1.

Diagnosis of patient with cardiovascular

disease Differential diagnosis of chest
pain
Differential diagnosis of chest pain:
- Cardiac: Aortic dissection, myocarditis,
pericarditis, stable angina, tamponade,
mitral valve prolapse, pulmonary
hypertension, aortic stenosis,
arrhythmias
- Respiratory: pulmonary embolism,
pneumonia, pleurisy
- Musculoskeletal
- Gastro-oesophageal reflux
- Anxiety/panic attack
- Oesophageal spasm
2. Non-invasive and invasive tests in cardiology from a blood vessel in the arm, groin or
neck to the heart.
Non-invasive:
a. Dye is injected from the
1. Electrocardiogram (ECG). This test catheter into blood vessels to
records the electrical activity of the make them visible by x-ray. It
heart, shows abnormal rhythms takes 2-3 hours.
(arrhythmias), and can sometimes detect
heart muscle damage b. Evaluation of chest pain to show if
plaque is narrowing or blocking
coronary arteries. This is called
2. Stress test (also called treadmill or coronary angiography.
exercise ECG). This test is done to
monitor the heart while you walk on a
treadmill or pedal a stationary bike. Your 3. Transesophageal echocardiogram
doctor also monitors your breathing and (TEE). In this test, pt will swallow a small
blood pressure. A stress test may be used probe, about the size of a little finger.
to detect coronary artery disease, or to The probe passes down the oesophagus
determine safe levels of exercise after a nearer to the heart.
heart attack or heart surgery. This test
can also be done using special medicines a. It allows a closer look at the
that stress the heart in a similar manner heart's structure and function.
as exercise does b. It also shows any abnormal tissue
around your heart valves, if blood
is leaking backward through a
3. Echocardiogram (also known as echo). An valve, and if blood clots are
echo is a non-invasive test that uses present in your heart chambers.
sound waves to evaluate your heart's
chambers and valves, as well as its
pumping function. The echo sound waves 4. PET F-18 FDG (fluorodeoxyglucose)
create an image on the monitor as an scan. This specialized PET scan uses a
ultrasound probe is passed across the skin form of glucose to help determine if any
over your heart. specific areas of heart tissue have
permanent damage.

Invasive: a. Used after a heart attack to

determine which procedure, such
1. Blood testing may include the following: as angioplasty, stenting, or bypass
Cardiac enzymes (including troponin and surgery, may be beneficial.
creatine kinase), C-reactive protein
(CRP), fibrinogen, homocysteine, b. Glucose solution injected through
lipoproteins, triglycerides, brain an IV into your blood.
natriuretic peptide (BNP) and c. Then a special camera takes
prothrombin. pictures of where the solution
a. Reason for Test: Confirms that a collects in your heart.
heart attack has occurred and
determines extent of damage.
b. Assesses future risk for coronary
artery disease.
c. Provides information on the time
it takes for the blood to clot.

2. Cardiac Catheterization: Test examines

inside of heart's blood vessels using
special X-rays called angiograms. A thin
hollow tube called a catheter is threaded
 3. Place of ECG in cardiological practice and o aVL lead: left arm
succession of reading the ECG
o aVF lead: left leg
The standard ECG uses 10 cables to obtain 12
electrical views of the heart. Chest leads:

- The different views reflect the angles at - Another six electrodes, placed in
which electrodes “look” at the heart and standard positions on the chest wall, give
the direction of the heart’s electrical rise to a further six unipolar leads – the
depolarization. chest leads (also known as precordial
leads), V1–V6.

-The
potential
difference of
a chest lead
is recorded
between the
relevant
chest
electrode
and an estimate of zero
potential – derived from the
average potential recorded from
the three limb leads.
Planes of view:
Limb leads look at the heart in a
vertical plane
Limb leads:
-Whereas the chest leads look at
- Three bipolar leads and the heart in a horizontal plane.
three unipolar leads are In this way a 3D electrical
obtained from three electrodes attached
to the left arm, the right arm, and the
left leg, respectively. (An electrode is
also attached to the right leg, but this is
an earth electrode.)
- The bipolar limb leads reflect the
potential difference between two of the picture of the heart is built up.
three limb electrodes:
o lead I: right arm–left arm
o lead II: right arm–left leg
o lead III: left leg–left arm
- The unipolar leads reflect the potential
difference between one of the three limb
electrodes and an estimate of zero
potential – derived from the remaining
two limb electrodes.
- These leads are known as augmented
leads. The augmented leads and their
respective limb electrodes are:
o aVR lead: right arm
 5. Determine QRS duration: normal 0.04 –
0.12s (1-3 boxes) – vertically count

Normal impulse conduction: SA node – AV node –

Bundle of His – Bundle branches – Purkinje fibers
- P wave: Atrial depolarization
- QRS: ventricular depolarization
- T: ventricular repolarization
- PR interval: atrial depolarization + delay
in AV junction (delay allows time for atria
to contract before the ventricles Normal sinus rhythm: presence of P wave =
contract) normal sinus rhythm – any deviation from the
above calculation = sinus tachycardia or sinus
- ST segment: It reflects the period of zero
bradycardia
potential between ventricular
depolarization and repolarization. - No P wave = arrhythmia
Pacemakers of the heart: o Arise from problems in SA, atrial
cells, AV junction, Ventricular
- SA node: dominant pacemaker – 60-100
cells
b/min
- Not whether QRS complexes are wide or
- AV node: back-up pacemaker – 40-60 b/
narrow, regular or irregular
min
o No P wave + irregular narrow QRS
- Ventricular cells: back-up pacemaker
= atrial fibrillation
20-45 b/min
Axis:
Interpreting ECG:
Every ECG reading should start with an - Net direction of electrical activity during
assessment of the rate, rhythm, and axis depolarization – altered by L or R
ventricular hypertrophy or by bundle
- ECH paper: branch blocks
o Horizontally: one small box = - Find QRS complex of lead I + aVF (look at
0.04s, large box = 0.20s heart at 00 + 900) – determine net
positivity = S (-ve) wave height – R (+ve)
o Vertically: one large box = 0.05mV wave height (of both leads) + plot on
o Every 3 sec (15 large boxes) is vector diagram - +ve downwards + -ve
marked by a vertical line – helps upwards
when calculating HR o Normal angle 00 - 120
Rhythm analysis:
1. Calculate rate – count no. of R waves in a
6s strip - (15 box = 3s) then x by 10
a. count the number of large squares
between one QRS wave and the
next & divide 300
2. Determine regularity: regular or irregular
(look at R-R distance) – equally apart Left axis
deviation =
3. Assess P waves: is there P wave – -30 - -90
presence = sinus rhythm
Right axis
4. Determine PR interval: normal 0.12-0.20s deviation =
(3-5 boxes) – horizontally count +90 - +180
ECG abnormalities:
 - Long PR interval (distance of more than 5 - Digoxin: ST depression – toxicity =
small squares) = 1st degree heart block dysrhythmias
o In presence of other abnormalities - Pulmonary Embolism: sinus tachycardia
might be sign of hyperkalaemia, or new RBBB
digoxin toxicity, cardiomyopathy
- Hyperkalaemia: tall T waves, long PR
interval, reduction of P wave height,
wide QRS, sinus wave QRS

- Normal ECG has very small Q waves –

downward deflection immediately
following P wave (wider than 2 small
squares) or greater than 1/3 of R wave =
previous infarction – (V1-V4) – there’s also
inverted T wave
- Large QRS complexes: left ventricular
hypertrophy – if sum of S wave in V1 + R
wave in V6 = >3.5mV i.e. 35 small or 7
big squares
o Right ventricular hypertrophy = R
wave bigger than following S wave
+ right axis deviation

- Broad QRS: Wide QRS despite P wave =

bundle branch block
o LBBB can make ECG look very
abnormal – calculate rate,
rhythm, axis + QRS (if >3 small
squares) = abnormal

▪ New LBBB can be

diagnostic of MI
o Check QRS in V1 + V6
- ST segment changes: elevation of >2
small squares plus characteristic history
indicates possibility of MI.
o ST depression = ischemia
- T wave = upright in every lead except
aVR – inversion = current ischemia or
previous infaction
- Long QT interval: hypokalaemia,
hypocalcamia, amiodarone, sotalol

Pattern combinations:
 4. Rheumatic Fever. Rheumatic Carditis
Aetiology and epidemiology
- Delayed immune mediated response to
Group A streptococci antigens that cross
react with cardiac myosin and
sacrolemmal membrane protein Dx:
- Therefore it can cause inflammation of Jones criteria (two or more major signs or 1
all layers of the cardium =endo- ,myo- major + 2 or more minor signs
and pericardium as well as joints + skin
because of the cross reaction
- Fibrinoid degeneration occurs and Aschoff - Throat swab
nodules in the heart are DD
- Chest X ray: cardiomegaly + pulmonary
- Bacteria causing this are usually from congestion
throat and rarely from infections of the
- ECG shows first and sometimes secondary
skin or other parts of the body
AV block, pericarditis features, T wave
- Affect children 5 -15 years or young inversion and reduction QRS voltages -
adults ; rare in America and western conduction defects may cause syncope
Europe but endemic in Asia, Africa and
- Echocardiogram shows cardiac dilatation
south America
and valve abnormalities
- It is the most common acquired heart
disease in children
Tx:
S+S:
- Single dose of benzyl pencillin 1.2 million
2-3 weeks after streptococcal pharyngitis
U IM or Oral phenoxymethypenicillin 250
mg 6 hourly for 10 days
- Aspirin reduces arthritis symptoms very
rapidly and important DD - 60mg/ kg
body weight/ day into six doses; max 8
grams
- Corticosteroids relieves pain even faster
and important in severe arthritis and
carditis
- Prednisolone 1-2mg/ Kg per day; in
divided doses until ESR drops
- Bed rest

- Secondary prevention with penicillin is a

must until the age of 21 but should be
extended if attack has occurred in last 5
years or if high exposure risk is present
- If heart disease is present then
prophylaxis continues 10 years after the
last episode or until 40 years of age
depending which one is longer

Complications: chronic fibrosis + valve damage

 5. Infective endocarditis - The acute forms has neutrophilic
infiltration then carries on with necrosis
Microbial infection of a heart valve, lining of and abscesses whereas subacute resolves
cardiac chamber or blood vessel, or congenital by healing
anomaly.

- 90 % Streptococci or staphylococci
S+S:
- Clinically, acute and subacute endocarditis
can be seen differing in duration , agents, - Fever, chills, weakness, malaise
severity and clinical presentation

- Post-operative endocarditis: Unexplained

fever after heart valve surgery, Morbidity
and mortality is high and redo surgery is
often required. Usually coagulase negative
staphylococcus , perioperative period

- Pre-disposing factors: bacteraemia +

septicaemia (inf from trauma, dental
procedure etc.), underlying heart disease - Cardiac complications: Valvular stenosis,
(coarctation, stenosis), rupture, aneurysm, myocardial abscess
immunocompromised
- Extra-cardiac complications: vegetations
are friable (crumble) – hence dislodge +
cause embolism – if in L heart may cause
Pathogenesis: infarct in spleen, kidneys, brain. R heart =
enter pulmonary circulation + cause
- Bacteria enter circulation and implant on abscess
endocardium via surface adhesion
molecules - In subacute ! Osler’s nodules can be seen
This may be helped by previously damaged which are at the finger tips and feet
valves (easier to hang on to), (tender and painful , Janeway lesions occur
haemodynamic stress which causes damage on the pulp of the fingers and hand
to the endothelium favouring platelet- (palmar) painless
fibrin thrombi which can get infected by
the bacteria or bacterial contamination of - Both are due to allergic inflammation of
non-bacterial thrombotic endocarditis vessel wall

- Found on atrial surface of atrioventricular Dx:

surface and ventricular surface of semi
- Elevation of EST, CRP
lunar valves and may extent to adjacent
endocardium - ECG: AV block – due to aortic root abscess
or infarct from emboli
- Subacute affects previous lesions,
vegetation’s are larger than the other types - X-ray: cardiac failure + cardiomegaly
of endocarditis , green and friable
Tx:

- Acute presentation ! staph: Flucloxacillin

i.v. (2g 4h (<85kg 6h 4wks native valve, 6
for prosthetic), and (met resistant)
gentamicin i.v. (1mg/kg 8h)

- Subacute ! benzyl penicillin i.v. (1.2g 4h)

and gentamicin (same)

- In case of penicillin allergy, prosthetic

valve or suspected MRSA, triple therapy
with vancomycin (1g 12h - enterococci),
gentamicin (staph + enterocci) oral
rifampicin

- Surgery: debridement of infected material

+ valve replacement
 6. Acquired Valvular disease heart diseases of infiltrate) in the endocardium and
mitral valve myocardium

1. Aetiology of mitral stenosis - With time, the valve apparatus becomes

thickened, calcified, and contracted, and
- The most common cause of mitral stenosis commissural adhesion occurs, ultimately
is rheumatic fever resulting in stenosis.
- 40% of RHD patients develop mitral - obstruction to left ventricular inflow at the
stenosis; 70 % are females level of mitral valve occurs due to
structural abnormality of the mitral valve
- The period between rheumatic carditis and
apparatus
symptomatic stenosis is 20 years
- This causes blood flow from LA TO LV to be
- Other causes include: Bacterial
restricted causing left atrial pressure to
endocarditis, Libman-Sacks endocarditis,
rise and thus leading to pulmonary venous
endocardial fibroelastosis and congenital
congestion and breathlessness
parachute mitral valve
- Dilatation and hypertrophy of LA occurs
- More causes: Lutembacher syndrome =
atrial septal defect + rheumatic mitral - This lack of flow means that the left
stenosis ventricular filling is more dependent on the
actual atrial contraction thus anything
- Some factors hasten/worsen mitral stenosis
decreasing diastole time such as exercise or
o Severe non-rheumatic mitral pregnancy increases atrial pressure even
annular calcification, infective further and decreases cardiac output
endocarditis with large vegetation,
- This is because the increase in heart rate,
left atrial mixoma, ball valve
decreases filling of the LV even further
thrombus
etc.

S+S:

Pathogenesis:

- The acute episodes of RHD lead to

formation of multiple inflammatory foci
(Aschoff bodies, perivascular mononuclear
 Complications:

- Pulmonary hypertension, emboli, pressure

from large LA on local structures, e.g.
hoarseness (recurrent laryngeal nerve),
dysphagia (oesophagus),

- Bronchial obstruction; infective

Dx:
endocarditis (rare).

- Acute RF: should be thought of in any

young pt presenting 1st time with MS:
penicillin 250mg b.d or sulfadiazine 500 mg
b.d. – continued in young women to age 40

2. Aetiology Mitral regurgitation/insufficiency

- 50 % of all cases are due to RHD

- All the causes mentioned in mitral stenosis

may cause insufficiency

- Mitral insufficiency is associated with some

degree of stenosis of the mitral valves

- However, in contrast with mitral stenosis ,

pure mitral insufficiency occurs in 75 % of
males

- Other
causes
include:
Non-

Tx:

- Digoxin: in AF only – if fast AF not slowed

by standard dose, either small dose of inflammatory calcification of mitral valve
verapamil or beta-blocking agent should be annulus (elderly); Myxomatous
added transformation of mitral valve (floppy valve
syndrome); Rupture of a leaflet /chordae
- Diuretics – reduce pre-load + pulmonary tendineae or of a papillary muscle
venous congestion – may help delay need
for surgery ( needed if valve area <1cm2) o E.g. after Ischaemia or infarct

o Open/Closed mitral valvotomy - Dilation of the mitral ring due to:

(commisurotomy), mitral valve Myocardial infarction, myocarditis and LV
replacement failure in hypertension

- Anticoagulants: only used on pts with prev - Other causes include: After Valvotomy or
pulmonary embolism, low CO with RHF valvuloplasty

- Cardioversion: amiodarone, beta-blockade

or flecainide help prevent development of
AF in pts who have been successfully Some clinical types
cardioverted
1. Chronic regurgitation
 - This causes gradual dilatation of the LA
with little increase in pressure and thus
less symptoms; however, the LV still dilates
but at a slower than in other types

- Left atrial pressure also increases gradually

as a result of chronic volume overload of
the LV

2. Acute mitral regurgitation

- Causes a rapid rise in left atrial pressure as

the atria compliance is normal and
symptoms are more severe and evident
when compared to the chronic
regurgitation

- This is a medical emergency

Dx:

3. Mitral prolapse aka floppy mitral valve Mitral

regurgitant
- Most common Valvular abnormality murmurs
may be:
- The valves remain competent but bulge pansystolic,
back in atrium during systole thus causing a late-
mid-systolic click but not a murmur crescendo
systolic or
- If regurgitation is present a late systolic
murmur can be heard

- With time, elongation of chordae tendineae

occurs, leading to mitral regurgitation and
chordal rupture

- murmur and regurgitation are very severe ;

usually 50-60 years of age
ejectionsystolic in quality
- It may also present with some benign
arrhythmias, atypical chest pain and very
small risk of emboli thus prognosis is
usually good

- Complications: Mitral regurgitation,

cerebral emboli, arrhythmias, sudden
death. Tests: Echocardiography is
diagnostic. ECG may show inferior T wave
inversion. Beta-blockers may help
palpitations and chest pain. In case of
severe mitral regurgitation, surgery is
needed.
Diff dx: Aortic valve stenosis: midsystolic click
S+S: occurs after carotid upstroke

HCM: does not have midsystolic click + more LV+

VSD
Tricuspid regurgitation: inspiratory murmur loudest
– prominent systolic waves in JVP

Tx:

- Control rate if fast AF. Tx with digoxin

- Anticoagulate if: AF; history of embolism;

prosthetic valve; additional mitral stenosis.

- Diuretics improve symptoms. Surgery for

deteriorating symptoms; aim to repair or
replace the valve before LV irreversibly
impaired. – annuloplasty ring

- SBE/IE prophylaxis for GI/GU infected

procedures.
7. Acquired Valvular heart diseases of aortic obstruction which leads to mismatch
valve. between oxygen demand and supply but
can also be due to coexisting coronary
1. Aortic stenosis- cause depends on age of artery disease, especially in old age.
patient. Infants, children,
adolescents - Exertional breathlessness suggests cardiac
decompensation as a consequence of the
- Occurs at 3 levels: valvar AS, subvalvular excessive pressure overload placed on the
AS, supravalvular AS. LV.
- Young adults to middle aged causes are: - Syncope because of exertion when CO fails
calcification and fibrosis of congenitally to rise to meet demand leading to a fall in
bicuspid aortic valve, rheumatic AS. BP.
- Middle aged to elderly it's due to senile - Mild mod stenosis; usually asympt.
calcification (most common), calcification
of bicuspid valve and rheumatic fever – - Exertional dyspnea, angina, exertional
inflammatory vulvulitis. syncope, sudden death, episodes of acute
pulmo oedema.
- Atherosclerosis: atheroma involves aortic
wall, major arteries, aortic valve + - Signs are ejection systolic murmur, slow
coronary arteries rising carotid pulse, narrow pulse pressure,
thrusting apex beat, signs of PVC
crepitations.
Pathogenesis:

- CO initially maintained due to steadily Dx:

increasing pressure gradient across the
aortic valve. - In advanced cases ECG, down sloping st
segments and T inversion seen in leads
- LV becomes hypertrophied and coronary reflecting LV. But ECG can be normal.
blood flow can decrease, patients may
therefore develop angina even in absence - Echo shows restricted valve opening. In
of concomitant coronary disease. patients with impaired LV velocities across
the aortic valve may be diminished because
- Outflow obstruction limits increase in CO of a reduced SV and in those where AR is
which is needed in exercise. present velocities are increased because of
an increased SV.
- Eventually LV can no longer overcome
obstruction so pulmonary oedema - Can calculate aortic valve area from
develops. Doppler measurements to see severity.
- AS patients stay asymptomatic for a long - CT and MRI useful to see valve calcification
time but when symptoms develop they and stenosis.
deteriorate rapidly and death within 3-5
years. Diff dx: hypertrophic cardiomyopathy

S+S: Tx:

- AS usually picked up in routine examination - In children: aortic Valvotomy or

in asympt patients. valvuloplasty is performed in symptomatic
pts or asymptomatic with severe stenosis
- 3 cardinal symptoms are angina,
breathlessness and syncope. o Ross operation: alternative -
pulmonary valve used as autograft
- Angina because of hypertrophied LV
working against the high pressure outflow
 - In adults AVR recommended once symptoms - This leads to hypertrophy and dilation
develop. Surgery is necessary, only 21% still producing massive enlargement of the
asymptomatic at 2 yrs heart ; it may weigh up to 1000 grams

o Severity of calcification also useful - The Left ventricle progressively fails to

prognostic guide compensate , and eventual pulmonary
hypertension and right heart failure occurs
- Aortic valvuloplasty: performed
percutaneously in catheter lab – small
group of elderly with severe AS considered
inoperable – best for child as they are too Cf:
small for AVR
- Symptoms: Exertional dyspnoea,
orthopnoea, and paroxysmal nocturnal
dyspnoea.
2. Aortic sclerosis is senile degeneration of the
valve. There is an ejection systolic murmur, no - Also: palpitations, angina, syncope, CCF.
carotid radiation, and normal pulse (character and
- Signs: Collapsing (water-hammer) pulse;
volume) and S2.
wide pulse pressure; displaced,
hyperdynamic apex beat; high-pitched
early diastolic murmur (heard best in
3. Aortic regurgitation- due to disease of aortic expiration, with patient sitting forward).
valve cusps or dilatation of the aortic root.
- Eponyms: Corrigan’s sign: carotid pulsation;
- LV dilates and hypertrophies to compensate de Musset’s sign: head nodding with each
for the regurg. heart beat; Quincke’s sign: capillary
pulsations in nail beds; Duroziez’s sign: in
- SV of LV may be doubled and major arteries the groin, a finger compressing the femoral
are then pulsatile. artery 2cm proximal to the stethoscope
gives a systolic murmur; if 2cm distal, it
- As disease progresses LV diastolic pressure
gives a diastolic murmur as blood flows
rises and breathlessness develops.
backwards; Traube’s sign: “pistol shot”
sound: over femoral arteries; an Austin
Flint murmur denotes severe AR.

- Acute: Infective endocarditis, ascending

aortic dissection, chest trauma.

- Chronic: Congenital, connective tissue

disorders (Marfan’s syndrome, Ehlers–
Danlos), rheumatic fever,

Pathogenesis:

- As a result of the regurgitant aortic orifice,

there is increase of the left Ventricular Dx:
end-diastolic volume
- ECG: LV hypertrophy + T wave inversion.
 - CXR: cardiomegaly; dilated ascending
aorta; pulmonary oedema.

- Echocardiography is diagnostic.

- Cardiac catheterization to assess: severity

of lesion; anatomy of aortic root; LV
function; CAD; other valve disease.

Tx:

- The main goal of medical therapy is to

reduce systolic hypertension. ACE-i are
helpful.

- Echo every 6–12 months to monitor

- Tx may be required for underlying

conditions like endocarditis or syphilis.

- Systolic BP should be controlled with

vasodilating drugs like nifedipine or ACE
inhibitors.

- Aortic root replacement can be necessary if

aortic root dilatation is the problem.
 8. Congenital Heart Disease in Adults - Cardiopulmonary exercise testing –
especially timing of re-intervention
- Holter ECG – 24h monitor
- Congenital heart defect is the term
given when one or more defects in the - Echocardiography
structure of the heart are present at
birth - Chest X-ray
- Cardiac CT + MRI (assessment of RV
volume + function, quantification of
- Approximately eight out of 1,000 infants valvular regurgitation)
are born with some type of congenital
heart defect - Invasive testing – catheterization –
haemodynamic (shunt quantification,
- In the past this meant shorter life span pulmonary pressure etc.) or
but now with advances in medicine pts electrophysiology testing
can live longer

Complications:
- 30-40% of all CHD = Ventricular Septal
Defect (VSD) 1. Heart failure (valcular defect, shunts,
volume +/or pressure overloading
o most common CHD ventricles, RV in systemic position
- Bicuspid Aortic Valve: 1-2% of General - Pharmacotherapy (ACEi, BB, diuretics)
Population
- Cardiac resynchronisation therapy (CRT) –
- Atrial Septal Defect: Most common CHD biventricular stimulation in case of
diagnosed in adulthood ineffective (dyssynchronic) contraction
o No exact evidence - Heart transplantation
- Complex CHD (e.g.TGA+VSD)
- Prevalence ~ 2800 CHD adults / 1mil 2. Arrhythmias and SCD (sudden cardiac
people death)
- Most CHD diagnosed in newborn + early - More difficult issue than in normal heart
childhood
- Risk stratification, investigation, and
- Some dx in adults: ASD, CoA, Ebtein choice of tx are often different from
disease of TV etc. those applied to the normally formed
heart (drugs poorly tolerated, side
effects)
Classification: - EP and ablation is prefer
1. Acyanotic heart disease - Onset of arrhythmias may be a signal of
a. Increase in pulmonary blood flow haemodynamic decompensation

b. Obstruction of blood flow - SCD especially in: ToF, TGA, ccTGA, aortic
stenosis (AS), and UVHs various risk
2. Cyanotic heart disease factors -ICD
a. Decrease in pulmonary blood flow
b. Mixed blood flow 3. Infectious endocarditis
- High risk particularly in:
Dx: o Cyanotic CHD without surgical
repair, residual defects, palliative
- History
shunts
- S+S
o Prosthetic valves
- ECG, Pulse oximetry
 o Residual defects (generally) after - volume hypertrophy of the left heart +
surgical or cath. Closure haemodynamic changes to mitral + aortic
valves
o Patients with previous IE

2. Left to right shunts

4. Pregnancy
- Blood escapes from left side to the right
- During pregnancy there is 50% increase in
plasma + 40% increase in whole blood - Volume overload of the right leading to
thus also CO – problems may arise with pulmonary hypertension +right
preg women who have CHD hypertrophy
- Generally well tolerated but extremely - The pressure increases in the right hence
high risk (high mortality 30-50%) more deoxygenated blood gets to the left
side leading to late cyanotic heart
- Severe pulmonary art. hypertension disease
(Eisenmenger sy) – cyanotic conditions
- Aka acyanotic; Includes VSD (up to 30 % )
- Cyanosis (esp. SpO2 <85%) ; ASD &PDA (patent ductus arteriosus) in
- Stenotic left valve disease (AS, MS) equal proportions 10-20 %

- Poor EF LV (<40%)
- Aortic roof dilation (Marfan sy) 3. PDA: Patent Ductus Arteriosus

- Arrhythmias - normal in newborns if it resolved within

first weeks of life
- Recurrence rate of CHD in offspring 2-50%
- If it stays beyond three months it is
o Highest in single gene disorder: abnormal
Marfan, Noonan, 22q11 deletion)
- Unknown cause but linked to PGE2 after
o Others 2-4% birth
o Aortic stenose 13-18% - In 90 % of PDA it is isolated but it may be
associated with VSD, coarctation of aorta
o VSD 6-10%
, pulmonary or aortic stenosis
- In mild to moderate forms it may be
Examples: asymptomatic

1. VSD - Effects : (increased pulmonary flow

- Volume hypertrophy of the right ventricle - Volume hypertrophy of right left heart +
and damaging effects on tricuspid and increase hemodynamic damage of mitral
pulmonary valves due to haemodynamic and pulmonary valves
changes
- Enlargement of ascending aorta
- endocardial hypertrophy of the right
ventricle + right atrial hypertrophy
4. ASD: Atrial Septal Defect
- goes unnoticed until pulmonary
hypertension develops leading to late
cyanotic heart disease + RHF
- Occurs more in females 2x compared to
males
- Effects : (primarily increased pulmonary
flow)
- Volume hypertrophy of the right atrium +
right ventricle as shunting occurs from LA
 to RA and then from RV to pulmonary
arteries
- In order to resist hypertrophy occurs even
of the pulmonary arteries
- Tricuspid + pulmonary valves experience
hemodynamic damage
- Endocardial hypertrophy of the right
heart causing volume hypertrophy of the
left heart
- Mitral and aortic orifices decrease in size
 9. Myocardial diseases. Myocarditis. - Most common symptoms 72 % dyspnoea,
32 & chest pain and 18 % arrhythmias
- Myocarditis is an acute inflammatory
condition. - Heart failure symptoms can also be seen

- Fever, palpitations, soft s1, s4 gallop.

Dx:

- Biochemical markers: elevation of

troponin I & T + CK, CRP + leucocytes

- ECG: common changes but non-specific –

may mimic acute MI or pericarditis ST
segment elevation

- Echo: may reveal ventricular dysfunction

Aetiology: - Positive troponin in absence of MI

confirms diagnosis. Can lead to fulminant
- Viral infections are common causes-
heart failure. If diagnosis uncertain,
Coxsackie and influenza a & b. Hepatitis,
endomyocardial biopsy. In most patients
mumps, HIV.
disease is self-limiting and immediate
- Bacterial- clostridia, diphtheria, TB, prognosis is good. But death may occur
meningococcus, mycoplasma, brucellosis, due to ventricular arrhythmia or rapidly
psittacosis. progressive HF.

- Spirochaetes- leptosirosis, syphilis, lyme. - Cause of sudden death in young athletes.

- Protozoa- Chagas. - Some forms of myocarditis can lead to

chronic low grade myocarditis or dilated
cardiomyopathy.

Pathogenesis:

- Can occur weeks after initial viral Tx:

symptoms. Susceptibility
increased by previous corticosteroid - Antimicrobial therapy if causative
treatment, immunosuppression, organism identified, but usually only
radiation, previous myocardial damage supportive therapy available.
and exercise.
- Treatment for cardiac failure or
- Certain drugs also precipitate myocarditis arrhythmias may be required and patients
such as anticancer drugs, herceptin, advised to avoid intense exercise because
penicillin, chloramphenicol, it can induce potentially fatal ventricular
sulfonamides, methyldopa, and cocaine. arrhythmias.

- Some AI conditions also associated with - ACEi or BB if HF – Indomethacin if

myocarditis such as SLE and rheumatoid myopericarditis present
arthritis.
- If autoimmunity Is cause: corticosteroids,
immunoglobulins + other
Immunosuppressants
S+S:

- Can be symptomless or recognised by

inappropriate tachycardia or abnormal
ECG.
 10. Myocardial diseases – Cardiomyopathies - Dx: ECG non-specific t wave changes,
echo is useful- dilated hypokinetic heart
Cardiomyopathy refers to disease of the heart with low EF.
muscles – there are many types:

- Tx: diuretics, dixogin, ACE i,

1. Dilated cardiomyopathy- characterised by anticoagulation, ICD.

2. Hypertrophic cardiomyopathy-

- Most common form. Elaborate LVH with

malalignment of myocardial fibres.
Hypertrophy can be generalised or
confined to IV septum or other regions.

dilatation and impaired contraction of LV.

Overall mass of LV increased but - HF can develop because of non-compliant
thickness of wall is normal or reduced. ventricles which impede diastolic filling.
Septal hypertrophy can cause LV outflow
obstruction- HOCM. Effort related
- Histo: myofibrillary loss, interstitial symptoms such as angina and
fibrosis and T cell infiltrates. breathlessness, arrhythmia and sudden
death are the dominant clinical
- DIFF dx: CAD, other cardiomyopathies. problems.

- PG unclear. Alcohol imp factor. 25% of - Genetic disorder with AD transmission,

cases are inherited as an AD trait and high degree of penetrance and variable
many single gene mutations have been expression. 3 common groups of
identified. Most mutations affect mutations with diff phenotypes-
cytoskeleton proteins of mycocyte-
dystrophin, lamin A and C, metavinculin. o Beta myosin heavy chain mut:
elaborate VH.
- X linked muscular dystrophies associated
with cardiomyopathy. o troponin mut: little or no
hypertrophy but myocardial fibre
- Late AI reaction to viral myocarditis disarray(high risk of sudden death)
thought to be main reason for dilated
cardiomyopathy. Men affected more than o myosin binding protein c mut:
twice than women. present late in life and assoc with
arrhythmias and HT
- Most patients present with HF on routine
investigation.

- Symptoms: Angina, dyspnoea, syncope on

effort, sudden death. Jerky pulse,
- Presentation: Fatigue, dyspnea, pulmo palpable left VH, palpable 4th heart
edema, emboli, AF, VT. Signs: Increase in sound due to left atrial hypertrophy.
pulse, decrease BP, Increase in JVP, Midsystolic murmur at the base,
displaced diffuse apex, s3 gallop, mitral/ pansystolic murmur at apex due to mitral
tricuspid regurgitation, jaundice, regurg.
hepatomegaly, ascites.
- Dx: ECG abnormal and shows signs of HF. Surgery with tricuspid or mitral
LVH. Progressive t wave inversion, deep q valve replacement with decortication
waves. Ventricular ectopics, VT. Echo is of endocardium may be helpful in
diagnostic, small LV cavity. Genetic some cases.
testing may facilitate diagnosis.
Hypertrophic

- Cardiomyopathy is most common cause of 5. Restrictive cardiomyopathy- rare

sudden death in young athletes. condition. Ventricular filling impaired
Ventricular arrhythmias responsible for because the ventricles are stiff, leads to
most deaths. high atrial pressures with atrial
hypertrophy, dilatation and later atrial
fibrillation.

- Tx: Beta blockers, calcium antagonists - Amyloidosis is most common cause in

verapamil and disopyramide can help to the UK. Idiopathic perimyocyte
relieve symptoms and prevent syncopal fibrosis and a familial form of
attacks. Outflow obstruction can be restrictive cardiomyopathy do occur.
improved by partial surgical resection or
septal ablation. ICD for patients with - Dx:Diagnosis is diff, doppler echo, CT
increased risk factors for sudden death. or MRI.

- Prognosis usually bad, transplantation

indicated.
3. Arrhythmogenic RV cardiomyopathy-
patches of RV myocardium are replaced
with fibrous and fatty tissue. AD trait.
- Dx: cardiac catheterization, MRI for
Leads to ventricular arrhythmias, sudden
exclusion of thick pericardium
death and RS HF.
(constrictive), X-ray, Echo
- Dx: ECG has broadened QRS complex and
- Tx: tx the cause
inverted T waves in right precordial
leads, o Chemotherapy for amyloidosis
- MRI is a useful diagnostic tool and is used o The most common used
to screen first degree relatives of medications are
affected individuals. Patients at high risk
of sudden death can be offered an ICD. ▪ Diuretics, vasodilators,
and ACEs as indicated,
as well as
anticoagulation (if not
4. Obliterative cardiomyopathy- involves
contraindicated).
endocardium of one or both of the
ventricles and is characterised by
thrombosis and elaborate fibrosis with
gradual obliteration of ventricular
cavities.

- Mitral and tricuspid regurg. HF and

pulmonary and systemic embolism are
prominent features, can sometimes
be associated with eosinophilia.

- In tropical countries the disease is

responsible for up to 10% of cardiac
deaths.

- Tx: Anticoagulation and antiplatelet

therapy and diuretics can help with
 11. Pericardial diseases: Pericarditis involve pericardium, TB, severe acute
infection
Acute pericarditis: This is inflammation of the
pericardium. It may be idiopathic or secondary
to:
Cf:
- Viruses (Coxsackie, flu, Epstein–Barr,
mumps, varicella, HIV) - Central chest pain worse on inspiration or
lying flat, +/- relief by sitting forward.
- Bacteria (pneumonia, rheumatic fever,
TB, staphs, streps, MAI in HIV, p410) - A pericardial friction rub may be heard.
Look for evidence of a pericardial
- Fungi effusion or cardiac tamponade.

- Myocardial infarction, Dressler’s (p712) - Fever may occur.

- Drugs: procainamide, hydralazine,

penicillin, cromolyn sodium, isoniazid
Dx:
- Others: uraemia, rheumatoid arthritis,
SLE, myxoedema, trauma, surgery, - ECG classically shows concave (saddle-
malignancy shaped) ST segment elevation, but may
be normal or non-specific (10%)
- (and antineoplastic agents), radiotherapy,
sarcoidosis - Blood tests: FBC, ESR, U&E, cardiac
enzymes (NB: troponin may be raised),
viral serology, blood cultures, and, if
indicated, autoantibodies, fungal
precipitins, thyroid function tests.
Cardiomegaly on CXR may indicate a
pericardial effusion.

- Echo (if suspected pericardial effusion).

Tx:

- Analgesia, e.g. ibuprofen 400mg/8h PO

with food.

- Treat the cause.

- Consider colchicine before steroids/

immunosuppressants if relapse or
Ranges from: continuing symptoms occur.

- Serous: high specific grafity + protein - 15–40% do recur. Steroids may increase
content – virus cause the risk of recurrence.

- Fibrous: most common type – cause

uremia, MI, rheumatic fever, bact
infection Pericardial effusion

- Purulent pericarditis: thick, creamy pus Accumulation of fluid in the pericardial sac.
coating pericardial surfaces – when it
- Causes: Any cause of pericarditis (see
heals adhesive or constrictive pericarditis
above).
– mainly pyogenic bact cause: staph,
strep Cf:
- Haemorrhagic pericarditis: inflammatory - Dyspnoea, raised JVP (with prominent x
effusion + blood – occurs when neoplasm descent), bronchial breathing at left base
 (Ewart’s sign: large effusion compressing
left lower lobe).

- Look for signs of cardiac tamponade.

Cardiac tamponade
Dx:
Accumulation of pericardial fluid raises
- CXR shows an enlarged, globular heart. intrapericardial pressure, hence poor ventricular
filling and fall in cardiac output.
- ECG shows low-voltage QRS complexes
and alternating QRS morphologies Causes: Any pericarditis (above); aortic
(electrical alternans). dissection; haemodialysis; warfarin; transseptal
puncture at cardiac catheterization; post cardiac
- Echocardiography: shows an echo-free biopsy.
zone surrounding the heart.

S+S: Pulse increased, BP low, pulsus paradoxus,

Tx: Treat the cause. Pericardiocentesis may be JVP high, Kussmaul’s sign, muffled S1 and S2.
diagnostic (suspected bacterial pericarditis) or
therapeutic (cardiac tamponade). Send
pericardial fluid for culture, ZN stain/TB
culture, and cytology. Dx:

- Beck’s triad: falling BP; rising JVP;

muffled heart sounds.
Chronic pericarditis:
- CXR: big globular heart (if >250mL fluid).
Constrictive pericarditis
- ECG: low voltage QRS +/- electrical
The heart is encased in a rigid pericardium. alternans. Echo is diagnostic: echo-free
zone (>2cm, or >1cm if acute) around the
Causes: Often unknown (UK); elsewhere TB, or heart +/- diastolic collapse of right
after any pericarditis. atrium and right ventricle.

Cf: These are mainly of right heart failure with Tx:

high JVP (with prominent x and y descents);
Kussmaul’s sign (JVP rising paradoxically with - The pericardial effusion needs urgent
inspiration); soft, diffuse apex beat; quiet heart drainage
sounds; S3; diastolic pericardial knock,
hepatosplenomegaly, ascites, and oedema. - Send fluid for culture, ZN stain/TB
culture and cytology.

Dx:
Cardiac tamponade, acute HF due to
- CXR: small heart, +/- pericardial compression of the heart by a large effusion.
calcification (if none, CT/MRI helps Raised JV pulse, hypotension, pulsus paradoxus
distinguish from other cardiomyopathies). and oliguria.
Echo; cardiac catheterization.

Pericardial aspiration - This is indicated for

Tx: Surgical excision. diagnostic purposes or for the treatment of
tamponade. Needle inserted under echo
guidance medial to the cardiac apex or below
the xiphoid process directing upwards towards
the left shoulder. Few ml for diagnostic purposes
and drain to relieve symptoms.

Complications of pericardiocentesis include

arrhythmias, damage to coronary artery and
bleeding with increased tamponade due to injury
of RV.
 12. Arterial Hypertension: Classification,
etiology, pathogenesis, clinical features
Hypertension is elevated arterial blood pressure;
which is a major cause of premature vascular
disease leading to cerebrovascular events,
ischaemic heart disease and peripheral vascular
disease.
- Hypertension major rf for stroke and MI
- 50% of all vascular death due to
hypertension

Pathogenesis:
Regulation of BP:
BP = Cardiac Output x Peripheral Resistance
- Endocrine Factors
o Renin, Angiotensin, ANP, ADH,
Aldosterone.
- Neural Factors

Aetiology: o Sympathetic & Parasympathetic

- The majority (80–90%) of patients with - Blood Volume

hypertension have primary elevation of o Sodium, Mineralocorticoids, ANP
blood pressure, i.e. essential
hypertension of unknown cause. - Cardiac Factors
- 2 types: Essential and secondary o Heart rate & Contractility.
o Essential: genetic factors, fetal - The pathogenesis of essential
factors (low birth weight), hypertension remains unclear.
environmental factors (obesity,
- In some young hypertensive patients,
alcohol intake, sodium intake,
there is an early increase in cardiac
stress), lack of exercise
output, in association with increased
pulse rate and circulating
catecholamines.
- This could result in changes in
baroreceptor sensitivity, which would
then operate at a higher blood pressure
level.

In established hypertension there are:

1. Cardiac changes:
- Resistance vessels (the small arteries and
- Secondary hypertension: arterioles) show structural changes in
hypertension with an increase in wall
thickness and a reduction in the vessel
lumen diameter.
- It is an increased peripheral resistance - Changes in the renal vasculature lead to
that maintains the elevated blood a reduced renal perfusion, reduced
pressure. glomerular filtration rate and, finally, a
reduction in sodium and water excretion.
- The cardiac output is normal.
- The decreased renal perfusion may lead
- There is also some evidence for to activation of the renin-angiotensin
rarefaction (decreased density) of these system (renin converts angiotensinogen
vessels. to angiotensin I, which is in turn
- These mechanisms would result in an converted to angiotensin II by
increased overall peripheral vascular angiotensin-converting enzyme) with
resistance. increased secretion of aldosterone and
further sodium and water retention – thus
blood volume increase - angiotensin II
increase peripheral resistance +
2. Large vessel changes occur:
vasoconstriction = thus increased BP
- There is thickening of the media, an
increase in collagen and the secondary
deposition of calcium. 6. Cerebral changes:
- These changes result in a loss of arterial - In small vessel cause lacunae (small
compliance, which in turn leads to a infarcts) and reversible neurological
more pronounced arterial pressure wave. deficits which do not show abnormalities
on imaging.
- This may lead to dementia and stroke.
3. Pulse wave velocity:
- Is a measure of arterial stiffness and is
inversely related to distensibility. Isolated systolic hypertension (ISH):
- With each systolic contraction a pulse - The most common form of hypertension
wave travels down the arterial wall —affects >50% of the over-60s, and
before the flow of blood. results from stiffening of the large
arteries (arteriosclerosis).
- Thus, the more rigid the arterial wall,
the faster the wave travels. - It is not benign: doubles risk of MI, triples
risk of CVA.
- It can be measured but is not in routine
use. - Tx reduces this excess risk and is as, if
not more, effective than treating
- Atheroma develops in the large arteries
moderate hypertension in middle-aged
owing to the interaction of these
patients.
mechanical stresses and low growth
factors
- Endothelial dysfunction with alternations Essential hypertension (primary, cause
in agents such as nitric oxide and unknown). ~95% of cases.
endothelins appear to be involved.

Secondary hypertension: ~5% of cases. Causes

4. Left ventricular hypertrophy: include:
- Results from increased peripheral - Renal disease: The most common
vascular resistance and increased left secondary cause.
ventricular load
o 75% are from intrinsic renal
- Significant prognostic indicator of future disease: glomerulonephritis,
cardiovascular events. polyarteritis nodosa (PAN),
systemic sclerosis, chronic
pyelonephritis, or polycystic
5. Renal changes: kidneys.
 o 25% are due to renovascular
disease, most frequently
atheromatous (elderly male
cigarette smokers, e.g. with
peripheral vascular disease) or
rarely fibromuscular dysplasia
(young females).

S+S:
- Essential hypertension usually
asymptomatic (except malignant
hypertension).
- Headache is no more common than in the
general population.
- Nocturia
- Signs of renal disease, radiofemoral
delay, or weak femoral pulses
(coarctation), renal bruits, palpable
kidneys, or Cushing’s syndrome?
- Look for end-organ damage: LVH,
retinopathy and proteinuria—indicates
severity and duration of hypertension and
associated with a poorer prognosis.
 13. Arterial Hypertension: diagnosis, Chronic kidney Pruritus, High serum
differential diagnosis disease edema, or creatinine,
Dx: change in chronic
urine anaemia, renal
- Take blood pressure from brachial artery output ultrasound
shows sclerotic
- To help quantify overall risk: Fasting or polycystic
blood glucose & cholesterol. ovaries
- Serum urea, creatinine + electrolytes Aortic Differential CT, angiogram,
coarctation BP in upper or MRI confirms
o If elevated: more specific renal + lower diagnosis.
investigations extremities
, absent
- To look for end-organ damage: ECG (any femoral
LV hypertrophy? past MI?); urine analysis pulses
(protein, blood).
Hyperaldostero Mild Unprovoked
- To ‘exclude’ secondary causes: U&E (e.g. nism metabolic hypokalaemia
K+ decreased in Conn’s – indicates alkalosis, Plasma
endocrine disorder); Ca2+ (high in relative aldosterone
hyperparathyroidism). hypernatre high.
mia, Plasma renin
- Special tests: Renal ultrasound/ potassium low.
arteriography (renal artery stenosis); 24h depletion, Failure to
urinary metanephrines; urinary free and suppress
cortisol (p217); renin; aldosterone; MR elevated aldosterone
aorta (coarctation). fasting with salt
glucose. loading.
o Clinical suspicion of
phaeochromocytoma should be
investigated further with Hypothyroidism Dry skin, TSH elevated
measurement of urinary cold
metanephrines and plasma or intolerance
, weight
urinary catecholamines.
gain,
- 24h ambulatory BP monitoring (ABPM) sluggishness
may help sometimes, e.g. in ‘white coat’ , and goiter
or borderline hypertension, and is now Hyperthyroidis Heat TSH suppressed
recommended for all newly diagnosed m intolerance and levels of
hypertensive. , weight free thyroid
loss, hormones
- Echocardiography: may be useful to hyperphagi elevated
assess end-organ damage (LV hypertrophy) a,
palpitations
Collagen Signs/ Elevated ESR,
Differential diagnosis:
Vascular symptoms abnormal
disease of SLE, complement
Disease Differentiat Differentiating rheumatoid levels, positive
ing S+S tests arthritis, anti-DNA,
Drug-induced Signs of Hypokalaemia if sclerodactly antiribonucleop
acute excessive , or Hx rotein (anti-
intoxication liquorice vasculitis. RNP), anti-
, hx of tx Smith
with or antibodies,
ingestion of positive
NSAID’s rheumatoid
factor.
Phaeochromocy Paroxysms 24-hour urine
toma of HTN, screen shows
flushing, elevated
and vanillylmandeli
headache c acid,
metanephrines,
and/or
catecholamines
Gestational Detected Urinary albumin
hypertension after 20 excretion of
weeks' 300mg/L/24
gestation in hours if pre-
a previously eclampsia
normotensi occurs
ve patient
Cushing Weight Abnormal
syndrome gain, moon dexamethasone
face, suppression,
dorsicocervi 24-hour urine
cal fat pad, free cortisol,
abdominal and/or late-
striae, and night salivary
easy cortisol
bruisability.
 14. Arterial hypertension: complications. - In the retina there may be flame-shaped
Malignant Arterial Hypertension. Hypertensive haemorrhages, cotton wool spots, hard
crisis. exudates and papilloedema.
Complications: - Without effective treatment there is a 1-
year survival of <20%.
1. Heart
- Tx: Pts with severe hypertension
- LV hypertrophy; Coronary artery disease; (diastolic pressure >140 mmHg),
Myocardial infarcts; Heart failure malignant hypertension (grades 3 or 4
retinopathy), hypertensive
encephalopathy or with severe
2. Brain hypertensive complications, such as
cardiac failure, should be admitted to
- Stroke or transient ischemic attacks,
hospital for immediate initiation of
infarction, sub arachnoid haemorrhage
treatment.
(splinter + lacunar)
- However, it is unwise to reduce the blood
pressure too rapidly, since this may lead
3. Kidney: to cerebral, renal, retinal or myocardial
infarction, and the BP response to
- Chronic kidney disease, kidney failure, therapy must be carefully monitored,
infarction, benign/malignant preferably in a high-dependency unit.
nephrosclerosis
- In most cases, the aim is to reduce the
diastolic blood pressure to 100–110 mmHg
4. Eyes: Hypertensive Retinopathy: over 24–48 hours.

- Retina; hypertensive retinopathy has 4 - This is usually achieved with oral

grades. Grade 1 includes arteriolar medication, e.g. amlodipine.
thickening and increased reflectiveness - The blood pressure can then be
known as silver wiring. Grade 2 focal normalized over the next 2–3 days.
arteriolar spasms, vein constriction.
Grade 3 has retinal ischaemia in form of - When rapid control of blood pressure is
flame blot haemorrhages and cotton wool required (e.g. in an aortic dissection),
exudates. Grade 4 plus pappiloedema. the agent of choice is intravenous sodium
nitroprusside.
- Alternatively, an infusion of labetalol can
Malignant hypertension: be used. The infusion dosage must be
- Malignant or accelerated hypertension titrated against the blood pressure
occurs when blood pressure rises rapidly response.
and is considered with severe
hypertension (diastolic blood pressure
>120 mmHg). Hypertensive crisis:

- The characteristic histological change is - Systolic pressure >180mmHg

Fibrinoid necrosis of the vessel wall and,
- Diastolic >120 mmHg
unless treated, it may lead to death from
progressive renal failure, heart failure, - 2 types: Urgency + emergency
aortic dissection or stroke.
o Urgency: no damage to end-organs
- The changes in the renal circulation (brain, heart, kidney, lungs)
result in rapidly progressive renal failure,
proteinuria and haematuria. o Emergency: damage to end-organs

- There is also a high risk of cerebral - S+S: confusion, drowsiness, chest pain +
oedema and haemorrhage with resultant breathlessness
hypertensive encephalopathy. - Provoking factor: physical activity,
stressful situation, inadequate treatment
(abrupt stopping of some drugs), rough
 dietary indiscretion) excessive Na in meal
and alcohol intake.
- It can be associated with NSAID intake
- HPT can be spontaneous
 15. Arterial hypertension – treatment. 1. Thiazide and other diuretics, can take
upto a month for total effect, daily dose
- First choice of tx is lifestyle changes – of 2.5mg bendroflumethiazide or 0.5mg
DASH diet (fruits, veg, low fat diet + cyclopenthiazide.
reduced Na intake, fish, nuts, poultry,
reduced red meat, sugar, total + a. More potent loop diuretics like
saturated fat + cholesterol), exercise, such as furosemide 40mg daily or
stress reduction bumetanide 1mg daily have few
advantages over thiazidesin
- BP goals <140/<90 and lower if tolerated treatment of HT unless there is
o <130/<80 in diabetics significant renal impairment or
they used with ACE inhibitors.
o <130/<85 in cardiac failure
o <130/<85 in renal failure
2. ACE inhibitors; enalapril 20mg daily,
o <125/<75 in renal failure with ramipril 5-10mg daily or lisinopril
10-40mg daily.
o proteinuria>1.0 g/24 hours
a. These inhibit the conversion of
- choice of drugs dictated by age + ethnic
angiotensin 1 to 2. Should be used
background
carefully in impaired renal
patients because they can reduce
the filtration pressure in the
glomeruli and precipitate renal
failure.
b. Side effects include first dose
hypotension, cough, rash,
hyperkalemia and renal
dysfunction.

3. Angiotensin receptor blockers; irbesartan

150-300mg daily, valsartan 40-160mg
daily.
a. These block angiotensin 2 type 1
receptor and have similar effects
to ACE inhibitors, they don't cause
cough and better tolerated.

4. Calcium channel blockers.

Dihydropyridines like amlodipine 5-10mg
daily, nifedipine 30-90mg daily are
effective and usually well tolerated
antihypertensive drugs and particularly
useful in older patients.
a. Side effects include flushing,
palpitations and fluid retention.
b. Rate limiting ca channel
antagonists like diltiazem
200-300mg daily, verapamil 240mg
daily can be useful when HT exists
with angina but they may cause
bradycardia.
Antihypertensive drugs:
c. Main side effect of verapamil is
constipation.
5. Beta blockers. No longer first line except
in patients with another indication for
the drug like angina.
a. Metoprolol 100-200mg daily,
atenolol 50-100mg daily,
bisoprolol 5-10mg daily
preferentially block cardiac beta 1
adrenoreceptors as opposed to
beta 2 adrenoreceptors that
mediate VD and
bronchodilatation.
b. Labetalol and carvedilol.
Labetalol 200mg-2.4g daily in
divided doses. Carvedilol
6.25-25mg 12 hourly are combined
beta and alpha adrenoceptor
antagonists which are sometimes
more effective than pure beta
blockers. Labetalol can be used as
an infusion in malignant phase HT.

6. Other drugs. Variety of VD can be used

like alpha blockers such as prazosin
0.5-20mg daily in divided doses.
Indoramin 25-100mg 12hourly and
doxazosin 1-16mg daily.
a. Drugs that act directly on SM such
as hydralazine 25-100mg 12 hourly
and minoxidil 10-50mg daily. Side
effects include first dose and
postural hypotension, headache,
tachycardia and fluid retention.
b. Minoxidil causes increased facial
hair so unsuitable for female
patients.
 16. Atherosclerosis. Ischemic heart disease / thrombus. Main growth mechanism is by
IHD/ classification. thrombosis and haematoma.
Can affect any artery in the body. In heart: it
can cause angina, MI and sudden death, in brain:
stroke and TIA, in limbs: claudication and Early AS: fatty streaks tend to occur at sites of
ischaemia. altered arterial shear stress like bifurcations and
associated with abnormal endothelial function.
- They develop when inflammatory cells
PP: AS progressive inflammatory disorder of mainly monocytes bind to receptors
arterial wall and its characterised by focal lipid expressed by endothelial cells, migrate
rich deposits of atheroma that are asymptomatic into the intima, take up oxidised LDL
until they become large enough to impair particles and become foam cells. EC lipid
perfusion or until ulceration and disruption of pools appear in the intimal space when
the lesion result in thrombotic occlusion or distal these foam cells die and release their
embolization of the vessel. contents.
- In response to cytokines and GF produced
by the activated macrophages , SM cells
AS begins early in life. Abnormalities in arteries migrate from media of arterial wall into
detected in high risk groups like those with the intima and change from a contractile
familial hyperlipidaemia or HT. However clinical to a repair phenotype in an attempt to
manifestations don't form till 7th and 8th stabilise the AS lesion.
decades of life.
- If they are successful the lipid core will
be covered by SM cells and matrix
6 stages of AS. producing a stable AS plaque that will
remain asymptomatic until it becomes
1. Type 1 (initial) lesion: isolated large enough to obstruct arterial flow.
macrophage foam cells, 1st decade and
clinical silent.
2. Type 2 (fatty streak) lesion, mainly Advanced AS: AS plaque, macrophages cause
intracellular lipid accumulation, and inflam and SM cells promote repair.
growth mainly by lipid accumulation like - If inflam predominates, the plaque
first and also from 1st decade. becomes active or unstable and may be
3. Type 3 (IM) lesion, changes and small EC complicated by ulceration and
lipid pools, mainly from 3rd decade but thrombosis.
still clinically silent. - Cytokines produced by macrophages like
4. Type 4 (atheroma) lesion, core of EC TNFalpha, PDGF, IL-1, they cause intimal
lipid. Can be clinically silent or overt. SM cells overlying the plaque to become
senescent and collagen within the plaque
5. Type 5 (fibroatheroma) lesion, lipid core to degrade which results in thinning of
and fibrotic layer, or multiple lipid cores the protective fibrous cap, which makes
and fibrotic layers r mainly calcific or the lesion vulnerable to mechanical
mainly fibrotic. Accelerated SM and stress that causes erosion of the plaque
collagen increase, from 4th decade. surface.
6. Type 6 (complicated) lesion. Surface - Breach in the integrity of the plaque can
defect, haematoma-haemorrhage, and expose it to the blood, cause platelet
aggregation and thrombus, can partially
occlude site of lesion or distal
embolisation, infarction or ischaemia of
affected organ.

Contrast between stable and unstable plaques,

depending on integrity of fibrous cap.
 - Rupture tends to occur at sites of
maximal mechanical stress and can be
triggered by a surge in BP such as during Primary prevention
exercise or emotional stress. - Modify risk factors of whole population
- AS may induce complex changes in the through diet and lifestyle advice.
media that lead to arterial remodelling. Legislation that restricts smoking in
Some can slowly constrict which is known public places is associated with reduction
as negative remodelling, and some in rates of MI.
enlarge which is positive remodelling.

Secondary prevention
Risk Factors: Impact of genetic risk is illustrated - Patients who already have evidence of
by twin studies. People with a combination of atheromatous vascular disease are at high
risk factors are at greatest risk. Relative risk and risk of future CV events and should be
absolute risk. offered treatments and measures to
- Age and sex: age most powerful improve their outlook. All patients with
independent risk factor for AS. coronary heart disease should be given
Premenopausal women have protective statin therapy irrespective of their serum
factor. cholesterol concentration.

- Family history, due to combination of

shared genetic lifestyle factors. Most Ischemic heart disease (Coronary heart disease)
common inherited risk factors like HT,
hyperlipidaemia, DM are polygenic. CHD is the most common form of heart disease
and the single most important cause of
- Smoking, most important avoidable cause premature death in Europe, the Baltic States,
of AS vascular disease. Russia, North and South America, Australia and
- HT, incidence of AS increases as BP rises. New Zealand.

- Hypercholesterolemia, risk rises with

increasing serum cholesterol Disease of the coronary arteries is almost always
concentrations. due to atheroma and its complications,
- DM, glucose intolerance accounts for a particularly thrombosis.
major part of the high incidence of Occasionally, the coronary arteries are involved
ischaemic heart disease in certain ethnic in other disorders such as aortitis, polyarteritis
groups like south asians. and other connective tissue disorders.
- Haemostatic factors, Platelet activation Classification:
and high levels of fibrinogen are
associated with increased risk of coronary
thrombosis. Antiphospholipid antibodies
are associated with recurrent arterial
thromboses.
- Physical activity, regular exercise has a
protective effect which can be related to
increased serum HDL, lower BP and
collateral vessel development.
- Obesity
- Alcohol reduces rate of coronary artery
disease but excess can be associated with
HT.
- Other dietary factors
- Personality, stress
- Social deprivation, health inequalities
 17. Ischemic heart disease /IHD/: Angina a. This is due to coronary artery
pectoris – classification, diagnosis, differential spasm, which can occur even in
diagnosis and treatment. normal coronary arteries.
This is due to myocardial ischaemia and presents b. Pain usually occurs during rest
as a central chest tightness or heaviness, which (rather than during activity).
is brought on by exertion and relieved by rest.
c. ECG during pain shows ST segment
- It may radiate to one or both arms, the elevation, which resolves as the
neck, jaw or teeth. pain subsides.
- Other precipitants: Emotion, cold d. Patients usually do not have the
weather, and heavy meals. standard risk factors for
atherosclerosis.
- Associated symptoms: Dyspnoea, nausea,
sweatiness, faintness. e. Tx: Calcium channel blockers +/-
long-acting nitrates.
i. Aspirin can aggravate the
Causes ischaemic attacks in these
- Mostly atheroma. Rarely: anaemia, AS; patients.
tachyarrhythmias; HCM (hypertrophic ii. B-blockers (esp non-
cardiomyopathy); arteritis/small vessel selective) should also be
disease (microvascular angina/cardiac avoided as they can
syndrome X). increase vasospasm.
iii. Prognosis is usually very
Classification: good.

1. Stable (classic) angina: induced by effort,

relieved by rest. Dx:
a. Associated with atherosclerotic - ECG: usually normal, but may show ST
disease that produces fixed depression; flat or inverted T waves
obstruction of the coronary
arteries. - Signs of past MI. See BOX 2 for other
investigations.
b. It occurs when the metabolic
needs of the myocardium exceed - Exclude precipitating factors: anaemia,
the ability of the occluded diabetes, hyperlipidaemia,
coronary arteries to deliver thyrotoxicosis, temporal arteritis.
adequate blood flow.
- If the patient has an acute coronary
c. Characterised by central chest syndrome, e.g. unstable angina,
pain, discomfort in chest, arms, emergency admission is indicated.
neck, jaw or breathlessness
- Pt categorised on whether there is known
d. Relieved within mins with rest or CAD, and the likelihood of CAD.
glyceryl trinitrate
o Known CAD and pain typical, no
2. Unstable (crescendo) angina: angina of further investigation.
increasing frequency or severity; occurs
on minimal exertion or at rest; associated
o If atypical pain, either exercise
with increased risk of MI. testing or functional imaging
(myocardial perfusion
a. Results from atherosclerotic scintigraphy, stress echo, or MRI).
plaque disruption.
- Unknown CAD stratify of likelihood of
3. Decubitus angina: precipitated by lying CAD
flat.
o >90% treat as known CAD
4. Variant (Prinzmetal’s) angina: caused by
coronary artery spasm (rare; may co-exist
o 61–90% angiography, or functional
with fixed stenoses). imaging if inappropriate
 o 30–60% functional imaging 180mg/12h PO (orally taken). They are
particularly useful if there is a
o 10–29% coronary artery contraindication to B-blockers.
calcification score1 with CT
7. K+ channel activator, e.g. nicorandil 10–
o <10% reconsider diagnosis. 30mg/12h PO, if still not controlled.
8. Others: ivabradine inhibits the
pacemaker (‘funny’) current in the SA
node and thus reduces heart rate. Useful
in those who cannot take a !-blocker,
having similar efficacy.
9. Trimetazidine inhibits fatty acid
oxidation, leading the myocardium to use
glucose, which is more efficient.
Ranolazine inhibits the late Na+ current.
10. Unstable angina requires admission and
urgent treatment

Differential dx:
Prognosis:
- Acute pericarditis
- 5 year mortality of patients with severe
- Aortic stenosis/dissection angina is nearly double that of patients
with mild symptoms.
- Hypertension
o Exercise testing and other forms
- Coronary artery vasospasm/
of stress testing are important
atherosclerosis
predictors of mortality.
- Mitral valve prolapse/regurgitation
o In general prognosis of CAD is
Tx: related to number of diseased
vessels and degree of LV
1. Modify risk factors: stop smoking, dysfunction.
encourage exercise, weight loss. Control
hypertension, diabetes - Angina with normal coronary arteries.
10% who report stable angina on effort
2. If total cholesterol >4mmol/L give a will have angiographically normal
statin arteries.
3. Aspirin (75–150mg/24h) reduces mortality o Mostly women, not too sure why.
by 34%. Coronary artery spasm-
4. B-blockers, e.g. atenolol 50–100mg/24h Prinzmetal’s angina.
PO, reduce symptoms unless o Syndrome X- angina on effort,
contraindicated (asthma, COPD, LVF, objective evidence of myocardial
bradycardia, coronary artery spasm). ischaemia on stress testing but
5. Nitrates: for symptoms, give GTN spray or normal coronary arteries.
sublingual tabs, up to every .h.
Prophylaxis: give regular oral nitrate,
e.g. isosorbide mononitrate 20–40mg PO
bd (2x) (have an 8h nitrate free period to
prevent tolerance) or slow-release
nitrate (e.g. Imdur 60mg/24h).
a. Alternatives: adhesive nitrate skin
patches or buccal pills. SE:
headaches, BP low.
6. Long-acting calcium antagonists:
amlodipine 10mg/24h; diltiazem-MR 90–
 18. IHD. Acute myocardial infarction: Pathogenesis:
aetiology, pathogenesis, clinical features,
diagnosis, differential diagnosis - As atherosclerotic lesions develop, they
become lipid laden and vulnerable to
Acute myocardial infarction (AMI), also known as rupture or fissuring with release of
a heart attack, refers to the ischemic death of substances that cause platelet activation
myocardial tissue associated with atherosclerotic an thrombin generation
disease of the coronary arteries.
o It is the resultant thrombus that
interrupts blood flow and leads to
myocardial infarction.
Aetiology + RF:
- Although AMI most often results from
Smoking, known cholesterol elevation, diabetes, atherosclerotic plaque disruption, some
hypertension, family history, alcohol persons may experience AMI because of
Types: prolonged severe vasospasm, as in
Prinzmetal’s variant angina.
- Type 1: spontaneous MI related to
ischemia due to a primary coronary event - Transmural infarct: involves full thickness
such as plaque erosion and/or rupture, of ventricular wall
fissuring, or dissection - Sub-endocardial: inner 1/3 – ½ of
- Type 2: MI secondary to ischemia due to ventricular wall
either increased oxygen demand or - 3 Zones of tissue damage: necrotic zone,
decreased supply, e.g. coronary artery surrounding injured zone or ischaemic
spasm, coronary embolism, anaemia, zone
arrhythmias, hypertension, or
hypotension
- Type 3: sudden unexpected cardiac Dx:
death, including cardiac arrest, often
with symptoms suggestive of myocardial WHO criteria have classically been used to dx MI;
ischemia, a patient is dx with MI if 2 (probable) or 3
(definite) of the following criteria are satisfied:
- Type 4: associated with coronary
angioplasty or stents 1. Clinical history of ischemic-type chest
pain lasting for more than 20 minutes
o Type 4a: MI associated with
percutaneous coronary 2. Changes in serial ECG tracings
intervention (PCI) 3. Rise and fall of serum cardiac biomarkers
o Type 4b: MI associated with stent - Physical examination: pt in distress,
thrombosis as documented by pallor, bradycardia or tachycardia (>120),
angiography or at autopsy elevated BP, hypotension – due to
- Type 5: MI associated with CABG vagotonia, dehydration, RV infarction,
(coronary artery bypass graft) splitting of 2nd heart sound, presence of
3rd or 4th heart sound, mitral regurgitant
murmur
- ECG: hyperacute tall T-wave, presence of
ST segment elevation 1 or >1mm in 2
consecutive leads 1-3, aVL, aVF, V4-6 or 2
or >2 mm in leads V1-3
- Blood: plasma levels of CK or CK-MB
increase 6hrs after MI – enzymes to be
assessed every 8hrs for 1st 24hrs – this
enzyme helpful in gauging size of MI
o Myoglobulin high within 1hr after
MI
o Troponin T & I: released during MI
 o LDH: high after 24-48hrs
- Angiography: helpful in difficult dx –
shows acutely occluded infarct vessel

S+S:
History: intense, oppressive, durable chest
pressure and radiation of the pain to the left
arm
- Indigestion is common, especially with
inferior wall MI. Nausea (particularly) and
vomiting are typical. Profuse diaphoresis
is also frequent. Dyspnea, palpitations or
syncope

Differential dx:
1. Aortic dissection, Pericarditis,
Esophagitis, Myocarditis, Pneumonia,
Cholecystitis, Pancreatitis
 19. IHD. Complications during acute - This section of the myocardium does not
myocardial infarction. contract with the rest of the ventricle
during systole.
Among the complications of AMI are:
- Instead, it increases the work of the left
- sudden death ventricle, predisposing the patient to
- heart failure and cardiogenic shock heart failure. Stasis of blood lead to
thrombus formation.
- pericarditis/Dressler’s syndrome
- thromboemboli
Arrhythmias
- rupture of the heart
1. Ventricular fibrillation
- ventricular aneurysms
This occurs in 5–10% of patients who reach
- post MI chest pain hospital and is thought to be the major cause of
death in those who die before receiving medical
- Arrhythmia’s
attention. Prompt defibrillation restores sinus
rhythm and is life-saving.

2. Atrial fibrillation
This is common but frequently transient, and
usually does not require emergency treatment.
However, if it causes a rapid ventricular rate
with hypotension or circulatory collapse, prompt
cardioversion by immediate synchronised DC
Sudden death from CHD is death that occurs
shock is essential. In other situations, digoxin or
within 1 hour of symptom onset.
a β-blocker is usually the treatment of choice.
- It usually is attributed to fatal
dysrhythmias, which may occur without
evidence of infarction. Pericarditis:
- About 30% to 50% of persons with AMI die This only occurs following infarction and is
of ventricular fibrillation within the first particularly common on the second and third
few hours after symptoms begin. days. The pt may recognise that a different pain
has developed, even though it is at the same
site, and that it is positional and tends to be
The acute post myocardial infarction period can worse or sometimes only present on inspiration.
be complicated by rupture of myocardium, the
- The post-MI syndrome (Dressler’s
interventricular septum, or a papillary muscle.
syndrome) is characterised by persistent
- Myocardial rupture, occurring on the fever, pericarditis and pleurisy, and is
fourth to seventh day when the injured probably due to autoimmunity.
ventricular tissue is soft and weak, often
- The symptoms tend to occur a few weeks
is fatal.
or even months after the infarct
- tx with high-dose aspirin, NSAIDs or even
An aneurysm is an outpouching of the ventricular corticosteroids.
wall.
- Scar tissue does not have the
Embolism:
characteristics of normal myocardial
tissue; when a large section of Thrombus often forms on the endocardial
ventricular muscle is replaced by scar surface of freshly infarcted myocardium.
tissue, an aneurysm may develop.
- This can lead to systemic embolism and
occasionally causes a stroke or ischaemic
limb.
- Venous thrombosis and pulmonary
embolism may occur but have become
less common with the use of prophylactic
anticoagulants and early mobilisation.
 20. Acute myocardial infarction –treatment.
The aim of management in AMI is: Fibrinolytic therapy:
- Primarily to prevent death All patients with ST-segment elevation MI who
present within 12 hours from the onset of
- Limit the extent of myocardial damage symptoms should be considered for myocardial
- Reduce subsequent morbidity and reperfusion therapy.
mortality from a damaged heart. - The only definite contraindications for
fibrinolytic therapy are

Myocardial infarction can be aborted if o any previous intracranial

reperfusion can be achieved before the heart haemorrhage
muscle is irreversibly damaged. o active bleeding
- Reperfusion can be achieved either: o recent stroke
o Mechanically by percutaneous o trauma
coronary intervention PCI
(angioplasty) o major surgery
o Pharmacologically by o Severe or uncontrolled
administration of a fibrinolytic hypertension (systolic blood
agent. pressure >180/110 mm Hg)
o Both methods have been shown to o Pregnancy
be successful.
o Active Menstruation
o GI haemorrhage
PCI for AMI:
1. The wire is guided into position across
the lesion in the diseased coronary Oxygen:
artery, and the deflated balloon is Supplemental oxygen should be administered to
advanced until it straddles the lesion. pts with arterial oxygen desaturation (SaO2<
2. The balloon is manoeuvred into position 90%)
across the middle of the stenosis. - During the first 6hrs
3. The balloon is repeatedly inflated to high
pressures (about 6-16 atmospheres),
compressing and cracking the stenosis. Nitroglycerin:

a. If a stent is to be deployed, the Patients with ongoing ischemic discomfort should

bare metal or drug-coated stent is receive sublingual NTG (0.4 mg) every 5 minutes
placed on a balloon catheter, for a total of 3 doses, after which an assessment
which is then threaded into the should be made about the need for intravenous
vessel and inflated. NTG.

b. The stent expands and embeds - Not administered to pts who have
itself on the inner lining of the received phosphodiesterase inhibitor in
artery. last 24hrs for erectile dysfunction (48hrs
for tadalafil)
4. The balloon is deflated and withdrawn
along the wire, leaving a good lumen o Systolic BP < 90 mmHg / ≥ to
with no significant obstructions to 30mmHg
o Severe bradycardia (< 50 bpm)
o tachycardia (> 100 bpm)
coronary blood flow. o suspected RV infarction
Angioplasty with stent
Analgesia:
Morphine sulfate (2 to 4 mg i.v. with increments
of 2 to 8 mg intravenously repeated at 5 to 15
minute intervals) is the analgesic of choice for
tx of pain associated with STEMI (ST elevate MI)

Antithrombotic & Anticoagulants

- Aspirin, LMW heparin 70–100 U/kg
- P2Y2 Inhibitor – if no risk of bleeding
- Pasugrel 60mg loading dose 10mg daily
- Clopidogrel 600mg loading dose 75 daily
 21. Cardiogenic Shock

Syndrome of inadequate blood supply to vital Dx:

organs with failure of elimination of metabolites
resulting in their functional and structural - General condition
disturbance.
- BP in both arms

- Pulse: volume, rhythm. Check all periph.

- usually results from massive MI with 40 or Pulses
> of myocardium involved
- Venous pressure
- mortality is approx. 85%
- Auscultation: S3 gallop, pansystolic
murmur

Aetiology:

- MI, causing pump failure, MR, VSD; Tx:

- Prosthetic valve dysfunction: acute - The most important factor in cardiogenic

obstruction or severe regurgitation; shock is time. If >6 h have elapsed from
the onset of the shock, then it is unlikely
- Massive pulmonary embolism; any intervention will make any
difference.
- Aortic dissection;
- Early coronary angiography is needed to
- Cardiac tamponade; identify those patients suitable for early
revascularization
- Acute myocarditis

Stage 1: General measures

Pathophysiology:
- Analgesia; oxygen via MC mask or
- Sympathetic-adrenal discharge and
ventilation; ECG monitoring; urine
vasoconstriction
catheter; blood gasses; cardiac enzymes
- Decreased tissue flow causes: tissue
- Endotracheal intubation and ventilation
hypoxia, anaerobic metabolism and lactic
acidosis - Insertion of monitoring lines: Swan-Ganz
(catheter inserted to right side of heart)
- Precapillary dilatation and post-capillary
to PA/PAW via subclavian vein; CVP;
constriction
- Echocardiography
- Mitochondrial damage, lysosome release
- Termodilution cardiac outputs can be
- Oxygen utilization is impaired
performed

Cf:
Stage 2: correction of filling pressure
- Hypotension
- To get filling pressure of LV to 16-18 mm
- Cool pale moist skin Hg

- Low volume rapid pulse - Filling pressure too high with

hypotension:
- Oliguria (<30mL/h)
o Use dopamine 5-10 µg/kg/min.
- Obtunded consciousness
 - Filling pressure too low: Give 200 ml - IABP (intra-aortic ballon) – inflation of
plasms and repeat measurements. ballon during diastole increases coronary
+ cerebral flow)

Stage 3: improvement of stoke volume

(Inotropes)

Drug receptor Increase HR Dose i.v.

affected (β1 effect)
Dopamine (β1, ++ 1-5µg/kg/min
α at high dose 5-10µg/kg/
min
Dobutamine + 2.5-15µg/kg/
(β2, small min
dose
Salbutamol – +++ 10-40 µg/kg/
β1, β2 min
Isoprenalin – +++ 1-10 µg/kg/
β1, β2 min
Adrenalin – +++ 1-12 µg/kg/
β1> β2 (α min
small dose)
Noradrenalin – - or + 1-12 µg/kg/
α (β small min
dose)

Dopamine – precursor to noradrenaline: Dose 1.0

–5.0 µg/kg/min. Dopamin (DA1) receptors
activated, resulting dilatation of coronary, renal,
cerebral and splanchic beds.

- “renal” dose of dopamine.

- Dopamin (DA2) receptors activated in the

periphery inhibit presynaptic release of
noradrenaline causing vasodilatation.

- Dose 5.0-10.0 µg/kg/min Inotropic dose –

Beta receptors activated – increase
contractility dose >10 cause arrhythmias

- Dose >15.0 alpha receptors activated

- Doputamine: HR lower for same increase

in output – pulmonary wedge pressure
lower with this

Stage 4: further measures

- PTCA – in pts with MI

 22. Acute Left Ventricular HF and Right = shift in intravascular fluids into
Ventricular HF interstitium of lung + development of
pulmonary edema
- Definition: Cardiac output is inadequate
for the body’s requirements. - Leads to: low renal flow ➔ Na retention
➔ oedema; pulmonary hypertension ➔
- Prognosis is poor with ~25–50% of patients pulmonary oedema + bronchospasm
dying within 5yrs of diagnosis.
- Symptoms: Dyspnoea, poor exercise
- Prevalence 1–3% of the general tolerance, fatigue, orthopnoea,
population; ~10% among elderly patients. paroxysmal nocturnal dyspnoea (PND),
nocturnal cough (+/- pink frothy sputum),
wheeze (cardiac “asthma”), nocturia,
Acute heart failure: characterized by pulmonary cold peripheries, weight loss, muscle
and/or peripheral oedema with or without signs wasting.
of peripheral hypoperfusion.
- Signs: tachypnoea, tachycardia, end-
inspiratory basal crackles, dullness to
percussion over lung bases, S3,
Systolic versus diastolic failure:
cardiomegaly, cyanosis, pleural effusion,
Systolic failure: raised JVP +/++, pitting edema +/++

- Inability of the ventricle to contract

normally, resulting in low cardiac output.
Right ventricular failure:
- Ejection fraction (EF) is <40%.
Causes: LVF, pulmonary stenosis, lung disease.
- Causes: IHD, MI, cardiomyopathy.
- LH failure ➔ pulmonary hypertension ➔
Diastolic failure: RV failure – accumulation of blood in
systemic venous system – increase RA +
- Inability of the ventricle to relax and fill RV end-diastolic pressure – edema in
normally, causing high filling pressures. peripheral tissues + congestion of
- EF is >50%. abdominal organs

- Causes: constrictive pericarditis, - RHF also produces a raised JVP +++ with
tamponade, restrictive cardio myopathy, hepatomegaly, ascites or pleural effusion
hypertension. NB: systolic and diastolic occurs in some patients, peripheral
failure usually coexist. edema
- Cor pulmonale (R ventricle increases
pressure due to disease of lung or
Left-sided versus right-sided failure pulmonary vasculature)
- Left ventricular failure (LVF) and right - Constrictive pericarditis
ventricular failure (RVF) may occur
independently, or together as congestive o Symptoms: Peripheral oedema (up
cardiac failure (CCF). to thighs, sacrum, abdominal
wall), ascites, nausea, anorexia,
facial engorgement, pulsation in
neck and face (tricuspid
Left ventricular failure:
regurgitation), epistaxis.
- Cause: ischaemic heart disease,
Dx:
hypertension, aortic + mitral valve (aortic
stenosis/rheumatic heart disease), - Blood: FBC, Cr, electrolyte, Trop I, U+E,
myocardial disease, hypertrophied L glucose, cholesterol
ventricle ➔ secondary atrial enlargement
➔ atrial fibrillation - ECG

- Low CO – increase in LA + LV end-diastolic - CXR: Kerley lines in LHF, cardiomegaly

pressure – congestion in pulmonary - Echo: indicate cause – confirm presence
circulation – when capillary pressure or absence of LV dysfunction
(10mmHg) > osmotic pressure (25mmHg)
Tx:
 23. Cardiac arrhythmias: classification, o Bradycardias cause symptoms that
aetiology, pathogenesis. show low CO: fatigue, light-
headedness and syncope.
- Heart beat initiated by electrical
discharge from the sinus node. - Broad complex: QRS >120ms or 0.12s
- Node acts as a pacemaker and its - Narrow complex: QRS <120ms or 0.12s
intrinsic rate is regulated by the ANS.
o Regular narrow complex:
- Vagal activity slows HR, sympathetic
activity accelerates HR.
o Atrial flutter with regular AV block

- If the sinus rate becomes slow, then

o Re-entrant tachycardia
another centre becomes pacemaker, this ▪ AV nodal (AVNRT)
is called an escape rhythm and may arise
in the AV node or His bundle or the ▪ Atrio ventricular (AVRT)
ventricles- idioventricular rhythm. o Atrial tachycardia

▪ Abnormal P wave
Classification: o Irregular narrow complex:
An abnormality of the cardiac rhythm is called a o Atrial fibrillation
cardiac arrhythmia.
o Atrial flutter
- It can be classified by whether it’s a sinus
rhythm (is there a P wave), the HR o Multifocal atrial tachycardia
(60-100), QRS duration (</> 120m/s),
regular or irregular NCT (is the R-R
distance equally apart) Another way to classify arrhythmias could be by
Arrhythmias may cause sudden death, syncope, site:
heart failure, chest pain, dizziness, palpitations - Supraventricular: sinus arrhythmia, atrial
or no symptoms at all. arrhythmia, junction arrhythmia
- 2 main types: - Ventricular
- Conduction: RBBB or LBBB

Etiology of cardiac arrhythmias:

Valvular heart disease, Ischemic heart disease,
Hypertensive heart diseases, Congenital heart
disease, Cardiomyopathies, Carditis, RV
dysplasia, Drug related, Pericarditis, Pulmonary
diseases, Others.

1) Sinus bradycardia: a sinus rate <60/min is

- HR >100/min tachycardia normal in healthy people at rest and
o Tachycardia’s: rapid palpitation, athletes.
dizziness, chest discomfort, a. Pathologies associated with this
breathlessness. are MI, sick sinus syndrome,
o Extreme tachycardia’s can cause hypothermia, hypothyroidism,
syncope because the heart is cholestatic jaundice, raised IC
unable to contract or relax pressure, drugs like beta blockers
properly at extreme rates. digoxin, verapamil.

- HR<60 is bradycardia b. Symptomatic acute sinus

bradycardia responds to IV
atropine (0.6-1.2mg) Patients who
have persistent, should be
 considered for pacemaker they are called ‘delayed after
implantation. depolarizations’ (D in fig B).
- The abnormal oscillations can be
exaggerated by pacing, catecholamines,
2) Sinus tachycardia: sinus rate > 100/min. electrolyte disturbances, hypoxia,
a. Increase in sympathetic activity acidosis and some medications, which
due to exercise, emotion, may then trigger arrhythmia.
pregnancy or pathology like - The atrial tachycardia produced by
anxiety, fear, anaemia, HF, digoxin toxicity are due to triggered
thyrotoxicosis, activity.
phaeochromocytoma and drugs
like beta agonists - - The initiation of ventricular arrhythmia
bronchodilators. in the long QT syndrome may be caused
by this mechanism.

Pathogenesis:
3 main mechanisms of tachycardia:
3.Re-entry
1. Accelerated automaticity: (most
- The normal mechanism of spontaneous common):
cardiac rhythmicity is slow depolarization -The
of the transmembrane voltage during
diastole until the threshold potential is
reached and the action potential of the
pacemaker cells takes off.
- This mechanism may be accelerated by mechanism
increasing the rate of diastolic of re-entry occurs when a ‘ring’ of
depolarization or changing the threshold cardiac tissue surrounds an in-excitable
potential. core (e.g. in a region of scarred
myocardium).
- For example, sympathetic stimulation
releases epinephrine (adrenaline), which - Tachycardia is initiated if an ectopic beat
enhances automaticity. finds one limb refractory (α), resulting in
unidirectional block, and the other limb
- Such changes are thought to produce excitable.
sinus tachycardia, escape rhythms and
accelerated AV nodal (junctional) - Provided conduction through the
rhythms. excitable limb (β) is slow enough, the
other limb (α) will have recovered and
will allow retrograde activation to
complete the re-entry loop.
2. Triggered activity:
- If the time to conduct around the ring is
- Myocardial damage can result in
longer than the recovery times
oscillations of the transmembrane
(refractory periods) of the tissue within
potential at the end of the action
the ring, circus movement will be
potential.
maintained, producing a run of
- These oscillations, which are called ‘after tachycardia.
depolarizations’, may reach threshold - The majority of regular paroxysmal
potential and produce an arrhythmia.
tachycardias are produced by this
- If they occur before the transmembrane mechanism.
potential reaches its threshold (at the
end of phase 3 of the action potential),
they are called ‘early after
depolarizations’ (E in fig B).
- When they develop after the
transmembrane potential is completed,
 23. Cardiac arrhythmias: classification, o Bradycardias cause symptoms that
aetiology, pathogenesis. show low CO: fatigue, light-
headedness and syncope.
- Heart beat initiated by electrical
discharge from the sinus node. - Broad complex: QRS >120ms or 0.12s
- Node acts as a pacemaker and its - Narrow complex: QRS <120ms or 0.12s
intrinsic rate is regulated by the ANS.
o Regular narrow complex:
- Vagal activity slows HR, sympathetic
activity accelerates HR.
o Atrial flutter with regular AV block

- If the sinus rate becomes slow, then

o Re-entrant tachycardia
another centre becomes pacemaker, this ▪ AV nodal (AVNRT)
is called an escape rhythm and may arise
in the AV node or His bundle or the ▪ Atrio ventricular (AVRT)
ventricles- idioventricular rhythm. o Atrial tachycardia

▪ Abnormal P wave
Classification: o Irregular narrow complex:
An abnormality of the cardiac rhythm is called a o Atrial fibrillation
cardiac arrhythmia.
o Atrial flutter
- It can be classified by whether it’s a sinus
rhythm (is there a P wave), the HR o Multifocal atrial tachycardia
(60-100), QRS duration (</> 120m/s),
regular or irregular NCT (is the R-R
distance equally apart) Another way to classify arrhythmias could be by
Arrhythmias may cause sudden death, syncope, site:
heart failure, chest pain, dizziness, palpitations - Supraventricular: sinus arrhythmia, atrial
or no symptoms at all. arrhythmia, junction arrhythmia
- 2 main types: - Ventricular
- Conduction: RBBB or LBBB

Etiology of cardiac arrhythmias:

Valvular heart disease, Ischemic heart disease,
Hypertensive heart diseases, Congenital heart
disease, Cardiomyopathies, Carditis, RV
dysplasia, Drug related, Pericarditis, Pulmonary
diseases, Others.

1) Sinus bradycardia: a sinus rate <60/min is

- HR >100/min tachycardia normal in healthy people at rest and
o Tachycardia’s: rapid palpitation, athletes.
dizziness, chest discomfort, a. Pathologies associated with this
breathlessness. are MI, sick sinus syndrome,
o Extreme tachycardia’s can cause hypothermia, hypothyroidism,
syncope because the heart is cholestatic jaundice, raised IC
unable to contract or relax pressure, drugs like beta blockers
properly at extreme rates. digoxin, verapamil.

- HR<60 is bradycardia b. Symptomatic acute sinus

bradycardia responds to IV
atropine (0.6-1.2mg) Patients who
have persistent, should be
 considered for pacemaker they are called ‘delayed after
implantation. depolarizations’ (D in fig B).
- The abnormal oscillations can be
exaggerated by pacing, catecholamines,
2) Sinus tachycardia: sinus rate > 100/min. electrolyte disturbances, hypoxia,
a. Increase in sympathetic activity acidosis and some medications, which
due to exercise, emotion, may then trigger arrhythmia.
pregnancy or pathology like - The atrial tachycardia produced by
anxiety, fear, anaemia, HF, digoxin toxicity are due to triggered
thyrotoxicosis, activity.
phaeochromocytoma and drugs
like beta agonists - - The initiation of ventricular arrhythmia
bronchodilators. in the long QT syndrome may be caused
by this mechanism.

Pathogenesis:
3 main mechanisms of tachycardia:
3.Re-entry
1. Accelerated automaticity: (most
- The normal mechanism of spontaneous common):
cardiac rhythmicity is slow depolarization -The
of the transmembrane voltage during
diastole until the threshold potential is
reached and the action potential of the
pacemaker cells takes off.
- This mechanism may be accelerated by mechanism
increasing the rate of diastolic of re-entry occurs when a ‘ring’ of
depolarization or changing the threshold cardiac tissue surrounds an in-excitable
potential. core (e.g. in a region of scarred
myocardium).
- For example, sympathetic stimulation
releases epinephrine (adrenaline), which - Tachycardia is initiated if an ectopic beat
enhances automaticity. finds one limb refractory (α), resulting in
unidirectional block, and the other limb
- Such changes are thought to produce excitable.
sinus tachycardia, escape rhythms and
accelerated AV nodal (junctional) - Provided conduction through the
rhythms. excitable limb (β) is slow enough, the
other limb (α) will have recovered and
will allow retrograde activation to
complete the re-entry loop.
2. Triggered activity:
- If the time to conduct around the ring is
- Myocardial damage can result in
longer than the recovery times
oscillations of the transmembrane
(refractory periods) of the tissue within
potential at the end of the action
the ring, circus movement will be
potential.
maintained, producing a run of
- These oscillations, which are called ‘after tachycardia.
depolarizations’, may reach threshold - The majority of regular paroxysmal
potential and produce an arrhythmia.
tachycardias are produced by this
- If they occur before the transmembrane mechanism.
potential reaches its threshold (at the
end of phase 3 of the action potential),
they are called ‘early after
depolarizations’ (E in fig B).
- When they develop after the
transmembrane potential is completed,
 24. Paroxysmal supraventricular cardiac - Dx: The ECG usually shows a tachycardia
arrhythmias: clinical, features, diagnosis, with normal QRS complexes but
treatment. occasionally there may be rate-
dependent bundle branch block.
- These arrhythmias are circus movement
or reciprocating tachycardia’s because
they utilize the mechanism of re-entry
- The onset is sudden, usually initiated by
a premature beat, and the arrhythmia
also stops abruptly - which is why they
are called paroxysmal
- They are usually narrow-QRS
tachycardia’s unless there is pre-existing
bundle branch block or rate-related
- Tx: episode may be terminated by carotid
aberrant ventricular conduction
sinus pressure or by the Valsalva
- There are several types of PSVT manoeuvre (increase in intrathoracic +
depending on the location of the re-entry intra-abdominal pressures by straining)
circuit. o Adenosine (3–12 mg rapidly IV in
o AVNRT and Wolff-Parkinson-White incremental doses until
syndrome tachycardia stops) or verapamil (5
mg IV over 1 min) will restore
sinus rhythm
Atrioventricular nodal re-entrant tachycardia o IV oral β-blocker, Verapamil or
(AVNRT): flecainide – avoided in pregnancy
- This is due to re-entry in a circuit o Severe haemodynamic
involving the AV node and its two right compromise, the tachycardia
atrial input pathways: a superior ‘fast’ should be terminated by DC
pathway and an inferior ‘slow’ pathway. cardioversion
o Recurrent SVT, catheter ablation
most effective therapy and will
-This permanently

Wolff-Parkinson-White syndrome:
- Abnormal band of conducting tissue
connects the atria and ventricles.
- This ‘accessory pathway’ comprises
rapidly conducting fibres which resemble
Purkinje tissue, in that they conduct very
rapidly and are rich in sodium channels.

produces a regular tachycardia with a - In around half of cases, this pathway only
rate of 120–240/min. conducts in the retrograde direction
(from ventricles to atria) and thus does
- It tends to occur in hearts that are not alter the appearance of the ECG in
otherwise normal and episodes may last sinus rhythm.
from a few seconds to many hours.
- This is known as a concealed accessory
- S+S: Anxiety, dizziness, dyspnoea, neck pathway.
pulsation, central chest pain + weakness,
polyuria (due to release of atrial - In the rest, the pathway also conducts
natriuretic peptide in response to high antegradely (from atria to ventricles) so
Atrial pressure), prominent jugular AV conduction in sinus rhythm is
venous pulsations, syncope in 10-15% of mediated via both the AV node and the
pts
 accessory pathway, excited atrial fibrillation and may cause
distorting the QRS collapse, syncope and even death.
complex.
- Tx: Procainamide best choice – slows the
- Premature ventricular accessory pathway, not use any meds
activation via the which will slow AV node: i.e. digoxin, B-
pathway shortens the blockers, adenosine or Ca channel
PR interval and blockers
produces a ‘slurred’
initial deflection of the
QRS complex, called a Other Supraventricular tachycardia’s:
delta wave (Fig. B).
1. Premature atrial complexes:
- This is known as a
manifest accessory - Rate: normal or accelerated
pathway.
- P wave: usually have a different
- As the AV node and morphology than sinus P waves because
accessory pathway have they originate from an ectopic
different conduction pacemaker
speeds and refractory
- QRS: normal
periods, a re-entry
circuit can develop, - Conduction: normal, however the ectopic
causing tachycardia beats may have a different P-R interval.
(Fig. 18.46C); when
associated with symptoms, the condition - Rhythm: PAC's occur early in the cycle
is known as Wolff–Parkinson–White and they usually do not have a complete
syndrome. compensatory pause.

- S+S: symptomatic tachycardia – - PAC's occur normally in a non-diseased

palpitations, shortness of breath, heart.
fainting, fatigue, anxiety, in babies ashen - However, if they occur frequently, they
colour may lead to a more serious atrial
- Dx: The ECG during this dysrhythmias.
tachycardia is almost - They can also result from CHF, ischemia
indistinguishable from and COPD
that of AVNRT (Fig.
18.46A).
o Short PR interval 2. Sinus tachycardia:
(<0.12), delta
- Rate: 101-160/min
wave + prolonged
QRS (>0.12) - P wave: sinus
o - QRS: normal
- Conduction: normal
Electrophysiologic
pathway helps identify re-entry - Rhythm: regular or slightly irregular
pathway + location of accessory - The clinical significance of this
pathway dysrhythmia depends on the underlying
- If atrial fibrillation cause. It may be normal.
occurs, it may produce a - Underlying causes include: increased
dangerously rapid circulating catecholamines, CHF, hypoxia,
ventricular rate because PE, increased temperature, stress,
the accessory pathway response to pain
lacks the rate-limiting
properties of the AV - Tx includes identification of the
node (Fig.D). underlying cause and correction

- This is known as pre-

3. Multifocal Atrial Tachycardia 5. Atrial flutter:
- Discrete, multifocal P' waves occurring at - Atrial activity of 240-320 with sawtooth
rates of 100-250/min and with varying P'R pattern.
intervals (should see at least 3 different P
wave morphologies in a given lead). - Usually a 2:1 conduction pattern; if it is
3:1 or higher, there is AV node damage
- Ventricular response is irregularly
irregular (i.e., often confused with A-fib). - Tx is to slow AV node conduction with
amiodarone, propafenone or sotalol
- May be intermittent, alternating with
periods of normal sinus rhythm. - DC cardiovert if <48 hours or unstable

- Seen most often in elderly patients with - You can also ablate the re-entry pathway
chronic or acute medical problems such within the atrium between the tricuspid
as hypoxia, COPD, atrial stretch and local and the IVC.
metabolic imbalance. atrial flutter in lead II
- If atrial rate is <100 bpm, call it
multifocal atrial rhythm
- Digoxin worsens it, so treat with oxygen
and slow channel blocker like verapamil
or diltiazem.

4. Atrial fibrillation:
- Rate: atrial rate usually between
400-650/bpm.
- P wave: not present; wavy baseline is
seen instead.
- QRS: normal
- Conduction: variable AV conduction; if
untreated the ventricular response is
usually rapid.
- Rhythm: irregularly irregular. (This is the
hallmark of this dysrhythmia)
- Atrial fibrillation may occur paroxysmally,
but it often becomes chronic.
- It is usually associated with COPD, CHF or
other heart disease.
- Tx: Digoxin to slow the AV conduction
rate. B-blockers, Ca CB – verapamil +
dilitiazem
 25. Paroxysmal ventricular arrhythmias:
clinical, features, diagnosis, treatment.
2. Ventricular tachycardia:
Ventricular rhythm disorders are divided into:
- Cause: acute MI, cardiomyopathy, chronic
- Premature ventricular complexes, IHD, particularly when it's associated with
ventricular tachycardia (monomorphic + a ventricular aneurysm or poor LV
polymorphic: Torsade’s de pointe), function.
ventricular fibrillation
- Can cause haemodynamic compromise or
degenerate into VF. Caused by abnormal
automaticity or by re-entry in scarred
1. V Ectopic beats (extrasystoles, premature ventricular tissue.
beats)
- S+S: palpitations or symptoms of low CO
- In sinus rhythms the QRS complexes are like dizziness, syncope, and dyspnea.
usually narrow because the ventricles are
activated rapidly and at the same time - Dx: ECG shows broad complex
via the His Purkinje system. tachycardia, abnormal QRS, >120/min.
- Complexes of ventricular ectopic beats o VT may be difficult to distinguish
are broad, premature, because ventricles from SVT with BBB or pre-
are activated one after the other rather excitation (WPW syndrome)
than simultaneously.
- Features in favour of VT diagnosis include
- Complexes can be unifocal which is history of MI, AV dissociation, capture/
identical beats arising from a single fusion beats, extreme left axis deviation,
ectopic focus or multifocal which is very broad QRS complexes >140ms, no
varying morphology with multiple foci. response to carotid sinus massage or IV
adenosine.
- Couplet or triplet are terms used to
describe a run of 2 or 3 ectopic beats
successively and ventricular “bigeminy”
is when you have a run of alternate sinus
and ectopic beats.
- Ectopic beats produce a low SV because
left ventricular contraction occurs before
filling is complete.
- Pulse is therefore irregular.
- S+S: Patients usually asymptomatic but - Tx: DC cardioversion is treatment of
may complain of an irregular beat, choice if systolic BP is <90mmHg.
missed beats or strong beats. – o IV amiodarone
prevalence increases with age
o IV lidocaine can be used but may
- Aetiology: coronary artery disease.
depress LV function causing
- Dx: Echo can tell us of any structural hypotension or acute HF.
heart issues, stress test to detect any o Beta blockers are effective at
underlying IHD. ECG
preventing VT by reducing
automaticity and by blocking
conduction in scar re-entry
circuits.
o Amiodarone can be added if
- Tx: B-blockers additional control is needed.
o VEBs common in HF patients. o Class Ic anti arrhythmic drugs
should not be used for prevention
o Also a feature of digoxin toxicity,
of VT in patients with IHD or HF
mitral valve prolapse, may occur
because they depress myocardial
as escape beats in presence of
underlying bradycardia.
 function and can be pro- - Ventricular fibrillation rarely reverses
arrhythmic. spontaneously.
o Pts at high risk of arrhythmic - Tx: The only effective treatment is
death can be given and implanted electrical defibrillation.
cardiac defibrillator- ICD.
o Basic and advanced cardiac life
support is needed.
3. Torsade’s de pointes: o If the attack of ventricular
fibrillation occurs during the first
- Form of polymorphic VT due to prolonged day or two of an acute MI, it is
ventricular repolarisation (prolonged QT probable that prophylactic
interval) therapy will be unnecessary.
- Cause: Twisting of the points” is usually o If it occurs w/o MI or severe
caused by medication (quinidine, metabolic disturbance -
disopyramide, sotalol, TCA), hypokalemia Implantable cardioverter-
or bradycardia especially after MI defibrillators (ICDs) are first-line
- Dx: ECG therapy in the management of
these pts

- Tx: Acute: Remove offending medication.

Shorten the QT interval with magnesium,
lidocaine, isoproterenol, or temporary
overdrive pacing
o Chronic: may need pacemaker/
ICD, amiodarone, beta-blockers

4. Ventricular fibrillation:
- This is very rapid and irregular
ventricular activation with no mechanical
effect.
- Cause: MI, severe metabolic disturbance
- S+S: Pt is pulseless and becomes rapidly
unconscious, and respiration ceases
(cardiac arrest).
- Dx: ECG shows shapeless, rapid
oscillations and there is no hint of
organized complexes

- It is usually provoked by a ventricular

ectopic beat.
26. Conduction disorders
- The conduction disturbance is classified
by severity into 3 categories:
o 1st degree heart block 2nd degree
HB: Morbitz type I (Wenckebach’s)
+ Morbitz type II - This occurs when some P waves conduct
o Complete or 3rd degree HB and others do not. – delay in AVN
- Mobitz I block (Wenckebach block
phenomenon) is progressive PR interval
1st degree HB: prolongation until a P wave fails to
conduct. The PR interval before the
- conduction time is prolonged but all
blocked P wave is much longer than the
impulses are conducted
PR interval after the blocked P wave.
- Every atrial impulse conducts to the
- Mobitz II block occurs when a dropped
ventricles and a regular ventricular rate
QRS complex is not preceded by
is produced
progressive PR interval prolongation.
- Prolonged PR interval > 0.20 second in
adults.
- Clinically important PR interval
prolongation can result from a
conduction delay in the AV node
- (ECG) (>200 msec in adults and >160
msec in young children) Usually the QRS complex is wide (>0.12
s). Occasional or repetitive sudden block
of conduction w/o prior measuring
lengthening of conduction time. The PR
interval remains constant before the
blocked P wave – involves block of HIS
- Cause: Acute MI may produce 2nd degree
block, drugs (e.g. digitalis, B-blockers, Ca
channel blockers) – effect AVN,
- May occur in healthy people infiltrative myocardial diseases:
sarcoidosis, myxedema, endocarditis,
- If the QRS width is normal then the block
hemochromatosis
is at the AV node, if the QRS shows
aberration (right (RBBB) or left bundle - S+S: 2nd degree HB usually asymptomatic,
branch block (LBBB)), then the block may in some pts there’s sensed irregularities
be at the AV node or the His–Purkinje of heart beat, syncope may occur
system.
- Cause of AV block: myocarditis, SLE, RA,
cardiomyopathies, congenital heart 3rd degree
block, MI, Drug (B-blockers, digitalis, Ca AV block
channel blockers) -Complete
heart block occurs when all atrial activity
fails to conduct to the ventricles
2nd degree HB:
Congenital CHB
- denotes

occasional or repetitive block of

conduction or impulse of an impulse Acquired CHB
 This is due to disease in the His–Purkinje system
causing a QRS > 120 ms.
- Common causes are conduction system
fibrosis (aging), IHD, hypertension,
cardiomyopathies, cardiac surgery,
infiltrative diseases (e.g. amyloid).

1. LBBB: often signifies important

underlying heart disease – LBB divided
into ant + post fascicle
a. LV depolarization is delayed,
-In
giving a wide QRS, large notched
this
R waves in leads I and V 6 , and a
deep S wave (may be preceded by
small R wave) in V 1 .
b. Block confined to the anterior or
posterior fascicles of the left
bundle gives left-axis or right-axis
deviation respectively on the ECG.
c. BBB leads to asynchronous
situation life is maintained by a contraction of the left and right
spontaneous escape rhythm. ventricle, which reduces cardiac
- Narrow complex escape rhythm (<0.12 s output, important in heart failure.
QRS complex) implies that it originates in 2. RBBB: can occur in healthy people
the His bundle and therefore that the
region of block lies more proximally in a. RV depolarization is delayed,
the AV node. giving wide QRS, an RSR pattern in
V 1, and a slurred S wave in I and
- The escape rhythm occurs with an V 6.
adequate rate (50–60 b.p.m.) and is
relatively reliable. b. This can be a normal variant but
more commonly as a result of
- S+S: fatigue, dizziness, light-headedness, causes listed above and, in
pre-syncope, and syncope most addition, ASD, pulmonary
commonly. Syncopal episodes due to slow embolism (PE), cor pulmonale.
heart rates are called Morgagni-Adams-
Stokes (MAS) episodes.
Tx of HB: - Bifasicular block = RBBB + left anterior
hemiblock (left-axis deviation on ECG)
- Acute inferior MI complicated by AV block
– if pt well no tx required - RBBB + left posterior hemiblock (right-
axis deviation on ECG), or LBBB.
- Symptomatic tx 2nd or 3rd degree block:
atropine (0.6mg i.v.) - All of these may progress to complete AV
block.
o If it fails temp pace maker
- Trifasicular block = bifasicular block +
o In most cases AV block resolves 1st-degree AV block.
within 7-10 days
RBBB
- If pt presents with asystole: i.v. atropine
3mg or i.v. isoprenline 2mg in 500ml 5%
dextrose, infused 10-60mL
- Permanent pacemaker for Morbitz type II
or 3rd degree block
Bundle branch blocks:
Bifascular block

Tx: pacemakers

LBBB

CF of BBB:
- BBB are usually asymptomatic.
- RBBB causes wide but physiological
splitting of the second heart sound.
- LBBB may cause reverse splitting of the
2nd sound.
- Pts with intraventricular conduction
disturbances may complain of syncope.
o This is due to intermittent
complete heart block or to
ventricular tachyarrhythmias.
- ECG monitoring and electrophysiological
studies are needed to determine the
cause of syncope in these patients.
 27. Chronic HF: aetiology, pathogenesis, - Also decreased respiratory function and
circulatory disturbances, classification renal function
- Chronic heart failure develops or 3. Precipitating factors unmask the
progresses slowly. subsequent reduced cardiac reserve, e.g.
arrhythmia, infarction, AF, infection,
- Venous congestion is common but arterial thyroid disease, anaemia, PE, COPD -
pressure is well maintained until very hypoxia, DRUGS, etc.
late.
4. Decreased perfusion due to decreased
pump action - ↓kidney perfusion -
Chronic HF sometimes associated with weight ↑renin/aldosterone - ↑blood volume to
loss - cardiac cachexia, caused by a combo of try and increase pre-load and push heart
anorexia and impaired absorption due to GI up the starling curve (however, they’re
congestion, poor tissue perfusion due to a low often into negative marginal gain from
CO and skeletal muscle atrophy due to increased volume). However, ↑ BP also
immobility. raises after-load and increases work of
the heart - ↑ischaemia
5. Cardiac dysfunction due to:
RF: Coronary disease, smoking, hypertension,
physical inactivity, male sex, obesity, diabetes, - Disruption of circulatory system
valvular heart disease
- Disorders of conduction
- Lesion preventing valve opening
Aetiology/pathogenesis:
- Pump failure (contraction/dilation) - ↓SV
1. Age associated changes: (stroke volume) and ↑EDV (end-diastolic
- Reduction in B-adrenergic responsiveness volume) - ↓CO (cardiac output)
– low inotropic response and low
6. Beriberi = heart failure due to deficiency
vasodilation
of Vitamin B1 (Thiamine): bradycardia,
- Increased arterial stiffness - low premature ventricular beats, VF
compliance – increase afterload (ventricular fibrillation), AF (atrial
fibrillation), and heart block
- Alterations in cardiac filling: increase
connective tissue content of myocardium
- stiffer ventricle - filling more
Circulatory disturbances:
dependent on atrial contraction -
increase pressure and size of left atrium - - Stroke volume = End-diastolic vol (filling
predisposes to AF (further filling pressure) x Ejection fraction (myocardial
problems) contractility)
- Failure of reserve capacity of - CO = SV x HR
mitochondria

2. Age associated diseases:

- Hypertension - risk factor for
atherosclerosis, and increase size and
stiffness of left ventricle. By the time
they have heart failure, may no longer
have hypertension as they can’t sustain
the cardiac output necessary to be
hypertensive
- Coronary artery disease: IHD accounts for
70% of pts with HF in the developed
world
 - Compensatory mechanism: 3. Pathophysiological classification: Acute/
Chronic HF, L or RV HF, Systolic or
1. Frank Starling law of heart - > increase vent. Diastolic
End diastolic volume (preload) ! ↑CO!
improve ejection - Diastolic and systolic dysfunction:
2. Neurohormonal balance HF can develop because of
- Sympathetic adrenergic - ↑ vent. impaired myocardial contraction
Force! ↑CO! spasm of perip. but also because of impaired
arteries! support perip. circ. Include ventricular filling and high filling
capillaries (depend on P gradient btw pressures caused by abnormal
arteries n venous system ventricular relaxation- stiff non-
- RAAS – #angiotensin II ! compliant ventricle, especially in
vasoconstrictor! ↑perip. Resistant patients with coronary artery
#aldostrone!prevent dehydration, V
disease.
of blood ↑! ↑venous return to heart
- Vasopressin!↓ diuresis, water
retention!↑venous return!↑CO

Classification of HF:
1. Symptoms alone can be used to classify
severity of CHF however the New York
Heart Association (NYHA) classification is
widely used

2. Stages of HF: - classification system

places emphasis on progressive nature of
HF (American College of Cardiology) – dx
can be made when multiples signs of ACC

are present
28. Chronic HF: differential diagnosis, clinical - Monitor U&E and add K+-sparing diuretic
features, treatment (e.g. spironolactone) if K+ <3.2mmol/L,
predisposition to arrhythmias, concurrent
digoxin therapy (low K+ increases risk of
Differential dx: digoxin toxicity), or pre-existing K+-losing
conditions.
- Must be able to prove the heart is the
problem - If refractory oedema, consider adding a
thiazide, e.g. metolazone 5–20mg/24h
- Otherwise consider: PO.
o Renal failure (e.g. nephritic
syndrome) - oedema
2. ACE-i: Consider in all those with left
o Liver disease or malnutrition – ventricular systolic dysfunction; improves
decreased albumin - oedema symptoms and prolongs life.
- Drug-induced ankle swelling - If cough is a problem, an angiotensin
(dihydropyridine ca blockers), drug- receptor blocker (ARB) may be
induced fluid retention (e.g. NSAID’s), substituted (e.g. candesartan 4mg/d;
hypoalbuminaemia, thyroid disease, max 32mg PO). SE: high K+.
severe anaemia, bilateral renal artery
stenosis 3. B-blockers (e.g. carvedilol) decrease
mortality in heart failure.
Clinical features: - These benefits appear to be additional to
those of ACE-i in patients with heart
- Low CO causes fatigue, listlessness and a
failure due to LV dysfunction.
poor effort tolerance, cold peripheries,
low BP. - Initiate after diuretic and ACE-i. Use with
caution: “start low and go slow”; (e.g.
- Fatigue and weakness because blood
carvedilol 3.125mg/12h - 25–50mg/12h);
diverted away from skeletal muscle.
wait ≥2weeks between each dose
- Hypotension, palpitations (tachycardia), increment.
chest pain
- Low mortality risk and improved tx rates.

Tx: 4. Spironolactone: Spironolactone (25mg/

24h PO) decrease mortality by 30% when
- Stop smoking. Eat less salt. Optimize addedto conventional therapy.
weight & nutrition.
5. Digoxin helps symptoms even in those
- Treat the cause (e.g. if dysrhythmias; with sinus rhythm
valve disease).
- Dose example: 125µg/24h PO if sinus
- Treat exacerbating factors (anaemia, rhythm.
thyroid disease, infection, high BP).
- Monitor U&E; maintain K+ at 4–5mmol/L.
- Avoid exacerbating factors, e.g. NSAIDS Digoxin levels
(fluid retention) and verapamil (–ve
inotrope). 6. Vasodilators: The combination of
hydralazine (SE: drug-induced lupus) and
isosorbide dinitrate should be used if
Drugs: intolerant of ACE-i and ARBS (angiotensin
receptor blockers) as it reduces
1. Diuretics: Diuretics can reduce the risk of mortality. It also reduces mortality when
death and worsening heart failure. added to standard therapy (including
ACE-i) in Black pts with heart failure.
- Give loop diuretics to relieve symptoms,
e.g. furosemide 40mg/24h PO or
bumetanide 1–2mg/24h PO. Increase dose
as necessary. SE (side effects): K+
decreased, renal impairment.
 29. Chronic cor pulmonale
Enlargement of right ventricle due to increase in
afterload which can be caused by diseases of the
thorax, lung or pulmonary circulation but it does
not always associate with right sided heart
failure

Aetiology:

-Symptoms
include dyspnoea, fatigue, and syncope.
- Signs: cyanosis; tachycardia; raised JVP
with prominent a and v waves; RV heave;
loud P2, pansystolic murmur (tricuspid
regurgitation); early diastolic Graham
Pathophysiology: Steell murmur; hepatomegaly and
oedema.
- The mechanism may vary but COPD can
be used to illustrate them all
- There is an increase in pulmonary Dx:
vascular resistance which leads to
pulmonary hypertension. - FBC: Hb and haematocrit high (secondary
polycythaemia). ABG: hypoxia, with or
- Initially this occurs in acute Respiratory without hypercapnia.
infection but with time the pulmonary
hypertension becomes persistent and - CXR: enlarged right atrium and ventricle,
worsens with time. prominent pulmonary arteries.

- The Pulmonary hypertension causes the - ECG: P pulmonale; right axis deviation;
vascular bed to be obliterated due to right ventricular hypertrophy/strain.
muscular hypertrophy of the arterioles
and thrombus formation
- All of the above causes an increase in
afterload as the right side of the heart
has to pump against a higher pressure;
the hypoxia that develops, further
worsens right ventricular function and
eventually the left ventricle will be
affected

S+S:
Tx:
- Treat underlying cause— e.g. COPD and
pulmonary infections.
- Treat respiratory failure—in the acute
situation give 24% oxygen if PaO2 <8kPa.
- Monitor ABG and gradually increase
oxygen concentration if PaCO2 is stable.
- In COPD patients, long-term oxygen
therapy (LTOT) for 15h/d increases
survival (p176).
- Patients with chronic hypoxia when
clinically stable should be assessed for
LTOT.
- Treat cardiac failure with diuretics such
as furosemide, e.g. 40–160mg/24h PO.
- Monitor U&E and give amiloride or
potassium supplements if necessary.
- Alternative: spironolactone.
- Consider venesection if haematocrit
>55%.
- Consider heart–lung transplantation in
young pts.

Prognosis:
- Poor 50% die within 5yrs.
 30. Acute aortic dissection - Factors that may predispose aortic
dissection:
A breach in the integrity of the aortic wall allows
arterial blood to enter the media, which is then o Hypertension (in 80%), aortic
split into two layers, creating a ‘false lumen’ atherosclerosis, aortic
alongside the existing or ‘true lumen’ coarctation, fibromuscular
dysplasia, previous aortic surgery,
trauma, iatrogenic (e.g. cardiac
catheterisation)

Pathogenesis:
- Aortic dissection usually begins with a
tear in the intima.
Classification:
- - Blood penetrates the diseased medial
Aortic dissection can be classified
according to the timing of diagnosis from layer and then cleaves the intimal
the origin of symptoms: acute <2 weeks, laminal plain leading to dissection.
subacute 2–8 weeks, chronic >8 weeks - IMH (intramural haematoma) is
with mortality and extension decreasing considered a precursor of dissection in
with time. which there is rupture of the vasa
- They can also be classified anatomically: vasorum in the aortic media with aortic
wall infarction.
o Type A: involving the aortic arch
- IMH is typically in the descending
and aortic valve proximal to the
left subclavian artery origin. thoracic aorta.
Includes De-Bakey type I (extends - Deep penetrating aortic plaques may lead
to the abdominal aorta) and De- to IMH, dissection or ulceration/
Bakey type II (localized to perforation.
ascending aorta)
- Aortic dissection is predisposed in
o Type B: involving the descending patients with autoimmune rheumatic
thoracic aorta distal to the left disorders and Marfan’s and Ehlers–Danlos
subclavian artery origin. De Bakey syndromes.
type III
S+S:
- Symptoms: sudden onset of severe +
central chest pain often that radiates to
the back and down the arms, mimicking
MI.
o The pain is often described as
tearing in nature and may be
migratory.
- Signs: Pts may be shocked + may have
neurological symptoms secondary to loss
of blood supply to the spinal cord.
o Develop aortic regurgitation,
coronary ischaemia + cardiac
tamponade. Distal extension may
produce acute kidney failure,
acute lower limb ischaemia or
Aetiology: visceral ischaemia.

- Aortic disease and hypertension are the

o Peripheral pulses may be absent.
most important aetiological factors Dx:
 - The mediastinum may be widened on
chest X-ray
- CT scan, transoesophageal
echocardiography or MRI will confirm dx

Tx:
- At least 50% of patients are hypertensive
thus urgent antihypertensive meds to
reduced bp <120 mmHg with i.v. B-
blockers (labetalol, metoprolol) and
vasodilators (GTN).
- Type A dissections: surgery (arch
replacement) – higher mortality 50%
within 2 weeks
o Type B: 89% at survival at 1 month
- Endovascular intervention with stents
may be indicated in pts with rapidly
expanding dissections (>1 cm/year),
critical diameter (>5.5 cm), refractory
pain or malperfusion syndrome, blunt
chest trauma, penetrating aortic ulcers
or IMH.
- Pts will require long-term follow-up with
CT or MRI.
 31. Inflammatory joint diseases – Rheumatoid - This leads to damage to Endothelium,
Arthritis synovial fibroblasts, bone cells and
chondrocytes
- Rheumatoid arthritis is an autoimmune
disease associated with autoantibodies to - Which results in swelling, congestion of
the Fc portion of immunoglobulin G synovial membrane and destruction of
(rheumatoid factor) and to citrullinated bone, cartilage and soft tissues
cyclic peptide.
- TNF-a is particularly important as it
- There is persistent synovitis, causing trigger production of other cytokines.
chronic symmetrical polyarthritis and
systemic inflammation. -Other damaging
agents include IL
- Genetic studies suggest that RA is a (interleukins) , MMP (
heterogeneous group of diseases. matrix
metalloproteinases),
- Before the modern drug era it was PGE and VEGF
rapidly disabling for most patients. ( vascular endothelial
growth factor)

Epidemiology: - Granulation tissue forms over and under

articular cartilage which gets eroded and
- Prevalence is ~1% (high in smokers). F: M destroyed this then triggers fibrous or
>2:1. Peak onset: 5th–6th decade. HLA bony ankylosis.
DR4/DR1 linked (associated with
increased severity). - Muscles surrounding those inflamed joints
may also be infiltrated and undergo
atrophy
Aetiology + pathogenesis: - Rheumatoid nodules
= central area of
The cause is multifactorial and genetic and
fibrinoid material
environmental factors play a part.
surround by
- More prevalent in women, genetic factors proliferating
account for 60% of RA mononuclear cells.

- Smoking is an environmental risk factor

for seropositive
- RA, possibly by
activation of the innate
immune system.
- It is thought that RA is
triggered by a specific
pathogen in a
genetically susceptible
pt
- The disease is caused by
infiltration of the S+S:
synovial membrane with
lymphocytes, plasma -Early (inflammation, no
cells and macrophages. joint damage): swollen
MCP, PIP, wrist, or MTP
- CD4+ T cells interact joints (often symmetrical).
with other cells in
synovium -Look for tenosynovitis or
bursitis.
- Activated T cells cause B cells to release
IGs including RF (rheumatoid - Later (joint damage, deformity): ulnar
factor=autoantibody) and also stimulate deviation of the fingers and dorsal wrist
macrophages to produce a range of subluxation.
inflammatory cytokines.
 o Boutonniere and swan-neck
deformities of fingers or Z-
deformity of thumbs occur. Tx:

o Hand extensor tendons may - Disease-modifying antirheumatic drugs

rupture. Foot changes are similar. (DMARDS) are 1st-line for treating RA and
should ideally be started within 3 months
o Larger joints can be involved. of persistent symptoms
o Atlanto-axial joint subluxation o Take 6–12 weeks for benefit.
may threaten the spinal cord
(rare).
o Combination of methotrexate,
sulfasalazine and
- Extra-articular Nodules—elbows & lungs; hydroxychloroquine.
lymphadenopathy; vasculitis; fibrosing
alveolitis, obliterative bronchiolitis;
o Pleural & pericardial effusion;
Raynaud’s; carpal tunnel
syndrome; peripheral neuropathy;
o Splenomegaly (seen in 5%; only 1%
have Felty’s syndrome: RA +
splenomegaly + neutropenia,
scleritis, amyloidosis, pericarditis,
myocarditis
Dx:
- Rheumatoid factor (RhF) is positive in
~70%
- A high titre is associated with severe
disease, erosions and extra-articular
disease.
- Anticyclic citrullinated peptide
antibodies (ACPA/anti-CCP) are highly
specific (~98%) for RA.
- There is often anaemia of chronic
disease. Inflammation causes increase
platelets, increase ESR, and increase CRP.
- X-rays show soft tissue swelling, juxta-
articular osteopenia and decreased joint
space.
- Later there may be bony erosions,
subluxation or complete carpal
destruction
- Ultrasound and MRI can identify synovitis
more accurately, and have greater
sensitivity in detecting bone erosions -
than conventional X-rays. Steroids rapidly reduce symptoms and
inflammation.
o They are useful for treating acute
exacerbations “flares”
o E.g. IM depot methylprednisolone
80–120mg.
o Intra-articular steroids have a
rapid but short-term effect
 o Oral steroids (e.g. prednisolone
7.5mg/d) may control difficult
symptoms, but side-effects
preclude routine long-term use.
- NSAIDS are good for symptom relief, but
have no effect on disease progression.
- Physio- and occupational therapy, e.g. for
aids and splints.
- Surgery may relieve pain, improve
function and prevent deformity.
 32. Inflammatory joint diseases – Juvenile - Uveitis (often with a positive ANA) occurs
rheumatoid arthritis and requires regular screening by slit-
lamp examination.
Referred to as Juvenile Idiopathic Arthritis is a
type of arthritis that causes joint inflammation - Blindness can occur if it is untreated.
and stiffness for more than six weeks in
- Prognosis is generally good, with
remission occurring eventually in most
patients.
1. Systemic onset JIA
- Still’s disease (which accounts for 10% of
cases of JIA) - Oligoarthritis (extended): In
approximately 25% of patients,
- Affects boys and girls equally up to 5 oligoarthritis extends to affect many
years of age; then girls are more more joints after around 6 months.
commonly affected.
o This form of arthritis can be very
- Adult-onset Still’s disease is extremely destructive.
rare.
CF:
- High (>39°) fever with an evanescent 3. Polyarthritis JIA
pink maculopapular rash and arthralgia,
arthritis, myalgia and generalized - The rheumatoid factor-positive form
lymphadenopathy. (usually also ACPA positive) occurs in
older girls, usually over 8 years.
- Hepatosplenomegaly, pericarditis and
pleurisy occur. - It is a systemic disease; the arthritis
commonly involves the small joints of the
Differential diagnoses: hands, wrists, ankles and feet initially,
and eventually larger joints.
- Malignancy, in particular leukaemia and
neuroblastoma, and infection. - It can be a very destructive arthritis and
needs aggressive treatment.
Dx:
- The rheumatoid factor-negative form is
- Laboratory tests show a high ESR and CRP,
commoner.
neutrophilia and thrombocytosis.
- It usually affects girls under 12 years but
- Autoantibodies are negative.
can occur at any age.
- Macrophage activation syndrome (an
- The arthritis is often asymmetrical, with
excessive proliferation of T cells and
a distribution similar to that seen in the
macrophages) is a rare but potentially
RF-positive form.
fatal complication.
- It may also affect the cervical spine,
- It can follow infection (often viral) or a
temporomandibular joints and elbows.
change in medication.
- Patients may be ANA positive, with a risk
2. Oligoarthritis (persistent) of chronic uveitis.

- Most common form of JIA (50–60%) but is - All children must have regular
still a relatively uncommon condition. ophthalmologic examination.

- It affects, by definition, four or fewer

joints, especially knees, ankles and 4. Enthesitis-related arthritis
wrists, often in an asymmetrical pattern.
- This affects teenage and younger boys
- It affects mainly girls, with a peak age of mainly, producing an asymmetrical
3 years. arthritis of lower-limb joints and
- The prognosis is generally good with most enthesitis.
going into remission. - It is associated with HLA-B27 and a risk of
CF: iritis.
 - It is the childhood equivalent of adult - NSAIDs reduce
ankylosing spondylitis but spinal pain and stiffness
involvement is rare in childhood. but disease-
modifying agents
- Approximately one in three develops such as
spinal disease in adulthood. methotrexate are
used to control
moderate and
5. Psoriatic arthritis severe disease.
- This occurs in children and is similar in - Corticosteroids
pattern to the adult form. are often
required in
- The arthritis can be very destructive.
systemic disease:
- Psoriasis may develop long after the intravenous
arthritis but is found commonly in a first- pulsed
degree relative.

Dx of JIA: methylprednisolone is used, followed by

methotrexate (10–15 mg/m2) weekly to
- Blood tests: ESR, C-reactive protein, Anti- control disease and prevent growth
nuclear ab, Rheumatoid factor, cyclic suppression.
citrullinated peptide
- Cytokine modulators are used if
- Imaging: X-ray, MRI methotrexate fails, and are highly
effective in all types except systemic-
onset JIA where the results are variable.
- Etanercept and adalimumab are the
commonest drugs used but anakinra,
tocilizumab and abatacept are being used
in systemic onset JIA.
o Anakinra, an IL-1β receptor
antagonist, helps in
methotrexate-resistant systemic
onset disease
- Sulfasalazine is used only in enthesitis-
related JIA.

Tx of JIA:
- Early recognition and aggressive
treatment prevents joint damage and
allows normal growth and development.
- There is no cure but clinical remission is
an achievable goal.
 33. Ankylosing Spondylitis aka Bechterew’s - Sacroiliitis is the earliest X-ray feature,
disease but may appear late: look for
irregularities, erosions, or sclerosis
- Ankylosing spondylitis (AS) is a chronic affecting the lower half of the sacroiliac
inflammatory disease of the spine and joints, especially the iliac side. Vertebral
sacroiliac joints, of unknown aetiology. syndesmophytes are characteristic (often
- Prevalence: 0.25–1%. Men present earlier: T11–L1 initially): bony proliferations due
M: F ≈ 6:1 at 16yrs old, and ~2:1 at 30yrs to enthesitis between ligaments and
old. ~90% are HLA B27 +ve. vertebrae.
- These fuse with the vertebral body
above, causing ankylosis.
S+S:
- In later stages, calcification of ligaments
- The typical patient is a man <30yrs old with ankylosis lead to a “bamboo spine”
with gradual onset of low back pain, appearance.
worse at night, with spinal morning stiff
ness relieved by exercise. - FBC (normocytic anaemia), high ESR, high
CRP (C - reactive protein), HLA B27+ve
- Pain radiates from sacroiliac joints to (not diagnostic).
hips/buttocks, and usually improves
towards the end of the day.
- There is progressive loss of spinal Tx:
movement (all directions)—hence - Exercise, not rest, for backache,
decreased thoracic expansion. including intense exercise regimens to
- The disease course is variable; a few maintain posture and mobility—ideally
progress to kyphosis, neck with a physiotherapist specializing in AS.
hyperextension and spino-cranial - NSAIDS (e.g. ibuprofen or naproxen)
ankylosis. usually relieve symptoms within 48h, and
- Other features include enthesitis, they may slow radiographic progression.
especially Achilles tendonitis, plantar - TNF α blockers Etanercept, adalimumab
fasciitis, at the tibial and ischial and golimumab are indicated in severe
tuberosities, and at the iliac crests. active AS if NSAIDS fail
- Anterior mechanical chest pain due to - Local steroid injections provide
costochondritis and fatigue may feature. temporary relief.
- Acute iritis occurs in ~⅓ of patients and - Surgery includes hip replacement to
may lead to blindness if untreated improve pain and mobility if the hips are
- AS is also associated with osteoporosis involved, and rarely spinal osteotomy.
(up to 60%), aortic valve incompetence - There is increased risk of osteoporotic
(<3%) and pulmonary apical fibrosis. spinal fractures (consider
bisphosphonates).

Prognosis:
- There is not always a clear relationship
between the activity of arthritis and
severity of underlying inflammation (as
for all the spondyloarthritides).
- Prognosis is worse if ESR >30; onset
<16yrs; early hip involvement or poor
response to NSAIDS.
Dx:
- Diagnosis is clinical, supported by
imaging (MRI is most sensitive and better
at detecting early disease).
 34. Crystal arthropathies – Gout Causes
- Gout is a true crystal deposition disease, - Hereditary, increase dietary purines,
and is defined as the pathological alcohol excess, diuretics, leukaemia,
reaction of the joint or periarticular cytotoxics (tumour lysis).
tissues to the presence of monosodium
urate monohydrate (MSU) crystals. - Associations: Cardiovascular disease,
hypertension, diabetes mellitus and
- Gout typically presents with an acute chronic renal failure.
monoarthropathy with severe joint
inflammation - Gout is a marker for these, therefore
seek out and treat if needed.
- >50% occur at the metatarsophalangeal
joint of the big toe (podagra). Dx:

- Other common joints are the ankle, foot, - Polarized light microscopy of synovial
small joints of the hand, wrist, elbow or fluid shows negatively birefringent urate
knee. crystals.

- It can be polyarticular. It is caused by - Serum urate is usually raised but may be

deposition of monosodium urate crystals normal.
in and near joints, precipitated, for - Radiographs show only soft-tissue
example, by trauma, surgery, starvation, swelling in the early stages.
infection or diuretics.
o Later, well-defined “punched out”
- It is associated with raised plasma urate. erosions are seen in juxta-
In the long term, urate deposits (= tophi, articular bone.
e.g. in pinna, tendons, joints) and renal
disease (stones, interstitial nephritis) - There is no sclerotic reaction, and joint
may occur. spaces are preserved until late.

- Prevalence: ~1%. M: F ≈ 4:1. Tx:

- Acute gout: presents - Acute gout: Use high-dose NSAID or coxib

typically in a middle- (e.g. etoricoxib 120mg/24h PO).
aged male with
- Symptoms should subside in 3–5d.
sudden onset of
agonizing pain, - If CI (e.g. peptic ulcer; heart failure;
swelling and redness anticoagulation), colchicine (0.5mg/6–
of the first MTP joint. 12h PO) is effective but slower to work
- Chronic gout: Large - NB: in renal impairment, NSAIDS and
MSU crystal deposits colchicine are problematic.
produce irregular firm
nodules (‘tophi’) - Steroids (oral, IM or intra-articular) may
around extensor also be used.
surfaces of fingers, - Rest and elevate the affected joint.
hands, forearm,
elbows, Achilles - Ice packs and “bed cages” can be
tendons and effective.
sometimes the
helix of the ear.
Prevention:

Differential diagnoses: - Lose weight. Avoid prolonged fasts,

Exclude septic arthritis in alcohol excess, purine-rich meats and
any acute low-dose aspirin (increase serum urate).
monoarthropathy. Then - Prophylaxis: Start if >1 attack in 12
consider haemarthrosis, months, tophi or renal stones.
CPPD and palindromic RA.
- The aim is to decrease attacks and
prevent damage caused by crystal
deposition.
- Pts to use allopurinol and titrate from
100mg/24h, increasing every 2 weeks
until plasma urate <0.3mmol/L (max

300mg/8h).
35. Reactive arthropathies – Reiter’s syndrome - Other extra articular changes include:

- Reactive Arthritis is commonly seen in o Balanitis of the penis; often

young men with a ratio of 15:1 and is the painless and can escape unnoticed
most common cause of inflammatory
o Keratoderma blennorrhagica
arthritis in men aged 16-35
usually occurring on palms and
- 1-2 percent of all patients complaining of soles but also scrotum, scalp and
non-specific urethritis have reactive trunk resembling psoriasis.
arthritis.
o Nail dystrophy, Mouth ulcers may
- When shigella dysentery becomes also be seen as red painless
epidemic in a region 20 % of HLA B 27 patches on tongue, palate, buccal
positive men acquire this disease. mucosa and lips.

Clinical findings o Conjunctivitis may accompany the

first acute episode.
Classical triad of
Reiter’s disease
1. Non-specific
urethritis
- Other rare complications are: heart
2. Conjunctivitis defects such as aortic incompetence,
conduction defects, pleuro-pericarditis,
3. Reactive peripheral neuropathy, seizures and
arthritis meningoencephalitis

Dx:
- Reiter’s cells are giant macrophages that
- Incomplete forms with one or two of the can be detected in the synovial fluid
aforementioned points, is more frequent - Body fluid assessments: EST AND CRP may
than the full syndrome be raised
- It is caused by bacterial dysentery - RF, CCP and ANA are negative ( explains
o Salmonella, shigella, their inclusion in seronegative group)
campylobacter or Yersinia or - Imaging techniques findings
Sexually acquired chlamydia
infection - X-rays may show some skeletal
abnormalities but usually only in chronic
- The first attack is usually self-limiting cases
with spontaneous remission within 2-4
months but chronic arthritis develops in 6 - Periostitis is characteristic especially in
the foot but also in pelvis
- DD in contract to AS the sacroiliitis is
- A common presentation is characterised unilateral, asymmetrical &
by: syndesmophytes are coarse and non-
- asymmetrical lower limb oligoarthritis marginal as they extend beyond the
typically knees, ankles, and feet (mid contours of the annulus unlike in AS
tarsal joints , metatarsophalangeal joint, - X- ray changes in peripheral joints and
Achilles tendinitis or plantar fasciitis ) spine are identical to those in psoriasis
- Fever and weight loss also occurs
- Low back pain and stiffness is not as Tx:
striking as in AS but present in 15-20 % of
patients with reactive arthritis - Anterior uveitis is an emergency and
needs to be treated with topical,
subconjunctival and systemic
corticosteroids
- NSAID and analgesics against
inflammation and pain
- Limited rest
- Injection of corticosteroid in synovium in
severe synovitis
- Tetracyclines are used to treat
chlamydial urethritis.
- DMARDs : when symptoms are persistent,
arthritis is recurrent if blennorrhagica is
present
 36. Connective Tissue diseases – Lupus 20%), autoimmune thyroid disease (5–
erythematoides 10%).
- SLE is an inflammatory, multisystem Dx: 3 best tests:
autoimmune disorder
1. Anti-dsDNA antibody titres.
- Immunopathology results in polyclonal B-
cell secretion of pathogenic auto anti 2. Complement: C3 low, C4 low (denotes
bodies causing tissue damage via multiple consumption of complement, hence C3
mechanisms including immune complex and C4 low, and C3d and C4d high, their
formation and deposition, complement degradation products).
activation and other direct effects. 3. ESR.
Prevalence: - BP, urine for casts or protein (lupus
- ~0.2%. F: M≈9:1, typically women of nephritis, below), FBC, U&E, LFTs,
child-bearing age. CRP (usually normal)

- Commoner in African-Caribbeans, Asians,

o high ESR + normal CRP = SLE
and if HLA B8, DR2 or DR3 +ve. o If high CRP = infection, serositis or
- ~10% of relatives may be affected. It may arthritis. Skin or renal biopsies
be triggered by EBV may be diagnostic.

Clinical features: - Dx SLE if 4/11 criteria present:

- It is a remitting and relapsing illness

o Malar rash (butterfly rash); discoid
rash, photosensitivity, oral ulcers,
- Immunology >95% are ANA +ve. non-erosive arthritis, serositis,
renal, CNS, haematological or
- ENA may be +ve in 20–30% (anti-Ro, anti- immunological disorder,
La, anti-Sm, anti-RNP); 40% are RhF +ve; antinuclear ab (ANA): +ve in 95%
antiphospholipid antibodies
(anticardiolipin or lupus anticoagulant)

Drug-
induced lupus:
- Causes (>50 drugs) include isoniazid,
hydralazine (if >50mg/24h in slow
acetylators), procainamide, quinidine,
chlorpromazine, minocycline, phenytoin.
- It is associated with antihistone
antibodies in ~100%.
- Skin and lung signs prevail (renal and CNS
are rarely affected).
- The disease remits if the drug is stopped.
- Sulfonamides or the oral contraceptive
pill may worsen idiopathic SLE.
Tx:

may also be +ve. - Severe flares: Acute SLE requires urgent

IV cyclophosphamide + high-dose
- SLE may be associated with other prednisolone.
autoimmune conditions: Sjogren’s (15–
- Cutaneous symptoms: treat rashes with
topical steroids.
- Prevent rashes with high-factor sunblock
creams. Sun exposure may also trigger
acute systemic flares.
- Maintenance: use NSAIDS and
hydroxychloroquine for joint and skin
symptoms.
- Low-dose steroids may be of value in
chronic disease. Azathioprine,
methotrexate and mycophenolate are
used as steroid-sparing agents.
- Lupus nephritis: (p314) May require more
intensive immunosuppression with
steroids and cyclophosphamide or
mycophenolate. NB: immunosuppressed
patients
- BP control is vital: ACE-i, α-blockers (e.g.
doxazosin) or Ca2+-channel blockers (e.g.
nifedipine).
 37. Connective Tissue diseases – Systemic - Intimal proliferation + vessel wall
sclerosis / Sclerodermia inflammation lead to arterial + arteriolar
narrowing
- Systemic sclerosis, or scleroderma, is a
generalised disorder of connective tissue - The following injury caused to the
affecting the skin, internal organs and endothelium triggers platelet activation
vasculature. and vasoconstriction leading to worsening
of the Ischaemia thereby worsening the
- It is characterised by sclerodactyly in fibrotic process
combination with Raynaud’s and digital
ischaemia CF:

- The peak age of onset is in the 4th and 5th

decades, and overall prevalence is 10–20
per 100 000, with a 4 : 1 female
preponderance.
- It is subdivided into diffuse cutaneous
systemic sclerosis (DCSS: 30% of cases)
and limited cutaneous systemic sclerosis
(LCSS: 70% of cases).
- Many patients with LCSS have features
that are phenotypically grouped into the
‘CREST’ syndrome (Calcinosis, Raynaud’s,
oEsophageal involvement, Sclerodactyly
and Telangiectasia).
- The prognosis in DCSS is poor, with a 5-
year survival of approximately 70%.
Pathophysiology:
- Cause of systemic sclerosis is poorly
understood
- It has a genetic component + associated
with certain alleles at the HLA locus
- However, there is a clear immunological
dysfunction as T lymphocytes infiltrate
the skin + there is an abnormal activation
of fibroblasts which causes excessive
production of extracellular matrix
especially type 1 collagen
- This causes the sclerodactyly which is
presented as thickened, tightened +
indurated lesions of the skin
 - Analgesics: if Joint pain is present

Dx:
- Blood tests
- The following are elevated:
o ESR, IgG, ANA positive (70%) and
topoisomerase 1 antibodies in 30
% of DCSS patients
o 60 % of patients with CREST
syndrome have anticentromere
antibodies
- U&E: urea + creatinine rise in kidney
injury
- Imaging:
o CXR: exclude other pathology, for
changes in cardiac size +
established lung disease
o Hands: deposits of Ca around
fingers
o Barium swallow: confirms
impaired oesophageal motility
o High resolution CT: demonstrate
fibrotic lung involvement
Tx:
- No tx against main cause - the fibrotic
changes caused in this disease
- However the organs can be targeted:
- Digital ulcers + Raynaud’s syndrome:
avoid cold exposure, use heated gloves +
ca antagonists or angiotensin 2 receptor
blockers
- Treatment of infection in ulcerated
lesions.
- Oesophageal reflux: PPIs + anti reflux
agents+ antibiotics if bacterial
overgrowth occurs
- Hypertension: ACE inhibitors even if renal
damage is present
- Pulmonary HP: endothelin 1 antagonist,
bosentan and even transplantation
- Corticosteroid are used people with
myositis and alveolitis
 38. Connective Tissue diseases –
Dermatomyositis and Polymyositis
- Polymyositis is characterised by an
inflammatory process affecting skeletal
muscle.
- Dermatomyositis describes the same
disease but with skin involvement.
- They are rare, with an incidence of 2–10
cases per million/year.
- Polymyositis can occur in isolation or in - Similar rashes occur on the upper back,
association with other autoimmune chest and shoulders (‘shawl’
diseases such as SLE, systemic sclerosis distribution).
and Sjögren’s syndrome.
- Periungual nail-fold capillaries are often
o The cause is unknown, although enlarged and tortuous.
there is evidence for a genetic
contribution. - There is about a threefold increased risk
of malignancy in patients with
dermatomyositis and polymyositis.
Clinical features: - This may be apparent at the time of
Polymyositis is with symmetrical proximal presentation, but the risk remains
muscle weakness, usually affecting the lower increased for at least 5 years following
limbs more than the upper. diagnosis.

- The onset is usually between 40 and 60

years of age Dx:
- Typically gradual, over a few weeks. - Muscle biopsy: shows the typical features
- Myositis is usually widespread but focal of fibre necrosis, regeneration and
disease can also occur. inflammatory cell infiltrate.

- Affected patients report difficulty rising

from a chair, climbing stairs and lifting,
sometimes in combination with muscle
pain.
- Systemic features of fever, weight loss
and fatigue are common.
- Respiratory or pharyngeal muscle
involvement can lead to ventilatory
failure or aspiration that requires urgent
treatment.
- Interstitial lung disease occurs in up to
30% of patients and is strongly associated - MRI is used to identify areas of abnormal
with the presence of antisynthetase muscle for biopsy.
(Jo-1) antibodies. - Serum levels of CK are usually raised and
Dermatomyositis presents similarly but in are a useful measure of disease activity,
combination with characteristic skin lesions. although a normal CK does not exclude
the diagnosis, particularly in juvenile
- These include Gottron’s papules, which myositis.
are scaly, erythematous or violaceous,
psoriaform plaques occurring over the - EMG can confirm the presence of
extensor surfaces of PIP and DIP joints, myopathy and exclude neuropathy.
and a heliotrope rash that is a violaceous - Screening for underlying malignancy
discoloration of the eyelid in combination should be undertaken
with periorbital oedema.
Tx:
- Oral corticosteroids (prednisolone 1 mg/
kg daily) initial tx
- High-dose intravenous
methylprednisolone (1 g/day for 3 days)
may be required in patients with
respiratory or pharyngeal weakness.
o Reduced by 25% if good response
to dose of 5–7.5 mg. Although
most patients respond
- Azathioprine and methotrexate additional
immunosuppressive therapy
39. Degenerative Joint diseases. Osteoarthritis - Abnormal stress and loading leading to
mechanical cartilage damage play a role
Osteoarthritis is the most common type of in secondary OA.
arthritis. Characterized by cartilage loss with an
accompanying periarticular bone response. - Obesity is a risk factor for developing OA
of the hand and knee, but not the hip in
later life. Increased skeletal mass
Epidemiology: increases cartilage volume.

- 50% of all rheumatic diseases - Collagenases (MMP-1 and MMP-13) cleave

collagen, and other metalloproteinases
- Affecting more than 50% of persons 65 such as stromelysin (MMP-3) and
years of age gelatinases (MMP-2 and MMP-9) are also
present in the extracellular matrix. MMPs
- Over 80% since '75 are affected by OA
are secreted by chondrocytes in an
- Dissociation between the X-ray changes inactive form. Extracellular activation
and clinical then leads to the degradation of both
collagen and proteoglycans around
chondrocytes.
- Tissue inhibitors of metalloproteinases
(TIMPs) regulate the MMPs. Disturbance
of this regulation may lead to an increase
in cartilage degradation over synthesis
and contribute to the development of
OA.
- IL-1 receptor antagonist genes are
associated with radiographic severity of
knee OA.
- Growth factors, including insulin-like
growth factor (IGF-1) and transforming
growth factor (TGF-β), are involved in
collagen synthesis, and their deficiency
Aetiology:
may play a role in impairing matrix
repair. However, increased TGF-β may
cause increased subchondral bone
density.
Clinical features:
Localized disease: (usually knee or hip): pain on
movement and crepitus, worse at end of day;
background pain at rest; joint gelling—stiff ness
after rest up to ~30min; joint instability.

Generalized disease (primary OA): with

Heberden’s nodes (“nodal OA”), seen mainly in
post-menopausal women), commonly affected
joints are the DIP joints, thumb carpo-
metacarpal joints and the knees. There may be
joint tenderness, derangement and bony
swelling (Heberden’s nodes at DIP, Bouchard’s
nodes at PIP), decreased range of movement and
mild synovitis. Assess effect of symptoms on
occupation, family duties, hobbies and lifestyle
expectations.
Pathogenesis: Dx:
Several mechanisms have been suggested:
 - Plain X-ray: assess severity of structural
change
- FBC, ESR, CRP normal
- Synovial fluid from knees shows –
predominantly viscous with low turbidity
Tx:
1. Patient education + Exercise
2. Reduction of adverse mechanical factors:
weight, shock absorbing footwear
3. Drug tx: paracetamol initially, Codeine,
NSAID’s, Opiates, tramadol
4. Surgery: joint replacement
40. Degenerative Joint disease – Osteoporosis Pathogenesis:
Osteoporosis: bone disease in which bone mass is - Results from increased bone breakdown
decreased, their microstructure is impaired, by osteoclasts and decreased bone
with the result that they become brittle, and formation by osteoblasts leading to loss
increasing the risk of fracture. of bone mass.
- Bone is composed of minerals - Bone mass decreases with age but will
(hydroxyapatite), to impart stiffness and depend on the ‘peak’ mass attained in
density, of the organic fraction (mainly adult life and on the rate of loss in later
collagen), and cells. life.
- To maintain the strength of the bone, it - Genetic factors are the single most
continuously replaces worn components significant influence on peak bone mass,
(remodeling). but multiple genes are involved,
including collagen type 1A1, vitamin D
Common disease – increasing with age + falls; receptor and oestrogen receptor genes.
women more prone than men
- Nutritional factors, sex hormone status
- Fractures occur during minor trauma or and physical activity also affect peak
even without falling. mass.
- Typical fractures of the spine, hip and
wrist.
Clinical features:
- Hip fractures are associated with high
mortality. - Fracture only cause of symptoms in
osteoporosis.
- Sudden onset of severe pain in the spine,
Aetiology: often radiating around to the front,
suggests vertebral crush fracture.
- However, only about one in three
vertebral fractures is symptomatic.
- Pain from mechanical derangement,
increasing kyphosis, height loss and
abdominal protuberance follow crushed
vertebrae.
- Colles’ fractures typically follow a fall on
an outstretched arm.
- Fractures of the proximal femur usually
occur in older individuals falling on their
side or back.
- Other causes of low-trauma fractures
must not be overlooked, including
metastatic disease and myeloma.

Dx:
- Plain radiographs, Ultrasound, CT
- Bone density: Dual energy X-ray
absorptiometry (DXA): OP dx when
T-score 2.5 or below
Tx:
- Life style changes – smoking, alcohol,
dietary Ca + exercise
- Vit D + Ca, Hormone replacement therapy
- Biphosphates: Alendronate, Risendronate,
Ibandronate
o Take on empty stomach in the
morning
- Protelos: Strontium ranelate
- Prolia: denosumab