AYAH ELAYAN

JENAN BANI ATA

 Chest pain

• 5 million emergency department visits.

• 2 million hospitalization annually with cost
of more than $8 billion.
• Cardiac etiology found less than one third.
• 2% of patients with acute MI are
unrecognized and discharged from the
ED.
 PATHOPHYSIOLOGY
• Pain in the chest may emanate from the
heart, great vessels, lungs, pleura, ribs,
shoulders, muscles, esophagus, or upper
abdomen. Pain can also be felt in the
chest as part of systemic processes such
as panic attacks, thyrotoxicosis, or
stimulant use.
 Tissues and organs that when disease is
present may result in chest pain
– Skin
– Chest muscles
– Bones (ribs, sternum,
and clavicles for
example)
– Heart
– Lungs
– Esophagus
– Nerves
– Pancreas
– Gastrointestinal tract
– Stomach
 Evaluation
• Rule out life threatening condition
• Assess vital sign
• History
• Physical exam
• Tests
• Diagnosis
• Management
 Chest pain; history
• Socrate (site, onset, character, radiation)
• Character:
– Constricting suggests angina, esophageal spasm, or anxiety;
– sharp pain may be from the pleura, pericardium, or chest wall.
– A prolonged (>.h), dull, central crushing pain or pressure suggests MI.
• Radiation:
– To shoulder, either or both arms, or neck/jaw suggests cardiac
ischemia.
– The pain of aortic dissection is classically instantaneous, tearing, and
interscapular, but may be retrosternal.
– Epigastric pain may be cardiac.
 History
• Associated factors (nausea, sweating, LOC, SOB,
light headedness, palpation, fever, cough, heart burn,
abdominal pain )
• Exacerbating factors inspiration, lying down, coughing,
physical activity
• Alleviating factors stopping physical activity, sitting up,
drugs
• Time course ,severity ,previous episodes of chest pain
• Elicits cardiac risk factors (FH , smoking , HTN , DM,
hyperlipidemia )
• Trauma to chest and any infections
 Cont’d
• Elicits risk factors of PE /DVT (calf pain or
swelling , recent travel, recent surgery , FH of
clotting disorders , malignancies, OCP,
pregnancy)
• PMH (MI , angina, stroke , PVD, asthma, COPD,
lung CA, DM)
• FH (cardiac diseases , PE, asthma , lung CA ,
sudden death)
• Drug history (alcohol, smoking , occupation, diet
and lifestyle )
• Idea, concerns, expectation
 Physical examination
• General look and vital signs
• Pulse ( irregularly irregular , tachycardia in VTACH , bradycardia in
heart block )
• O2sat
• Carotid and femoral pulses (maybe absent in aortic dissection)
• BP( hypo in acute MI)
• JVP
• Tracheal position and apex beat for shifting in pneumothorax
• Chest examination :
• Inspection ( scar , deformities, dilated vein )
• Percussion (dullness)
• Auscultation (new onset murmurs, gallob rhythm, breath sound ,
pericardial rub )
• Abdominal palpation and auscultation
• Extremities and tenderness
 ACS
• The clinical manifestation of
atherosclerotic plaque rupture and
coronary occlusion
• Refers to USA ,STEMI,NSTEMI
• The pain of an ACS is typically dull, aching,
pressing, squeezing, or heavy and steady. It is
seldom sharp or burning. Pain or pressure may
be located in the chest (angina pectoris) with
radiation elsewhere, or it may be located
entirely outside the chest in the upper
epigastrium, shoulder, upper arm (left or right),
jaw, or neck. Pain is often severe, but some
patients describe their discomfort as pressure or
heaviness rather than pain. Asking only about
pain will fail to identify many of these patients.
• Chest symptoms are often accompanied by
palpitations, diaphoresis, pallor, dyspnea,
and a feeling of impending doom (angor
animi). Less severe and less persistent pain
of the same type, triggered by activity and
not relieved by rest
• Women are more likely to report their
ischemic cardiac pain in the neck, back, or
epigastrium .
• Diabetic patients may have little or no pain,
and elderly patients often present with
shortness of breath rather than chest pain .
 Unstable angina
• Oxygen demand is unchanged ,supply is decreased due
to reduced resting coronary flow and it is significant
because it indicates stenosis has enlarged by
thrombosis , rupture of plaque and hemorrhage
• Pt with chronic angina with increasing frequency,
duration, or intensity of pain
• Pt with new onset angina that is sever or worsening
• Pt with angina at rest
• Unrelieved by rest and nitroglycerin
• USA and NSTEMI lack ST segment elevation and
pathological Q wave so we differentiate between them
by cardiac enzymes (CK-MB and troponin ) which not
elevated in USA
 Diagnosis
• PE
• ECG
• Stress ECG
• Stress echo
• Pharmacological stress test
• Cath and coronary angiography
(definitive test)
 Treatment
• Admission to floor
• Aggressive medical management is indicated
• Aspirin
• Clopidogrel
• BB
• LMWH
• Nitrates are first line therapy
• Oxygen if pt hypoxic
• Glycoprotein IIb/IIIa inhibitors (abiciximab, tirofiban )
• Morphine
• Replacement of deficit electrolytes
• Cardiac cath
 Myocardial infarction
• Is due to necrosis of myocardium as a result
of an interruption of BS
1. Most cases are due to acute coronary
thrombosis
2. MI is associated with 30% mortality rate
3. Most pt with MI have Hx of angina , RF for
CAD , or Hx of arrhythmia
 Clinical features
• Chest pain
1. Intense substernal pressure sensation often
describing as crushing or elephant standing on
my chest
2. Radiation to neck ,jaw , arms or back
commonly to the left side
3. Similar to angina pectoris in character and
distribution but much more sever and lasts
longer usually not respond to nitroglyceride
4. Epigastric discomfort
• Can be asymptomatic in up to one third of pt
• Other symptoms
1. Dyspnea
2. Diaphoresis
3. Weakness , fatigue
4. Nausea and vomiting
5. Sense of impending doom
6. Syncope
• Sudden cardiac death due to VFIB
 Category of infarcts
• STEMI
• Transmural involve wall thickness and
tends to be larger
• NON STEMI
• Subendocardial , tends to be smaller and
presentation similar to USA
 Diagnosis
• ECG markeres of ischemia /infarction include
• Peaked T wave : occur very early and maybe missed
• ST segment elevation indicates transmural injury and
can be diagnostic of acute infarct
• Qwave : evidence for necrosis (specific ) are usually
seen late typically not seen acutely
• T wave inversion is sensitive but not specific
• ST segment depression subcondrial injury
• New BBB
• Cardiac enzymes
• Troponins (I and T) MOST IMPORTANT
enzyme test to order
Greater sensitivity and specificity and reach peak
in 24 to 48 hours
• CK-MB less commonly used
95% sensitivity and specificity and reach peak in
24 hours
Most helpful in detecting recurrent infarction
 Treatment of ACS
• MOVE (monitor, o2, venous access,
ECG)
Admission to the CCU
 Treatment of ACS
• Anti-platelet therapy (Aspirin):
- All patients with suspected ACS should
receive Aspirin [325mg] swallowed or chewed ,
immediately and then continued daily
indefinitely .
- It should only be withheld for absolute CI,
such as anaphylaxis , other major allergic
reaction , or active GI bleeding. Patients with
true CI should receive Clopidogrel 300mg as a
loading dose as soon as an ACS is diagnosed
and 75mg daily thereafter .
• Clopidolgrel should also be considered in
addition to Aspirin for patents with UA or
NSTEMI , as the combination lower risk of
death or urgent revascularization versus
aspirin alone . The duration of therapy is
guided by subsequent evaluation and
intervention.
• Oxygen
• Nitroglycerin; can be given sublingually every 5 minutes for
three doses before consideration of intravenous or
transdermal administration.
• Morphine can provide important analgesia and anxiety relief.
• B-blockers can improve both short- and long-term mortality in
patients with ACS, and should be administered orally within
the first 24 hours of onset.
• Anticoagulant therapy has become standard for higher risk
UA/NSTEMI patients because it decreases infarction
• (ACE) inhibitors are indicated within 24 hours of onset for
patients who sustain MI, but not for ACS patients in general.
ACE inhibitors should not be given to patients with
hypotension, hyperkalemia, or rising creatinine.
• Statin as a lipid lowering agent.
• Reperfusion therapy.
 REPERFUSION THERAPY
• Reperfusion therapy either by PTCA (
cath ) or
Thrombolytic (streptokinase or recombinant
tissue plasminogen activator—rtPA)
• characteristic pain onset within 6 hours of
presentation (perhaps up to 12 hours, but
with lesser benefit) plus either ST
segment elevation in more than two
contiguous leads or new LBBB.
Thrombolytics CI
• Emergent PCI yields better short- and long-term
outcomes than thrombolysis for patients with
STEMI.
• PCI is not superior in hospitals with lower
volumes, and if a “door-to-balloon” time of 90
minutes cannot be achieved
• platelet inhibition with intravenous glycoprotein
IIb/IIIa receptor antagonists (abciximab,
eptifibatide, or tirofiban) can improve early
survival
 Coronary Artery Disease Therapy

• Aspirin should be given to all patients who do

not have absolute contraindications , Likewise,
B-blockers are standard of care because of their
long-term mortality benefit, and they are also
effective antianginal drugs.

• Smokers with CAD who quit reduce their

absolute risk of death over the ensuing decade
by 11% to 16%, making smoking cessation the
single most important intervention in this group .
• In patients with known CAD and baseline LDL
levels above 130 mg/dL on diet alone, reduction
in LDL cholesterol to below 100 mg/dL can
prevent 4 deaths in 100 patients treated for 5
years

• Statins used in combination with diet are the

preferred agents because they are the only
agents shown to achieve this level of benefit
• Nitrates and CCBs are also used for symptomatic relief
• Chronic use of NSAIDs increases risk for MI and cardiac
death for patients with CAD, in direct proportion to the
agent’s degree of COX-2 inhibition
• Higher risk NSAIDs include not only those marketed as
“COX-2 selective inhibitors” such as rofecoxib, celecoxib,
and valdecoxib, but also relatively COX-2 selective
drugs such as diclofenac and nabumetone—all should
be avoided in patients with CAD.
• First-line analgesic medications for CAD patients should
include acetaminophen, non-acetylated salicylates (e.g.,
salsalate)and aspirin
 Aortic dissection
• A serious condition in which there is a tear in the inner layer of
aorta
• Type A (Dissection of ascending aorta)
• Type B (Dissection of descending aorta)
• Features:
– Sudden severe pain, tearing in nature
– Anterior chest may radiate to back
– Occurs in patient with HTN, Marfans syndrome, cocaine use,
coarctation of the aorta.
– Branch artery involvement lead to neurological sign , absent pulses and
unequal BP
• Diagnosis :
– CXR : widened mediastinum
– TEE (TransEsophageal Echocardiograh) Very sensitivite and specific.
– CT scan & MRI
Treatment
Immediate medical Tx :
IV BB , sodium nitroprusside,

Type A surgical
management
Type B medical
management like IV BB and
morphine
ESOPHAGEAL RUPTURE (PERFORATION):
• Etiology: blunt trauma, medical instrumentation &
BOERHAAVE SYNDROME: forceful vomiting that is associated with
alcoholic binges and bulimia.
• Clinical features: pain(severe, retrosternal , shoulder pain)
tachycardia, hypotension, tachypnea, dyspnea, fever, hamman sign
• Dx: contrast esophagram ( definitive diagnostic study)
CXR: air in the mediastinum
• Tx:
• Stable pt with small perforation: IV fluid,NPO, antibiotics & H2
blockers
• Ill pt with large perforation: surgery within 24 hours
 PULMONARY EMBOLISM:

• Occurs when a thrombus in another region of the body (

usually lower extremity DVT) embolizes to the
pulmonary vasculature and pulmonary artery blood flow
distal to embolus is obstructed.

• Clinical features:
• Symptoms: dyspnea, pleuritic chest pain, cough ,
hemoptysis syncope , only 1/3 of pt have DVT
symptoms
• Signs: tachypnea, tachycardia, S4, increased P2,
shock in massive PE
• Dx:
• ABG levels: not diagnostic >> PaO2 & PaCO2 are low,
PH is high >> respiratory alkalosis.
• CXR: usually normal , atelectasis or pleural effusion
classical signs: Hampton hump or Westermarck sign
• ECG: sinus tachycardia, S1Q3T3,Rt axis deviation,
RBBB,Ppulmonale & others
• Venous duplex ultrasound of lower extremity
• V/Q scan: NL scan rules out PE, high probability: very
senstive ,treat with heparin
• CTA:the test of choice in most medical centers
• Pulmonary angiograophy: gold standard
• D-dimer assay
Score <= 4 indicate that PE is unlikely, score >4
indicates that PE is likely.
• Tx:
– O2 supplement to correct hypoxemia, severe
cases may require intubation and mechanical
ventilation.
– Acute anticoagulant therapy : unfractionated
or LMWH.
– Oral anticogulation.
– Thrombolytic therapy: streptokinase,tPA
– IVC filter placement
– Surgical thrombectomy.
PNEUMOTHORAX:
• Accumulation of air within the pleural space
• Spontaneous (primary & secondary) and traumatic( often
iatrogenic).
• Clinical feature:
– Symptoms: sudden onset ipsilateral chest pain, dyspnea &
cough.
– Signs: decrease breathing sounds over affected side,
hyperresonance.
• Dx: CXR: visceral pleural line
• Tx:
– if small & pt asymptomatic: observation, resolve spontaneously
– If large & pt symptomatic: admission, O2 supplement, chest tube
TENSION PNEUMOTHORAX:
• Accumulation of air under postive
pressure in pleural space collapses the
ipsilateral lung and shift mediastinum
away from side of pneumothorax
• Clinical features: hypotension, distended
neck veins, dec. breathing sounds, hyper
resonance on percussion , tracheal shift
• Tx: a medical emergency
– Chest decompression with a large pore
neddle
– Chest tube insertion
NON LIFE-THRETEANING CONDITIONS
 Musculoskeletal causes:
• That is, chest pain related to the muscles ,
ligaments, cartilage and bones of the chest wall.
• Causes : traumatic and non-traumatic.
• usually result from muscle strain due to physical
activity
• clinical features : pain usually localized, acute &
positional . Pain often reproducible by palpation
or by movement. With No other associated
symptoms
• Topical agents relief pain(heat rub, ice back)
• Treatment : NSAID , muscle relaxent.
Costochondritis: (costosternal syndrome or anterior chest wall
syndrome)
• is inflammation of the junctions where the upper ribs join the costal
cartilage that attaches them to the sternum
• Clinical features: localized chest wall pain and tenderness that can
be reproduced by pushing on the involved cartilage in the front of
the rib cage.
• Costochondritis is a relatively harmless musculoskeletal chest pain
and usually resolves without treatment.
• The cause is usually unknown.
• Different types of infectious diseases can cause costochondritis but
are un common,it also can occur with certain form of arthritis :
ankylosig spondylitis and psoriatic arthritis
• Costochondritis affects females more often than males (70% versus
30%).
• Investigation : CBC,CXR
• Lower rib pain syndrome: (slipping rib syndrome)
usually complain of pain in the lower part of the chest or in
the abdomen.
In this syndrome, one of the lower ribs (eighth, ninth or
tenth rib) becomes loosened from its fibrous connection
to the breastbone, usually following some type of
trauma.
The "moving" rib impinges on nearby nerves producing
pain. This condition is usually treated conservatively
with advice to avoid activities that reproduce the pain in
an attempt to allow the ribs to heal, but surgery may be
required to stabilize the slipping rib.
Precordial catch :
• is a completely benign and very common condition,
generally seen in children or young adults
• Clinical feature: sudden, sharp chest pain occurs,
usually on the left side of the chest, lasting for a few
seconds to a few minutes. It typically occurs at rest, and
during the episode, the pain increases with breathing.
After a few seconds or a few minutes, the pain resolves
completely.
• The cause of this condition is unknown, and it has no
known medical significance.
Rheumatic Diseases Associated With Chest Wall
Pain
• Chest wall pain associated with inflammation of the
spine or rib joints can be seen with several rheumatic
conditions, in particular, rheumatoid arthritis, ankylosig
spondylitis and psoriatic arthritis.
Stress Fractures
• Stress fracture of the ribs can be seen in athletes who
engage in strenuous, repetitive motions involving the
upper body, such as rowers or baseball pitchers. Stress
fractures can also be seen in people with osteoporosis
or vitamin D deficiency.
Gastrointestinal causes:
GERD:
• Reflux of gastric contents into the esophagus is a normal event.
Clinical symptoms only occur when there is prolonged contact of
gastric contents with esophageal mucosa.
• Clinical features: heartburn (major symptom),regurgitation and
odynophagia. Cough and nocturnal asthma can occur from
aspiration of gastric contents
• Investigation :
– Usually clinically
– Oesophago-Gastro-Duodenoscopy (OGD): new-onset
heartburn over 55 years of age, alarming symptoms:( weight
loss, dysphagia, haematemesis,anemia),documentation of
reflux complications
– 24-hour pH monitoring :gold standard but usually reserved for
confirmation of GERD prior to surgery
• Tx:
– Elevation of head of bed
– Dec. fat intake
– Avoidance of chocolate, onions peppermint & garlic
– PPI, H2 receptor antagonist
– Surgery
• Complication : esophageal stricture and
barretts' esophagus
ESOPHAGEAL SPASM:
• Nonperistalitic spontaneous contraction of
esophageal body.
• Clinical features: chest pain that mimics
angina and may radiate to the jaw, arms,
and back.
• Dx: esophageal manometry(diagnostic),
barium swallow (corkscrew esophagus).
• Tx: nitrates, CCB,TCA
corkscrew esophagus
Cardiovascular causes:
STABLE ANGINA:( angina pectoris)
• Is due to fixed atherosclerotic lesion that narrow the major coronary
artries.occurs when O2 demand exceeds blood supply
• Risk factors: DM (worst), HTN, hyperlipidemia, smoking, family Hx
of premature CAD(M<55,F<65) & age(M>45, F>55)
• Clinical features:
• Retrosternal chest pain, pressure sensation radiated to left shoulder
lasts 10 to 15 min , brought by factors that increase myocardial O2
demand (predictable precipitating factors) and relieved by rest or
nitroglycerine may be associated by nausea & mild sweating.
• Pain doesn't change with breathing nor with body position . Pt
doesn’t have chest tenderness
• Dx:
– Physical examination usually normal in most patient.
– Resting ECG: usually NL, if ST segment or T-wave abnormalities are
present treat as USA
– Stress test: ECG, echocardiography
– Holter monitoring
– Cardiac catheterization with coronary angiography: definitive test
• Tx: risk factor modification and aspirin indicated in all pt
– Mild disease : (NL EF,mild angina,single-vessel) : nitrate , B-blocker
– Moderate : (NL EF , moderate angina,two-vessels): previous regimen
and coronary angiography (to assses pt for revascularization)
– Severe: (dec EF, severe angina, three-vessels or lt main or LADA):
coronary angiography and consider for CABG
PERICARDITIS:
• Acute inflammation of the pericardium , most commonly due to viral
infection(coxsackie B, echovirus, HIV infection) or follow myocardial
infarction . Other causes: uraemia,rheumatic disease,malignancy.
• Clinical features: sharp, retrosternal chest pain that radiates to neck
and shoulders which characteristically relieved by leaning forward
and worse on inspiration.
• Cardinal sign is a pericardial friction rub
• Dx: ECG is diagnostic : concave upwards(saddle shaped) ST
segment elevation across all leads
• Tx: treat underlying cause plus NSAID (shouldn’t used within few
days following MI)
Diffuse ST elevation
Dermatological cause:
SHINGLES:
• Reactivation of varicella zoster
infection
• Clinical feature: pain and tingling in a
dermatomal distribution preceed the
rash by few days(papules & vesicles
in same dermatome)
• Risk factors : elderly,
immunocompromised
• Investigation: tzank smear
• Tx: antiviral (acyclovir, valaciclovir),
analgesia
Psychological causes:
Anxiety:
• Common cause of chest pain.
• Accessional presentations are dramatic with patient
represent intense symptoms.
• Associated features include breathlessness with inability
to take enough air and tingling around the mouth.
• The onset of symptoms may coincidence with stressful
stimulators or emotional distress.
• Treatment : stress management and relaxation
techniques, antidepressant and benzodiazepines
Psychological causes:
Panic attack:
A panic attack is the abrupt onset of intense fear or
discomfort that reaches a peak within minutes and
includes at least four of the following symptoms:
• what differentiates a panic attack from other
anxiety symptoms is the intensity and duration
of the symptoms. Panic attacks typically reach
their peak level of intensity in 10 minutes or less
and then begin to subside.
• Tx:
– Psychotherapy
– Medications: SSRI(fluoxetine , paroxetine and
sertraline), SNRI(venlafaxine hydrochloride)
Benzodiazepines( alprazolam and clonazepam)
THANK YOU ☺