RANK ONE REVIEWER

- OXYGENATION

ACQUIRED
I. CARDIOVASCULAR SYSTEM
● Most common cause is atherosclerosis
● Main function is for tissue perfusion ● Atheromatous plaques in the lining of blood vessels that
start off as fatty deposits
A. 3 COMPONENTS FOR TISSUE PERFUSION ● Nicotine is also deposited in the blood vessels
● Irreversible
BLOOD ● Sclerosis means hardening
○ Plaque becomes hard because calcium is also
● Carries oxygen deposited in the lining of blood vessels
● Most common site is the aorta
HEART
● Arteries - resistance vessels
○ Greater pressure
● Pumps blood to different parts of the body
○ Largest: aorta
● Veins - capacitance vessels
BLOOD VESSELS
○ Less pressure but greater surface to carry more
blood (carries blood back to the heart)
● Distributes blood towards the body
○ Largest: Inferior vena cava
● Maintains vascular tone
● Capillaries - exchange vessels; largest surface area
○ Tunica intima - innermost layer
○ Tunica media - smooth muscles of the blood
ATHEROSCLEROSIS
vessels
■ When smooth muscles contract, blood
● Atheromatous plaques in the lining of blood vessels that
vessels constrict. When smooth
start off as fatty deposits
muscles relax, blood vessels dilate.
● Risk factors:
○ Tunica externa/adventitia - outermost layer
○ Age - blood vessels become less elastic,
● When the blood vessels lose the vascular tone, smooth
making it more prone to injury
muscles relax → dilatation → BP lowers → decreased
○ Obesity
tissue perfusion → shock.
○ Sedentary lifestyle
○ Smoking
B. SHOCK
○ Diabetes Mellitus
○ Uncontrolled Hypertension
● A collapse in the cardiovascular system will results in
■ Blood pressure - the pressure of the
shock
blood against the walls of the blood
● Shock - inadequate tissue perfusion
vessels
○ Hypovolemic - decreased tissue perfusion
■ Blood vessels are elastic. An increase
○ Cardiogenic - pump failure
in the blood pressure will be able to
■ Coronary (CAD, MI)
be compensated by the blood
■ Non-coronary (CHD, Endocarditis) HD
vessels.
■ Obstructive - compression in the heart
■ Atherosclerosis in the blood vessels
(Tension pneumothorax)
will make the blood vessels hard,
○ Distributive - loss of vascular tone
damaging its elasticity. When there is
■ Infection → inflammation →
increased blood pressure, the inner
vasodilation → Septic Shock
wall of the blood vessels can no
■ Allergy → inflammation →
longer distend. Instead, the outer wall
vasodilation → Anaphylactic Shock
will be distended.
■ Spinal cord injury → inflammation →
■ Abnormal dilatation of the wall →
vasodilation → loss of sympathetic
Aneurysm
reflexes → Neurogenic shock
AORTIC ANEURYSM
II. VASCULAR DISEASES

=
A. ANEURYSM

● Disease of the artery

● Abnormal dilatation and sac formation in the wall of an
artery
○ Easily ruptures

CONGENITAL

● Idiopathic (cause is unknown)

● Most common location is the cerebral vessels
● Common hemorrhagic stroke among young people is ● Ascending Aortic Aneurysm
peripheral aneurysm ● Descending Aortic Aneurysm
○ Thoracic Aortic Aneurysm
○ Abdominal Aortic Aneurysm
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SIGNS AND SYMPTOMS
Assess the skin: Assess the skin:
● Pale ● Dark
● Usually, it is asymptomatic ● Cool to touch (there ● Pigmented
● Abdominal Aortic Aneurysm - pulsating mass in the is no blood flow) ● Cyanotic
abdomen ● Thinning of hair (unoxygenated
blood cannot go up)

BOARD EXAM QUESTIONS Palpate for pulses/edema: Palpate for pulses/edema:

● Abnormal pulses ● Pulses are normal
What is the difference between Type A and Type B ● No edema ● Pulses are difficult to
Dissecting Aneurysm? palpate due to
● Type A Dissecting Aortic Aneurysm - Ascending Aorta edema
● Type B Dissecting Aortic Aneurysm - Descending
Aorta Skin lesions (vascular Skin lesions (vascular
ulcers): ulcers):
Type A: ● Ulcers are small but ● Ulcers are larger
● Admit to surgery ward (management is surgery as soon deep with well with irregular
as possible) circumscribed edges borders
● Very painful ● Less painful
Type B: ● Less or no ● Several granulation
● Medical ward (control blood pressure first before granulations tissues
surgery)

Surgery - endovascular surgery Position the legs: Position the legs:

● Stent will be put inside and blood vessel will be stabled ● Dependent ● Elevated
to prevent rupture
Nursing Diagnosis:
Acute/Chronic Pain
COMPLICATIONS
Impaired Tissue Perfusion
Risk for Impaired Skin Integrity
● Ruptured aneurysm - most dangerous
○ Massive internal bleeding may lead to Arteriosclerosis Obliterans Varicose veins
hypovolemic shock Raynaud’s Disease Deep Vein Thrombosis/
○ May be caused by uncontrolled hypertension Venous Thromboembolism

CLINICAL MANIFESTATION OF Buerger’s Disease/ Thromboangiitis obliterans- may affect both

IMPENDING RUPTURED ANEURYSM arteries and veins

● Dissection of the aorta - tearing of the wall due to

uncontrolled hypertension
● Ascending Aorta: ● Most common in the lower extremities
○ Severe chest pain (similar to myocardial ● Manifestation: Leg Pain
infarction) ● If the patient has both Diabetes Mellitus and Vascular
● Thoracic Aorta: Insufficiency, he/she is more prone to gangrene formation.
○ Severe epigastric pain
● Abdominal Aorta: VENOUS INSUFFICIENCY
○ Severe low back pain
VARICOSE VEINS
B. PERIPHERAL VASCULAR DISEASES
● Abnormal dilatation and tortuous formation in the walls of
● Involves small and medium-sized blood vessels, arteries, the superficial veins
and veins of the upper and lower extremities ● Etiology: Incompetent valves/ destruction of valves
● Arterial Insufficiencies ● Risk factor: Prolonged standing/sitting/crossing of legs
● Venous Insufficiencies ○ Prolonged standing may cause destruction of
valves
○ Crossing of legs impede the circulation
ARTERIAL INSUFFICIENCY VENOUS INSUFFICIENCY
● Other Risk Factors: Obesity, Pregnancy, Family history
○ Anything that increases intra-abdominal
There is not enough function of There is not enough function of
the arteries. the veins. pressure
● Irreversible
Blood flow goes downward Blood flow goes upward ● Diagnostic Exam: Venography, Venous doppler, Venous
duplex
Clinical Manifestations: Clinical Manifestations: ● Prevention:
Severe pain Venous congestion ○ Avoid prolonged standing/sitting
● Due to ischemia to Increased pressure ○ Exercise
the lower extremity ● Due to venous
○ Weight reduction
Claudication - pain with congestion, injuring
movement the wall of blood ○ Elevate the legs
vessels → ○ Compression stockings - compresses the
inflammation → pain muscles and help the blood to go up
● Can also be caused ● Management:
by phlebitis ○ Elevate the legs
○ Sclerotherapy - inject a chemical or do laser to
harden the blood vessels/vein to straighten it
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 ■ Not enough for bigger varicosities ● Risk Factors: Exposure to cold temperature; Young adult
○ Surgery: Vein stripping and ligation women; Smoking; Stress
■ No more varicose veins/veins, so the ● Other Contributing Factors: Hypertension, Diabetes
blood will flow in the collateral vessels Mellitus
● Signs/Symptoms: Cyanosis/Bluish discoloration
DEEP VEIN THROMBOSIS ○ Severe vasospasm → white fingertips;
numbness; tingling sensation (paresthesia); pain
● Deep veins are found inside the muscles ● Ischemia → Risk for Impaired Skin Integrity
● Deep veins also have valves, but they also have muscles ● Management:
● When muscles contract, blood vessels will be constricted ○ Avoid exposure to cold temperature
which helps the blood go up ○ Always wear gloves/boots
● When muscles do not contract, stasis of blood flow will ○ Avoid smoking
occur ○ Avoid stress
● Stasis of blood → hypercoagulable → endothelial injury = ○ Avoid trauma
thrombus formation ○ Analgesic as ordered
○ Virchow’s triad - stasis, hypercoagulation, ○ Vasodilators are given as ordered (Diltiazem)
endothelial injury ● Raynaud’s Phenomenon - secondary causes (known
● Etiology: Unknown causes)
○ Atherosclerosis - causes thrombus formation ○ Scleroderma
● Risk Factors: Immobilization, Oral Contraception, Obesity ■ Calcinosis
○ Common to post-operative patients, bed-ridden ■ Raynaud’s Phenomenon
patients ■ Esophageal Dysmotility
● Signs and Symptoms: ■ Syndactyly
○ Phlebothrombosis - asymptomatic ■ Telangiectasia (formation of abnormal
■ Sudden onset of leg pain vessels)
■ Homan’s Sign - pain in the calf ○ Rheumatoid arthritis
muscle upon dorsiflexion of foot ○ Systemic Lupus Erythematosus
● Not very reliable
○ Thrombophlebitis - pain, warmth, redness ARTERIOSCLEROSIS OBLITERANS &
● Complications: Possible dislodgment of the thrombus THROMBOANGITIS OBLITERANS (BUERGER’S DISEASE
○ Dislodgement of the thrombus from the vein will
make it an embolus, which can travel to other
ARTERIOSCLEROSIS THROMBOANGITIS
parts of the body, which may block the
OBLITERANS (ASO) OBLITERANS/ BUERGER’S
pulmonary artery → pulmonary embolism DISEASE (TAO)
○ Venous thromboembolism
● Prevention: Hardening of small and Inflammation and thrombus
○ Mobilize the legs medium-sized arteries formation in the walls of small
○ Exercise and medium-sized arteries and
○ Compression stockings veins
○ Elevate the legs
Affects arteries more than
● Management:
veins
○ Immobilize - moving may cause dislodgement of
thrombus → pulmonary embolism
Common in lower extremities
○ Analgesic IV Etiology: Idiopathic
○ Surgery: Endovascular surgery
○ Medical Management: Thrombolytic therapy - Risk Factors: Risk Factors:
dissolves thrombus ● Ae (60 y.o. and above) ● Cigarette Smoking
■ Urokinase ● Men ● Tobacco products
■ Streptokinase ● Smoking ● Young adult men
■ Alteplase ● Stress ● Stress
● Sedentary Lifestyle
○ Medical Management: Antithrombotic drugs -
● Obesity
prevents thrombus ● Increased cholesterol
■ Antiplatelet - Aspirin/Clopidogrel ● Hypertension
■ Anticoagulant - Heparin/Warfarin ● Diabetes Mellitus
● TED hose can be removed when the patient will lie down.
Elevate the legs. Then wear the hose before standing. Common Signs and Symptoms:
● Leg Pain
● Claudication
ARTERIAL INSUFFICIENCY
● Abnormal pulses
● Pallor
RAYNAUD’S DISEASE
Other Signs and Symptoms:
● “Blue - White - Red Disease” ● Edema
● Characterized by arteriolar vasospasm ● Cyanosis/Pigmentation
● Reversible
○ After some time, blood vessels dilate → more
Management: Management:
blood flow → more red than usual extremities
● Avoid smoking ● Avoid smoking
● Commonly affects upper extremities (tips of fingers, ● Weight reduction ● Avoid stress
hands) ● Mobilize ● Avoid trauma
● Etiology: Idiopathic/Unknown ● Low-fat, low-sugar, ● Analgesic as ordered

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 low-cholesterol diet ● Vasodilators are rarely
● Valvular repair (valvuloplasty)
● Control blood pressure given (only dilates
● Control sugar normal vessels) ● Valvular replacement (prosthesis)
● Analgesic as ordered ● Amputation (if there is ● Support cardiac function
● Vasodilators are rarely gangrene formation) ○ Provide rest
given ○ Administer cardiac drugs
● Amputation (if there is ● Manage heart failure
gangrene formation)
B. INFLAMMATORY HEART DISEASES

C. DIAGNOSTIC TESTS ● Endocardium - innermost layer of the heart

● Myocardium - middle layer of the heart
ANGIOGRAPHY ● Epicardium - outermost layer of the heart
● Pericardium - sac that covers the heart
● Most definitive type of diagnostic test ○ Visceral - covers the heart muscle
● Occluded blood vessels are visualized ○ Parietal - covers the pericardial cavity
● Dye is injected ○ Pericardial space - contains pericardial fluid
● Invasive and done under cardiac catheterization which decreases the friction as the heart pumps
● Local anesthesia is done blood

ULTRASOUND ● Myocarditis - common in children

● Doppler / Duplex Ultrasound ENDOCARDITIS

● Non-invasive
● Commonly done for peripheral vascular diseases ● Inflammation of the endocardium
● Common cause: Infection
III. HEART - CARDIOLOGIC ANATOMY ○ Group A beta-hemolytic streptococcus,
Staphylococci
● Heart - hollow muscular organ located in the middle ● Risk Factors:
mediastinum ○ Immunocompromised
● Function of the valves: to prevent backflow ○ Existing cardiac disease RH -

● Using the bell of the stethoscope, auscultate: ○ Invasive procedure/surgery

○ 2nd ICS right parasternal area – aortic valve ● Pathogenesis:
○ 2nd ICS left parasternal area – pulmonic valve ○ When a patient is immunocompromised and has
○ 4th ICS left parasternal area – tricuspid valve an existing cardiac disease or has undergone
○ 5th & 6th ICS left midclavicular line – mitral invasive procedure/surgery, since the blood
valve (apex) PMI (point of maximum impulse) vessels are open after surgery, there is a
● Valvular defect (Destruction of valves/backflow) – murmurs tendency for the bacteria to enter the blood.
Since the patient is immunocompromised, there
A. VALVULAR HEART DISEASES is a tendency for the bacteria to proliferate,
multiply, and cause damage. Since there is a
cardiac disease/valvular defect, the bacteria can
● Common causes are congenital heart defects and
enter the heart and cause damage in the lining
acquired (Rheumatic fever, Kawasaki Disease).
of the heart → inflammation (endocarditis).
■ Systemic inflammation - since it is
TYPES OF VALVULAR HEART DISEASES
already in the blood
■ Manifestations:
● Valvular insufficiency/Valvular regurgitation - inability
Increased WBC (Leukocytosis)
of the valves to close completely → backflow
Intermittent fever
○ Backflow - regurgitation
Fatigue
○ Murmurs
Weakness
● Valvular stenosis - inability of the valves to open
Chest pain
completely
Elevated ESR (Erythrocyte
○ Increased turbulence
sedimentation rate) - indicates
● Mitral Valve Prolapse - bulging or ballooning of the mitral
systemic inflammation
valve onto the left atrium
○ Bacteria already proliferate in the endocardium
○ (+) systolic click/mitral click
→ injury and bleeding in the endothelial lining.
○ Etiology: Unknown
Microorganisms will be covered by the fibrin
○ Risk factor: Women, family history
which is part of the clotting mechanism, and the
○ Signs and Symptoms: Palpitation, chest pain,
microorganism can’t be identified by the WBC.
easy fatigability
This is an abnormal clotting since it cannot
○ Complications: Mitral regurgitation, Dysrhythmia
dissolve by itself. If the clot is already abnormal,
it is referred to as thrombus.
DIAGNOSTIC TEST
○ Thrombus formation in the lining of the
endocardium and valves = microthrombi
● 2D Echocardiography formation/vegetations.
○ Dislodgement of thrombus → embolus
■ Right ventricle - pulmonary embolism
■ Left ventricle - embolic stroke
MANAGEMENT ■ Manifestations of embolization:
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 Osler’s Nodes - painful nodules in ○ Acute pain r/t inflammation of pericardial sac
fingertips and toes ● Diagnostic Test:
Janeway Lesions - painless macules ○ 2D Echocardiography
on palms and soles of the feet ○ Chest X-Ray
Roth’s Spot - hemorrhages with pale ○ Elevated ESR
center in the retina ○ Culture and Sensitivity Test - for infection cause
Splinter hemorrhages - brown streaks ○ Antinuclear antibody test (ANA) - positive in
in fingernails and toenails autoimmune problem; for SLE cause
● Manifestations: ○ Coronary angiography - for M.I. cause
○ Fever (Intermittent) ○ Biopsy - for cancer cause
○ Roth’s Spots ● Management:
○ Osler’s Nodes ○ Orthopneic position
○ Murmurs (existing valvular defects) ○ Pain reliever - NSAIDs
○ Janeway lesions ○ Anti-inflammatory drugs (e.g. steroids)
○ Anemia ○ Manage the cause
○ Nail changes ○ Prevent and manage complications
○ Ecchymosis/Embolization) ● Complications:
● Diagnostic Test: ○ Pericardial effusion
○ Culture and sensitivity test - most definitive ○ Cardiac tamponade
○ CBC
○ ESR PERICARDIAL EFFUSION
○ 2D Echo - to check the vegetations and
microthrombi ● When the fluid in the pericardial sac accumulate more
○ Chest X-Ray than 20 ml → pericardial effusion
● Nursing Management: ● Fluid may be compressed in the heart
○ Manage fever ● Referred to as “constrictive pericarditis”
○ Assess for changes in murmur ● Pericardiocentesis - aspiration of fluid from the
○ Monitor vital signs pericardial sac
○ Provide rest periods ○ Chest X-Ray before pericardiocentesis
○ Support cardiac functions ○ X-ray/ultrasound-guided
● Medical Management: ○ ECG-guided
○ Prevention - prophylaxis antibiotics prior to ■ Needle is connected to the ECG. The
invasive procedure (e.g. penicillin, monitoring of ECG will indicate if the
erythromycin/azithromycin) needle punctures the heart muscle →
■ Patients with mitral valve prolapse do abnormal impulses seen in ECG.
not need prophylaxis.
○ Administer anti-infective drugs
○ Administer antipyretic drugs BOARD EXAM QUESTION
○ Administers drugs to support cardiac function
○ Prevent complications: How to position a patient during pericardiocentesis?
■ Cardiogenic shock Answer: Semi-fowler’s position
■ Septic shock
■ Congestive heart failure CARDIAC TAMPONADE

PERICARDITIS ● Life-threatening complication characterized by too much

pericardial fluid causing obstructive shock
● Inflammation of the pericardium/pericardial sac ● Manifestations/Beck’s Triad (of Cardiac Tamponade):
○ Increased friction which can be assessed by ○ Decreased BP
auscultation (friction rub) - most prominent sign ○ Increased venous pressure
■ 4th ICS left parasternal border – ■ Distended neck veins
scratching and leather sound heard ○ Distant/muffled heart sounds
best at the end of expiration while ● Management:
sitting/leaning forward ○ Refer to physician
● Etiology: ■ Emergency pericardiocentesis
○ Idiopathic
○ Infection IV. HEART - CARDIOLOGIC PHYSIOLOGY
○ Trauma
○ Systemic Lupus Erythematosus
A. PROPERTIES OF THE HEART
○ Myocardial Infarct
○ Malignancy
● Contractility
● Manifestations:
● Conductivity
○ Chest pain - most prominent symptom
● Excitability
■ M.I.: constant and not
● Rhythmicity
affected/relieved by breathing or
● Automaticity
movement of chest
■ Pericarditis: worsens with deep
inspiration, lying down, turning; B. CONDUCTING SYSTEM OF THE HEART
relieved by sitting/leaning forward
(orthopneic positioning) ● SA node - pacemaker of the heart; initiates impulse
● Nursing Diagnosis: ○ Between right atrium and superior vena cava

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 ● AV Node ○ After the blood has been ejected, the pressure
● Bundle of His in the ventricles will go down + all valves are
● Purkinje Fibers closed.
● Rapid ventricular filling
ACTION POTENTIAL ○ Filling of atria with too much blood
○ Pressure in the atria > pressure in the ventricles
● Action potential - a rapid change in the membrane = opening of valves → blood will flow = S3
potential (inaudible).
● In the body, we have electrical charges. ■ Can be heard with patients with CHF
○ Cations (+) (lub dub dub – ventricular gallop)
○ Anions (-) ● Diastasis
● More sodium (Na) outside the cell. ● Another atrial systole
● More potassium (K) inside the cell. ○ S4 (inaudible)
● The difference of concentration between cations and ■ Atrial gallop (lub lub dub)
anions create electrical charges.
○ (-) inside the cell ● Stroke volume - volume of blood released by the heart in
○ (+) outside the cell one beat (50-100 ml)
● -60 to -90 mv – electrical charge at rest (resting ○ Ejection fraction
membrane potential) ● Preload - volume of blood that is already in the heart
before it contracts
HOW IMPULSES TRAVEL (ACTION POTENTIAL)
FACTORS AFFECTING STROKE VOLUME
NERVE
● Preload - volume of blood that is already in the heart
● Upon stimulus, the sodium channels (+) open and enter before it contracts
the cell. Therefore, the membrane potential becomes ○ Positioning
more positive → depolarization. ■ Standing - decreased
● Potassium channels (-) open and leave the cell. Therefore, ■ Supine - increased
the cell goes back to the resting phase → repolarization. ○ Breathing pattern
■ Deep - more blood goes back to the
HEART heart
■ Valsalva maneuver - less blood that
goes back to the heart
● When the SA node initiates an impulse, it travels to AV
● Afterload - pressure that must be exceeded by the heart
nodes, then to Bundle of His, then to Purkinje fibers.
before it contracts
● Sodium channels open and enter the cell. Membrane
○ Hypertensive - difficulty of the heart to pump →
potential becomes more positive → depolarization.
decreased SV
● Calcium channels open and enter the cell → plateau
○ Atherosclerosis of the aorta
formation.
● Contractility - the lesser the contraction, the lesser the
○ Calcium enters the cell in the heart because it is
stroke volume
needed for muscle contraction.
● Heart rate
● Potassium channels open and leave the cell. Membrane
○ SNS - increases heart rate
potential goes back to resting → repolarization.
○ PNS - decreases heart rate
○ Thyroid Hormones
● When impulse travels from SA node to AV node, it
○ Exercise
stimulates the atria to contract.
○ Temperature
○ Atrial depolarization - P Wave
○ Atrial repolarization goes with ventricular
depolarization.
● Stroke volume x HR
● When impulse travels from AV node to Purkinje fibers, it
○ Vol/beat x beats/min = Volume of blood ejected
stimulates the ventricles to contract.
in one heartbeat (CARDIAC OUTPUT vol/min)
○ Ventricular depolarization - QRS
● MAP = CO x TPR (SVR)
● Contraction of atria + Contraction of ventricles = one
○ SP + 2DP / 3
heartbeat/cardiac cycle
● Total peripheral resistance (TPR)
○ Diameter of the blood vessels
C. EVENTS IN ONE CARDIAC CYCLE
■ Vasoconstriction - increased
■ Vasodilation - decreased
● Atrial systole
○ Viscosity of the blood
○ When atria contracts, the blood is pumped into
■ Viscous - increased pressure
the ventricles → closing of AV valves to prevent
backflow = S1 “lub.”
V. BLOOD PRESSURE
● Isovolumetric ventricular contraction
○ Valves are closed and the pressure in the
ventricles are high. Classification Systolic Pressure Diastolic Pressure
● Maximum ejection
○ Pressure in the ventricles > aortic pressure = Normal <120 <80
valves will open → blood flows.
○ Valves close to prevent backflow → closure of Prehypertension <120 - 139 80 - 89
semilunar valves = S2 “dub.”
● Isovolumetric ventricular relaxation Stage 1 140 - 159 90 - 99

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 Stage 2 =/> 160 =/> 100
● Renin - enzyme released by the kidneys that converts
angiotensinogen to become angiotensin I.
● If there is an increase in BP twice, at least two weeks ● Angiotensin I → Angiotensin II by ACE which is released
apart → Hypertensive by the lungs.
● Primary/Essential Hypertension - unknown cause ● Angiotensin II binds with its receptor → vasoconstriction
○ Family history → increased BP.
● Secondary Hypertension - there is a known cause; sign ● Angiotensin II will stimulate the release of aldosterone →
of disease increased Na and water retention → increased blood
○ Pheochromocytoma - tumor of the adrenal volume → increased BP.
medulla → releases catecholamines
(epinephrine and norepinephrine) → increases 4. ACE Inhibitors
SNS response ● Captopril, Quinapril, Enalapril
○ Malignant hypertension
○ Diabetes Mellitus 5. Angiotensin II receptor blockers
○ Renal Disease ● Losartan, Valsartan, Candesartan
● Modifiable risk factor ● A/E: GI toxicity (given after meals)
● Goal in Management: Control BP
● Pathogenesis: 6. Diuretics
○ Increased pressure in the systemic circulation ● Decreases blood volume → decreases BP
will cause increased pressure in the cerebral ● Thiazide D.
circulation → CVA. ● Hydrochlorothiazide
○ Increased pressure in the coronary circulation
→ CAD. 7. Vasodilators
○ Increased pressure in the peripheral circulation ● Direct acting vasodilators - directly relax the smooth
→ PVD. muscles of the blood vessels → relaxation → dilatation
○ Increased pressure in the microcirculation → ● Hydralazine, Nitrates, Nitroglycerin, Isosorbide,
retinal vessels → retinopathy / renal vessels → Nitroprusside
nephropathy ● Indirect acting vasodilators - causes smooth muscles
● Signs and Symptoms: relaxation by decreasing release of calcium (decreases
○ Asymptomatic → poor compliance in contraction)
medications ○ Calcium-channel blockers
○ Headache ■ Nifedipine, Felodipine, Amlodipine,
○ Dizziness Verapamil, Diltiazem
○ Blurring of vision
○ Epistaxis VI. CORONARY ARTERY DISEASES
● Independent Interventions:
○ Diet - restrict sodium, low-fat, low cholesterol, ● Also referred to as “Ischemic Heart Disease” or
low sugar diet “Atherosclerotic Cardiovascular Disease”
○ Exercise ● Coronary arteries - comes from descending aorta
○ Weight reduction ○ Left coronary artery - lateral and anterior portion
○ Avoid stress (stress increased catecholamines) of the heart
○ Avoid smoking ■ Left anterior descending branch -
○ Avoid alcohol most commonly affected by CAD
○ Restrict caffeine ■ Circumflex branch
○ Relaxation techniques ○ Right coronary artery - inferior and posterior wall
of the heart
A. ANTIHYPERTENSIVE DRUGS ■ Posterior interventricular branch
■ Marginal branch
● Problem: High blood pressure ● Venous drainage
● Action: Normalize BP ○ Great cardiac vein
● Primary Adverse Effects: Hypotension ○ Middle cardiac vein
● Etiology: Idiopathic
Pheochromocytoma - increased BP due to increased ● Risk Factors - (Atherosclerosis):
catecholamines → increased SNS response ○ Deposition of calcium in the plaque makes it
hard → blood vessels are less elastic →
1. Alpha 1 antagonist (blockers) narrowing → decreased perfusion → ischemia
● Vasodilators ● Non-Modifiable Risk Factors:
● Prazosin, Terazosin, Doxazosin ○ Age - atypical symptoms
○ Sex - males > reproductive females
2. Alpha 2 agonists (CNS) ■ Estrogen - cardioprotective effects
● Decreases norepinephrine flow → decreases SNS (increase HDL)
response ■ Male = menopausal women
● Clonidine, Methyldopa ○ Family History
■ Atherosclerotic genes - 3x more prone
3. Beta antagonist/blockers to develop CAD
● A/E: Slows down HR ○ Past Health History
● Metoprolol, Propranolol
● Modifiable Risk Factors:
RENIN - ANGIOTENSIN - ALDOSTERONE SYSTEM (RAAS) ○
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 ● Signs and Symptoms: ○ Knowledge Deficit
○ Chest pain (angina - due to ischemia) ○ Ineffective Health Maintenance
○ Atypical symptoms (elderly): ○ Non-compliance
■ Shortness of breath ● Nursing Interventions:
■ Confusion ○ Stable Angina: Provide rest periods
○ Unstable Angina/Prinzmetal Angina:
ANGINA PECTORIS VS. MYOCARDIAL INFARCTION ■ Nitroglycerin FIRST because oxygen
will not enter the heart if the blood
vessels are not dilated.
Angina Pectoris Myocardial Infarction ■ Oxygen administration
● Diagnostic Test:
Imbalance between oxygen Ischemia and necrosis of the ○ Coronary angiography - done by cardiac
supply and cardiac workload cardiac cells catheterization under local anesthesia
○ ECG - non-invasive yet definitive
■ T-Wave Inversion - sign of
Reversible Irreversible
myocardial ischemia
■ Done during the pain
TYPES OF ANGINA ○ Blood tests
■ No enzyme elevation yet because
1. Stable Angina - due to increased cardiac workload there is no necrosis/injury yet.
2. Unstable Angina - due to severe atherosclerosis ■ Elevated homocysteine levels
● May occur even during rest ■ Elevated C-reactive proteins
● Preinfarction angina ■ Will indicate inflammation and risk for
3. Prinzmetal Angina - due to coronary vasospasm CAD
● May happen during resting/sleeping ■ Not definitive
4. Intractable Angina - severe pain ● Management:
● Levine Sign ○ Provide rest periods
5. Silent Ischemia - asymptomatic ○ Oxygen therapy
● Drug Therapy:
ASSESSMENT ○ Nitroglycerin - sublingual (acute attack - 3-5
mins); patch (chronic)
● Position/Location ■ Coronary vasodilator → increase O2
○ Chest/Substernal pain supply
● Provocation/Precipitating Factors ■ Peripheral vasodilator → decrease BP
○ Anger → decrease cardiac workload
○ Excitement ■ Can be given 3 times, with an interval
○ Exhaustion of 3-5 minutes.
● Quality ■ Sensitive to light, easily gets expired
○ M.I. - Constant, Not relieved by ■ Kept on a dark container
movement/breathing ■ Monitor BP before and after
○ “Crushing/excruciating pain” administration
○ “Feeling of impending doom” ■ S/E: Headache
○ “Heaviness on the chest” ○ Isosorbide Dinitrate/Mononitrate
● Radiation ■ Vasodilators
○ Radiates to the left shoulder, left neck, and left ■ Slow onset of action
jaw ○ Beta Blockers (--olol)
● Relieving Factors ■ Decrease HR → decrease cardiac
○ Angina pectoris - Rest, Nitroglycerin workload
○ M.I. - None ■ Monitor HR
● Severity ○ Calcium-channel blockers
○ Pain Scale ■ Vasodilators → decrease BP →
● Symptoms associated with other conditions decrease cardiac workload
○ Diaphoresis ■ Monitor BP
○ Palpitations ■ Diltiazem, Verapamil v
○ Tachycardia ● Surgical Management:
○ Restlessness ○ (PTCA) Percutaneous Transluminal Coronary
● Timing/Duration Angioplasty
○ Angina - less than 15 minutes ■ A balloon is inflated in the area of
○ M.I. - More than 30 minutes atherosclerosis.
■ Stent is inserted inside to keep the
A. ANGINA PECTORIS blood vessels open.

● Imbalance between oxygen supply and cardiac workload SITUATION

● Nursing Diagnosis:
○ Ineffective myocardial tissue perfusion A patient is experiencing unstable angina but has a BP of 80/60
○ Acute pain mmHg.
● Withhold nitroglycerin because it can further decrease
○ Anxiety r/t fear of unknown
BP.
■ May cause physical symptoms: ● Position the patient in modified trendelenburg.
restlessness → increase cardiac
workload
8
 B. MYOCARDIAL INFARCTION ■ Anticoagulant drugs (Low molecular
weight Heparin, Warfarin)
● Nursing Diagnosis: ○ Support cardiac function
○ Acute Pain ■ Vasodilators
■ Pain causes restlessness → increase ■ Calcium-channel blockers
cardiac workload ■ Beta blockers
○ Ineffective Myocardial Tissue Perfusion ○ Manage risk factors
■ Even administering oxygen will not ○ PTCA
relieve the pain. ○ CABG (Coronary Artery Bypass Graft) - open
○ Anxiety r/t fear of death heart surgery done under general anesthesia
● Complications: ■ Graft (saphenous veins/ internal
○ Risk for dysrhythmia thoracic/mammary artery) is attached
○ Risk for shock to the occluded vessel
○ Risk for decreased cardiac output
● Diagnostic Test: VII. HEART FAILURE
○ Angiography
○ ECG (taken during pain) ● A syndrome - group of signs and symptoms
■ Area of necrosis/infarction - ST ● A complication that led to inability of the heart to pump
segment elevation - early sign of MI ineffectively
■ Area/zone of injury - ST segment ● Causes:
depression ○ Cardiac
■ Zone of ischemia - T-Wave inversion ○ Non-Cardiac (e.g. COPD)
■ Old sign of M.I. - Inverted Q / ● Cardiac decompensation - heart grew so big that it can no
Pathologic Q Wave longer compensate
● Types:
○ Systolic HF - inability of the heart to contract
○ Diastolic HF - inability of the heart to relax
○ Left-Sided HF - left ventricle fails, most
common
○ Right-Sided HF - right ventricle fails
● Pathogenesis:
○ The heart grew so big (cardiac decompensation)
○ Cardiac Enzymes Elevation - protein released ○ LSHF: When left ventricle fails → decreased
by the cardiac cells in the blood as response to cardiac output → pressure in the left ventricle
injury (necrosis) increases → blood in the left atrium can’t be
■ CK MB Isoenzyme - most indicative pumped down → left atrium will have increased
and the most specific enzyme pressure → blood from the lungs can’t go to the
released by the cardiac cells; left atrium → backward pressure in the lungs →
increased level 4-6 hours after onset increased pressure in the pulmonary capillaries
of pain → fluid leaks out in the pulmonary capillaries →
■ Troponin - most reliable and most pulmonary edema
sensitive blood test; increased level ■ Paroxysmal nocturnal dyspnea
4-6 hours after onset of pain (or ■ Orthopnea
earlier than CK MB); persists to be ■ Dyspnea
elevated within 3 weeks ■ (+) Crackles/rales – fluid-filled alveoli
■ Myoglobin - earliest to be elevated (2 ■ Progressive cough
hours), but not definitive ○ RSHF: High pressure in the lungs → difficulty
■ CPK - enzyme released by all for the right ventricle to pump to the lungs →
muscles, not definitive increased pressure in the right ventricles and
■ LDH atrium → increased venous pressure → fluid
■ AST leaks out in the systemic circulation → Bipedal
● 2 Types of Myocardial Infarction edema
○ STEMI - ST elevation M.I. ■ Systemic edema
○ NSTEMI - Non-ST Elevation M.I. ■ Nursing Diagnosis: Fluid volume
■ Atypical sign of M.I. excess
■ Common in elderly ● Classification of Congestive Heart Failure:
● Management: ○ Class I - can do ordinary physical activities
○ Pain control is PRIORITY ! without S/S
■ Dependent: Morphine ■ Risk for activity intolerance
○ Oxygen administration ■ If a patient can tolerate one flight of
○ Within 3 hours, administer thrombolytic therapy stair after M.I., patient can resume
(USA) to dissolve the thrombus and provide sex activity
reperfusion ○ Class II - slight limitation of ADLs
■ Urokinase ■ Activity intolerance
■ Streptokinase ○ Class III - marked limitation of ADLs, no
■ Alteplase symptoms at rest
○ Administer antithrombotic drugs to prevent ■ Decreased cardiac output
formation of thrombus ○ Class IV - symptoms at rest
■ Antiplatelet drugs (Aspirin, ● Diagnostic Test:
Clopidogrel) ○ 2D Echocardiography - most definitive
9
 ○ Chest X-Ray - most initial ● Upper respiratory tract
○ Elevated BNP (Brain Natriuretic Peptide) - ○ Nose → larynx
protein released by the ventricles in response to ○ Kept open by cartilages
congestion ● Lower respiratory tract
● Nursing Diagnosis & Management: ○ Trachea → alveoli
○ Ineffective Airway Clearance/Ineffective ○ Bronchi and bronchioles are lined by smooth
Breathing Pattern/Impaired Gas Exchange muscles
■ Position - High Fowler’s ■ Smooth muscles contract → constrict
■ Oxygen administration ■ Smooth muscles relax → dilate
■ IV line ● Respiratory center (brainstem)
■ Furosemide - 40 mg IV stat ● Stimuli for respiration: Increased PCO2 (best stimuli for
■ Catheterize normal)
■ Monitor intake and output ○ Decreased PO2 (patients with COPD)
■ Monitor V/S (BP) ■ Keep oxygen in low flow
○ Fluid Volume Excess ● Diaphragm - supplied by phrenic nerve (C3 and C4)
■ Restrict fluid intake ○ Major muscle of respiration
■ Restrict sodium
■ Monitor intake and output RESPIRATION, VENTILATION, PERFUSION
■ Monitor V/S
■ Diuretics (Furosemide oral/ ● Respiration - gas exchange
Spironolactone) ● Ventilation - entry of air into the lungs/alveoli
■ Monitor K level ○ Compromise: Atelectasis
○ Decreased cardiac output r/t inability of the ● Perfusion - blood flows to the lungs
heart to pump effectively ○ Compromise: Pulmonary embolism
■ Increase cardiac contractility and
decrease cardiac workload MECHANICS OF BREATHING
● Interventions to decrease cardiac workload:
○ Provide rest periods ● Inspiration - active process for muscles to contract
○ Support cardiac functions ○ Diaphragm, External intercostals
■ ACE Inhibitors - vasodilator ○ Muscles contract → diaphragm flattens →
■ Angiotensin II receptor blockers increased thoracic cage → expansion of
■ Calcium channel blockers thoracic cage → expansion of lungs →
■ Beta blockers decreased pressure in the alveoli → air enters
○ Manage risk factors lungs
● Interventions to increase cardiac contractility: ● Expiration - passive process for recoil of the lungs
○ Cardiotonic drugs/Inotropic drugs ○ Stretch receptors prevent too much stretching to
■ Sympathomimetic drugs - enhance prevent collapse
SNS; (+) inotropic drugs - increase ○ Accessory muscles: Sternocleidomastoid,
cardiac contractility; (+) chronotropic internal intercostals (only used during labored
drugs - increase HR breathing)
➢ Dopamine, Dobutamine
➢ Cons: Heart is not yet fully ASSESSMENT
filled but the heart is
already pumping fast
● Inspection
■ Cardiac Glycosides - (+) inotropic
● Palpation
effects; increase release of calcium
● Percussion
from the cardiac cells for contraction;
● Auscultation
(-) chronotropic effect - slow down
○ Upper - bronchial
heart rate by prolonging cardiac
○ Middle - bronchovesicular
repolarization (slowly releasing
○ Lower - vesicular
potassium)
○ Adventitious sound - abnormal
➢ Digoxin, Digitalis (Monitor
■ Crackles
HR, ECG, K level; Maintain
■ Wheezing
therapeutic levels 0.5 - 2.0
■ Rhonchi/stridor
ng/ml; Do not combine with
■ Absent - atelectasis
calcium-channel blockers,
amiodarone; monitor for
DIAGNOSTIC TEST
signs of toxicity –
● Chest X-Ray
bradycardia, visual
● Thoracic cage X-Ray – check fracture
disturbances, lack of
● CT Scan/MRI – identify soft tissue muscles
appetite, nausea and
● Bronchoscopy – visualization of bronchioles
vomiting, ECG changes;
○ Assess gag reflex
anticipate antidote
● ABG
administration – digibind)
● Pulse oximeter
VIII. RESPIRATORY SYSTEM
● Pulmonary function test
○ Spirometry - volume and capacity of the lungs
ANATOMY AND PHYSIOLOGY
VOLUME
● An open system and has communication with outer
environment
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 ● Tidal Volume - the volume air that gets in and out of the DIAGNOSTIC TEST
lungs
○ 500 ml ● Chest X-Ray - hyperinflation of lungs due to trapping of air
● Inspiratory reserve volume - air that can still be inhaled (bronchospasm during expiration)
after normal inspiration ● ABG - respiratory alkalosis → respiratory acidosis
○ 3000 ml ● Pulse oximetry - low O2 saturation
● Expiratory reserve volume - air that can still be exhaled ● Spirometry - decreased ERV, increased RV, increased
after normal expiration FRC
○ 1100 ml ● Peak flow meter - determine degree of obstruction
● Residual volume - the air that is left in the lungs after
forceful expiration P MANAGEMENT
○ 1200 ml
● Dead space volume - volume of air that does not ● (1) Position: Orthopneic to promote expansion of alveoli
participate in gas exchange ● (2) Bronchodilator - inhalation
○ 150 ml ● (3) Oxygen administration
● Functional volume - volume of air that participates in the ● Provide rest
gas exchange ● Prevent infection
○ 350 ml ○ Handwashing
○ Physical distancing
CAPACITY ○ Wear mask, face shield
○ Avoid crowded places
● Inspiratory capacity - volume of air that is maximally ○ Avoid sick people
inhaled ○ Immunization
○ TV + IRV ● Treat infection
● Functional residual capacity - volume of air that is left in ○ Antibacterial/Antiviral
the lungs after normal expiration ● Support lung function: Bronchodilators
○ ERV + RV ○ Xanthines derivatives (Methylxanthines) -
● Vital capacity - volume of air that is maximally inhaled directly relax smooth muscles (e.g.
and maximally exhaled aminophylline, theophylline)
○ TV + IRV + ERV ■ A/E: Caffeine containing –
● Total lung capacity - total volume of air the lungs can tachycardia, palpitations, tremors
hold ○ Sympathomimetic bronchodilators/ beta-agonist
○ VC + RV (e.g. salbutamol, terbutaline)
○ Anticholinergic bronchodilators (e.g.
IX. OBSTRUCTIVE DISORDERS ipratropium/atrovent, tiotropium)
● Steroids - anti-inflammatory effect and decrease swelling
● Problem with air going in of bronchioles
● Bronchial Asthma - pulmonary disease characterized by ○ Beclomethasone, budesonide, prednisone,
bronchospasm; reversible and non-progressive dexamethasone, hydrocortisone
○ Acute attack of asthma ● Leukotriene receptor antagonists - block leukotriene
● Chronic Obstructive Pulmonary Disease - irreversible that causes bronchospasm → treatment of bronchospasm
and progressive ○ Montelukast
○ Acute exacerbation ● Hook to mechanical ventilator
● Prevent complications:
BRONCHIAL ASTHMA ○ Infection (Pneumonia)
○ Status asthmaticus - uncontrolled asthma attack
● Chronic pulmonary disease characterized by ○ Acute respiratory failure (ARF)
bronchospasm; reversible and non-progressive ■ PCO2 > 50 mmHg
● Chronic asthma can lead to emphysema ■ PO2 < 50 mmHg
● Etiology: Allergens - extrinsic asthma ○ Emphysema - due to air trapping that causes
○ Idiopathic - intrinsic asthma overdistension of alveoli
○ Allergens → antigen antibody formation → ● Manage complications
induce inflammation of the bronchioles → ● Prevent another attack
release of chemical mediators (histamine - will ○ Avoid allergens
cause swelling of the bronchioles; leukotriene - ○ Prophylaxis (Mast cell stabilizers to prevent
cause bronchospasm during expiration) → histamine release e.g. cromolyn sodium,
airway obstruction nedocromil)
○ Bronchospasm during expiration → wheezing
■ Air is trapped inside
○ Swelling of bronchioles → swelling of goblet
cells → increased mucus production → cough
and risk for infection
○ Airway obstruction → dyspnea → use of
accessory muscles (intercostal retraction) → CHRONIC OBSTRUCTIVE PULMONARY DISEASES
fatigue
○ Impaired gas exchange CHRONIC BRONCHITIS
on
■ Initially: respiratory alkalosis
■ Later: Respiratory acidosis ● Chronic bronchitis - chronic inflammation of bronchioles
○ More than 6 months

11
 ○ Permanent, irreversible, and progressive ● Collapse of alveolar wall → impaired gas exchange →
● Etiology: Environmental pollutants (smoking) decreased PO2 (hypoxemia), and increased PCO2
○ Pollutants → injury to the bronchioles → (hypercapnia) → stimulate of release of erythropoietin →
inflammation of bronchioles → hypertrophy of production of RBC → polycythemia → flushing of face
goblet cells → increased production of mucus → ○ “PINK PUFFER”
cough
○ Inflammation of bronchioles → swelling → DIAGNOSTIC EXAM
airway obstruction → dyspnea → use of
accessory muscles → intercostal retractions, ● Chest X-Ray - barrel chest, pneumonia
fatigue ● ABG - respiratory acidosis
○ Airway obstruction → impaired gas exchange → ● Pulse oximetry - low O2 saturation
respiratory acidosis (increased PCO2 and ● Spirometry - decreased ERV, increased RV, increased
decreased PO2) FRC, increased TLC
■ Hypoxemia - cyanosis, nail clubbing
■ “BLUE BLOATER” MANAGEMENT
● Clinical definition: Productive cough for 3 months for 2
consecutive years (despite normal Chest X-Ray) ● Position: Orthopneic
● Bronchodilator
DIAGNOSTIC EXAM ● O2 administration (low flow)
● Treat infection
● Chest X-Ray – pneumonia ● Manage dyspnea
● ABG – respiratory acidosis ○ Pursed lip breathing
● Pulse oximeter – low O2 saturation

MANAGEMENT PURPOSE OF PURSED LIP BREATHING:

● Prolong expiration
● Prevent alveolar collapse
● Position: Orthopneic ● Promote gas exchange
● Bronchodilator - inhalation ● Promote CO2 elimination
● O2 administration ● Strengthen respiratory muscles
○ Low flow oxygen ● Keep the airway open
● Treat infection
● Manage cough ● Support lung function
○ Increase OFI ○ Bronchodilators
○ Chest physiotherapy ○ Steroids
○ Postural drainage ○ Mechanical ventilator
○ Suction secretion ● Slow down progression of disease
○ Mucolytics - carbocysteine, acetylcysteine ○ Stop smoking
● Support lung function ○ Avoid infection and fatigue
○ Bronchodilators ● Prevent and manage complication:
○ Steroids ○ Pneumonia
○ Mechanical ventilation ○ Acute respiratory failure
● Prevent and manage complications: ○ Polycythemia (Erythrocytosis)
○ Pneumonia ■ Secondary and does not need direct
○ Acute respiratory failure treatment (treat COPD!)
○ Bronchiectasis ○ Simple/Spontaneous Pneumothorax - due to
● Slow down progression of disease: rupture of bleb or bullae
○ Stop smoking ■ Managed by thoracentesis
○ Avoid fatigue ○ Pulmonary hypertension - increased pulmonary
pressure > 25/9 mmHg
Bronchiectasis - complication of COPD and cystic fibrosis ■ Primary - idiopathic
● Characterized by permanent dilatation and destruction ■ Secondary - known causes (COPD,
of bronchi and bronchioles → buildup of mucus pulmonary embolism, kyphoscoliosis,
● Etiology: Repeated bacterial infection morbid obesity)
● Manifestations: Foul smelling sputum; Yellow, green,
rusty sputum; Halitosis (bad breath)
● Management: Massive antibacterial therapy; COPD → chronic hypoxemia → pulmonary vasoconstriction →
mechanical ventilator pulmonary hypertension
Manifestations:
● Dyspnea
EMPHYSEMA ● Tachypnea
● Tachycardia
● Emphysema - inflammation of alveoli ● Syncope
● Overdistension and destruction of alveolar wall
● Etiology: Environmental pollutants (smoking), chronic
asthma, Alpha 1 antitrypsin deficiency ○ Cor pulmonale
○ A1A - chemical that protects the lining of alveoli ○ Right-sided heart failure
● Air enters → inspiration followed by short expiratory phase ■ Pulmonary hypertension → difficult for
→ collapse of the alveolar wall → air trapping → dyspnea right ventricle to pump blood →
→ use of accessory muscles → hypertrophy of muscles pumping too much → enlargement of
● Air trapping → hyperinflated lungs (+ hypertrophy of right ventricle → cor pulmonale →
muscles) → barrel chest, fatigue
12
 right sided heart failure (bipedal C. PNEUMOTHORAX
edema) → pulmonary heart disease
● Air in the pleural space
X. RESTRICTIVE DISORDERS ● Classifications:
○ Close/Open
● Problem with expansion of lungs ○ Simple/Spontaneous Pneumothorax - due to
● Poor compliance: Elasticity, stretchability, and distensibility rupture of bleb/bullae
○ Traumatic Pneumothorax - opening → air will
A. FLAIL CHEST enter the pleural space → air is also getting out
○ Tension Pneumothorax - opening → air will
● Etiology: Chest trauma keep on entering the pleural space and not exit
○ Led to multiple rib fracture → collapse → deviated trachea → compression
○ Chest cavity failed to expand → pain of heart → obstructive shock
● Air enters the unaffected side → expansion of unaffected
side → affected side is drawn inwards and collapse SIGNS AND SYMPTOMS
● Air leaves the unaffected side and affected lung expands
→ PARADOXICAL BREATHING ● Dyspnea
○ Inhalation: affected side collapses ● Tachypnea
○ Exhalation: affected side expands ● Pain
● Cough
DIAGNOSTIC TEST ● Asymmetrical chest expansion
● Unequal tactile and vocal fremitus
● Chest X-Ray ● Absent breath sounds
● Thoracic Cage X-Ray ● Percussion: hyperresonant to tympanic

SIGNS AND SYMPTOMS MANAGEMENT

● Dyspnea ● Thoracentesis - aspirating fluid/air from the pleural space

● Tachypnea ○ Air - between 2nd and 3rd ICS (UP)
● Severe pain ○ Fluid - between 8th and 9th ICS (DOWN)
○ Superior border of the inferior rib - where needle
MANAGEMENT is injected
○ After: Position to unaffected side
● Support lung function ● Pleurodesis - injecting sticky substance in the cavity to
● Relief of pain slow down accumulation of fluid
● Manage fracture ● Chest Tube Thoracostomy
● Surgery (Open reduction with internal fixation) ○ Bottle 1: air and blood
■ Monitor amount and characteristic of
B. PLEURAL EFFUSION the drainage

● Accumulation of fluid
● “Hydrothorax”
● Normally, the pleural cavity has negative pressure. But
due to accumulation of fluid, there is increased pressure
(positive) and the lungs can no longer expand, and it will
collapse (atelectasis).
● Absent breath sounds
● Classifications:
○ Primary - idiopathic
○ Secondary - known causes (pneumonia, PTB,
malignancy

SIGNS AND SYMPTOMS

Bottle 1 (Air and Blood)
● Dyspnea ● Monitor amount and characteristic of the drainage
● Tachypnea
● Dry cough Bottle 2
● Pain - chest/back ● Monitor if bottle is normally functioning
○ Intermittent bubbling
● Asymmetrical chest expansion
○ Fluctuation or tidalling
● Unequal tactile and vocal fremitus
● Absent or diminished breath sounds
Bottle 3
● Percussion: Flat to Dull (normal: resonance) ● Monitor for continuous bubbling

DIAGNOSTIC TEST
NURSING CARE PLAN FOR CTT
● Chest X-Ray
● Ultrasound - approximate amount of fluid in the pleural ● Place the system below the level of chest
space ● Always have an extra bottle with sterile water at bedside

13
● If tubings are removed or disconnected from the bottle,
REINSERT.
● If tubings are dislodged from the chest wall, COVER.
● Avoid too much manipulation of the tubings as it may
cause tension pneumothorax.
● If there is no intermittent bubble in the 2nd bottle, assess
for LEAKAGE.
○ To assess leakage, get a clamp and temporarily
clamp the tubing near the insertion site.
● If there is no fluctuation in the 2nd bottle, assess for
OBSTRUCTION and RE-EXPANSION of lungs.
○ To assess obstruction:
■ Check KINKING of tubing. Reposition
the patient.
■ Check for CLOT. Refer.
○ To assess re-expansion:
■ Assess breath sounds.
■ Repeat Chest X-Ray.
● If there is no continuous bubbling in the 3rd bottle, check
the SUCTION (OFF).
● Palpate the area near the catheter for crepitus – sign of
subcutaneous emphysema.
○ Mark the area then reassess to check
worsening of crepitus, and refer.
● Assist in the removal.
○ Analgesic before and after.
○ After: Position to unaffected side to promote
lung expansion.
○ Chest X-Ray after 2 weeks

14