Download - Cardiac Pathophysiology
![Page 1: Cardiac Pathophysiology](https://reader031.vdocuments.us/reader031/viewer/2022012922/56813472550346895d9b55af/html5/thumbnails/1.jpg)
1
Cardiac Pathophysiology
![Page 2: Cardiac Pathophysiology](https://reader031.vdocuments.us/reader031/viewer/2022012922/56813472550346895d9b55af/html5/thumbnails/2.jpg)
2
Pericarditis
• Often local manifestation of another disease
• May present as:
– Acute pericarditis
– Pericardial effusion
– Constrictive pericarditis
![Page 3: Cardiac Pathophysiology](https://reader031.vdocuments.us/reader031/viewer/2022012922/56813472550346895d9b55af/html5/thumbnails/3.jpg)
3
Acute Pericarditis
• Acute inflammation of the pericardium
• Cause often unknown, but commonly caused by infection, uremia, neoplasm, myocardial infarction, surgery or trauma.
• Membranes become inflamed and roughened, and exudate may develop
![Page 4: Cardiac Pathophysiology](https://reader031.vdocuments.us/reader031/viewer/2022012922/56813472550346895d9b55af/html5/thumbnails/4.jpg)
4
Symptoms:• Sudden onset of severe chest pain that
becomes worse with respiratory movements and with lying down.
• Generally felt in the anterior chest, but pain may radiate to the back.
• May be confused initially with acute myocardial infarction
• Also report dysphagia, restlessness, irritability, anxiety, weakness and malaise
![Page 5: Cardiac Pathophysiology](https://reader031.vdocuments.us/reader031/viewer/2022012922/56813472550346895d9b55af/html5/thumbnails/5.jpg)
5
Signs• Often present with low grade fever and
sinus tachycardia
• Friction rub (sandpaper sound) may be heard at cardiac apex and left sternal border and is diagnostic for pericarditis (but may be intermittent)
• ECG changes reflect inflammatory process through PR segment depression and ST segment elevation.
![Page 6: Cardiac Pathophysiology](https://reader031.vdocuments.us/reader031/viewer/2022012922/56813472550346895d9b55af/html5/thumbnails/6.jpg)
6
![Page 7: Cardiac Pathophysiology](https://reader031.vdocuments.us/reader031/viewer/2022012922/56813472550346895d9b55af/html5/thumbnails/7.jpg)
7
Treatment• Treat symptoms
• Look for underlying cause
• If pericardial effusion develops, aspirate excess fluid
• Acute pericarditis is usually self-limiting, but can progress to chronic constrictive pericarditis
![Page 8: Cardiac Pathophysiology](https://reader031.vdocuments.us/reader031/viewer/2022012922/56813472550346895d9b55af/html5/thumbnails/8.jpg)
8
Pericardial effusion• Accumulation of fluid in the pericardial cavity
– May be transudate– May be exudate– May be blood
• Not clinically significant other than to indicate underlying disorder, unless:
• Pressure becomes sufficient to cause cardiac compression – cardiac tamponade
![Page 9: Cardiac Pathophysiology](https://reader031.vdocuments.us/reader031/viewer/2022012922/56813472550346895d9b55af/html5/thumbnails/9.jpg)
9
• If development is slow, pericardium can stretch
• If develops quickly, even 50 -100 ml of fluid can cause problems
• When pressure in pericardium = diastolic pressure, get ↓ filling of right atrium, ↓ filling of ventricles, ↓ cardiac output → circulatory collapse.
Outcome depends on how fast fluid accumulates.
![Page 10: Cardiac Pathophysiology](https://reader031.vdocuments.us/reader031/viewer/2022012922/56813472550346895d9b55af/html5/thumbnails/10.jpg)
10
Clinical manifestations
• Pulsus paradoxus – B.P. higher during expiration than inspiration by 10 mm Hg
• Distant or muffled heart sounds
• Dyspnea on exertion
• Dull chest pain
• Observable by x-ray or ultrasound
![Page 11: Cardiac Pathophysiology](https://reader031.vdocuments.us/reader031/viewer/2022012922/56813472550346895d9b55af/html5/thumbnails/11.jpg)
11
Treatment
• Pericardiocentesis
• Treat pain
• Surgery if cause is aneurysm or trauma
![Page 12: Cardiac Pathophysiology](https://reader031.vdocuments.us/reader031/viewer/2022012922/56813472550346895d9b55af/html5/thumbnails/12.jpg)
12
Constrictive (chronic) pericarditis
• Years ago, synonymous with T.B.
• Today, usually idiopathic, or associated with radiation exposures, rheumatoid arthritis, uremia, or coronary bypass graft
![Page 13: Cardiac Pathophysiology](https://reader031.vdocuments.us/reader031/viewer/2022012922/56813472550346895d9b55af/html5/thumbnails/13.jpg)
13
• Fibrous scarring with occasional calcification of pericardium
• Causes parietal and visceral layers to adhere
• Pericardium becomes rigid, compressing the heart →↓ C.O.
• Stenosis of veins entering atria
• Always develops gradually
Pathophysiology:
![Page 14: Cardiac Pathophysiology](https://reader031.vdocuments.us/reader031/viewer/2022012922/56813472550346895d9b55af/html5/thumbnails/14.jpg)
14
Symptoms and Signs
• Exercise intolerance
• Dsypnea on exertion
• Fatigue
• Anorexia
![Page 15: Cardiac Pathophysiology](https://reader031.vdocuments.us/reader031/viewer/2022012922/56813472550346895d9b55af/html5/thumbnails/15.jpg)
15
Clinical manifestations
• Weight loss
• Edema and ascites
• Distention of jugular vein (Kussmaul sign)
• Enlargement of the liver and/or spleen
• ECG shows inverted T wave and atrial fibrillation
• Can be seen on imaging
![Page 16: Cardiac Pathophysiology](https://reader031.vdocuments.us/reader031/viewer/2022012922/56813472550346895d9b55af/html5/thumbnails/16.jpg)
16
Treatment
• Drugs and diet
– Digitalis
– Diuretics
– Sodium restriction
• Surgery to remove restrictive pericardium
![Page 17: Cardiac Pathophysiology](https://reader031.vdocuments.us/reader031/viewer/2022012922/56813472550346895d9b55af/html5/thumbnails/17.jpg)
17
Cardiomyopathies• Disorders of the heart muscle
• Most cases idiopathic
• Many due to ischemic heart disease and hypertension.
• Three categories:– Dilated ( formerly, congestive)– Hypertrophic– Restrictive
• Heart loses effectiveness as a pump
![Page 18: Cardiac Pathophysiology](https://reader031.vdocuments.us/reader031/viewer/2022012922/56813472550346895d9b55af/html5/thumbnails/18.jpg)
18
Dilated cardiomyopathy
↓ C.O.; ↑ thrombi formation ; ↓ contractility, and mitral valve incompetence, arrhythmias Tx: relieve symptoms of heart failure, decrease workload, and anticoagulants; transplants
![Page 19: Cardiac Pathophysiology](https://reader031.vdocuments.us/reader031/viewer/2022012922/56813472550346895d9b55af/html5/thumbnails/19.jpg)
19
Hypertrophic Cardiomyopathy
C.O. is normal,↑ inflow resistance, and mitral valve incompetence, arrhythmais and sudden death.
![Page 20: Cardiac Pathophysiology](https://reader031.vdocuments.us/reader031/viewer/2022012922/56813472550346895d9b55af/html5/thumbnails/20.jpg)
20
Restrictive cardiomyopathy
Reduced diastolic compliance of the ventricle. C.O. is normal or↓; ↑ formation of thrombi, dilation of left atrium, and mitral valve incompetence.
![Page 21: Cardiac Pathophysiology](https://reader031.vdocuments.us/reader031/viewer/2022012922/56813472550346895d9b55af/html5/thumbnails/21.jpg)
21
Disorders of the Endocardium:Valvular dysfunction
• Endocardial disorders damage heart valves
• Changes can lead to :
– Valvular Stenosis = too narrow
– Valvular Regurgitation = too leaky
(or insufficiency or incompetence)
![Page 22: Cardiac Pathophysiology](https://reader031.vdocuments.us/reader031/viewer/2022012922/56813472550346895d9b55af/html5/thumbnails/22.jpg)
22
![Page 23: Cardiac Pathophysiology](https://reader031.vdocuments.us/reader031/viewer/2022012922/56813472550346895d9b55af/html5/thumbnails/23.jpg)
23
• Valves that are most often affected are the mitral and aortic valves, but in I.V. drug users and in athletes that inject performance enhancing drugs, > 50 % involve only the tricuspid valve.
• Heart Murmur – sound caused by turbulent blood flow through damaged valves.
![Page 24: Cardiac Pathophysiology](https://reader031.vdocuments.us/reader031/viewer/2022012922/56813472550346895d9b55af/html5/thumbnails/24.jpg)
24
Both types of valve disorders:• Cause increased cardiac work, and
increased volumes and pressures in the chambers.
• This leads to chamber dilation and hypertrophy.
• Chamber dilation and myocardial hypertrophy are compensatory mechanisms to increase the pumping capability of the heart.
• Eventually, the heart fails from overwork
![Page 25: Cardiac Pathophysiology](https://reader031.vdocuments.us/reader031/viewer/2022012922/56813472550346895d9b55af/html5/thumbnails/25.jpg)
25
Aortic Stenosis
• Three common causes:– Rheumatic heart disease -Streptococcus
infection – damage by bacteria and auto-immune response
– Congenital malformation– Degeneration resulting from calcification
![Page 26: Cardiac Pathophysiology](https://reader031.vdocuments.us/reader031/viewer/2022012922/56813472550346895d9b55af/html5/thumbnails/26.jpg)
26
• Blood flow obstructed from LV into aorta during systole
Causes increased work of LV→ LV dilation & hypertrophy as
compensation→ prolonged contractions as
compensationFinally heart overwhelmed
• → increased pressures in LA, then lungs, then right heart
Aortic Stenosis
![Page 27: Cardiac Pathophysiology](https://reader031.vdocuments.us/reader031/viewer/2022012922/56813472550346895d9b55af/html5/thumbnails/27.jpg)
27
Clinical manifestations• Develops gradually
• Decreased stroke volume
• Reduced systolic blood pressure
• Narrowed pulse pressure
• Heart rate often slow and pulse faint
• Crescendo-decrescendo heart murmur
• Angina, dizziness, syncope, fatigue
• Can lead to dysrhythmias, myocardial infarction, and left heart failure
![Page 28: Cardiac Pathophysiology](https://reader031.vdocuments.us/reader031/viewer/2022012922/56813472550346895d9b55af/html5/thumbnails/28.jpg)
28
Mitral Stenosis• Most common of all valve disorders
• Usually the result of rheumatic fever or bacterial endocarditis
• During healing the orifice narrows, the valves become fibrous and fused, and chordae tendineae become shortened
• Get decreased flow from LA to LV during filling
• Results in hypertrophy of LA
![Page 29: Cardiac Pathophysiology](https://reader031.vdocuments.us/reader031/viewer/2022012922/56813472550346895d9b55af/html5/thumbnails/29.jpg)
29
• By causing LA to become pump:
• Get increased pulmonary vascular pressures; pressures increase through LA into lung
• →pulmonary congestion• →lung tissue changes to accommodate
increased pressures• →increased pressure in pulmonary artery• →increased pressure in right heart• →right heart failure
![Page 30: Cardiac Pathophysiology](https://reader031.vdocuments.us/reader031/viewer/2022012922/56813472550346895d9b55af/html5/thumbnails/30.jpg)
30
Clinical Manifestations • Atrial enlargement can be seen on x-ray
• Rumbling decrescendo diastolic murmur, and accentuated first heart sound
• Dyspnea
• Tachycardia and risk of atrial fibrillation
• Other signs and symptoms are of pulmonary congestion and right heart failure
![Page 31: Cardiac Pathophysiology](https://reader031.vdocuments.us/reader031/viewer/2022012922/56813472550346895d9b55af/html5/thumbnails/31.jpg)
31
Aortic Regurgitation
• Caused by acute or chronic lesion of rheumatic fever, bacterial endocarditits, syphilis, hypertension, connective tissue disorder (e.g.Marfan syndrome) or atherosclerosis
![Page 32: Cardiac Pathophysiology](https://reader031.vdocuments.us/reader031/viewer/2022012922/56813472550346895d9b55af/html5/thumbnails/32.jpg)
32
• Reflux of blood from aorta to LV during ventricular relaxation.
• Causes LV to pump more blood w/ each contraction
• → LV hypertrophy
– LV takes on “globular shape”• → increased pressures in LA, lung, right
heart
![Page 33: Cardiac Pathophysiology](https://reader031.vdocuments.us/reader031/viewer/2022012922/56813472550346895d9b55af/html5/thumbnails/33.jpg)
33
Clinical manifestations• Widened pulse pressure
• Prominent carotid pulsations and throbbing peripheral pulses
• Palpitations
• Fatigue
• Dyspnea
• Angina
• High-pitched or blowing heart sound during diastole
![Page 34: Cardiac Pathophysiology](https://reader031.vdocuments.us/reader031/viewer/2022012922/56813472550346895d9b55af/html5/thumbnails/34.jpg)
34
Mitral Regurgitation • Causes: mitral valve prolapse, rheumatic
heart disease, infective endocarditis, connective tissue disorders, and cardiomyopathy
• Permits backflow of blood from the LV into the LA during ventricular systole
• Loud pansystolic murmur that radiates into the back and axilla
![Page 35: Cardiac Pathophysiology](https://reader031.vdocuments.us/reader031/viewer/2022012922/56813472550346895d9b55af/html5/thumbnails/35.jpg)
35
• Causes blood to flow simultaneously to aorta and back to LA.
• Both LV and LA pump harder to move same blood twice– →LV hypertrophy and dilation as
compensation– Compensation works awhile, then see ↓C.O.– → heart failure– Also →LA hypertrophy
• → increased pressures through lungs → ↑ pressures in right heart →right heart failure
• Can see edema, shock
![Page 36: Cardiac Pathophysiology](https://reader031.vdocuments.us/reader031/viewer/2022012922/56813472550346895d9b55af/html5/thumbnails/36.jpg)
36
Clinical Manifestations
• Weakness and fatigue
• Dyspnea
• Palpitations
![Page 37: Cardiac Pathophysiology](https://reader031.vdocuments.us/reader031/viewer/2022012922/56813472550346895d9b55af/html5/thumbnails/37.jpg)
37
Mitral Valve Prolapse
• Cusps of valve billow upward into the LA during ventricular systole
• Mitral regurgitation can occur
• Most common valve disorder in U.S.
• Studies suggest an autosomal dominant inheritance pattern
• Many cases completely asymptomatic
• Regurgitant murmur or midsystolic click
![Page 38: Cardiac Pathophysiology](https://reader031.vdocuments.us/reader031/viewer/2022012922/56813472550346895d9b55af/html5/thumbnails/38.jpg)
38
Clinical manifestations
• Palpitations
• Tachycardia
• Light-headedness, syncope, fatigue, weakness
• Chest tightness, hyperventilation
• Anxiety, depression, panic attacks
• Atypical chest pain
![Page 39: Cardiac Pathophysiology](https://reader031.vdocuments.us/reader031/viewer/2022012922/56813472550346895d9b55af/html5/thumbnails/39.jpg)
39
• Once considered to be a psychiatric malady
• May have an autonomic dysfunction in which large quantities of catecholamines are produced.
• May be a normal variant
• Can see:–chorda rupture–ventricular failure–systemic emboli and sudden death
• actually associated with minimal morbidity and mortality
![Page 40: Cardiac Pathophysiology](https://reader031.vdocuments.us/reader031/viewer/2022012922/56813472550346895d9b55af/html5/thumbnails/40.jpg)
40
Management
• Echocardiography for diagnosis
• Related to degree of regurgitation
• Antibiotics before invasive procedures blockers to relieve syncope, severe chest
pain, or palpitations
• Avoid hypovolemia
• Surgical repair
![Page 41: Cardiac Pathophysiology](https://reader031.vdocuments.us/reader031/viewer/2022012922/56813472550346895d9b55af/html5/thumbnails/41.jpg)
41
General Treatment for Valve disorders
• Antibiotics for Strep
• Anti-inflammatories for autoimmune disorder
• Analgesics for pain
• Restrict physical activity
• Valve replacement surgery
![Page 42: Cardiac Pathophysiology](https://reader031.vdocuments.us/reader031/viewer/2022012922/56813472550346895d9b55af/html5/thumbnails/42.jpg)
42
Heart failure
• Definition – When heart as a pump is insufficient to meet the metabolic requirements of tissues.
• Acute heart failure– 65% survival rate
• Chronic heart failure – Most common cause is ischemic heart
disease
![Page 43: Cardiac Pathophysiology](https://reader031.vdocuments.us/reader031/viewer/2022012922/56813472550346895d9b55af/html5/thumbnails/43.jpg)
43
Ischemic Heart Disease
• Coronary Artery Disease (CAD), myocardial ischemia and myocardial infarction are progression of conditions that impair the pumping ability of the heart by depriving it of oxygen and nutrients.
![Page 44: Cardiac Pathophysiology](https://reader031.vdocuments.us/reader031/viewer/2022012922/56813472550346895d9b55af/html5/thumbnails/44.jpg)
44
Coronary Artery Disease• Any vascular disorder that narrows or
occludes the coronary arteries.
• Most common cause is atherosclerosis
![Page 45: Cardiac Pathophysiology](https://reader031.vdocuments.us/reader031/viewer/2022012922/56813472550346895d9b55af/html5/thumbnails/45.jpg)
45
• The arteries that supply the heart are the first branches off the aorta
• Coronary artery disease decreases the blood flow to the cardiac muscle.
• Persistent ischemia or complete occlusion leads to hypoxia.
• Hypoxia can cause tissue death or infarction, which is a “heart attack,” which accounts for about one third of all deaths in U.S.
![Page 46: Cardiac Pathophysiology](https://reader031.vdocuments.us/reader031/viewer/2022012922/56813472550346895d9b55af/html5/thumbnails/46.jpg)
46
Risk Factors• Hyperlipidemia
• Hypertension
• Diabetes mellitus
• Genetic predisposition
• Cigarette smoking
• Obesity
• Sedentary life-style
• Heavy alcohol consumption
• Higher risk for males than premenopausal women
![Page 47: Cardiac Pathophysiology](https://reader031.vdocuments.us/reader031/viewer/2022012922/56813472550346895d9b55af/html5/thumbnails/47.jpg)
47
Myocardial Ischemia• Myocardial cell metabolic demands not met• Time frame of coronary blockage:
• 10 seconds following coronary block–Decreased strength of contractions–Abnormal hemodynamics
• See a shift in metabolism, so within minutes: –Anaerobic metabolism takes over–Get build-up of lactic acid, which is toxic within
the cell–Electrolyte imbalances–Loss of contractibility
![Page 48: Cardiac Pathophysiology](https://reader031.vdocuments.us/reader031/viewer/2022012922/56813472550346895d9b55af/html5/thumbnails/48.jpg)
48
• 20 minutes after blockage–Myocytes are still viable, so–If blood flow is restored, and increased
aerobic metabolism, and cell repair,– →Increased contractility
• About 30-45 minutes after blockage, if no relief
–Cardiac infarct & cell death
![Page 49: Cardiac Pathophysiology](https://reader031.vdocuments.us/reader031/viewer/2022012922/56813472550346895d9b55af/html5/thumbnails/49.jpg)
49
Clinical Manifestations
• May hear extra, rapid heart sounds
• ECG changes:
– T wave inversion
– ST segment depression
![Page 50: Cardiac Pathophysiology](https://reader031.vdocuments.us/reader031/viewer/2022012922/56813472550346895d9b55af/html5/thumbnails/50.jpg)
50
Chest Pain• First symptom of those suffering myocardial
ischemia.
• Called angina pectoris (angina – “pain”)
• Feeling of heaviness, pressure
• Moderate to severe
• In substernal area
• Often mistaken for indigestion
• May radiate to neck, jaw, left arm/ shoulder
![Page 51: Cardiac Pathophysiology](https://reader031.vdocuments.us/reader031/viewer/2022012922/56813472550346895d9b55af/html5/thumbnails/51.jpg)
51
• Due to :– Accumulation of lactic acid in myocytes or– Stretching of myocytes
• Three types of angina pectoris:– Stable, unstable and Prinzmetal
![Page 52: Cardiac Pathophysiology](https://reader031.vdocuments.us/reader031/viewer/2022012922/56813472550346895d9b55af/html5/thumbnails/52.jpg)
52
Stable angina pectoris
• Caused by chronic coronary obstruction
• Recurrent predictable chest pain
• Gradual narrowing and hardening of vessels so that they cannot dilate in response to increased demand of physical exertion or emotional stress
• Lasts approx. 3-5 minutes
• Relieved by rest and nitrates
![Page 53: Cardiac Pathophysiology](https://reader031.vdocuments.us/reader031/viewer/2022012922/56813472550346895d9b55af/html5/thumbnails/53.jpg)
53
Prinzmetal angia pectoris(Variant angina)
• Caused by abnormal vasospasm of normal vessels (15%) or near atherosclerotic narrowing (85%)
• Occurs unpredictably and almost exclusively at rest.
• Often occurs at night during REM sleep
• May result from hyperactivity of sympathetic nervous system, increased calcium flux in muscle or impaired production of prostaglandin
![Page 54: Cardiac Pathophysiology](https://reader031.vdocuments.us/reader031/viewer/2022012922/56813472550346895d9b55af/html5/thumbnails/54.jpg)
54
Unstable Angina pectoris
• Lasts more than 20 minutes at rest, or rapid worsening of a pre-existing angina
• May indicate a progression to M.I.
![Page 55: Cardiac Pathophysiology](https://reader031.vdocuments.us/reader031/viewer/2022012922/56813472550346895d9b55af/html5/thumbnails/55.jpg)
55
Silent Ischemia
• Totally asymptomatic
• May be due abnormality in innervation
• Or due to lower level of inflammatory cytokines
![Page 56: Cardiac Pathophysiology](https://reader031.vdocuments.us/reader031/viewer/2022012922/56813472550346895d9b55af/html5/thumbnails/56.jpg)
56
Treatment• Pharmacologically manipulate blood
pressure, heart rate, and contractility to decrease oxygen demands
• Nitrates dilate peripheral blood vessels and
• Decrease oxygen demand
• Increase oxygen supply
• Relieve coronary spasm
![Page 57: Cardiac Pathophysiology](https://reader031.vdocuments.us/reader031/viewer/2022012922/56813472550346895d9b55af/html5/thumbnails/57.jpg)
57
blockers:
– Block sympathetic input, so
– Decrease heart rate, so
– Decrease oxygen demand
• Digitalis
– Increases the force of contraction
• Calcium channel blockers
• Antiplatelet agents (aspirin, etc.)
![Page 58: Cardiac Pathophysiology](https://reader031.vdocuments.us/reader031/viewer/2022012922/56813472550346895d9b55af/html5/thumbnails/58.jpg)
58
Surgical treatment
• Angioplasty – mechanical opening of vessels
• Revascularization – bypass
– Replace or shut around occluded vessels
![Page 59: Cardiac Pathophysiology](https://reader031.vdocuments.us/reader031/viewer/2022012922/56813472550346895d9b55af/html5/thumbnails/59.jpg)
59
Myocardial infarction
• Necrosis of cardiac myocytes– Irreversible– Commonly affects left ventricle– Follows after more than 20 minutes of
ischemia
![Page 60: Cardiac Pathophysiology](https://reader031.vdocuments.us/reader031/viewer/2022012922/56813472550346895d9b55af/html5/thumbnails/60.jpg)
60
Structural, functional changes• Decreased contractility
• Decreased LV compliance
• Decreased stroke volume
• Dysrhythmias
• Inflammatory response is severe
• Scarring results –– Strong, but stiff; can’t contract like healthy
cells
![Page 61: Cardiac Pathophysiology](https://reader031.vdocuments.us/reader031/viewer/2022012922/56813472550346895d9b55af/html5/thumbnails/61.jpg)
61
Clinical manifestations• Sudden, severe chest pain
– Similar to pain with ischemia, but stronger– Not relieved by nitrates– Radiates to neck, jaw, shoulder, left arm
• Indigestion, nausea, vomiting
• Fatigue, weakness, anxiety, restlessness and feelings of impending doom.
• Abnormal heart sounds possible (S3,S4)
![Page 62: Cardiac Pathophysiology](https://reader031.vdocuments.us/reader031/viewer/2022012922/56813472550346895d9b55af/html5/thumbnails/62.jpg)
62
• Blood test show several markers:– Leukocytosis– Increased blood sugar– Increased plasma enzymes
• Creatine kinase• Lactic dehydrogenase• Aspartate aminotransferase (AST or
SGOT)
– Cardiac-specific troponin
![Page 63: Cardiac Pathophysiology](https://reader031.vdocuments.us/reader031/viewer/2022012922/56813472550346895d9b55af/html5/thumbnails/63.jpg)
63
ECG changes
• Pronounced, persisting Q waves
• ST elevation
• T wave inversion
![Page 64: Cardiac Pathophysiology](https://reader031.vdocuments.us/reader031/viewer/2022012922/56813472550346895d9b55af/html5/thumbnails/64.jpg)
64
Treatment
• First 24 hours crucial
• Hospitalization, bed rest
• ECG monitoring for arrhythmias
• Pain relief (morphine, nitroglycerin)
• Thrombolytics to break down clots
• Administer oxygen
• Revascularization interventions: by-pass grafts, stents or balloon angioplasty