Cardiac Pathophysiology

Cardiac Pathophysiology

1

Pericarditis

• Often local manifestation of another

disease

• May present as:

– Acute pericarditis

– Pericardial effusion

– Constrictive pericarditis

2

Acute Pericarditis

• Acute inflammation of the pericardium

• Cause often unknown, but commonly

caused by infection, uremia, neoplasm, caused by infection, uremia, neoplasm,

myocardial infarction, surgery or trauma.

• Membranes become inflamed and

roughened, and exudate may develop

3

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 • 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 malaise4

Signs

• Often present with low grade fever and sinus

tachycardia

• Friction rub (sandpaper sound) may be

heard at cardiac apex and left sternal border 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.5

6

Treatment

• Treat symptoms

• Look for underlying cause

• If pericardial effusion develops, aspirate

excess fluidexcess fluid

• Acute pericarditis is usually self-limiting,

but can progress to chronic constrictive

pericarditis

7

Pericardial effusion

• Accumulation of fluid in the pericardial cavity

– May be transudate

– May be exudate

8

– May be blood

• Not clinically significant other than to indicate

underlying disorder, unless:

• Pressure becomes sufficient to cause cardiac

compression – cardiac tamponade

Outcome depends on how fast

fluid accumulates.

• If development is slow, pericardium can

stretch

• If develops quickly, even 50 -100 ml of • 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.9

Clinical manifestations

• Pulsus paradoxus – B.P. higher during

expiration than inspiration by 10 mm Hg

• Distant or muffled heart sounds

• Dyspnea on exertion • Dyspnea on exertion

• Dull chest pain

• Observable by x-ray or ultrasound

10

Treatment

• Pericardiocentesis

• Treat pain

• Surgery if cause is aneurysm or trauma

11

Constrictive (chronic)

pericarditis

• Years ago, synonymous with T.B.

• Today, usually idiopathic, or associated

with radiation exposures, rheumatoid

arthritis, uremia, or coronary bypass graft

12

Pathophysiology:

• Fibrous scarring with occasional

calcification of pericardium

• Causes parietal and visceral layers to

adhereadhere

• Pericardium becomes rigid, compressing

the heart C.O.

• Stenosis of veins entering atria

• Always develops gradually 13

Symptoms and Signs

• Exercise intolerance

• Dsypnea on exertion

• Fatigue

• Anorexia• Anorexia

14


• Weight loss

• Edema and ascites

• Distention of jugular vein (Kussmaul sign)

• Enlargement of the liver and/or spleen • Enlargement of the liver and/or spleen

• ECG shows inverted T wave and atrial

fibrillation

• Can be seen on imaging

15

Treatment

• Drugs and diet

– Digitalis

– Diuretics

– Sodium restriction– Sodium restriction

• Surgery to remove restrictive pericardium

16

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 pump17

Dilated cardiomyopathy

18

↓

Hypertrophic Cardiomyopathy

19

C.O. is normal,↑ inflow resistance, and

mitral valve incompetence, arrhythmais

and sudden death.

Restrictive cardiomyopathy

20

Reduced diastolic compliance of the ventricle.

C.O. is normal or ↑ formation of thrombi,

dilation of left atrium, and mitral valve

incompetence.

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)

21

22

• 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 enhancing drugs, > 50 % involve only the

tricuspid valve.

• Heart Murmur – sound caused by turbulent

blood flow through damaged valves.

23

Both types of valve disorders:

• Cause increased cardiac work, and increased volumes and pressures in the chambers.

• This leads to chamber dilation and hypertrophy.hypertrophy.

• Chamber dilation and myocardial hypertrophy are compensatory mechanisms to increase the pumping capability of the heart.

• Eventually, the heart fails from overwork

24

Aortic Stenosis

• Three common causes:

– Rheumatic heart disease -Streptococcus

infection – damage by bacteria and auto-

immune responseimmune response

– Congenital malformation

– Degeneration resulting from calcification

25

Aortic Stenosis

• Blood flow obstructed from LV into aorta during systole

• Causes increased work of LV

→ LV dilation & hypertrophy as compensation→ LV dilation & hypertrophy as compensation

→ prolonged contractions as compensation

Finally heart overwhelmed

• → increased pressures in LA, then lungs, then right heart

26


• Develops gradually

• Decreased stroke volume

• Reduced systolic blood pressure

• Narrowed pulse 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 27

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 LA28

• By causing LA to become pump:

• Get increased pulmonary vascular pressures;

pressures increase through LA into lung

– →pulmonary congestion– →pulmonary congestion

– →lung tissue changes to accommodate increased

pressures

– →increased pressure in pulmonary artery

– →increased pressure in right heart

– →right heart failure29

Clinical Manifestations

• Atrial enlargement can be seen on x-ray

• Rumbling decrescendo diastolic murmur,

and accentuated first heart soundand accentuated first heart sound

• Dyspnea

• Tachycardia and risk of atrial fibrillation

• Other signs and symptoms are of pulmonary

congestion and right heart failure 30

Aortic Regurgitation

• Caused by acute or chronic lesion of

rheumatic fever, bacterial endocarditits,

syphilis, hypertension, connective tissue

disorder (e.g.Marfan syndrome) or disorder (e.g.Marfan syndrome) or

atherosclerosis

31

• Reflux of blood from aorta to LV during

ventricular relaxation.

• Causes LV to pump more blood w/ each • Causes LV to pump more blood w/ each

contraction

LV hypertrophy

– LV takes on “globular shape”

increased pressures in LA, lung, right

heart32


• Widened pulse pressure

• Prominent carotid pulsations and

throbbing peripheral pulses

• Palpitations• Palpitations

• Fatigue

• Dyspnea

• Angina

• High-pitched or blowing heart sound

during diastole 33

Mitral Regurgitation

• Causes: mitral valve prolapse, rheumatic

heart disease, infective endocarditis,

connective tissue disorders, and

cardiomyopathycardiomyopathy

• Permits backflow of blood from the LV

into the LA during ventricular systole

• Loud pansystolic murmur that radiates

into the back and axilla34

• Causes blood to flow simultaneously to aorta and back to LA.

• Both LV & LA pump harder to move same blood twice

– →LV hypertrophy and dilation as compensation– →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, shock35


• Weakness and fatigue

• Dyspnea

• Palpitations• Palpitations

36

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 37


• Palpitations

• Tachycardia

• Light-headedness, syncope, fatigue, • Light-headedness, syncope, fatigue,

weakness

• Chest tightness, hyperventilation

• Anxiety, depression, panic attacks

• Atypical chest pain

38

• 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 • May be a normal variant

• Can see:

– chorda rupture

– ventricular failure

– systemic emboli and sudden death

• actually associated with minimal morbidity and mortality 39

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

40

General Treatment for Valve

disorders

• Antibiotics for Strep

• Anti-inflammatories for autoimmune

disorder

• Analgesics for pain

• Restrict physical activity

• Valve replacement surgery

41

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 disease42

Explanation of the termsExplanation of the terms

• Myocardial failure = abnormalities reside in the myocardium and

lead to inability of myocardium to fulfilling its function

•• Circulatory failureCirculatory failure = = any abnormality of the circulationany abnormality of the circulation•• Circulatory failureCirculatory failure = = any abnormality of the circulationany abnormality of the circulation

responsible for the inadequacy in bodyresponsible for the inadequacy in body tissue perfusion, e.g. tissue perfusion, e.g.

decreased blood volume, changesdecreased blood volume, changes of vascular tone, heart of vascular tone, heart

functiones functiones disordersdisorders

•• Congestive heart failureCongestive heart failure = clinical syndrome which is= clinical syndrome which is

developed due to developed due to accumulation of the blood inaccumulation of the blood in frontfront of the of the

left or right parts of the heartleft or right parts of the heart

General pathomechanisms involved in heart

failure development

Cardiac mechanical dysfunction can develop as a

consequence in preload, contractility and afterload

disorders

Disorders of preloadDisorders of preloadDisorders of preloadDisorders of preload

↑↑↑↑↑↑↑↑↑↑↑↑↑↑↑↑ preloadpreload→→ length of length of sarcomeresarcomere is more than is more than

optimal optimal →→→→→→→→↓↓↓↓↓↓↓↓ strength of contractionstrength of contraction

↓↓↓↓↓↓↓↓↓↓↓↓↓↓↓↓ preloadpreload→→ length of length of sarcomeresarcomere is well below theis well below the

optioptimalmal→→→→→→→→↓↓↓↓↓↓↓↓ strength of contractionstrength of contraction

Important: failing ventricle requires higher end-diastolicvolume to achieve the same improvement of CO

that normal ventricle achieves with lower

ventricular volumes

Disorders of contractility

In the most forms of heart failure the contractility of

myocardium is decreased (ischemia, hypoxia, acidosis,myocardium is decreased (ischemia, hypoxia, acidosis,

inflammation, toxins, metabolic disorders... )

Disorders of afterload due to:

•• fluid retentionfluid retention in the bodyin the body

•• ↑↑↑↑↑↑↑↑ arterial resistancearterial resistance

•• valvularvalvular heart diseases ( heart diseases ( stenosisstenosis ))

� ventricular dilatation

� reducing ventricular contractility (either generalized or

localized)

� diminished ejection fraction (i.e., that fraction of end-

Characteristic features of systolic dysfunction

(systolic failure)

� diminished ejection fraction (i.e., that fraction of end-

diastolic blood volume ejected from the ventricle

during each systolic contraction – les then 45%)

� in failing hearts, the LV end-diastolic volume (or

pressure) may increse as the stroke volume (or CO)

decreases

� ventricular cavity size is normal or small

� myocardial contractility is normal or hyperdynamic

� ejection fraction is normal (>50%) or supranormal

Characteristic features of diastolic dysfunctions

(diastolic failure)

� ejection fraction is normal (>50%) or supranormal

� ventricle is usually hypertrophied

� ventricle is filling slowly in early diastole (during the

period of passive filling)

� end-diastolic ventricular pressure is increased

Causes of heart pump failureCauses of heart pump failure

A. MECHANICAL ABNORMALITIESA. MECHANICAL ABNORMALITIES

1.1. Increased pressure loadIncreased pressure load

� central (aortic stenosis, aortic coarctation...)

� peripheral (systemic hypertension)� peripheral (systemic hypertension)

2. Increased volume load2. Increased volume load

� valvular regurgitation

� hypervolemia

3. Obstruction to ventricular filling3. Obstruction to ventricular filling

� valvular stenosis

� pericardial restriction

B. MYOCARDIAL DAMAGEB. MYOCARDIAL DAMAGE

1.1. PrimaryPrimary

a) a) ccardiomyopathyardiomyopathy

b) b) mmyocarditisyocarditisb) b) mmyocarditisyocarditis

c) c) ttoxicityoxicity ((e.g. e.g. alcohol)alcohol)

d) d) mmetabolicetabolic abnormalities (abnormalities (e.g. e.g. hyperthyreoidismhyperthyreoidism))

2. Secondary2. Secondary

a) a) ooxygenxygen deprivation (deprivation (e.g. e.g. coronary heart disease)coronary heart disease)

b) b) iinflammationnflammation ((e.g. e.g. increased metabolic demands)increased metabolic demands)

c) c) cchronichronic obstructive lung diseaseobstructive lung disease

C. ALTERED CARDIAC RHYTHMC. ALTERED CARDIAC RHYTHM

1. 1. vventricularentricular flutter and flutter and fibrilationfibrilation

2. 2. eextremextreme tachycardiastachycardias2. 2. eextremextreme tachycardiastachycardias

3. 3. eextremextreme bradycardiasbradycardias

Pathomechanisms involved in heart failurePathomechanisms involved in heart failure

A. A. PathomechanismsPathomechanisms involved in myocardial failureinvolved in myocardial failure

1.1. Damage of Damage of cardiomyocytescardiomyocytes →→→→→→→→ ↓↓↓↓↓↓↓↓ contractility, contractility,

↑↓↑↓↑↓↑↓↑↓↑↓↑↓↑↓ compliancecompliance

Consequences:Consequences:

•• defect in ATP production and utilisationdefect in ATP production and utilisation•• defect in ATP production and utilisationdefect in ATP production and utilisation

•• changes in contractile proteinschanges in contractile proteins

•• uncoupling of excitation uncoupling of excitation –– contraction processcontraction process

•• ↓↓↓↓↓↓↓↓ number of number of cardiomyocytescardiomyocytes

•• impairment of relaxation of impairment of relaxation of cardiomyocytescardiomyocytes withwith decrease decrease

compliance of myocardiumcompliance of myocardium

•• impaired of impaired of sympatosympato--adrenal system (SAS) adrenal system (SAS) →→→→→→→→ ↓↓↓↓↓↓↓↓ numbernumber of of

ββββββββ11--adrenergic receptors on the surface of adrenergic receptors on the surface of cardiomycytescardiomycytes

2. Changes of 2. Changes of neurohumoralneurohumoral control of the heart control of the heart

functionfunction

•• Physiology:Physiology: •• SNSSNS →→→→→→→→ ↑↑↑↑↑↑↑↑ contractilicontractilityty

↑↑↑↑↑↑↑↑ HRHR

↑↑↑↑↑↑↑↑ activactivity of ity of physiologic physiologic pacemakerspacemakers

•• PathophysiologyPathophysiology:: normal normal neurohumoralneurohumoral control iscontrol is

changed and creationchanged and creation of of

pathologicpathologic nneurohumoraleurohumoral

mechanismsmechanisms are presentare present

Pathophysiology of diastolic heart failurePathophysiology of diastolic heart failure

• systolic heart failure = failure of ejecting function of

the heart

• diastolic heart failure = failure of filling the • diastolic heart failure = failure of filling the

ventricles, ↑↑↑↑ resistance to filling of ventricles

But,But, wwhichhich of the cardiac cycle isof the cardiac cycle is realreal diastole ?diastole ?

Diastolic failure is a widely recognized

clinical entity

Definition of diastolic heart failureDefinition of diastolic heart failure

It is pathophysiological process characterized by symptoms and signs of

CHF, which is caused by ↑ filling resistance of ventricles and ↑

intraventricular diastolic pressure

Primary diastolic heart failurePrimary diastolic heart failurePrimary diastolic heart failurePrimary diastolic heart failure

- no signs and symptoms of systolic dysfunction is present

- ! up to 40% of patients suffering from heart failure!

Secondary diastolic heart failureSecondary diastolic heart failure

- diastolic dysfunction is the consequence of primary

systolic dysfunction

Main causes and pathomechanisms of

diastolic heart failure

1.1. structural disordersstructural disorders→↑→↑passive chamber stiffnesspassive chamber stiffness

a)a) intramyocardialintramyocardial

–– e.g. myocardial fibrosis, e.g. myocardial fibrosis, amyloidosisamyloidosis,, hypertrophy, hypertrophy,

myocardial ischemiamyocardial ischemia......myocardial ischemiamyocardial ischemia......

b) b) extramyocardialextramyocardial –– e.g. constrictive e.g. constrictive pericarditispericarditis

2. functional disorders 2. functional disorders →→→→→→→→ ↓↓↓↓↓↓↓↓ relaxation of chambersrelaxation of chambers e. g. myocardial e. g. myocardial

ischemia, advanced hypertrophy of ventricles,ischemia, advanced hypertrophy of ventricles,

failing myocardium, asynchronyfailing myocardium, asynchrony in heart in heart

functionsfunctions

Causes and mechanism participating on Causes and mechanism participating on

impaired ventricular relaxationimpaired ventricular relaxation

a) physiological changes in chamber relaxation due to:

– prolonged ventricular contraction

Relaxation of ventricles is not impaired !

b) pathological changes in chamber relaxation

due to: Impaired relaxation process

•••••••• delayed relaxation (retarded)delayed relaxation (retarded)

•••••••• incomplete (slowed) relaxationincomplete (slowed) relaxation

•••••••• Consequences of impaired ventricular relaxationConsequences of impaired ventricular relaxation

- filling of ventricles is more dependent on diastasis

and on the systole of atrias than in healthy subjects

SSymptomsymptoms and signs:and signs:

•••••••• exercise intoleranceexercise intolerance = = early sign of diastolic failureearly sign of diastolic failure

•••••••• ↓↓↓↓↓↓↓↓ coronary blood flow during diastolecoronary blood flow during diastole

• Causes and mechanisms involved in

development of ventricular stiffness

•••• ventricular compliance = passive property of ventricle

Source of compliance: cardiomyocytes and other heart

tissue to stretching

↓↓↓↓↓↓↓↓ VVentricularentricular compliance is caused by structuralcompliance is caused by structural

abnormalities abnormalities llocalizedocalized in myocardium and in in myocardium and in

extramyocardialextramyocardial tissuetissue

a) Intramyocardial causes : myocardial fibrosis,

hypertrophy of ventricular wall,restrictive

cardiomyopathy

b. Extramyocardial causes : constrictive pericarditis

The role of myocardial remodelling in genesis of

heart failure

•••• adaptive remodelling of the heart

•••• pathologic remodelling of the heart

Main causes and mechanisms involved in Main causes and mechanisms involved in

pathological pathological remodelationremodelation of the heartof the heart

1.Increased amount and size of myocytes = hypertrophy

Due to: - ↑↑↑↑ volume and/or pressure load

(excentric, concentric hypertrophy)

- hormonal stimulation of cardiomyocytes by

norepinephrine, angiotenzine IInorepinephrine, angiotenzine II

2. Increased % of non-myocytic cells in myocardium

and their influence on structure and function of heart

a. endothelial cells – endothelins : mitogenic ability →→ stimulation growth of smooth muscle cells of vessels,

fibroblasts

b. fibroblasts - ↑ production of kolagens

Symptoms and signs of heart failureSymptoms and signs of heart failure

1. forward failure: symptoms result from inability of the heart to pump

enough blood to the periphery (from left heart), or to

the lungs (from the right heart)

a) forward failure of left heart:- muscle weakness, fatigue,

dyspepsia, oliguria....

•••• general mechanism: tissue hypoperfusion

b) forward failure of right heart: - hypoperfusion of the

lungs →→→→ disorders of gas

exchange

- decreased blood supply

to the left heart

2. backward failure:

– symptoms result from inability of the heart to accept

the blood comming from periphery and from lungs

a. backward failure of left heart:

– increased pulmonary capillary pressure→ dyspnoea

and tachypnoea, pulmonary edema (cardiac asthma) →

→→ arterial hypoxemia and hypercapnia....

b. backward failure of right heart:

– increased pressure in systemic venous system→

→ peripheral edemas, hepatomegaly, ascites

→↑nocturnal diuresis....

Ischemic Heart Disease

• Coronary Artery Disease (CAD),

myocardial ischemia and myocardial

infarction are progression of conditions

that impair the pumping ability of the that impair the pumping ability of the

heart by depriving it of oxygen and

nutrients.

62

Coronary Artery Disease

• Any vascular disorder that narrows or

occludes the coronary arteries.

• Most common cause is atherosclerosis

63

• The arteries that supply the heart are the first branches

off the aorta

• Coronary artery disease decreases the blood flow to

the cardiac muscle.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. 64

Risk Factors

• Hyperlipidemia

• Hypertension

• Diabetes mellitus

• Genetic predisposition• Genetic predisposition

• Cigarette smoking

• Obesity

• Sedentary life-style

• Heavy alcohol consumption

• Higher risk for males than premenopausal women 65

Myocardial Ischemia

• Myocardial cell metabolic demands not met

• Time frame of coronary blockage:

– 10 seconds following coronary block

• Decreased strength of contractions• 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 66

• 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 67


• May hear extra, rapid heart sounds

• ECG changes:

– T wave inversion– T wave inversion

– ST segment depression

68

Chest Pain

• First symptom of those suffering myocardial ischemia.

• Called angina pectoris (angina – “pain”)

• Feeling of heaviness, pressure• Feeling of heaviness, pressure

• Moderate to severe

• In substernal area

• Often mistaken for indigestion

• May radiate to neck, jaw, left arm/ shoulder 69

• Due to :

– Accumulation of lactic acid in myocytes or

– Stretching of myocytes– Stretching of myocytes

• Three types of angina pectoris:

– Stable, unstable and Prinzmetal

70

Stable angina pectoris

• Caused by chronic coronary obstruction

• Recurrent predictable chest pain

• Gradual narrowing and hardening of vessels • 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 71

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.• 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 72

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.

73

Silent Ischemia

• Totally asymptomatic

• May be due abnormality in innervation

• Or due to lower level of inflammatory

cytokinescytokines

74

Treatment

• Pharmacologically manipulate blood pressure, heart

rate, and contractility to decrease oxygen demands

• Nitrates dilate peripheral blood vessels and• Nitrates dilate peripheral blood vessels and

• Decrease oxygen demand

• Increase oxygen supply

• Relieve coronary spasm

75

• � blockers:

– Block sympathetic input, so

– Decrease heart rate, so

– Decrease oxygen demand– Decrease oxygen demand

• Digitalis

– Increases the force of contraction

• Calcium channel blockers

• Antiplatelet agents (aspirin, etc.) 76

Surgical treatment

• Angioplasty – mechanical opening of

vessels

• Revascularization – bypass

– Replace or shut around occluded

vessels

77

Myocardial infarction

• Necrosis of cardiac myocytes

– Irreversible

– Commonly affects left ventricle

– Follows after more than 20 minutes of – Follows after more than 20 minutes of

ischemia

78

Structural, functional

changes

• Decreased contractility

• Decreased LV compliance

• Decreased stroke volume• Decreased stroke volume

• Dysrhythmias

• Inflammatory response is severe

• Scarring results –

– Strong, but stiff; can’t contract like healthy cells 79


• Sudden, severe chest pain

– Similar to pain with ischemia, but stronger

– Not relieved by nitrates

– Radiates to neck, jaw, shoulder, left arm– 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)

80

• Blood test show several markers:

– Leukocytosis

– Increased blood sugar

– Increased plasma enzymes

• Creatine kinase

• Lactic dehydrogenase

• Aspartate aminotransferase (AST or SGOT)

– Cardiac-specific troponin 81

ECG changes

• Pronounced, persisting Q waves

• ST elevation

• T wave inversion• T wave inversion

82

Treatment

• First 24 hours crucial

• Hospitalization, bed rest

• ECG monitoring for arrhythmias• ECG monitoring for arrhythmias

• Pain relief (morphine, nitroglycerin)

• Thrombolytics to break down clots

• Administer oxygen

• Revascularization interventions: by-pass grafts, stents

or balloon angioplasty 83

Documents

Cardiac Pathophysiology