79
1 Cardiac Cardiac Pathophysiology Pathophysiology

Cardiac Pathophysiology

  • Upload
    tanith

  • View
    63

  • Download
    0

Embed Size (px)

DESCRIPTION

Cardiac Pathophysiology. Pericarditis. Often local manifestation of another disease May present as: Acute pericarditis Pericardial effusion Constrictive pericarditis. Acute Pericarditis. Acute inflammation of the pericardium - PowerPoint PPT Presentation

Citation preview

Page 1: Cardiac Pathophysiology

1

Cardiac Cardiac PathophysiologyPathophysiology

Page 2: Cardiac Pathophysiology

2

PericarditisPericarditis

Often local manifestation of Often local manifestation of another diseaseanother disease

May present as:May present as:– Acute pericarditisAcute pericarditis– Pericardial effusionPericardial effusion– Constrictive pericarditisConstrictive pericarditis

Page 3: Cardiac Pathophysiology
Page 4: Cardiac Pathophysiology

4

Acute PericarditisAcute Pericarditis

Acute inflammation of the Acute inflammation of the pericardiumpericardium

Cause often unknown, but commonly Cause often unknown, but commonly caused by infection, uremia, caused by infection, uremia, neoplasm, myocardial infarction, neoplasm, myocardial infarction, surgery or trauma.surgery or trauma.

Membranes become inflamed and Membranes become inflamed and roughened, and exudate may roughened, and exudate may developdevelop

Page 5: Cardiac Pathophysiology

5

Symptoms:Symptoms: Sudden onset of severe chest pain that Sudden onset of severe chest pain that

becomes worse with respiratory becomes worse with respiratory movements and with lying down.movements and with lying down.

Generally felt in the anterior chest, but Generally felt in the anterior chest, but pain may radiate to the back.pain may radiate to the back.

May be confused initially with acute May be confused initially with acute myocardial infarctionmyocardial infarction

Also report dysphagia (difficulties Also report dysphagia (difficulties swallowing), restlessness, irritability, swallowing), restlessness, irritability, anxiety, weakness and malaiseanxiety, weakness and malaise

Page 6: Cardiac Pathophysiology

6

SignsSigns Often present with low grade fever Often present with low grade fever

and sinus tachycardiaand sinus tachycardia Friction rubFriction rub (sandpaper sound) may (sandpaper sound) may

be heard at cardiac apex and left be heard at cardiac apex and left sternal border and is sternal border and is diagnosticdiagnostic for for pericarditis (but may be intermittent)pericarditis (but may be intermittent)

ECG changes reflect inflammatory ECG changes reflect inflammatory process through PR segment process through PR segment depression and ST segment elevation.depression and ST segment elevation.

Page 7: Cardiac Pathophysiology

7

Page 8: Cardiac Pathophysiology

8

TreatmentTreatment Treat symptomsTreat symptoms Look for underlying causeLook for underlying cause If pericardial effusion develops, If pericardial effusion develops,

aspirate excess fluidaspirate excess fluid

Acute pericarditis is usually self-Acute pericarditis is usually self-limiting, but can progress to chronic limiting, but can progress to chronic constrictive pericarditisconstrictive pericarditis

Page 9: Cardiac Pathophysiology

9

Pericardial effusionPericardial effusion

Accumulation of fluid in the Accumulation of fluid in the pericardial cavitypericardial cavity– May be transudateMay be transudate– May be exudateMay be exudate– May be bloodMay be blood

Not clinically significant other than to Not clinically significant other than to indicate underlying disorder, unless:indicate underlying disorder, unless:

Pressure becomes sufficient to cause Pressure becomes sufficient to cause cardiac compression – cardiac cardiac compression – cardiac tamponadetamponade

Page 10: Cardiac Pathophysiology
Page 11: Cardiac Pathophysiology

11

If development is slow, pericardium If development is slow, pericardium can stretchcan stretch

If develops quickly, even 50 -100 ml If develops quickly, even 50 -100 ml of fluid can cause problemsof fluid can cause problems

When pressure in pericardium = When pressure in pericardium = diastolic pressure, get diastolic pressure, get ↓ ↓ filling of filling of right atrium, right atrium, ↓↓ filling of filling of ventricles, ventricles, ↓↓ cardiac output cardiac output →→ circulatory collapse.circulatory collapse.

Outcome depends on how Outcome depends on how fast fluid accumulates.fast fluid accumulates.

Page 12: Cardiac Pathophysiology

12

Clinical manifestationsClinical manifestations

Pulsus paradoxusPulsus paradoxus – B.P. higher – B.P. higher during expiration than inspiration during expiration than inspiration by 10 mm Hgby 10 mm Hg

Distant or muffled heart soundsDistant or muffled heart sounds Dyspnea on exertion Dyspnea on exertion Dull chest painDull chest pain Observable by x-ray or ultrasoundObservable by x-ray or ultrasound

Page 13: Cardiac Pathophysiology

13

TreatmentTreatment

PericardiocentesisPericardiocentesis Treat painTreat pain Surgery if cause is aneurysm or Surgery if cause is aneurysm or

traumatrauma

Page 14: Cardiac Pathophysiology

14

Constrictive (chronic) Constrictive (chronic) pericarditispericarditis Years ago, synonymous with T.B.Years ago, synonymous with T.B. Today, usually idiopathic, or Today, usually idiopathic, or

associated with radiation associated with radiation exposures, rheumatoid arthritis, exposures, rheumatoid arthritis, uremia, or coronary bypass grafturemia, or coronary bypass graft

Page 15: Cardiac Pathophysiology

15

Fibrous scarring with occasional Fibrous scarring with occasional calcification of pericardiumcalcification of pericardium

Causes parietal and visceral layers Causes parietal and visceral layers to adhereto adhere

Pericardium becomes rigid, Pericardium becomes rigid, compressing the heart compressing the heart →↓ →↓ C.O.C.O.

Stenosis of veins entering atriaStenosis of veins entering atria Always develops graduallyAlways develops gradually

Pathophysiology:Pathophysiology:

Page 16: Cardiac Pathophysiology

16

Symptoms and SignsSymptoms and Signs

Exercise intoleranceExercise intolerance Dsypnea on exertionDsypnea on exertion Fatigue Fatigue AnorexiaAnorexia

Page 17: Cardiac Pathophysiology

17

Clinical manifestationsClinical manifestations

Weight lossWeight loss Edema and ascitesEdema and ascites Distention of jugular vein (Kussmaul Distention of jugular vein (Kussmaul

sign)sign) Enlargement of the liver and/or Enlargement of the liver and/or

spleen spleen ECG shows inverted T wave and ECG shows inverted T wave and

atrial fibrillationatrial fibrillation Can be seen on imagingCan be seen on imaging

Page 18: Cardiac Pathophysiology

18

TreatmentTreatment

Drugs and diet Drugs and diet – DigitalisDigitalis– DiureticsDiuretics– Sodium restrictionSodium restriction

Surgery to remove restrictive Surgery to remove restrictive pericardiumpericardium

Page 19: Cardiac Pathophysiology

19

CardiomyopathiesCardiomyopathies Disorders of the heart muscleDisorders of the heart muscle Most cases idiopathicMost cases idiopathic Many due to ischemic heart disease Many due to ischemic heart disease

and hypertension.and hypertension. Three categories:Three categories:

– Dilated ( formerly, congestive)Dilated ( formerly, congestive)– HypertrophicHypertrophic– RestrictiveRestrictive

Heart loses effectiveness as a pumpHeart loses effectiveness as a pump

Page 20: Cardiac Pathophysiology

20

Dilated cardiomyopathyDilated cardiomyopathy

AKA: congestive, ↓ C.O.; ↑ thrombi formation, slow blood flow ; ↓ contractility, and mitral valve incompetence, arrhythmias

Page 21: Cardiac Pathophysiology

Treatment: relieve symptoms of Treatment: relieve symptoms of heart failure, decrease workload, heart failure, decrease workload, and anticoagulants; transplantsand anticoagulants; transplants

Page 22: Cardiac Pathophysiology

22

Hypertrophic Hypertrophic CardiomyopathyCardiomyopathy

Often inherited, C.O. is normal,↑ inflow resistance,

and mitral valve incompetence, arrhythmais and sudden death.

Page 23: Cardiac Pathophysiology

Chest painChest pain DizzinessDizziness Fainting, especially during Fainting, especially during

exercise exercise

Page 24: Cardiac Pathophysiology

major cause of death in young major cause of death in young athletes who seem completely athletes who seem completely healthy but die during heavy healthy but die during heavy exercise exercise

Page 25: Cardiac Pathophysiology

The goal of treatment is to control The goal of treatment is to control symptoms and prevent symptoms and prevent complications complications

Page 26: Cardiac Pathophysiology

26

Restrictive Restrictive cardiomyopathycardiomyopathy

Reduced diastolic compliance of the ventricle. C.O. is normal or↓; ↑ formation of thrombi, dilation of left atrium, and mitral valve incompetence.

Page 27: Cardiac Pathophysiology

27

Disorders of the Disorders of the Endocardium:Endocardium:Valvular dysfunctionValvular dysfunction

Endocardial disorders damage heart Endocardial disorders damage heart valvesvalves

Changes can lead to :Changes can lead to :– Valvular StenosisValvular Stenosis = too narrow = too narrow– Valvular RegurgitationValvular Regurgitation = too = too

leakyleaky(or insufficiency or incompetence)(or insufficiency or incompetence)

Page 28: Cardiac Pathophysiology

28

Page 29: Cardiac Pathophysiology

29

Valves that are most often affected Valves that are most often affected are the mitral and aortic valves, but are the mitral and aortic valves, but in I.V. drug users and in athletes that in I.V. drug users and in athletes that inject performance enhancing drugs, inject performance enhancing drugs, > 50 % involve only the tricuspid > 50 % involve only the tricuspid valve.valve.

Heart Murmur – sound caused by Heart Murmur – sound caused by turbulent blood flow through turbulent blood flow through damaged valves.damaged valves.

Page 30: Cardiac Pathophysiology

30

Both types of valve Both types of valve disorders:disorders:

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

This leads to chamber dilation and This leads to chamber dilation and hypertrophy.hypertrophy.

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

Eventually, the heart fails from overworkEventually, the heart fails from overwork

Page 31: Cardiac Pathophysiology

31

Aortic StenosisAortic Stenosis

Three common causes:Three common causes:– Rheumatic heart disease -Rheumatic heart disease -StreptococcusStreptococcus infection – damage by infection – damage by bacteria and auto-immune responsebacteria and auto-immune response

– Congenital malformationCongenital malformation– Degeneration resulting from Degeneration resulting from

calcificationcalcification

Page 32: Cardiac Pathophysiology

32

Blood flow obstructed from LV into aorta Blood flow obstructed from LV into aorta during systoleduring systole

Causes increased work of LVCauses increased work of LV

→→ LV dilation & hypertrophy as LV dilation & hypertrophy as compensationcompensation

→→ prolonged contractions as prolonged contractions as compensationcompensation

Finally heart overwhelmedFinally heart overwhelmed →→ increased pressures in LA, then lungs, then increased pressures in LA, then lungs, then

right heartright heart

Aortic StenosisAortic Stenosis

Page 33: Cardiac Pathophysiology

33

Clinical manifestationsClinical manifestations Develops graduallyDevelops gradually Decreased stroke volumeDecreased stroke volume Reduced systolic blood pressureReduced systolic blood pressure Narrowed pulse pressureNarrowed pulse pressure Heart rate often slow and pulse faintHeart rate often slow and pulse faint Crescendo-decrescendo heart Crescendo-decrescendo heart

murmurmurmur Angina, dizziness, syncope, fatigueAngina, dizziness, syncope, fatigue Can lead to dysrhythmias, myocardial Can lead to dysrhythmias, myocardial

infarction, and left heart failureinfarction, and left heart failure

Page 34: Cardiac Pathophysiology

34

Mitral StenosisMitral Stenosis Most common of all valve disordersMost common of all valve disorders Usually the result of rheumatic fever Usually the result of rheumatic fever

or bacterial endocarditisor bacterial endocarditis During healing the orifice narrows, During healing the orifice narrows,

the valves become fibrous and fused, the valves become fibrous and fused, and chordae tendineae become and chordae tendineae become shortenedshortened

Get decreased flow from LA to LV Get decreased flow from LA to LV during fillingduring filling

Results in hypertrophy of LAResults in hypertrophy of LA

Page 35: Cardiac Pathophysiology

35

By causing LA to become pump:By causing LA to become pump: Get increased pulmonary vascular Get increased pulmonary vascular

pressures; pressures increase pressures; pressures increase through LA into lungthrough LA into lung

→→pulmonary congestionpulmonary congestion →→lung tissue changes to lung tissue changes to

accommodate increased pressuresaccommodate increased pressures →→increased pressure in pulmonary increased pressure in pulmonary

arteryartery →→increased pressure in right heartincreased pressure in right heart →→right heart failureright heart failure

Page 36: Cardiac Pathophysiology

36

Clinical Manifestations Clinical Manifestations Atrial enlargement can be seen on x-rayAtrial enlargement can be seen on x-ray Rumbling decrescendo diastolic Rumbling decrescendo diastolic

murmur, and accentuated first murmur, and accentuated first heart soundheart sound

DyspneaDyspnea Tachycardia and risk of atrial fibrillationTachycardia and risk of atrial fibrillation Other signs and symptoms are of Other signs and symptoms are of

pulmonary congestion and right heart pulmonary congestion and right heart failurefailure

Page 37: Cardiac Pathophysiology

37

Aortic RegurgitationAortic Regurgitation

Caused by acute or chronic lesion Caused by acute or chronic lesion of rheumatic fever, bacterial of rheumatic fever, bacterial endocarditits, syphilis, endocarditits, syphilis, hypertension, connective tissue hypertension, connective tissue disorder (e.g.Marfan syndrome) or disorder (e.g.Marfan syndrome) or atherosclerosisatherosclerosis

Page 38: Cardiac Pathophysiology

38

Reflux of blood from aorta to LV Reflux of blood from aorta to LV during ventricular relaxation.during ventricular relaxation.

Causes LV to pump more blood w/ Causes LV to pump more blood w/ each contractioneach contraction

→→ LV hypertrophyLV hypertrophy– LV takes on “globular shape”LV takes on “globular shape”

→→ increased pressures in LA, lung, increased pressures in LA, lung, right heartright heart

Page 39: Cardiac Pathophysiology

39

Clinical manifestationsClinical manifestations

Widened pulse pressureWidened pulse pressure Prominent carotid pulsations and Prominent carotid pulsations and

throbbing peripheral pulsesthrobbing peripheral pulses PalpitationsPalpitations FatigueFatigue DyspneaDyspnea AnginaAngina High-pitched or blowing heart High-pitched or blowing heart

sound during diastolesound during diastole

Page 40: Cardiac Pathophysiology

40

Mitral Regurgitation Mitral Regurgitation Causes: mitral valve prolapse, Causes: mitral valve prolapse,

rheumatic heart disease, infective rheumatic heart disease, infective endocarditis, connective tissue endocarditis, connective tissue disorders, and cardiomyopathydisorders, and cardiomyopathy

Permits backflow of blood from the Permits backflow of blood from the LV into the LA during ventricular LV into the LA during ventricular systolesystole

Loud pansystolicLoud pansystolic murmur that murmur that radiates into the back and axillaradiates into the back and axilla

Page 41: Cardiac Pathophysiology

See the animated

Page 42: Cardiac Pathophysiology

42

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

Both LV and LA pump harder to move Both LV and LA pump harder to move same blood twicesame blood twice– →→LV hypertrophy and dilation as LV hypertrophy and dilation as

compensationcompensation– Compensation works awhile, then see Compensation works awhile, then see

↓↓C.O.C.O.– →→ heart failureheart failure– Also Also →→LA hypertrophyLA hypertrophy

→→ increased pressures through lungs increased pressures through lungs → → ↑↑ pressures in right heart pressures in right heart →→right heart failureright heart failure

Can see edema, shockCan see edema, shock

Page 43: Cardiac Pathophysiology

43

Clinical ManifestationsClinical Manifestations

Weakness and fatigueWeakness and fatigue DyspneaDyspnea PalpitationsPalpitations

Page 44: Cardiac Pathophysiology

44

Mitral Valve ProlapseMitral Valve Prolapse

Cusps of valve billow upward into the LA Cusps of valve billow upward into the LA during ventricular systoleduring ventricular systole

Mitral regurgitation can occur Mitral regurgitation can occur Most common valve disorder in U.S.Most common valve disorder in U.S. Studies suggest an autosomal dominant Studies suggest an autosomal dominant

inheritance patterninheritance pattern Many cases completely asymptomaticMany cases completely asymptomatic Regurgitant murmur or Regurgitant murmur or midsystolic midsystolic

clickclick

Page 45: Cardiac Pathophysiology
Page 46: Cardiac Pathophysiology

46

Clinical manifestationsClinical manifestations

PalpitationsPalpitations TachycardiaTachycardia Light-headedness, syncope, Light-headedness, syncope,

fatigue, weaknessfatigue, weakness Chest tightness, hyperventilationChest tightness, hyperventilation Anxiety, depression, panic attacksAnxiety, depression, panic attacks Atypical chest painAtypical chest pain

Page 47: Cardiac Pathophysiology

47

Management Management

Echocardiography for diagnosisEchocardiography for diagnosis Related to degree of regurgitationRelated to degree of regurgitation Antibiotics before invasive Antibiotics before invasive

proceduresprocedures Beta blockers to relieve syncope, Beta blockers to relieve syncope,

severe chest pain, or palpitationssevere chest pain, or palpitations Avoid hypovolemia Avoid hypovolemia Surgical repairSurgical repair

Page 48: Cardiac Pathophysiology

48

General Treatment for General Treatment for Valve disordersValve disorders

Antibiotics for StrepAntibiotics for Strep Anti-inflammatories for Anti-inflammatories for

autoimmune disorderautoimmune disorder Analgesics for painAnalgesics for pain Restrict physical activityRestrict physical activity Valve replacement surgeryValve replacement surgery

Page 49: Cardiac Pathophysiology

49

Heart failureHeart failure

Definition – When heart as a pump Definition – When heart as a pump is insufficient to meet the is insufficient to meet the metabolic requirements of tissues.metabolic requirements of tissues.

Acute heart failureAcute heart failure– 65% survival rate65% survival rate

Chronic heart failure Chronic heart failure – Most common cause is ischemic Most common cause is ischemic

heart diseaseheart disease

Page 50: Cardiac Pathophysiology

Right heart failureRight heart failure

Systemic symptomsSystemic symptoms– Edema, ascitesEdema, ascites– Enlarged liver, spleenEnlarged liver, spleen– Swollen feet, anklesSwollen feet, ankles– NauseaNausea– Swollen internal jugular veinsSwollen internal jugular veins

Page 51: Cardiac Pathophysiology

Left hear failureLeft hear failure

Fluid accumulation in lungs Fluid accumulation in lungs – Shortness of breathShortness of breath– Orthopnea Orthopnea – Coughing, foaming sometimesCoughing, foaming sometimes– TirednessTiredness– weaknessweakness

Page 52: Cardiac Pathophysiology

52

Ischemic Heart Ischemic Heart DiseaseDisease Coronary Artery Disease (CAD), Coronary Artery Disease (CAD),

myocardial ischemia and myocardial ischemia and myocardial infarction are myocardial infarction are progression of conditions that progression of conditions that impair the pumping ability of the impair the pumping ability of the heart by depriving it of oxygen heart by depriving it of oxygen and nutrients.and nutrients.

Page 53: Cardiac Pathophysiology

53

Coronary Artery Coronary Artery DiseaseDisease

Any vascular disorder that narrows or Any vascular disorder that narrows or occludes the coronary arteries.occludes the coronary arteries.

Most common cause is Most common cause is atherosclerosisatherosclerosis

Page 54: Cardiac Pathophysiology

54

The arteries that supply the heart are the The arteries that supply the heart are the first branches off the aortafirst branches off the aorta

Coronary artery disease decreases the blood Coronary artery disease decreases the blood flow to the cardiac muscle.flow to the cardiac muscle.

Persistent ischemia or complete occlusion Persistent ischemia or complete occlusion leads to hypoxia.leads to hypoxia.

Hypoxia can cause tissue death or infarction, Hypoxia can cause tissue death or infarction, which is a “heart attack,” which accounts for which is a “heart attack,” which accounts for about one third of all deaths in U.S. about one third of all deaths in U.S.

Page 55: Cardiac Pathophysiology

55

Risk FactorsRisk Factors HyperlipidemiaHyperlipidemia HypertensionHypertension Diabetes mellitusDiabetes mellitus Genetic predispositionGenetic predisposition Cigarette smokingCigarette smoking ObesityObesity Sedentary life-styleSedentary life-style Heavy alcohol consumptionHeavy alcohol consumption Higher risk for males than Higher risk for males than

premenopausal womenpremenopausal women

Page 56: Cardiac Pathophysiology

56

Myocardial IschemiaMyocardial Ischemia Myocardial cell metabolic demands not metMyocardial cell metabolic demands not met Time frame of coronary blockage:Time frame of coronary blockage:

10 seconds following coronary block10 seconds following coronary block– Decreased strength of contractionsDecreased strength of contractions– Abnormal hemodynamics Abnormal hemodynamics

See a shift in metabolism, so within minutes: See a shift in metabolism, so within minutes: – Anaerobic metabolism takes overAnaerobic metabolism takes over– Get build-up of lactic acid, which is toxic Get build-up of lactic acid, which is toxic

within the cellwithin the cell– Electrolyte imbalancesElectrolyte imbalances– Loss of contractibilityLoss of contractibility

Page 57: Cardiac Pathophysiology

57

20 minutes after blockage20 minutes after blockage– Myocytes are still viable, soMyocytes are still viable, so– If blood flow is restored, and If blood flow is restored, and

increased aerobic metabolism, and increased aerobic metabolism, and cell repair,cell repair,

– →→Increased contractilityIncreased contractility About 30-45 minutes after blockage, if About 30-45 minutes after blockage, if

no reliefno relief– Cardiac infarct & cell death Cardiac infarct & cell death

Page 58: Cardiac Pathophysiology

58

Clinical ManifestationsClinical Manifestations

May hear extra, rapid heart May hear extra, rapid heart soundssounds

ECG changes: ECG changes: – T wave inversionT wave inversion– ST segment depressionST segment depression

Page 59: Cardiac Pathophysiology
Page 60: Cardiac Pathophysiology

60

Chest PainChest Pain First symptom of those suffering First symptom of those suffering

myocardial ischemia.myocardial ischemia. Called angina pectoris (angina – Called angina pectoris (angina –

“pain”)“pain”) Feeling of heaviness, pressureFeeling of heaviness, pressure Moderate to severeModerate to severe In substernal areaIn substernal area Often mistaken for indigestionOften mistaken for indigestion May radiate to neck, jaw, left arm/ May radiate to neck, jaw, left arm/

shouldershoulder

Page 61: Cardiac Pathophysiology

61

Due to :Due to :– Accumulation of lactic acid in myocytes Accumulation of lactic acid in myocytes

oror– Stretching of myocytesStretching of myocytes

Three types of angina pectoris:Three types of angina pectoris:– Stable, unstable and PrinzmetalStable, unstable and Prinzmetal

Page 62: Cardiac Pathophysiology

62

Stable angina pectorisStable angina pectoris

Caused by chronic coronary Caused by chronic coronary obstructionobstruction

Recurrent predictable chest painRecurrent predictable chest pain Gradual narrowing and hardening of Gradual narrowing and hardening of

vessels so that they cannot dilate in vessels so that they cannot dilate in response to increased demand of response to increased demand of physical exertion or emotional stressphysical exertion or emotional stress

Lasts approx. 3-5 minutesLasts approx. 3-5 minutes Relieved by rest and nitratesRelieved by rest and nitrates

Page 63: Cardiac Pathophysiology

63

Prinzmetal angia pectorisPrinzmetal angia pectoris(Variant angina)(Variant angina)

Caused by abnormal vasospasm of Caused by abnormal vasospasm of normal vessels (15%) or near normal vessels (15%) or near atherosclerotic narrowing (85%)atherosclerotic narrowing (85%)

Occurs unpredictably and almost Occurs unpredictably and almost exclusively at rest.exclusively at rest.

Often occurs at night during REM Often occurs at night during REM sleepsleep

May result from hyperactivity of May result from hyperactivity of sympathetic nervous system, sympathetic nervous system, increased calcium flux in muscle or increased calcium flux in muscle or impaired production of prostaglandin impaired production of prostaglandin

Page 64: Cardiac Pathophysiology

64

Unstable Angina Unstable Angina pectorispectoris Lasts more than 20 minutes at Lasts more than 20 minutes at

rest, or rapid worsening of a pre-rest, or rapid worsening of a pre-existing anginaexisting angina

May indicate a progression to M.I.May indicate a progression to M.I.

Page 65: Cardiac Pathophysiology

65

Silent IschemiaSilent Ischemia

Totally asymptomaticTotally asymptomatic May be due abnormality in May be due abnormality in

innervationinnervation Or due to lower level of Or due to lower level of

inflammatory cytokinesinflammatory cytokines

Page 66: Cardiac Pathophysiology

66

TreatmentTreatment Pharmacologically manipulate blood Pharmacologically manipulate blood

pressure, heart rate, and contractility pressure, heart rate, and contractility to decrease oxygen demandsto decrease oxygen demands

Nitrates dilate peripheral blood Nitrates dilate peripheral blood vessels andvessels and

Decrease oxygen demand Decrease oxygen demand Increase oxygen supplyIncrease oxygen supplyRelieve coronary spasmRelieve coronary spasm

Page 67: Cardiac Pathophysiology

67

Beta blockers:Beta blockers:– Block sympathetic input, soBlock sympathetic input, so– Decrease heart rate, soDecrease heart rate, so– Decrease oxygen demandDecrease oxygen demand

DigitalisDigitalis– Vagal effectVagal effect

Calcium channel blockersCalcium channel blockers– Decrease force of contraction, decrease Decrease force of contraction, decrease

blood pressureblood pressure Antiplatelet agents (aspirin, etc.)Antiplatelet agents (aspirin, etc.)

Page 68: Cardiac Pathophysiology

68

Surgical treatmentSurgical treatment

Angioplasty – mechanical opening Angioplasty – mechanical opening of vesselsof vessels

Revascularization – bypassRevascularization – bypass– Replace or shut around Replace or shut around

occluded vesselsoccluded vessels

Page 69: Cardiac Pathophysiology

69

Myocardial infarctionMyocardial infarction

Necrosis of cardiac myocytesNecrosis of cardiac myocytes– IrreversibleIrreversible– Commonly affects left ventricleCommonly affects left ventricle– Follows after more than 20 minutes Follows after more than 20 minutes

of ischemiaof ischemia

Page 70: Cardiac Pathophysiology

70

Structural, functional Structural, functional changeschanges

Decreased contractilityDecreased contractility Decreased LV complianceDecreased LV compliance Decreased stroke volumeDecreased stroke volume DysrhythmiasDysrhythmias Inflammatory response is severeInflammatory response is severe Scarring results –Scarring results –

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

Page 71: Cardiac Pathophysiology

71

Clinical manifestationsClinical manifestations

Sudden, severe chest painSudden, severe chest pain– Similar to pain with ischemia, but strongerSimilar to pain with ischemia, but stronger– Not relieved by nitratesNot relieved by nitrates– Radiates to neck, jaw, shoulder, left armRadiates to neck, jaw, shoulder, left arm

Indigestion, nausea, vomitingIndigestion, nausea, vomiting Fatigue, weakness, anxiety, Fatigue, weakness, anxiety,

restlessness and feelings of impending restlessness and feelings of impending doom.doom.

Abnormal heart sounds possible (S3,S4)Abnormal heart sounds possible (S3,S4)

Page 72: Cardiac Pathophysiology

72

Blood test show several markers:Blood test show several markers:– LeukocytosisLeukocytosis– Increased blood sugarIncreased blood sugar– Increased plasma enzymesIncreased plasma enzymes

Creatine kinaseCreatine kinase Lactic dehydrogenaseLactic dehydrogenase Aspartate aminotransferase (AST or Aspartate aminotransferase (AST or

SGOT)SGOT)

– Cardiac-specific troponinCardiac-specific troponin

Page 73: Cardiac Pathophysiology

73

ECG changesECG changes

Pronounced, persisting Q wavesPronounced, persisting Q waves ST elevationST elevation T wave inversionT wave inversion

Page 74: Cardiac Pathophysiology

74

TreatmentTreatment First 24 hours crucialFirst 24 hours crucial Hospitalization, bed restHospitalization, bed rest ECG monitoring for arrhythmiasECG monitoring for arrhythmias Pain relief (morphine, nitroglycerin)Pain relief (morphine, nitroglycerin) Thrombolytics to break down clotsThrombolytics to break down clots Administer oxygenAdminister oxygen Revascularization interventions: by-pass Revascularization interventions: by-pass

grafts, stents or balloon angioplastygrafts, stents or balloon angioplasty

Page 75: Cardiac Pathophysiology

Tetralogy of Fallot Tetralogy of Fallot

Most common cause of blue baby Most common cause of blue baby syndrome. syndrome.

Tetralogy of Fallot has four key features. Tetralogy of Fallot has four key features. – obstruction from the right ventricle to the obstruction from the right ventricle to the

lungs (pulmonary stenosis) are the most lungs (pulmonary stenosis) are the most important. Aimportant. A

– Also, the aorta lies directly over the Also, the aorta lies directly over the ventricular septal defect, overriding aorta Bventricular septal defect, overriding aorta B

– A ventricular septal defect (a hole between A ventricular septal defect (a hole between the ventricles) -- C see next imagethe ventricles) -- C see next image

– and the right ventricle develops thickened and the right ventricle develops thickened muscle, right ventricular hypertrophy Dmuscle, right ventricular hypertrophy D

Page 76: Cardiac Pathophysiology
Page 77: Cardiac Pathophysiology
Page 78: Cardiac Pathophysiology

SymptomsSymptoms

high pressure from right ventricle high pressure from right ventricle related to right hypertrophy A and Drelated to right hypertrophy A and D

Mixing of oxygenated and Mixing of oxygenated and deoxygenated blood (B and C)deoxygenated blood (B and C)

Left to right shunt first (septal Left to right shunt first (septal defect), then right to left shunt defect), then right to left shunt when pressure in the right is higher when pressure in the right is higher than leftthan left

Page 79: Cardiac Pathophysiology

TreatmentTreatment

SurgerySurgery– Palliative, not used common nowPalliative, not used common now– Total repairTotal repair