Cardiac Pathology 2: Congenital and Ischemic Heart Disease - - PowerPoint PPT Presentation

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Cardiac Pathology 2: Congenital and Ischemic Heart Disease - - PowerPoint PPT Presentation

Nov 09, 2022 294 likes •715 views

Cardiac Pathology 2: Congenital and Ischemic Heart Disease Kristine Krafts, M.D. Cardiac Pathology Outline Blood Vessels Heart I Heart II Cardiac Pathology Outline Blood Vessels Heart I Heart Failure Congenital Heart

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SLIDE 1

Cardiac Pathology 2:

Congenital and Ischemic Heart Disease

Kristine Krafts, M.D.

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SLIDE 2
  • Blood Vessels
  • Heart I
  • Heart II

Cardiac Pathology Outline

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SLIDE 3
  • Blood Vessels
  • Heart I
  • Heart Failure
  • Congenital Heart Disease
  • Ischemic Heart Disease

Cardiac Pathology Outline

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SLIDE 4
  • Blood Vessels
  • Heart I
  • Heart Failure

Cardiac Pathology Outline

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SLIDE 5
  • End point of many heart diseases
  • Common!
  • 5 million affected each year
  • 300,000 fatalities
  • Most due to systolic dysfunction
  • Some due to diastolic dysfunction,

valve failure, or abnormal load

  • Heart can’t pump blood fast enough

to meet needs of body

Heart Failure

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SLIDE 6
  • System responds to failure by
  • Releasing hormones (e.g., norepinephrine)
  • Frank-Starling mechanism
  • Hypertrophy
  • Initially, this works
  • Eventually, it doesn’t
  • Myocytes degenerate
  • Heart needs more oxygen
  • Myocardium becomes vulnerable to ischemia

Heart Failure

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SLIDE 7

R L

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SLIDE 8

Main clinical consequences

  • f left and right

heart failure

peripheral edema ascites hepatomegaly pulmonary edema splenomegaly

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SLIDE 9
  • Left ventricle fails; blood backs up in lungs
  • Commonest causes
  • Ischemic heart disease (IHD)
  • Systemic hypertension
  • Mitral or aortic valve disease
  • Cardiomyopathy
  • Heart changes
  • LV hypertrophy, dilation
  • LA may be enlarged too (risk of atrial fibrillation)

Left Heart Failure

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SLIDE 10
  • Dyspnea
  • Orthopnea and paroxysmal nocturnal dyspnea
  • Enlarged heart, increased heart rate, fine rales

at lung bases

  • Later: mitral regurgitation, systolic murmur
  • If atrium is big, “irregularly irregular”

heartbeat

Left Heart Failure

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SLIDE 11
  • Right ventricle fails; blood backs up in body
  • Commonest causes
  • Left heart failure
  • Lung disease (“cor pulmonale”)
  • Some congenital heart diseases
  • Heart changes
  • RV hypertrophy, dilation
  • RA enlargement

Right Heart Failure

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SLIDE 12
  • Peripheral edema
  • Big, congested liver (“nutmeg liver”)
  • Big spleen
  • Most chronic cases of heart failure are bilateral

Right Heart Failure

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SLIDE 13

Hepatic blood flow

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SLIDE 14

“Nutmeg” liver Nutmeg

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SLIDE 15
  • Blood Vessels
  • Heart I
  • Heart Failure
  • Congenital Heart Disease

Cardiac Pathology Outline

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SLIDE 16
  • Abnormalities of heart/great vessels

present from birth

  • Faulty embryogenesis, weeks 3-8
  • Broad spectrum of severity
  • Cause unknown in 90% of cases

Congenital Heart Disease

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SLIDE 17

Left-to-right shunts

  • Atrial septal defect
  • Ventricular septal defect
  • Patent ductus arteriosus

Right-to-left shunts

  • Tetralogy of Fallot

Obstructions

  • Aortic coarctation

Congenital Heart Disease

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SLIDE 18

Left-to-right shunts

Atrial septal defect Ventricular septal defect Patent ductus arteriosus

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SLIDE 19

Left-to-right shunts

Atrial septal defect

  • Small ASD: asymptomatic
  • Large ASD: big left-to-right shunt
  • Eventually, may develop

Eisenmenger syndrome

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SLIDE 20

Left-to-right shunts

Atrial septal defect

  • Small ASD: asymptomatic
  • Large ASD: big left-to-right shunt
  • Eventually, may develop

Eisenmenger syndrome

Eisenmenger syndrome: Big left-to-right shunt puts extra pressure on pulmonary circulation. Eventually, pulmonary vessels constrict, and the shunt reverses (becomes right-to-left).

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SLIDE 21

Left-to-right shunts

Ventricular septal defect

  • Most common congenital heart anomaly
  • Small VSD: asymptomatic
  • Large VSD: big left-to-right shunt
  • Eventually, may develop Eisenmenger syndrome
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SLIDE 22

Left-to-right shunts

Patent ductus arteriosus

  • In utero: ductus lets blood flow from PA to aorta
  • After birth: ductus closes
  • Small PDA: asymptomatic
  • Large PDA: big left-to-right shunt
  • Eventually, may develop Eisenmenger syndrome
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SLIDE 23

Right-to-left shunt

Tetralogy of Fallot

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SLIDE 24

Right-to-left shunt

Tetralogy of Fallot

  • Most common cyanotic congenital

heart disease

  • Main problem: infundibular septum

is pushed up and to the right

  • Four features:

1.

VSD

2.

Overriding aorta

3.

RV outflow obstruction

4.

RV hypertrophy

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SLIDE 25

Obstruction

Coarctation of the aorta

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SLIDE 26

Obstruction

Coarctation of the aorta

  • Coarctation = narrowing
  • With PDA: unoxygenated blood gets dumped into aorta,

causing cyanosis of lower extremities shortly after birth.

  • Without PDA: hypertension of upper extremities, hypotension
  • f lower extremities; usually asymptomatic until adulthood.
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SLIDE 27
  • Blood Vessels
  • Heart I
  • Heart Failure
  • Congenital Heart Disease
  • Ischemic Heart Disease

Cardiac Pathology Outline

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SLIDE 28
  • Myocardial perfusion can’t meet demand
  • Usually caused by decreased coronary

artery blood flow due to atherosclerosis (“coronary artery disease”)

  • Two main clinical syndromes: angina and

myocardial infarction

Ischemic Heart Disease

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SLIDE 29

How atherosclerosis leads to angina and MI

Normal vessel No symptoms

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SLIDE 30

Vessel <70% occluded by plaque No symptoms

How atherosclerosis leads to angina and MI

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SLIDE 31

Vessel >70% occluded by plaque Stable angina

How atherosclerosis leads to angina and MI

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SLIDE 32

Disrupted plaque Uh oh

How atherosclerosis leads to angina and MI

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SLIDE 33

Thrombus partially

  • ccluding vessel

Unstable angina

How atherosclerosis leads to angina and MI

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SLIDE 34

Thrombus completely

  • ccluding vessel

Myocardial infarction

How atherosclerosis leads to angina and MI

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SLIDE 35
  • Intermittent chest pain caused by

transient, reversible ischemia

  • Stable angina
  • Pain on exertion
  • Cause: fixed narrowing of coronary artery
  • Unstable angina
  • Increasing pain with less exertion
  • Cause: plaque disruption and thrombosis

Angina Pectoris

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SLIDE 36
  • Necrosis of heart muscle caused by ischemia
  • 1.5 million people get MIs each year
  • Usually due to acute coronary artery thrombosis
  • sudden plaque disruption
  • platelets adhere
  • coagulation cascade activated
  • thrombus occludes lumen within minutes
  • irreversible injury/cell death in 20-40 minutes
  • Prompt reperfusion can salvage myocardium

Myocardial Infarction

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SLIDE 37

4-12 hours 12-24 hours Days 2-7

Myocytes undergo coagulative necrosis Neutrophils arrive Macrophages come in and eat dead cells; neutrophils leave

What happens to the heart after an MI?

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SLIDE 38

What happens to the heart after an MI?

Week 2 Weeks 3-8

Granulation tissue forms Granulation tissue replaced by collagen, forming a scar

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SLIDE 39

Clinical features

  • Severe, crushing chest pain ± radiation
  • Not relieved by nitroglycerin, rest
  • Sweating, nausea, dyspnea
  • Sometimes no symptoms

Serum markers

  • Troponins increase within 2-4 hours,

remain elevated for a week.

  • CK-MB increases within 2-4 hours,

returns to normal within 72 hours.

Myocardial Infarction

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SLIDE 40

Complications

  • contractile dysfunction
  • arrhythmias
  • rupture
  • chronic progressive heart failure

Prognosis

  • verall 1 year mortality: 30%
  • 3-4% mortality per year thereafter

Myocardial Infarction