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CV II Exam 2 > 9-3 Pathology of the Heart > Flashcards

9-3 Pathology of the Heart Flashcards

1
Q

What does the SA node consist of?

A

Small, modified mm cells which generate the electrical signal that controls the heart

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2
Q

What are intercalated discs?

A

specialized end-to-end junctions of adjoining cells

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3
Q

What are the histological layers of a heart valve?

A

ventricularis

spongiosa

fibrosa

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4
Q

What are some changes in the chambers associated with the aging heart?

A

Increased left atrial cavity size
Decreased left ventricular cavity size
Sigmoid-shaped ventricular septum

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5
Q

What are some changes in the valves associated with the aging heart?

A

Aortic valve calcific deposits
Mitral valve annular calcific deposits
Fibrous thickening of leaflets
Buckling of mitral leaflets toward the left atrium
Lambl excrescences

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6
Q

What are some changes in the epicardial coronary aa associated with the aging heart?

A

Tortuosity - heart tends to shrink A-P diameter, so aa no longer straight
Diminished compliance
Calcific deposits
Atherosclerotic plaque

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7
Q

What are some changes associated with the myocardium in the aging heart?

A

Decreased mass
Increased subepicardial fat
Brown atrophy
Lipofuscin deposition (aging pigment)
Basophilic degeneration (glycogen breakdown)
Amyloid deposits

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8
Q

What change is associated with the aorta in the aging heart?

A

Dilated ascending aorta with rightward shift

  • often due to sigmoid shaped venticular septum that can obstruct outflow tract

to aortic valve
Elongated (tortuous) thoracic aorta
Sinotubular junction calcific deposits
Elastic fragmentation and collagen accumulation
Atherosclerotic plaque

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9
Q

Mortality related to heart disease is on the decline, and cancer is on the rise. Why?

A

heart disease is better controlled, and less fatal

people are living long enough to get cancer

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10
Q

How has the picture of mortality from cardiac death changed from 1999-2010?

A

number of deaths declined 18%

death rate declined 33% (total deaths to total population)

↑ Congenital heart disease deaths

↑ Hypertensive heart disease deaths

↓ Ischemic heart disease deaths (prevention)

↓ Valvular heart disease deaths (↓ rheumatic heart disease)

↓ Nonischemic (primary) myocardial disease deaths

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11
Q

How is someone able to lose a significant amount of cardiac function before becoming sick?

A
  • Cardiac output is ~10-20% of maximum at rest in normal adults
  • “Cardiac Reserve” 5-fold margin for increased output
  • Have lost 70-80% of cardiac function by the time patient is symptomatic!

Heart disease is predominantly a long-term chronic disease with superimposed acute episodes

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12
Q

What are the 6 different basic causes of cardiac dysfxn?

A

1.Pump failure - diminished myocardial contractility

Primary cardiomyopathy; ischemic cardiac disease

2.Obstruction to blood flow through the heart

Stenotic valvular disease; hypertensive disease

3.Regurgitant flow

Valvular disease with incompetence

4.Shunted flow

Congenital heart diseases

5.Disorders of cardiac conduction

Atrial fibrillation; ventricular tachycardia

6.Disruption of continuity of the circulatory system

Gunshot wound; ventricular rupture; ruptured aneurysm

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13
Q

What are 3 methods of cardiac compensation?

A
  1. Activation of neurohumoral systems
    •Norepinephrine from adrenergic nerves
    •Renin-angiotensin-aldosterone system
    •Natriuretic peptides
  2. Myocardial adaptations - ventricular remodeling
  3. Frank-Starling mechanism - enhance contractility and stroke volume
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14
Q

How is A-type natriuretic peptide produced?

A

A-type natriuretic peptide produced by specialized atrial myocytes with specific atrial granules and released with atrial distension

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15
Q

How is B-type natriuretic peptide produced?

A

B-type natriuretic peptide (BNP) produced by ventricles (2ry to increased pressure) and is used for determination of CHF/stressed out heart

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16
Q

How is C-type natriuretic peptide produced?

A

C-type produced by endothelial cells (secondary to shear stress)

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17
Q

What do natriuretic peptides do? What hormones do they oppose?

A

Cause vasodilation, natriuresis and diuresis

Antithesis of renin-angiotensin-aldosterone system

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18
Q

What leads to increases in cardiac work and wall stress?

A

HTN - pressure overload

Valvular disease - pressure and/or volume overload

MI - regional dysfxn with volume overload

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19
Q

Increased cardiac work and wall stress will lead to what downstream cellular response?

A

cell stretch, leading to hypertrophy and/or dilation

leads to remodeling

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20
Q

What does remodeling of the heart include?

A

Increased heart size and mass

increased protein synthesis

inducton of immediate-early genes

induction of fetal gene program

abnormal proteins

fibrosis

inadequate vasculature

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21
Q

Remodeling has happened, what is the proper term for “you’re screwed, you’re heart doesn’t work no good no more”?

A

Cardiac dysfxn, happens due to remodeling

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22
Q

What is cardiac dysfxn characterized by?

A
  • inability to pump blood at a rate necessary for metabolizing tissues

Includes:

heart failure (systolic/distolic)

arrhythmias

neurohumoral stimulation

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23
Q

How is CHF and cardiac dysfxn related?

A

CHF is a type of cardiac dysfxn

  • chronic and symptomatic
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24
Q

What are the main causes of increased workload to myocardial myocytes?

A
  1. Increased physiologic need by a normal heart (aerobic exercise)
  2. Cardiac failure increases workload per myocyte due to overall decreased intrinsic myocardial contractility (ischemia, etc.)
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25
Q

Why do myocytes undergo hypertrophy instead of hyperplasia in response to stress?

A

Myocyte hypertrophy

  • Response available for increased cardiac workload per myocardial fiber
  • Myocytes are terminally differentiated, cannot undergo significant amounts of regeneration
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26
Q

What is the difference between cardiac hypertrophy and cardiomegaly?

A

Cardiac hypertrophy – increase in ventricular thickness or weight

Cardiomegaly - increase in heart size or weight

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27
Q

A heart weight of 350-600 g indicates what?

A

•350-600 gm: Pulmonary HTN, IHD

Normal: Male 300-350 gm; Female 250-300 gm

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28
Q

A heart weight of 400-800g indicates what?

A

•400-800 gm: Systemic HTN, aortic stenosis, mitral regurgitation, dilated cardiomyopathy

Normal: Male 300-350 gm; Female 250-300 gm

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29
Q

A heart weight of 600-1000 gm indicates what?

A

•600-1000 gm: Aortic regurgitation, hypertrophic cardiomyopathy

Normal: Male 300-350 gm; Female 250-300 gm

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30
Q

“pressure overload” hypertrophy is also known as concentric hypertrophy.

What is this?

A

Increase in the thickness of wall subjected to the increased work load

Left ventricle - systemic HTN or Aortic stenosis

Right Ventricle - Pulmonary HTN

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31
Q

Volume overload hypertrophy is also known as?

Characterize the cardiac muscle mass!

A

Volume overload hypertrophy

Overall cardiac muscle mass is increased

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32
Q

Cardiac failure in CHF is due to either or both…

A
  • Insufficient pump rate to meet metabolic demands
  • Pump can marginally meet demands with elevated filling pressure
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33
Q

CHF can be caused by forward failure. What is this?

A

Diminished cardiac output.

Systolic dysfunction- progressive deterioration of myocardial contractility

Diastolic dysfunction- Inability of the heart chambers to relax (distend) sufficiently to allow filling during diastole

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34
Q

CHF can also be caused by backward failure. What is this?

A

Damming of blood in the venous system

  • Left-side failure leads to accumulation of fluid within the lungs and pleural cavities
  • Right-side failure leads to accumulation of fluid in all other body sites and all body cavities
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35
Q

Left sided heart failure can be acute or chronic. What are the 4 most common causes?

A

Ischemic heart disease

Hypertensive heart disease

Aortic and mitral valvular disease

Primary nonischemic myocardial disease (cardiomyopathy)

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36
Q

A BNP > 500 pg/mL is most consistent with?

A

CHF

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37
Q

BNP < 100 pg/mL is…

A

unlikely to be CHF

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38
Q

What are the extracardiac effects of left sided heart failure on the following…

  1. Lungs
  2. Kidney
  3. Brain
A
  1. Lungs
    • Dyspnea
    • Orthopnea
    • Paroxysmal nocturnal dyspnea
    • Pulmonary congestion and edema
    • Long-term get siderophages (heart failure cells)
  2. Kidney
    • Renal hypoperfusion
  3. Brain
    • hypoxic encephalopathy
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39
Q

What is right sided heart failure most commonly a consequence of?

A

Left sided heart failure

↑ pressure in the pulmonary circulation →↑workload right ventricle →right-sided heart failure

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40
Q

Pure, or isolated right sided heart failure is uncommon, but will present with cardiac hypertrophy and dilatation confined to the right atrium and ventricle.

What causes this?

A

Cor Pulmonale - heart disease secondary to lung disease

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41
Q

What are the right sided heart failure cardiac effects on…

  1. Subcutaneous tissues
  2. Liver
  3. Spleen
  4. Pleura
  5. Peritoneum
  6. Pericardium
A
  1. Subcutaneous tissues
    • pitting edema of lower extremities or generalized anasarca
  2. Liver
    • Congestive hepatomegaly
    • Chronic passive congestion in hepatic sinusoids
    • cardiac cirrhossis - increased fibrous tissue in the centrilobular zone
  3. Spleen
    • congestive splenomegaly
  4. Pleura, Peritoneum, Pericardium effusions - transudates
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42
Q

In order, what are the congenital heart defects associated with Trisomy 21?

A
  1. AVSD
  2. VSD
  3. ASD
  4. PDA
  5. TOF (tetrology of fallot)
  6. TGA (transposition of great arteries)
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43
Q

What are the top three congenital cardiac malformations?

A

Bicuspid aortic valve

VSD

ASD

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44
Q

What gene defect is responsible for ASD or conduction defects?

A

NKX2.5

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45
Q

What gene defect is responsible for DiGeorge syndrome?

A

TBX1 (Deletion 22q11.2)

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46
Q

What gene defect is responsible for Marfan syndrome?

A

FBN1

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47
Q

What are the defects associated with Digeorge syndrome?

A

“CATCH-22”

Cardiac

Abnormal facies

Thymic aplasia

Cleft palate

Hypocalcemia (d/t parathyroid hypoplasia)

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48
Q

What are the left to right shunts?

A

ASD

VSD

PDA

AVSD

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49
Q

What is Eisenmenger syndrome?

A

The muscular pulmonary arteries develop medial hypertrophy and vasoconstriction to normalize distal pressure.

Eventually develop pulmonary HTN, leading to shift from left to right shunt to right to left shunt, and late cyanotic congenital heart disease, occurring months to years after birth.

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50
Q

90% or VSD involves what?

A

The membranous septum

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51
Q

What type of defect is shown here?

A

VSD, membranous type

Note proximity to the valve

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52
Q

What are the three major types of ASD?

Where are these each located?

A
  1. Secundum (90%) - involves fossa ovalis
  2. Primum (5%) - adjacent to AV valve
  3. Sinus venosus (5%) - near superior vena cava
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53
Q

The ductus arteriosis typically closes at 1-2 days secondary to what three changes?

A
  • ↑O2
  • ↓ Pulmonary vasculature resistance
  • ↓ Prostaglandin E2
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54
Q

What would you use to tx a PDA?

A

NSAID (Indomethacin or ibuprofen) to close

or prostaglandin E to keep open until surgery

but, don’t do this before looking for other defects, you might kill the baby.

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55
Q

What is this?

In what population is this particularly common?

A

Atrioventricular Septal Defect (AVSD)

more than 30% of down syndrome patients have this.

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56
Q

What are the types of AVSD?

A

Partial - ASD and cleft anterior mitral leaflet with mitral insufficiency

Complete - large combined AV septal defect and large common AV valve, all 4 chambers communicate and develop volume hypertrophy.

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57
Q

Right to left shunts cause?

A

cyanotic congenital heart disease.

  • mixing of unoxygenated blood with blood in systemic circulation
  • decreased amount of blood going to lungs to be oxygenated
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58
Q

What are some presentations we might see with right to left shunts?

A
  1. Clubbing tips of fingers and toes (hypertrophic osteoarthropathy)
  2. polycythemia d/t hypoxia
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59
Q

What is a paradoxical embolism?

A

•emboli from periphery bypass lungs through cardiac defect and enter systemic circulation

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60
Q

What… is the tetralogy of fallot?

A
  1. Ventricular Septal Defect (VSD)
  2. Subpulmonic (+/- pulmonic valve) stenosis with obstruction of right ventricular outflow tract
  3. Aorta overrides the VSD
  4. Right ventricular hypertrophy
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61
Q

Direction of shunting in tetralogy of fallot is dependent upon?

A

Severity of subpulmonic stenosis

When severe, a right to left shunt results

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62
Q

How does Pink tetralogy of fallot differ?

A

mild subpulmonic stenosis

with well perfused lungs (behaves like VSD)

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63
Q

What is this radiographic finding referred to as? What does this patient have?

A

“Boot shaped” heart

Tetralogy of fallot

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64
Q

Is this a normal heart?

A

Nope, this is an example of transposition of the great arteries. Note the aorta arising from the right ventricle.

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65
Q

TGA creates two seperate circulatory circuits.

What can allow a patient with transposition of the great arteries to survive?

A

A patent ductus arteriosis, VSD or patent foramen ovale are the only ways a patient with this can survive. For a while.

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66
Q

What is the defect that leads to TGA?

A

Truncal and aortapulmonary septae

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67
Q

What are the obstruvtive congenital cardiac anomolies?

A
  1. Aortic stenosis and atresia
  2. Pulmonary stenosis and atresia
  3. Coarctation of the aorta
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68
Q

What are the types of congenital aortic stenoses?

A
  1. Valvular aortic stenosis
  2. subaortic stenosis
  3. supravalvular aortic stenosis
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69
Q

What is abnormal in valvular aortic stenosis?

What can happen if this is severe?

A

Abnormal valve cusps

if severe, get hypoplastic left heart syndrome

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70
Q

What is stenosed in subaortic stenosis?

A

Ring or collar above the cusps

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71
Q

Supravalvular aortic stenosis arises due to the ring or collar above the cusps. What is the mutation that commonly leads to this?

What is the syndrome associated with this?

A

Elastin gene mutation with aortic dysplasia (thickening)

William-Beuren Syndrome -
•deletion of about 28 genes from chromosome 7 with ELN gene (elastin) haploinsufficiency, hypercalcemia, glucose intolerance, facial and cognitive defects

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72
Q

What are the two forms of coarctation of the aorta?

A

Infantile - hypoplasia of aorta prior to patent ductus arteriosus. See cyanosis of the inferior body and weak femoral pulses.

Adult - Ridge like fold opposite ligamentum arteriosus. See HTN in the upper extremities with low pressure and pulses in lower extremities.

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73
Q

What type of coarctation of the aorta is shown here?

A

Infantile form

Stenosis is just proximal to the patent ductus arteriosis. So, upper extremities are oxygenated, and lower extremeties are getting deoxygenated blood.

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74
Q

What would you see in this patient as far as blood pressures?

A

Adult form coarctation of the aorta, causing HTN in the upper extremities and low pressure and pulses in the lower extremeties.

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75
Q

What are some other important associated anomalies that are common with coarctation of the aorta?

A

More than half also have a bicuspid aortic valve

Sometimes see coexisting circle of willis aneurysms

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76
Q

This is an example of postductal, adult type coarctatoin of the aorta. What would you see on x-ray?

A

Subcostal notching, d/t increased flow through the intercostal arteries.

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77
Q

What are the four clinical syndromes associated with IHD?

A
  1. Sudden Cardiac death
  2. angina pectoris
  3. chronic IHD with heart failure
  4. MI
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78
Q

What is the most common cause of ischemic heart disease?

A

90% of cases are d/t atherosclerotic coronary arterial obstruction

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79
Q

As mentioned before, atherosclerosis is the major cause of IGD. What are some other causes?

A
  1. Localized platelet aggregation
  2. Thrombosis overlying a disrupted plaque
  3. Vasospasm
  4. Emboli
  5. Hypotension
  6. Coronary artery vasculitis
80
Q

What level of fixed obstruction is required to cause IGD symptoms during exercise?

A

75% or greater obstruction

81
Q

What level of obstruction is required to produce IHD symptoms at rest?

A

90% obstruction or greater

82
Q

Acute atherosclerotic plaque change can play a role in IHD, what are the types of changes that can be problematic?

A

Rupture/Fissuring

Erosion/Ulceration

Hemorrhage into an atheroma (plaque)

83
Q

What is prinzmental angina?

A

Sustained vasospasm that causes angina

84
Q

What is cardiac Raynaud?

A

cold or emotion induced cardiac vasospasm

85
Q

What is Takotsubo cardiomyopathy?

A

dilated cardiomyopathy secondary to emotional or physical stress with normal coronary angiogram (sometimes due to vasospasm)

86
Q

What is the most common mechanism of sudden cardiac death (SCD)?

Most common cause?

A

Most often a lethal arrhythmia from

  1. electrical instability
  2. ventricular fibrillation
  3. asystole

Most common cause is IHD

87
Q

What pathologies should you suspect non-ischemic SCD in young people? (More of an FYI card)

A

Possibilities (% are from study on deaths in young athletes)

  • Hypertrophic cardiomyopathy (18%)
  • Coronary artery anomalies (9%)
  • Myocarditis (3%)
  • Arrhythmogenic right ventricular cardiomyopathy (2%)
  • Ion channelopathies (2%)
  • Commotio cordis (3%) due to sudden v-fib caused by blunt impact to the heart
  • Congenital structural abnormalities (<1%)
  • Dilated cardiomyopathy (<1%)
  • Aortic valve stenosis
  • Mitral valve prolapse
  • Pulmonary hypertension
  • Cardiac hypertrophy of any cause (e.g., hypertension)
  • Systemic metabolic and hemodynamic alterations (vasculitis)
  • Catecholamines and drugs of abuse (cocaine and methamphetamine)
88
Q

What is another name for ischemic cardiomyopathy?

A

Chronic Ischemic Heart Disease

89
Q

What does ischemic cardiomyopathy usually present with?

A

with insidious onset of congestive heart failure

90
Q

In addition to CHF, what also frequently presents with ischemic cardiomyopathy?

A
  • Cardiomegaly with left ventricular hypertrophy & dilatation
  • Evidence of previous healed MIs or ischemia (areas of myocardial fibrosis)
  • Develop arrhythmias, congestive heart failure and MIs
91
Q

Chronic ischemia that does not cause necrosis can lead to what?

A

hypokinetic myocardium with myocyte hibernation that can become functional after reperfusion

92
Q

What is angina pectoris?

A

Paroxysmal and usually recurrent attacks of substernal or precordial chest discomfort

93
Q

What causes angina pectoris?

A

transient myocardial ischemia that falls short of inducing the cellular necrosis that defines infarction

94
Q

What is stable/typica angina?

What provokes it?

How common is it?

What relieves it?

A

Stable (Typical) Angina: ↓perfusion 2ry to fixed-narrowing

  • Most common form of angina
  • Can be provoked by increased cardiac demand (emotion, exercise)
  • Usually relieved by rest or sublingual nitroglycerin
95
Q

What is unstable/crescendo/pre-infarction angina?

A

Caused by transient myocardial ischemia that falls short of inducing the cellular necrosis that defines infarction

Usually have acute plaque change

96
Q

How are the attacks characterized in terms of frequency with unstable angina? How are they provoked?

A
  • Progressive increase in frequency and severity of attacks
  • Provoked by progressively less effort and may occur at rest

Still have angina symptoms of:

Paroxysmal and usually recurrent attacks of substernal or precordial chest discomfort

97
Q

How are crescendo angina attacks relieved?

A

Sometimes they are not relieved by rest or nitroglycerin

98
Q

What the heck is Prinzmetal angina?

A

Prinzmetal Angina: episodic angina due to coronary artery spasm

99
Q

How is Prinzmetal angina relieved?

A

Nitroglycerin or Ca++ channel blockers

100
Q

What is the definition of an MI?

A

The death of cardiac muscle from ischemia

101
Q

What are some facts about the epidemiology of MI that you might want to remember?

Think age, gender, risk factors, genetics…

A

Frequency of MI rises progressively with increasing age

  • 10% MIs occur in individuals under age 40
  • 40-45% occur in individuals under age 65

Men at far higher risk than women – women are protected during premenopausal period (but not post menopause w/ or w/o estrogen)

Lipid risk factors account for 50-60 % of MIs

Genetic risk factors for thrombosis (e.g., prothrombin mutations, hyperhomocystenemia) account for another 10-20%

102
Q

What is a transmural infarction? What is it frequently associated with?

A

Ischemic necrosis involves >50% of the ventricular wall thickness

  • Commonly associated with acute plaque change with thrombosis
103
Q

What is a subendocardial infarction?

A

Subendocardial infarction:

Area of ischemic necrosis limited to inner 1/2

104
Q

What can cause a subendocardial infarct?

A

May occur as a result of acute plaque change and thrombosis

May result from reduction in systemic blood pressure (shock)

105
Q

Why does a small band of subendocardial tissue remain viable?

A

Perfusion still present - myocardium right underneath endocardium is perfused via diffusion from the ventricle

106
Q

What does triphenyltetrazolium chloride staining reveal on gross specimens?

A

lactate dehydrogenase leakage following cell death

  • necrotic areas won’t take up stain
  • helpful in dx’ing MI in gross specimens
107
Q

What is the typical sequence of events for the pathogenesis of an MI?

A

Typical Sequence of Events (90% Patients)

•Sudden change in plaque →

•Immediate formation of platelet plug →

  • Vasospasm (vasoactive substances from platelets)
  • Propagation of platelet plug and formation of stable clot (clotting system)

•→Coronary artery occlusion within minutes

108
Q

What type of stimulation can induce an MI?

A

Adrenergc stimulation:

  • peak incidence 6am-noon, cortisol levels increase just prior to wake
  • intense emotional stress
109
Q

How does an MI happen in patients with no associated atherosclerosis?

A
  • Vasospasm (e.g., cocaine)
  • Emboli (e.g. mural thrombus, valve vegetations, paroxysmal emboli)
  • Vasculitis
  • Hemoglobinopathy
  • Etc.
110
Q

An MI has happened. What is the first thing that happens, and how quickly does it happen?

A

Onset of ATP depletion (↓ glycolysis)

happens in seconds

111
Q

An MI has occurred and ATP depletion has started. What is next? When does it happen

A

Loss of contractility

< 2 min after MI

112
Q

An MI has occurred, with ATP depletion and loss of contractility. What happens next? Timeframe?

A

ATP reduced:

50% of normal - 10 min

down to 10% of normal - 40 min.

113
Q

Along with grossly reduced ATP levels and loss of contractility, what also happens after an MI?

A

Irreversible cell injury/necrosis

- starts 20-40 min.

114
Q

An MI has occurred, and there is loss of contractility, depletion of ATP, and irreversible cell injury. What 2 things can happen to the heart tissue now, and when?

A

Microvascular injury - >1 hour

Complete unsalvageable necrosis 6-12 hours

115
Q

Summarize the changes that take place following an MI on the cellular level. (I know, repetition, but I think there might be TQ stuff here.)

A

Onset of ATP depletion (↓ glycolysis) - Seconds

Loss of contractility - < 2 min

ATP reduced:

to 50% of normal - 10 min

to 10% of normal - 40 min

Irreversible cell injury (necrosis) - 20-40 min

Microvascular injury - >1 hr

Complete unsalvageable necrosis - 6 -12 hours

116
Q

What are some early biochemical findings after MI?

A

Increasing/accumulating lactate

decreased/depleted ATP

117
Q

When is MI potentially reversible?

A

~30 min after onset of ischemia

118
Q

When is reperfusion most effective after an MI?

A

Earlier the better - more myocytes saved

119
Q

A coronary aa has become occluded, and myocardial necrosis has set in. Where does necrosis set in first? Where are myocytes ‘at risk’?

A

Necrosis begins in a small zone of the myocardium beneath the endocardial surface in the center of the ischemic zone.

The area that depends on the occluded vessel for perfusion is the “at risk” myocardium

Note that a very narrow zone of myocardium immediately beneath the endocardium is spared from necrosis because it can be oxygenated by diffusion from the ventricle.

120
Q

What layer of the heart mm do most MIs start? Why? What kinds of infarcts result from full versus partial blockages?

A

most MIs start on subendocardial region and travel towards outside

  • Heart tends to get better perfusion on the outside

partial blockage will not result in transmural infarct, often results in subendocardial infarct

  • complete blockage = transmural MI
121
Q

How is the location of MIs determined? What arteries are at the most risk for occlusion?

A

1.Specific coronary artery obstructed

LAD 40-50%; RCA 30-40%; LCX 15-20%

122
Q

How is the size of tissue deemed at risk from MI determined? What factors should you keep in mind?

A

Consider aa blocked and:

  • Duration of occlusion (spontaneous or therapeutic lysis of initial thrombus)
  • Metabolic requirements of affected myocardium
  • Presence, site and severity of associated vasospasm
  • Extent of collateral blood supply
123
Q

What regions would you expect to be at risk (left or right ventricle, ant or posterior) from the following transmural infarcts?

LAD

left circumflex

right coronary aa

  • or post descending branch
A

LAD = anterior left ventricle

left circumflex = lateral left ventricle

right coronary = post left ventricle

post descending branch RCA = post left ventricle

124
Q

What regions would you expect to at risk for ischemic necrosis from the following non-transmural infarcts?

transient/partial obstruction

global hypotension

small intramural vessel occlusions

A

transient/partial obstruction =

  • regional subendocardial infarct
  • anterior left ventricle wall

global hypotension=

  • circumferential subendocardial infarct
  • entire wall of left ventricle

small intramural vessel occlusions=

  • microinfarcts
  • small areas of necrosis scattered throughout
125
Q

A patient with no previous symptoms of cardiac ischemia gets a septic infection, then has an MI. Why did this happen?

A

Patient probably had a significant occlusion - 75% or so - on a coronary aa

  • hypotension secondary to sepsis, trauma, etc, can result in too little blood flow, ischemia and MI to tissue downstream of stenosis
126
Q

How do myocytes get collateral circulation?

A
  • chronic ischemia of the heart leads to better collateralization of vessels due to VEG-F expression
  • no ischemia, no collateralization
  • oft better on posterior heart, LAD area not good
127
Q

What is the time frame for a reversible ischemic injury in MI? Associated histological findings?

A

time: 0-30 min.

no gross or light microscopy changes

EM changes:

Relaxation of myofibrils; glycogen loss; mitochondrial swelling

128
Q

When does irreversible injury from MI start to occur?

A

After 30 min mark

129
Q

In the half hour - 4 hour timeframe, what would you expect to find as far as:

gross features

light microscopy findings

A

gross features

none

light microscopy findings

  • Usually none; variable waviness of fibers at border
130
Q

In the 12-24 hour timeframe after an MI, what would you expect to find as far as morphological changes in:

gross features

light microscope findings

A

gross features

  • dark mottling

light microscope findings

  • Ongoing coagulation necrosis; pyknosis of nuclei; myocyte hypereosinophilia; marginal contraction band necrosis; early neutrophilic infiltrate
131
Q

In the 1-3 days timeframe after an MI, what would you expect to find as far as morphological changes in:

gross features

light microscope findings

A

gross features:

mottling with yellow-tan infarct center

Light microscope:

Coagulation necrosis, with loss of nuclei and striations; brisk interstitial infiltrate of neutrophils

132
Q

What is the goal of MI infarct modification by reperfusion?

A

•salvage ischemic myocardium from potential infarction by restoration of tissue perfusion as quickly as possible (reperfusion)

133
Q

What intervention techniques are available for MI modification by reperfusion?

A
  • Intervention techniques include:
  • Lysis of thrombus by fibrinolytic therapy (streptokinase, urokinase, or tissue plasminogen activator (TPA)
  • Balloon angioplasty
  • Coronary artery bypass graft
134
Q

If flow is restored to ischemic heart tissue following MI, what happens?

A

If flow is restored, then some necrosis is prevented, myocardium is salvaged, and at least some function will return.

The earlier reperfusion occurs, the greater the degree of salvage.

However, the process of reperfusion itself may induce some damage (reperfusion injury), and return of function of salvaged myocardium may be delayed for hours to days (post-ischemic ventricular dysfunction).

135
Q

At what time point does reperfusion not change the MI infarct size?

A

Reperfusion beyond 6 hours does not appreciably reduce myocardial infarct size

136
Q

What is myocardiocyte stunning?

A

a type of reversible injury - cells viable but not functional

137
Q

What are some pathological changes associated with reperfusion of an MI?

A
  • Reperfusion-induced arrhythmias
  • Myocardial hemorrhage with contraction bands
  • Reperfusion injury – additional permanent myocardial damage
  • No-reflow - Microvascular injury with endothelial swelling
  • Reversible “myocardial stunning” (prolonged ischemic dysfunction with CHF)
138
Q

What are the classic acute onset symptoms, signs and findings with an MI?

A

•Severe substernal chest pain with radiation of pain down left arm, neck, jaw, epigastrium
•Weak, rapid pulse
•Sweating profusely (diaphoretic)
•Nausea
•Dyspnea secondary to pulmonary congestion and edema
•STEMI –ST segment Elevation Myocardial Infarct (transmural)
•NSTEMI – Non-ST segment Elevation Myocardial Infarct (subendocardial)

139
Q

What percent of MI patients are asymptomatic? How do you find MI on these people?

A

10-25% asymptomatic

  • seen with DM, transplant patients

•MI discovered by EKG (Q waves, ST-segment changes, T-wave inversion) or other types of testing

140
Q

What cardiomyocyte proteins are released following MI? When?

A

myoglobin - peaks ~6 hours after MI

CK-MB - peaks 10-24 hrs after MI

MB isofroms - peaks 4-12 hr aft MI

Troponin I/cTnI - peaks 10-24 hours after MI

Troponin T/cTnT - peaks 12-24 hrs aft MI

141
Q

In addition to MI, what can elevate myoglobins? What do you use in addition to this biomarker for suspected MI dx?

A

can be elevated by trauma

use with EKG to rule out MI:

normal myoglobin + normal EKG = no MI

142
Q

According to Dr. Gomez, how should you order cardiac enzyme labs and why?

A

Order cardiac enzymes x3 every 2 hours

  • will climb gradually, get total pic over time to get full clinical picture
  • go ahead and use other things to treat MI and start reperfusion immediately, use labwork later to confirm MI
143
Q

What biomarkers start to increase first after an MI?

A

1 hour:

myoglobin

MB-isoforms

3 hours:

CK-MB

troponins

144
Q

What biomarkers return to baseline when after an MI?

A

myoglobin - 18-24 hours

MB-isoforms - 38 hours

CK-MB - 48-72 hours

cTnI - 5-10 days

cTnT - 5-14 days

145
Q

What enzyme markers will change after an MI, in addition to myoglobin and troponins?

A

liver enzymes - AST - peaks in ~1.5 days, done by 5 days

lactate dehydrogenase - LDH - peaks in ~2 days, done by 6 days

146
Q

What is the clinical outcome from MIs?

A

½ of deaths occur in patients within one hour of onset symptoms

vast majority of these patients never reach Emergency Department

5% In-hospital death rate (once was 30%)

  • 2/3 die from cardiogenic shock (which has a 70% mortality rate)

¾ of MI patients have one or more complications of an acute MI

147
Q

What are some physiological complications of MIs?

A

Contractile dysfunction: Severe pump failure occurs in 10-15% of patients

Arrhythmias: Conduction disturbances along with myocardial “irritability”

Papillary muscle dysfunction: mitral regurgitation

148
Q

What are some pathological/morphological complications of acute MI?

A

Myocardial rupture (1-5% of MIs)

  • Free wall (usually anterior) → cardiac tamponade
  • Interventricular septum → VSD/ASD
  • Papillary muscle → acute valvular regurgitation

Pericarditis (fibrinous or hemorrhagic)

Right ventricular infarction (isolated in 1-3% of cases)

Infarct extension (enlargement) and expansion (thinning and dilation)

Mural thrombus

Ventricular aneurysm (usually anteroseptal)

Progressive late heart failure (IHD)

149
Q

What is the criteria for Dx for systemic HTN heart disease? What side of the heart does this affect?

A

Affects left side

Criteria for Dx:

  1. Left ventricular hypertrophy (usually concentric) in the absence of other cardiovascular pathology that may have induced it
  2. A history of HTN (BP > 140/90 mm Hg) or pathologic evidence of systemic hypertension in other organs
150
Q

What does left sided HTN heart disease present with, clinically?

A

CHF or atrial arrythmias

151
Q

Someone has died from complications of systemic HTN heart disease (i.e. CHF). What gross changes would you expect to see to the heart?

A

There is marked concentric thickening of the left ventricular wall causing reduction in lumen size.

  • many patients will also have small infarcts too, i.e. subendocardial infarct
152
Q

A patient of yours doesn’t look good/very healthy, and has a 10 year Hx of COPD. What cardiac changes should you look out for?

A

Pulmonary/Right sided HTN heart disease

Namely. chronic C**or pulmonale

153
Q

How does chronic Cor pulmonale happen? What gross changes to the heart would you expect?

A

results from pulmonary disorders that cause chronic severe pulmonary hypertension

  • thick and dilated RV & RA
  • RV has a thickened free wall and hypertrophied trabeculae
  • LV has been distorted by the enlarged right ventricle
154
Q

What is acute Cor pulmonale? What gross changes would you expect?

A

occurs from massive pulmonary thromboembolism (saddle embolus, etc.)

  • acutely dilated RV and RA
155
Q

PHTN = what cardiac change?

A

PHTN = Pulmonary Hypertension

PHTN = hypertrophy of right side of heart

heart has to work harder to perfuse lung for gas exchange, leading to eccentric hypertrophy of RV

  • often see jet lesions (white and fatty plaques) on RV outflow tract
156
Q

What types of diseases predispose someone to Cor pulmonale?

A

Diseases of pulmonary parenchyma

Disease of pulmonary vessels

Disorders affecting chest movement

Disorders inducing pulmonary arterial constriction

157
Q

What are the 2 main types of cardiac valve dysfxn?

A

“pure” = only stenosis or regurg

158
Q

Like professors, cardiac valves are often dysfxnal in multiple ways. What is mixed cardiac valve dysfxn?

A

have stenosis and insufficiency in same valve

159
Q

What is cardiac valve stenosis? Is it an acute or chronic problem? Where is the abnormality?

A

Stenosis: failure of valve to open – leaflet problem

Virtually always a chronic disease

Almost always a cusp abnormality

160
Q

What is valve insufficiency? Is it an acute or chronic problem?

A

Insufficiency (regurgitation or incompetence): failure of a valve to close

Chronic disease or acute insufficiency syndromes may occur

Intrinsic disease of valve cusp or acquired abnormality of the supporting structures

161
Q

What is functional regurg?

A

normal valve leaflets but problem with supporting structures (e.g. dilated annulus from ventricular dilatation)

162
Q

What is a major cause of mitral stenosis?

A

postinflammatory scarring - rheumatic heart disease

163
Q

What are some major structural causes of mitral regurg?

A

abnormalities of leaflets and commissures

abnormalities of tensor apparatus

abnormalities of left ventricular cavity and/or annulus

164
Q

What are some major pathologies that cause mitral valve regurg?

A

abnormalities of leaflets and commissures

postinflamm scarring

infective endocarditis

mitral valve prolapse

drugs - fen-phen

abnormalities of tensor apparatus

rupture of papillary mm

papillary mm dysfxn/fibrosis

rupture of chordae tendinae

abnormalities of left ventricular cavity and/or annulus

LV enlargement - myocarditis, dilated cardiomyopathy

calcification of mitral ring

165
Q

What are some major causes of aortic stenosis?

A

postinflamm scarring - rheumatic heart disease

senile calcific aortic stenosis

calcification of congenitaly deformed valve

166
Q

What are some major causes of aortic regurg?

A

postinflamm scarring

infective endocarditis

Marfan syndrome

167
Q

What are some major causes of aortic disease?

A

degenerative aortic dilation

syphilitic aortitis

ankylosing spondylitis

RA

Marfan syndrome

168
Q

Aortic stenosis most commonly is caused by what?

A

calcification - normal or bicuspid valves

169
Q

Aortic insufficiency most frequently results from what?

A

Dilated ascending aorta

due to HTN and aging

170
Q

Mitral stenosis most frequently occurs from what?

A

rheumatic valvular disease

  • due to valve scarring
171
Q

Mitral insufficiency most frequently results from what?

A

Myxomatous degeneration - mitral valve prolapse

172
Q

2/3 of all valvular disease is what?

A

Acquired stenoses of aortic and mitral valves

173
Q

Calcific aortic stenosis results from what?

A

Most common of all valvular abnormalities

Consequence of dystrophic calcification and ossification owing to chronic valve abuse (years of use)

174
Q

What are the pathological features of senile calcific aortic stenosis?

A

Nodular masses of calcium are heaped up within the sinuses of Valsalva

175
Q

What are the clinical features of calcific aortic stenosis?

A
  • Clinical symptoms do not occur until 7th (60s) to 9th (80s) decades
  • Crescendo-decrescendo systolic murmur (crescendo with severe disease)
  • Pressure hypertrophy results from flow obstruction and patient develops significant left ventricular concentric hypertrophy
176
Q

Patients with calcific aortic stenosis are at risk for developing left ventricular cardiac mass. This puts them at risk for what sequelae?

A

•Left ventricular cardiac mass tends to be ischemic and leads to:
•Congestive heart failure (die within 2 yrs)
•Syncope (die within 3 years)
Angina pectoris (die within 5 yrs)

177
Q

Calcific stenosis of the aortic valve can happen due to old age, or to what congenital anomaly that is in 2% of the population?

A

Bicuspid aortic valve

178
Q

What problems is a bicuspid aortic valve at greater risk of acquiring?

A
  • Bicuspid valves more susceptible to progressive degenerative calcification; develop significant calcification earlier
  • Develop clinical symptoms and signs of cardiac dysfunction earlier, 5th and 6th decades (7th to 9th decades with tricuspid aortic valves)
  • May have coexisting abnormalities of aortic wall
179
Q

What types of patients does mitral annular calcification occur in?

A

1) Women over 60 years of age
2) Individuals with myxomatous mitral valves
3) Patients with elevated left ventricular pressure – e.g., hypertension

180
Q

How does mitral annular calcification affect valvular function? What is it occasionally associated with?

A

Generally does not affect valvular function

Occasionally associated with arrythmias

181
Q

How is mitral annular calcification frequently dx’ed?

A

Large calcium deposits are incidentally detected on radiography done for other reasons

  • see it on CXR incidentally
  • most are clinically silent - rare arrhythmias d/t calcification of conduction system, valvular dysfxn d/t extensive calcification causing stenosis
182
Q

What changes does mitral annular calcification have on the valve?

A

calcific nodules at the base of the anterior mitral leaflet

183
Q

What happens to the valves (grossly) during mitral valve prolapse? How does this cause the characteristic heart sounds?

A

Mitral valve leaflet(s) is (are) floppy and prolapse into the left atrium during systole

  • create midsystolic click, regurgitant murmur

hooding with prolapse of the posterior mitral leaflet into the left atrium

thrombotic plaques at sites of leaflet-left atrium contact

184
Q

What populations is mitral valve prolapse more common in?

A
  • Affects ~2-3% adults in US, most often young women (7F:1M)
  • Seen in Marfan syndrome (fibrillin-1/elastic fibers)
  • Vast majority patients clinically asymptomatic
185
Q

Myxomatous degeneration of the mitral valve is often clinically silent. What complications can develop?

A
  • Small subset (3%) may develop complications
  • Infective endocarditis
  • Mitral insufficiency
  • Stroke or other systemic infarct
  • Arrhythmias (both atrial and ventricular, rare sudden death)
  • Atypical chest pain
186
Q

How is myxomatous degneration of the mitral valve dx’ed?

A

echocardiogram

auscultation

187
Q

What are the primary changes associated with myxomatous degeneration of the mitral valve?

A
  • Intercordal ballooning of mitral valve leaflets
  • Leaflets enlarge (thick and rubbery)
  • Thinned fibrosa; thickened spongiosa with mucoid (myxoid) material
  • Concomitant involvement of tricuspid valve in 20-40% of cases

Valve weakens due to mucoid instead of fibrous material à leads to stretching and ballooning, doesn’t work normally

188
Q

What are the secondary changes associated with myxomatous degeneration of the mitral valve?

A

Secondary changes

  • Dilation of annulus
  • Jet lesions with fibrosis of endocardial surfaces
  • Fibrosis of valve leaflets
  • Thrombi on atrial surfaces of mitral leaflets
  • Focal calcification at base of posterior leaflet
189
Q

How does strep pharyngitis cause chronic rheumatic valvular disease?

A

Beta-hemolytic strep infection -> imm response, with anti-group A strep antigens

  • fever and migratory polyarthritis results
  • same infection, several weeks later -or- after new strep infection
  • deposition of cross-reactive Ab on heart valves, chordae tendinae, myocardium, and cause of fibrinous pericarditis

Chronic rheumatic heart disease = deformity of heart valves

190
Q

What clinical signs and symptoms would you expect with chronic rheumatic valvular heart disease?

A

pericardial rub - fibrinous pericarditis

Usually occurs 10 days to 6 weeks post strep throat

  • can get pancarditis – endocardium and valves,

myocardium and epicardium get granulomas called Aschoff bodies that show acute rheumatic fever

– can hear murmurs or pericardial rub

Aschoff body - Collection of large activated histiocytes

Anitschkow cells – “mononuclear”

Aschoff cells - multinucleated forms

caterpillar” cells - unique linear chromatin pattern

191
Q

What are the signs and symptoms of acute rheumatic fever?

A

Acute rheumatic fever: Acute systemic disease

  • Migratory polyarthritis of large joints (swollen, painful joints)
  • Acute carditis with cardiac enlargement and diminished function
  • Subcutaneous nodules
  • Erythema marginatum of skin
  • Sydenham chorea (involuntary, purposeless movements of extremities)
192
Q

What is the Jones criteria for dx of acute rheumatic fever?

A

Jones Criteria” for diagnosis

Evidence prior group A Strep infection plus

  • 2 major system findings (from above list of 5)
  • Or 1 major system finding plus 2 minor manifestations
  • Fever
  • Arthralgia
  • Evidence of acute phase reactants
  • elevated sedimentation rate
  • elevated C-reactive protein
193
Q

What kind of a reaction is acute rheumatic fever?

A

•Hypersensitivity reaction to M protein cross-reacting with tissue glycoproteins

194
Q

How are subsequent attacks of rheumatic fever prevented after initial episode?

A
  • After initial episode have increased risk of subsequent attacks with repeat group A Strep infections
  • Patients may receive long-term antibiotic prophylaxis
195
Q

What is rheumatic heart disease? What valves does it affect?

A

Rheumatic Heart Disease (RHF)

  • Term used for the chronic valvular disease that occurs years after ARF
  • Commonly affects mitral and aortic valves
  • Mitral valve only: 65 – 70 %
  • Mitral valve plus aortic valve: 25%
  • Uncommonly the tricuspid
  • rarely the pulmonic valve
  • 99% of all mitral stenosis is caused by RHD
196
Q

What are MacCallum plaques?

A

subendocardial fibrosis from regurgitant jets in RHD

197
Q
A

CV II Exam 2 (8 decks)

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