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CV 2 Exam 2 > heart 1 > Flashcards

heart 1 Flashcards

1
Q

Myocardium histology includes

A

intercalated discs

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2
Q

Valve histology

A

(ventricularis* [v], spongiosa [s], and fibrosa [f]).

Pulmonary valve histology is similar but the atrioventricular valves will be thinner and have an atrialis, instead of a ventricularis, layer.

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3
Q

Chambers in the aging heart

A

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

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4
Q

Valves in 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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5
Q

epicardial coronary arteries in the aging heart

A

** Tortuosity
Diminished compliance
Calcific deposits
** Atherosclerotic plaque

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6
Q

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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7
Q

the aging aorta

A

** Dilated ascending aorta with rightward shift
Elongated (tortuous) thoracic aorta
Sinotubular junction calcific deposits
Elastic fragmentation and collagen accumulation
atherosclerotic plaque

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8
Q

cardiac death statistics– what have gone up?

A

↑ Congenital heart disease deaths

↑ Hypertensive heart disease deaths

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9
Q

Normal Cardiac Function and Cardiac Reserve

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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10
Q

Cardiac Dysfunction Six Basic Causes

A

Pump failure - diminished myocardial contractility
Primary cardiomyopathy; ischemic cardiac disease
Obstruction to blood flow through the heart
Stenotic valvular disease; hypertensive disease
Regurgitant flow
Valvular disease with incompetence
Shunted flow- Congenital heart diseases
Disorders of cardiac conduction- Atrial fibrillation; ventricular tachycardia
Disruption of continuity of the circulatory system- Gunshot wound; ventricular rupture; ruptured aneurysm

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11
Q

Cardiac Compensation

A

Activation of neurohumoral systems

  • Norepinephrine from adrenergic nerves
  • Renin-angiotensin-aldosterone system
  • Natriuretic peptides

Myocardial adaptations - ventricular remodeling

Frank-Starling mechanism - enhance contractility and stroke volume

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12
Q

Natriuretic Peptides

A

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

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

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

** Cause vasodilation, natriuresis and diuresis
Antithesis of renin-angiotensin-aldosterone system

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13
Q

causes and consequences of cardiac hypertrophy

A

pressure overload/ volume overload (Hypertension, valve disease, MI) –> increased work and wall stress and cell stretch –> hypertrophy and/ or dilation

“Congestive Heart Failure” (CHF)
When dysfunction is chronic and symptomatic

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14
Q

Cardiac Hypertrophy Pathophysiology

A

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

Myocyte hypertrophy - Response available for increased cardiac
workload per myocardial fiber
(Myocyte hyperplasia does not occur in adult ventricle)

Cardiac hypertrophy – increase in ventricular thickness or weight
Cardiomegaly - increase in heart size or weight

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15
Q

heart: weight in grams for normal and abnormal

A

Normal: Male 300-350 gm; Female 250-300 gm
350-600 gm: Pulmonary HTN, IHD
400-800 gm: Systemic HTN, aortic stenosis, mitral regurgitation, dilated cardiomyopathy
600-1000 gm: Aortic regurgitation, hypertrophic cardiomyopathy

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16
Q

Cardiac Hypertrophy Pathologic Findings

A

“Pressure Overload” Hypertrophy = Concentric Hypertrophy
-increase in the thickness of wall subjected to the increased workload
Left ventricle: systemic hypertension or aortic stenosis
Right ventricle: cor pulmonale

“Volume Overload” Hypertrophy = Eccentric Hypertrophy
- chamber dilatation caused by volume overload stimulus
Overall cardiac muscle mass is increased
Ventricular wall thickness is near normal
Can be seen with ischemia, valve disorders, congenital heart disease, etc.

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17
Q

Congestive Heart Failure (CHF)

A

Cardiac Failure due to insufficient pump rate to meet metabolic demands and/or pump can marginally meet demands with elevated filling pressure

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18
Q

Forward and Backward failure in CHF

A

Forward failure - Diminished cardiac output
Systolic dysfunction - progressive deterioration of myocardial contractility
Diastolic dysfunction - Inability heart chambers to relax (distend) sufficiently to fill during diastole

Backward failure - 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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19
Q

Left-Sided Heart Failure

A

Chronic: Slowly progressive failure (insidious onset) which may over time develop sufficient severity to cause right sided heart failure
Acute: Rapidly progressive fatal course (with acute pulmonary edema) – Medical Emergency with 50% mortality

Most commonly caused by 
	Ischemic heart disease
	Hypertensive heart disease
	Aortic and mitral valvular disease
	Primary nonischemic myocardial disease (cardiomyopathy)
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20
Q

Lab testing for left-sided heart failure

A

Laboratory testing : B-type natriuretic peptide produced by ventricles (2ry to increased pressure); BNP and NT pro-BNP tests available
BNP >500 pg/mL are most consistent with CHF
BNP less than 100 pg/mL unlikely to be CHF

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21
Q

Left-Sided Heart Failure Cardiovascular Pathologic Findings

A

Cardiomegaly: Hypertrophy +/- chamber dilatation

Secondary enlargement of the left atrium (eccentric hypertrophy)
Can lead to mitral valve regurgitation and atrial fibrillation

Tachycardia – increased adrenergic activity
Third heart sound (S3 gallup) - occurs during ventricular filling (diastole)
Systolic murmur - if develop mitral regurgitation
Hepatojugular reflux - distention of the jugular vein induced by applying manual pressure over the liver (elevated filling pressure in left-sided heart failure)

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22
Q

Left-Sided Heart Failure Extracardiac Effects

A

Lung pathology: pulmonary basilar crackles (rales) +/- pleural effusions
Flash pulmonary edema
siderophages (heart failure cells)- long-term

Dyspnea
Orthopnea
Paroxysmal nocturnal dyspnea

Kidney- renal hypoperfusion

Brain- hypoxic encephalopathy

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23
Q

Right-Sided Heart Failure

A

Most commonly a consequence of left-sided heart failure
↑ pressure in the pulmonary circulation →↑workload right ventricle →right-sided heart failure

“Pure” or isolated (no left-sided dysfunction) right-sided failure

  • Uncommon
  • Cardiac hypertrophy and dilatation confined to the right atrium and ventricle
  • Sequela of severe chronic pulmonary hypertension
  • ** Cor Pulmonale = Heart disease secondary to lung disease
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24
Q

Right-Sided Heart FailureExtra-cardiac Effects

A

Subcutaneous tissues
“Pitting edema” lower extremities or generalized anasarca

Congestive hepatomegaly

 - Chronic passive congestion in hepatic sinusoids
 - Cardiac cirrhosis - increased fibrous tissue in centrilobular zone  
 - Centrilobular necrosis (more with concurrent LV failure)

Congestive splenomegaly - usually mild with only doubling in size

Pleural, peritoneal and pericardial effusions - transudates

25
Q

Congenital Heart Disease

A

Defects occur between 3 and 8 weeks gestational age

Chromosomal disorders- 1 in 200, 30% with CHD

Trisomy 21 - 1 in 700- 50% with CHD
AVSD>VSD>ASD>PDA>TOF>TGA

26
Q

Bicuspid aortic valve ?

A

seen in 2% of population

27
Q

most common malformations

A

bicuspid aortic valve
Ventricular septal defect
Atrial septal defect

28
Q

Heart disease genes

A

ASD- NKX2.5

DiGeorge- TBX1(del22aq11.2)

Marfan syndrome- FBN1

29
Q

Cardiac Defects Related to Neural Crest Abnormalities

A

Abnormal development of neural-crest derived cells (4th branchial arch and 3rd and 4th pharyngeal pouches)

“CATCH-22”-cardiac, abnormal facies, thymic aplasia, cleft palate, hypocalcemia – Chr22 (TBX-1)

DORV- double-outlet right ventricle
TGA- transposition of the great arteries

30
Q

Left to Right Shunts

A

ASD, VSD, PDA, AVSD (the letter D is in them all)
Increased pulmonary blood flow with no initial cyanosis

Muscular pulmonary arteries develop medial hypertrophy and vasoconstriction to normalize distal pressure
Eventually develop pulmonary hypertension leading to right to left shunt and late cyanotic congenital heart disease (Eisenmenger syndrome)

31
Q

Ventricular Septal Defect (VSD)

A

large ones have a murmur, pulmonary hypertension and Eisenmenger syndrome (Pulmonary HTN → ↑ right ventricular pressure → right-to-left shunt (shunt reversal)

32
Q

Atrial Septal Defect (ASD)

A

Three major types
Secundum (90%) - involves fossa ovalis
Primum (5%) - adjacent to AV valve
Sinus venosus (5%) - near superior vena cava

10% of untreated develop pulmonary HTN

May have murmur (flow increased 2-4x across pulmonary valve)
Some may present as adults with pulmonary HTN

Probe patent foramen ovale is not an ASD

33
Q

Patent (Persistant) Ductus Arteriosus (PDA)

A

Ductus usually closes at 1-2 days 2ry to
↑O2
↓ Pulmonary vasculature resistance
↓ Prostaglandin E2

90% are isolated defects
Continuous harsh machine-like murmur
If chronic, develop pulmonary HTN and cyanosis
Narrow ductus defect will be asymptomatic

Rx – NSAID (Indomethacin or ibuprofen) to close
or prostaglandin E to keep open until surgery

34
Q

Atrioventricular Septal Defect (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

(>1/3 of these patients have Down syndrome)

35
Q

Right to Left Shunts

A

Cause cyanotic congenital heart disease
Mixing of unoxygenated blood with blood in systemic circulation
Decreased amount of blood going to lungs to be oxygenated

Develop clubbing of the tips of fingers and toes (hypertrophic osteoarthropathy) and polycythemia due to hypoxia

** Paradoxical embolism – emboli from periphery bypass lungs through cardiac defect and enter systemic circulation

36
Q

Tetralogy of Fallot

A

Anterosuperior displacement of infundibular septum
Ventricular Septal Defect (VSD)
Subpulmonic (+/- pulmonic valve) stenosis with obstruction of right ventricular outflow tract
Aorta overrides the VSD
Right ventricular hypertrophy

** Direction of shunting depends on severity of subpulmonic stenosis
When severe, a right-to-left shunt results (arrow)

Subpulmonic stenosis protects lung from increase pressure and pulmonary arteries may be hypoplastic

Pink tetralogy of Fallot- mild subpulmonic stenosis
with well perfused lungs (behaves like VSD)

37
Q

Transposition of the great arteries

A

Defect with truncal and aortapulmonary septae

Separation of pulmonary and systemic circulations

Incompatible with live if no VSD, patent foramen
ovale or patent ductus arteriosus present

38
Q

Other Anomalies with

Right to Left Shunt

A

Truncus arteriosus – failure of truncus to separate into aorta and pulmonary artery
Have VSD
Cyanosis, increased pulmonary flow (pulmonary hypertension)

Tricuspid atresia – complete occlusion of tricuspid valve orifice
Right ventricle usually hypoplastic
ASD or patent foramen ovale allows right to left shunt
VSD allows right ventricle blood into common great artery

Total anomalous pulmonary venous connection -
No pulmonary veins enter left atrium
Drainage into innominate (brachiocephalic) vein or sinus venosus
Patent foramen ovale or ASD always present

39
Q

Aortic stenosis and atresia

A

Valvular aortic stenosis –abnormal valve cusps
if severe get hypoplastic left heart syndrome
Subaortic stenosis – ring or collar below cusps
Supravalvular aortic stenosis – ring or collar above cusps
elastin gene mutation with aortic dysplasia (thickening)

40
Q

Pulmonary stenosis and atresia

A

smaller the valve orifice the worse the cyanosis

41
Q

Coarctation of the aorta

A

Infantile form
hypoplasia of aorta prior to patent ductus arteriosus
cyanosis of inferior body and weak femoral pulses

Adult form
ridge-like fold opposite ligamentum arteriosus
HTN upper extremities with low pressure and pulses in lower extremities

42
Q

Ischemic Heart Disease (IHD)

A

Cardiac ischemia = imbalance between the supply (perfusion) and demand of the heart for oxygenated blood
90% due to atherosclerotic coronary arterial obstruction

4 clinical syndromes:

  • sudden cardiac death
  • angina pectoris
  • chronic IHD with heart failure
  • MI
43
Q

Ischemic Heart Disease (IHD) Role of Acute Atherosclerotic Plaque Change

A

The dominant cause of IHD syndromes is insufficient coronary perfusion relative to myocardial demand; in the vast majority of cases, this is due to chronic, progressive atherosclerotic narrowing of the epicardial coronary arteries, and variable degrees of superimposed acute plaque change, thrombosis, and vasospasm.”

Acute plaque change tends to occur in plaques with large cores and thin caps!

Acute plaque change:

- Rupture/Fissuring
- Erosion/Ulceration
- Hemorrhage into an atheroma (plaque)

Acute plaque change does not usually occur in severely stenotic portions of arteries

44
Q

Ischemic Heart Disease (IHD)Pathogenesis

A

Fixed atherosclerotic narrowing (stenosis) of coronaries

    • C-reactive protein - acute phase reactant; non-specific measure of chronic inflammation
    • When elevated has predictive value for risk of coronary heart disease (1-3 mg/L moderate risk)

Localized platelet aggregation

Thrombosis overlying a disrupted plaque

Vasospasm

Fixed obstruction >75% required to cause symptoms with exercise
Fixed obstruction > 90% can lead to ischemia at rest

45
Q

Ischemic Heart Disease (IHD)Role of Vasoconstriction

A

Prinzmetal (variant) angina – sustained vasospasm causing angina

Cardiac Raynaud – cold or emotion induced cardiac vasospasm
- If vasospasm is > 20 minutes can lead to myocardial infarction

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

Vasodilators (nitroglycerin, etc.) are effective treatment for angina pectoris of any etiology

46
Q

Sudden Cardiac Death (SCD)

A

Definition: Unexpected death from cardiac causes early after onset of symptoms (1 to 24 hours) or sudden death from cardiac cause without antecedent acute symptoms

Mechanism: Most often a lethal arrhythmia

Most commonly caused by Ischemic Heart Disease (IHD)

47
Q

Chronic Ischemic Heart Disease (Ischemic Cardiomyopathy)

A

usually presents with insidious onset of CHF

cardiomegaly w/ left ventricular hypertrophy

evidence of previous healed MIs or ischemia (areas of ** myocardial fibrosis)

Chronic ischemia that does not 
    cause necrosis  can lead to
    hypokinetic myocardium with
    myocyte hibernation ** that can 
    become functional after reperfusion
48
Q

Angina Pectoris- 4 types

A

Paroxysmal and usually recurrent attacks of substernal or precordial chest discomfort
- Caused by transient myocardial ischemia that falls short of inducing the cellular necrosis that defines infarction

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

Unstable (Crescendo, Pre-infarction) Angina
- Usually have acute plaque change

Prinzmetal Angina: episodic angina due to coronary artery spasm **

49
Q

Myocardial Infarction (MI)

A

The death of cardiac muscle from ischemia

transmural- over 50% of the ventricular wall thickness

subendocardial- limited to inner 1/2

50
Q

Myocardial Infarction (MI)Pathogenesis

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

Adrenergic stimulation can induce MI
Peak incidence between 6 am and noon (awakening)
Intense emotional stress

10% of transmural MI patients have NO associated atherosclerosis

51
Q

timing of bad things in MI

A

irreversible cell injury (necrosis) in 20-40 minutes

complete unsalvageable necrosis in 6-12 hours

usually find no gross features or light microscopic findings in the first 4 hours.

52
Q

most MIs happen in what artery?

A

LAD 40-50%

53
Q

Myocardial Infarction (MI) Infarct Modification by Reperfusion

A

Goal- salvage myocardium by reperfusion

techniques: lysis of thrombus, balloon agnioplasty, coronary artery bypass graft

Reperfusion beyond 6 hours does not appreciably reduce myocardial infarct size

54
Q

Myocardial Infarction (MI) Pathologic Changes Associated with Reperfusion

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)

55
Q

Myocardial Infarction (MI) Clinical Features

A

Severe substernal chest pain with radiation of pain down left arm, neck, jaw, epigastrium

STEMI –ST segment Elevation Myocardial Infarct (transmural)
NSTEMI – Non-ST segment Elevation Myocardial Infarct (subendocardial)

10-25% of MI patients may be asymptomatic

56
Q

Release of myocyte proteins in myocardial infarction.

A

Some of these proteins are used as diagnostic biomarkers (e.g., troponin I, C, or T and creatine phosphokinase, MB fraction [CK-MB])

57
Q

Myocardial Infarction (MI) Clinical Outcome

A

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

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

58
Q

Myocardial Infarction (MI) Complications of Acute MI

A

Physiologic
Contractile dysfunction: Severe pump failure occurs in 10-15% of patients
Arrhythmias: Conduction disturbances along with myocardial “irritability”
Papillary muscle dysfunction: mitral regurgitation

Pathologic (Morphologic)
Myocardial rupture (1-5% of MIs)
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)

CV 2 Exam 2 (10 decks)

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