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CPR Exam 1 > Cardiac Specialization, Aging, Heart Failure > Flashcards

Cardiac Specialization, Aging, Heart Failure Flashcards

1
Q

What is the #1 worldwide cause of mortality?

A

Cardiovascular Dz (CAD, stroke, peripheral vascular dz)

1/3 of deaths in USA

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2
Q

How does heart weight vary from person to person?

A

Varies with body habitus

Approx 0.4-0.5% body weight

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3
Q

Describe the thickness of right an left ventricles.

A 
Rt = 0.5 cm thickness
Lt = 1.5 cm thickness
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4
Q

What is hypertrophy of the heart?

A

Increased ventricular thickness

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5
Q

What is dilation of the heart?

A

Enlarged chamber size

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6
Q

What is cardiomegaly of the heart?

A

Increase in cardiac weight

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7
Q

Describe the myocardium. What hormone does it release? What does this hormone do?

A

Atrial myocytes have storage granules that contain atrial natriuretic peptide (ANP)

Promotes arterial vasodilation and stimulates renal salt and water elimination (natriuresis and diuresis) –> beneficial in setting of HTN and CHF

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8
Q

How are myocytes arranged in the ventricles and atrium?

A

Lt ventricle = arranged circumferentially in spiral orientation that helps generate coordinated wave of contraction the spreads from apex to base of heart

Rt ventricle = Less structured, contractile apparatus organized in series of subunits called sarcomeres

Atrial myocytes = haphazardly arranged, generate weaker contractile forces

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9
Q

Describe the structure of valves.

A

Lined by endothelium and share similar tri-layered architecture:

  • fibrosa = dense collagesous core at outflow surface
  • spongiosa = central core of loose CT
  • ventricularis/atrialis = rich laryer of elastin on inflow surface
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10
Q

How do valves receive their nutrient?

A

Due to thin structure, derive most of nourishment via Diffusion

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11
Q

What are 3 types of damage that can happen to valves?

A

Damage to collagen = weakens (ex: mitral prolapse)

Nodular calcification (ex: calcific aortic stenosis)

Fibrotic thickening (ex: rheumatic heart dz)

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12
Q

Describe the conduction of the heart.

A 
Responsible = 
SA node (Pacemaker)
AV node
Bundle of His
Purkinje network

Normal rate spontaneous depolarization of SA node (60-100 bpm) is faster, thus sets pace typically

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13
Q

What are the main arteries supplying blood to the heart?

A

3 major epicardial coronary arteries, form corona (crown) at base of heart:

  • LAD (left anterior descending) - diagonal branches
  • LCX (left circumflex) - marginal branches
  • RCA (right coronary)
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14
Q

What happens during ventricular diastole?

A

Aortic valves closes leading to blood flow to the myocardium

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15
Q

What are cardiac stem cells? How much of the heart do they replace? Can they undo necrosis?

A

Bone marrow derived precursors and stem cells present in myocardium

Only replaces ~1% each yr

No significant recovery in zones of necrosis

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16
Q

What changes can occur in the myocardium and chambers with aging?

A

Increase in LV cavity/volume is reduced

Increase in epicardial fat

Myocardium changes =

  • Lipofuscin granules (the more you have, more stress heart is under)
  • Basophilic degeneration
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17
Q

What changes can occur to the valves with aging?

A

Aortic and mitral valves annular calcification

Fibrous thickening

Mitral leaflets buckle towards Lt atrium –> increase in left atrium size

Lambl excrescences = small filiform processes form on the closure lines of aortic and mitral valves, probably resulting from organization of small thrombi

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18
Q

What changes could occur to the cardiac vasculature with aging?

A

Coronary atherosclerosis

Stiffening of the aorta

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19
Q

What is pump failure?

A

Myocardium contracts weakly during systole and there is inadequate cardiac output.

It may also relax insufficiently during diastole to permit adequate ventricular filling

20
Q

What is flow obstruction?

A

When lesions:

  • obstruct blood flow through a vessel
  • prevent valve opening
  • cause increased ventricular chamber pressure

Valvular blockage causes increased pressure overloading the chamber that pumps against obstruction

21
Q

What is regurgitant flow?

A

Portion of the output from each contraction flows backward through incompetent valve, adding volume overload to affected atria or ventricles

22
Q

What is shunted flow?

A

Blood can be diverted from one part of heart to another through defects that can be congenital or acquired.

Can also occur between blood vessels (ex: Patent Ductus Arteriosus)

23
Q

What are disorders of cardiac conduction?

A

Conduction defects or arrhythmias due to uncoordinated generation or transmission of impulses lead to nonuniform and inefficient myocardial contractions

24
Q

What happens with rupture of the heart or major vessel?

A

There is a cataclysmic exsanguination either into body cavities or externally

25
Q

When does Congestive Heart Failure (CHF) occur?

A

Occurs when heart is unable to pump blood at a rate to meet peripheral demand, or can only do so with increase filling pressure

26
Q

When may CHF occur?

A

Loss of myocardial contractile function (systolic dysfunction)

Loss of ability to fill the ventricles during diastole (diastolic dysfunction)

27
Q

When do cardiac myocytes become hypertrophic?

A

Sustained pressure or volume overload (systemic HTN or aortic stenosis)

Sustained trophic signals (B-adrenergic stimulation)

28
Q

During cardiac hypertrophy, What happens when you have pressure overload? volume overload?

A

Pressure overload hypertrophy:
-myocytes become thicker & LV increases thickness concentrically

Volume overload hypertrophy:
-myocytes elongate & ventricular dilation is seen

29
Q

What is the best measure of hypertrophy in a dilated heart?

A

Heart weight

30
Q

Does hypertrophy indicate an increase in blood supply?

A

No.

Hypertrophy of myocytes is not accompanied by a matching increase in blood supply, despite increase energy demand

31
Q

Hypertrophy leaves the heart vulnerable to what?

A

ischemia-related decompensation

32
Q

What happens to the heart during pregnancy?

A

Physiologic hypertrophy

33
Q

Is left-sided heart failure systolic or diastolic?

A

Can be systolic or diastolic

34
Q

What is left-sided heart failure commonly a result of?

A

MI
HTN
Left-sided value dz
Primary myocardial dz

35
Q

What are the clinical effects of left-sided heart failure due to?

A

Congestion in pulmonary circulation

Decrease in tissue perfusion

36
Q

What clinical sx can you see w/ left-sided heart failure?

A

Morphologic changes are variable (depends on inciting events)

Pulmonary congestion (cough, crackles, wheezes, etc.)
Edema
Restlessness, confusion
Tachycardia
Cyanosis
Exertional dyspnea, fatigue
Paroxysmal nocturnal dyspnea
37
Q

What can you see on imaging w/ LSHF?

A

Left ventricular hypertrophy

38
Q

What can left ventricular dysfunction eventually lead to?

A

Left atrial dilation

-this can lead to atrial fibrillation, stasis, thrombus

39
Q

Describe the change in ejection fraction in relation to LSHF.

A

EF decreases - may result in decreased glomerular perfusion

  • stimulating release of renin = increased volume
  • prerenal azotemia
40
Q

What can advanced CHF lead to?

A

Decreased cerebral perfusion

-hypoxic encephalopathy

41
Q

On a biopsy, what is characteristic of LSHF?

A

Heart failure cells = hemosiderin-laden macrophages

42
Q

What is the most common cause of right-sided heart failure?

A

left-sided heart failure

43
Q

What does ISOLATED right-sided heart failure result from?

A

Any cause of pulmonary HTN

  • parenchymal lung dz
  • primary pulmonary HTN
  • pulmonary vasoconstriction
44
Q

What happens during PRIMARY right-sided heart failure?

A

Pulmonary congestion minimal

Venous system markedly congested

45
Q

What results in the venous system being congested during primary RSHF?

A

Liver congestion (nutmeg liver)

Splenic congestion = splenomegaly

Effusions involving peritoneal, pleural, & pericardial spaces

Edema, esp. in dependent area (ex: ankle)

Renal congestion

CPR Exam 1 (11 decks)

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