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CPR II > (4) Heart failure, congenital & ischemic disease (Martin) > Flashcards

(4) Heart failure, congenital & ischemic disease (Martin) Flashcards

1
Q

What is the number 1 worldwide cause of mortality?

A

Cardiovascular disease (CAD, stroke, and peripheral vascular disease)

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2
Q

Define: (in relation to the heart)

Hypertrophy=

Dilation =

Cardiomegaly=

A

Hypertrophy= increase in ventricular thickness

Dilation = enlarged chamber size

Cardiomegaly= increased cardiac weight

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3
Q

Where is atrial natriuretic peptide (ANP) found?

What is ANP’s significance?

A

ANP is found in storage granules within atrial myocytes of the myocardium

ANP promotes arterial vasodilation and stimulates renal salt and water elimination (natriuresis & diuresis)

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4
Q

What are the three types of heart damage?

A

Collagen = mitral prolapse

Nodular calcification = calcific aortic stenosis

Fibrotic thickening = rheumatic heart disease

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5
Q

Significance of lipofucin?

A

Yellow-brown pigment granules composed of residues of lysosomal digestion

They are considered the “wear and tear” pigments

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6
Q

Significance of basophilic degeneration?

A

As the myocardium looses material, it gets replaced by basophilic deposits

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7
Q

What is congestive heart failure (CHF)?

A

Occurs when the heart is unable to pump blood at a rate to meet peripheral demand OR can only do so with increasing filliing pressure

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8
Q

What can cause CHF?

A

Loss of myocardial contractile function (systolic function)

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

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9
Q

When does cardiac hypertrophy occur?

A
  • Sustained pressure or volume overload (systemic HTN or aortic stenosis)
  • Sustained trophic signals (Beta-adrenergic stimulation)
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10
Q

What is the best way to measure hypertrophy?

A

Heart weight

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11
Q

Is there an increase in the blood supply with a hypertrophic heart?

A

NO!

Hypertrophy of myocytes isn’t accompanied by a matching increase in blood supply, despite the increase in energy demand

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12
Q

Hypertrophied hearts are vulnerable to…

A

Ischemia-related decompensation

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13
Q

What is a major histologic marker for left sided heart failure?

A

HEART FAILURE CELLS

Hemosiderin-laden macrophages

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14
Q

Make this association RIGHT NOW…

Heart failure cells only occur with…

A

LEFT sided heart failure

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15
Q

What is the most common cause of Right sided heart failure?

A

Left-sided heart failure

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16
Q

What would cause an isolated right sided heart failure?

A

Pulmonary hypertension

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17
Q

Left sided heart failure is most commonly due to…

A

Ischemic heart disease, systemic hypertension, mitral or aortic valve disease

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18
Q

The most common genetic cause of congenital heart disease is…

A

Trisomy 21 (Down syndrome)

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19
Q

What is the most common congenital cardiac malformation?

A

Ventricular septal defect

20
Q

What is the most common form of ventricular septal defects?

A

Left-to-Right Shunts

21
Q

What are the common forms of left to right shunts?

A

Atrial septal defect (ASD)

Ventricular septal defect (VSD)

Patent ductus arteriosus (PDA)

22
Q

What does left-to-right shunting cause?

A

Volume overload on the right side which can lead to…

  • Pulmonary hypertension
  • Right heart failure
  • Paradoxical embolization
23
Q

What is a PFO?

A

Patent foramen ovale

Most of the time, it permanently closes by 2y/o

24
Q

What is this an example of?

A

VSD membranous type

25
Q

What is the clinical sign of a patent ductus arteriosus (PDA)?

A

Harsh, machinery-like murmur

26
Q

What is a common presentation for the teralogy of fallot (TOF)?

A

Squatting

Cyanosis

Clubbing

Syncope

27
Q

What are the four cardinal features of tetralogy of fallot?

A
  1. VSD
  2. Pulmonary stenosis
  3. Aorta overrides the VSD
  4. RV hypertrophy

*Heart is enlarged and “boot shaped” because of RIGHT ventricular hypertrophy

28
Q

Transposition of the great vessels (TGA)

Discuss

A

Incompatible with life after birth unless a shunt is present for mixing of blood

*With TGA, pt gets two separate systemic and pulmonary circulations

29
Q

Coarctation of the aorta is highly associated with?

A

Turner Syndrome

30
Q

Major clinical manifestations of Coarctation of the aorta WITH a PDA?

A

Cyanosis in the lower half of the body

31
Q

What are the major clinical manifestations of aortic coarctation WITHOUT a PDA?

A

Murmurs throughout systole

Usually asymptomatic

HTN upper extremities and hypotension in lower extremities

NOTCHING on undersurface of ribs

32
Q

What causes ischemic heart disease?

A

Results from insufficient perfusion to meet the metabolic demands of the myocardium

*Blood to the myocardium is supplied by the coronary arteries, so any disruption of coronary flow may result in ischemia

33
Q

What is angina pectoris?

A

Transient, often recurrent chest pain induced by myocardial ischemia insufficient to induce myocardial infarction

34
Q

What are the three clinical varients of angina pectoris?

A

Stable angina

Prinzmetal variant angina

Unstable (or “crescendo”) angina

35
Q

What are the sx of stable angina?

A

“Squeezing” or burning sensation

Relieved by rest or vasodilators

Induced by physical activity or stress

36
Q

What is prinzmetal variant angina?

A

Episodic coronary artery spasm

Relieved with vasodilators

Unrelated to physical activity HR or BP

37
Q

What is unstable/crescendo angina?

A

Frank pain that increases in frequency, duration and severity at progressively lower levels of physical activity

Usually rupture of atherosclerotic plaque which causes

38
Q

How can you tell that a heart is experiencing irreversible injury?

A

Increase in lactate, decrease in ATP

39
Q

What is the most common coronary vessel associated with infarct?

A

LAD

40
Q

Describe the appearance of:

An Old MI

Necrotic tissue

Cardiac rupture

A

An Old MI = White reveals scarring

Necrosis = yellowish appearance

Cardiac rupture = blackish

41
Q

What are the tests you’d perform to confirm an MI?

A

CK-MB

Troponin I and T (cTnI and CTnT) *most sensitive and specific

42
Q

What is the most common complication of MI?

A

Arrhythmia

43
Q

Time to elevation of CKMB, cTnT and cTnl?

A

3 to 12 hours

44
Q

CKMB and cTnL peak at?

A

24 hours

45
Q

CKMB returns to normal levels at?

A

48-72 hours

46
Q

cTnl returns to normal levels after?

A

5-10 days

47
Q

cTnT returns to normal levels after?

A

5-14 days

CPR II (30 decks)

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