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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
What is the clinical sign of a patent ductus arteriosus (PDA)?
Harsh, machinery-like murmur
26
What is a common presentation for the **teralogy of fallot (TOF)?**
Squatting Cyanosis Clubbing Syncope
27
What are the four cardinal features of **tetralogy of fallot?**
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
Transposition of the great vessels (TGA) Discuss
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
Coarctation of the aorta is highly associated with?
Turner Syndrome
30
Major clinical manifestations of **Coarctation of the aorta** WITH a PDA?
Cyanosis in the **lower half of the body**
31
What are the major clinical manifestations of **aortic coarctation** WITHOUT a PDA?
Murmurs throughout systole Usually asymptomatic HTN upper extremities and hypotension in lower extremities **NOTCHING** on undersurface of ribs
32
What causes **ischemic heart disease?**
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
What is **angina pectoris?**
Transient, often **recurrent chest pain** induced by myocardial ischemia _insufficient to induce myocardial infarction_
34
What are the three clinical varients of **angina pectoris?**
Stable angina Prinzmetal variant angina Unstable (or "crescendo") angina
35
What are the sx of **stable angina?**
"Squeezing" or burning sensation Relieved by rest or vasodilators Induced by **physical activity** or **stress**
36
What is **prinzmetal variant angina?**
Episodic coronary artery spasm Relieved with vasodilators **Unrelated to physical activity HR or BP**
37
What is **unstable/crescendo** angina?
Frank pain that **increases in frequency, duration and severity** at progressively lower levels of physical activity Usually rupture of **atherosclerotic plaque** which causes
38
How can you tell that a heart is experiencing irreversible injury?
Increase in lactate, decrease in ATP
39
What is the most common coronary vessel associated with infarct?
LAD
40
Describe the appearance of: An Old MI Necrotic tissue Cardiac rupture
An Old MI = White reveals scarring Necrosis = yellowish appearance Cardiac rupture = blackish
41
What are the tests you'd perform to confirm an MI?
CK-MB **Troponin I and T (cTnI and CTnT)** \*most sensitive and specific
42
What is the most common complication of MI?
Arrhythmia
43
Time to elevation of CKMB, cTnT and cTnl?
3 to 12 hours
44
CKMB and cTnL peak at?
24 hours
45
CKMB returns to normal levels at?
48-72 hours
46
cTnl returns to normal levels after?
5-10 days
47
cTnT returns to normal levels after?
5-14 days

CPR II (30 decks)

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