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CRAAB 2 > Nordgren: Cardiac Abnormalities > Flashcards

Nordgren: Cardiac Abnormalities Flashcards

1
Q

What happens when valves don’t function properly?

A
  1. Impaired pumping action of heart

2. Abnormal heart sounds (murmurs) caused by abnormal pressure gradients and turbulent blood flow patterns.

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2
Q

What are the two types of valvular abnormalities?

A
  1. Stenotic- doesn’t open fully.

2. Insufficient- doesn’t close completely

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3
Q

How can a stenotic valve lead to hypertrophy?

A

The chamber upstream has to develop more pressure during the systolic phase in order to achieve a given flow through the valve. The increased pressure (work) leads to hypertrophy.

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4
Q

How can an insufficient valve lead to chamber dilation?

A

Regurgitant blood flow represents an additional volume that must be ejected in order to get sufficient forward flow. It increases the “volume” work leading to chamber dilation.

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5
Q

How does an increase in atrial pressure (d/t stenosis/insufficiency) affect upstream capillary beds?

A

It causes HIGHER pressure in the upstream capillary beds.

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6
Q

What happens if capillary hydrostatic pressures are elevated?

A

Tissue edema–> effects functioning of upstream organs

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7
Q

What are the 4 common valve defects in the left heart?

A
  1. Aortic stenosis
  2. Mitral stenosis
  3. Aortic insufficiency (regurge)
  4. Mitral insufficiency

**similar stenotic and regurge abnormalities can occur in the RV w/ similar consequences

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8
Q

What is aortic stenosis?

A

When the aortic valve doesn’t open fully leading to increased resistance to flow.

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9
Q

What are the characteristic signs of aortic stenosis?

A
  1. Significant pressure difference between the LV and the aorta.
  2. Intraventricular pressure rises VERY High during systole.
  3. Aortic pressure is subnormal in systole.
  4. Low pulse pressure
  5. High ejection velocity of blood leads to systolic murmur
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10
Q

What causes cardiac muscle hypertrophy and increases left ventricular mass?

A

Aortic stenosis

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11
Q

What is the primary physiologic consequence of aortic stenosis?

A

high ventricular afterolad

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12
Q

What happens when the mitral valve doesn’t fully open?

A

Increased resistance to flow

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13
Q

What are the characteristic signs of mitral stenosis?

A
  1. Pressure difference of more than a few mmHg across teh mitral valve during diastole.
  2. Elevated atrial pressure
  3. Turbulent flow of blood leads to diastolic murmur
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14
Q

What may induce hypertrophy of the left atrial muscle?

A

Mitral stenosis

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15
Q

What is the primary physiological consequence of mitral stenosis?

A

High left atrial and pulmonary capillary pressures (can cause pulmonary edema nd interference w/ gas exchange in lungs–> SOB)

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16
Q

What causes aortic insufficiency?

A

Leaflets of the aortic valve don’t seal causing blood to regurgitate back into the LV during diastole.

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17
Q

What are characteristic signs of aortic insufficiency?

A
  1. Aortic pressure falls faster/farther than normal during diastole
  2. low diastolic pressure
  3. Large pulse pressure
  4. Ventricular EDV and EDP are higher than normal because extra blood reenters the chamber.
  5. Turbulent flow of blood reentering LV cuasi
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18
Q

What causes a diastolic murmur in aortic insufficiency?

A

turublent flow of blood reentering LV

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19
Q

What is the primary physiological consequence of aortic insufficiency?

A

Reduced ejection fraction, increased volume workload

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20
Q

What happens if an aortic valve is BOTH stenotic and insufficient?

A

Both systolic and diastolic murmurs will be heard.

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21
Q

What causes mitral regurgitation?

A

Leaflets of the mitral valve don’t seal so blood regurgitates back into the left atrium during systole.

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22
Q

What are the characteristic signs of mitral regurgitation?

A
  1. Left atrial pressure is abnormally high
  2. Left ventricular EDV and EDP increase
  3. Systolic murmur
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23
Q

What is the primary physiologic consequence of mitral regurgitation?

A

Ejection fraction from the left ventricle is compromised causing an increased volume workload on the LV

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24
Q

Mitral regurgitation primarily affects what system?

A

It primarily has pulmonary effects and can cause SOB

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25
Q

What is the most common form of mitral regurgitation?

A

Prolapse–> valve leaflets evert into the left atrium during systole.

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26
Q

What lead is usually used to diagnose a majority of cardiac excitation problems?

A

Lead II

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27
Q

Physiological consequences of abnormal excitation and conduction depend on what two cardiac abnormalities?

A
  1. If it evokes tachycardia- limits time for cardiac filling between beats
  2. Decreases coordination of myocyte contraction (reduce stroke volume)
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28
Q

What are indicators of normal lead II tracing?

A
  1. Frequency of QRS about 1/sec
  2. Shape of QRS is normal for Lead II and duration is less than 100 msec
  3. Each QRS preceded by a P wave of proper configuration
  4. PR interval is less than 200 msec
  5. QT interval is less than half of hte R to R interval
  6. No extra P waves
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29
Q

What will you see on EKG of a heart with aortic stenosis?

A

Left axis deviation

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30
Q

A frequency of QRS that is about 1/sec is indicative of…

A

Normal beating rate

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31
Q

The shape of QRS is normal for Lead II and duration is less than 100ms is indicative of…

A

Rapid repolarization of the ventricles via normal conduction pathways

32
Q

Each QRS is preceded by a P wave of proper configuration is indicative of…

A

SA nodal origin of excitation

33
Q

PR interval less than 200 msec is indicative of…

A

Proper conduction delay of hte impulse propagation through the AV node

34
Q

QT interval less than half of the R to R interval is indicative of…

A

Normal ventricular repolarizatoin

35
Q

No extra P waves is indicative of…

A

No AV nodal block is present

36
Q

When are elevated or depressed ST segments often observed?

A

With tissue injury (ischemia)

37
Q

What happens to the direction of the ST segments if the injury is non-transmural?

A

ST depression

PARTIAL depth of the tissue..

38
Q

Non transmural ST depression is associated with what type of ischemia?

A

Demand ischemia (exertional angina)

39
Q

What happens to the direction of the ST segment if the injury is transmural?

A

ST elevation

FULL depth of tissue region

40
Q

ST elevation is associated with what type of ischemia?

A

Supply ishemia (coronary occlusion)

41
Q

How does injury lead to an altered ST segment?

A

Injury current (depolarization) is active even when the ventricle is in resting and repolarized states.

This means that there is a slight depolarizing current from the injured region even when there should be no current.

42
Q

How does non-transmural (partial depth) ischemia lead to a depressed ST?

A

Generally, the bit before the QRS is isoelectric, but the underlying current will raise the voltage baseline. During the ST segments the ventricles are depolarized (even the injured tissue). This means that the second isoelectric phase, the voltage recording is truly zero, but the net effect of the elevated baseline (PR interval) is that the ST segment APPEARS depressed.

43
Q

How does current move when an injury is continuous throughout the tissue (transmural)?

A

Current moves laterally, instead of outward first, then laterally around. So the depolarizing current is traveling AWAY from the + electrode and registers as a NEGATIVE shift in the ECG tracing.

44
Q

How does transmural ischemia lead to an elevated ST?

A

Before the QRS should be isoelectric, but the underlying current lowers the voltage of the baseline. SO, during the ST segment, the ventricles are depolarized. This means that hte second isoelectric phase hte voltage recording is truly zero. The net effect of hte depressed baseline (PR interval) is that hte ST segment appears elevated.

45
Q

Where do supraventricular abnormalities originate?

A

In the atria or AV node

46
Q

What is supraventricular tachycardia (PAT)?

A

When the atria are abnormally excited and drive ventricles at a rapid rate.

47
Q

What does PAT look like on an ECG?

A
  1. Begin abruptly and end abruptly
  2. QRS normal (but frequent)
  3. P and T wave may be superimposed because of high heart rate.
48
Q

What are common symptoms of PAT?

A

Low bp and dizziness

49
Q

What causes PAT?

A
  1. Ectopic focus activated

2. Reentry–> atrial flutter

50
Q

What is a first degree conduction block?

A

Unusually slow conduction (slow HR)

51
Q

What does a first degree conduction block look like on and ECG?

A
  1. Abnormally long PR interval (>.2 sec)

2. Otherwise normal ECG

52
Q

What is a second degree block?

A

When some atrial impulses transmit through the AV node slower than normal conduction. Results in some independent P waves.

53
Q

What is a third degree block?

A

When NO impulses are transmitted through the AV node, and the packemaker defaults to HIS, so atrial and ventricular rates are independent

54
Q

What does a third degree block look like on an ECG?

A
  1. P waves and QRS are totally dissociated
  2. Ventricular rate is likely slower than normal because of alternate pacemaker> often slow enough to impair cardiac output
55
Q

What is atrial fibrillation?

A

The complete loss of the normally close synchrony of excitation and resting phases between individual and atrial cells.

56
Q

What causes atrial fibrillation?

A

Depolarization/repolarization happen randomly throughout atria
2.

57
Q

How does A. fib appear on an ECG?

A
  1. P wave may be rapid, irregular, small wave apparent throughout diastole
  2. Ventricular rate is irregular
  3. self sustaining process
58
Q

Does atrial fibrillation kill yoU?

A

Nope. It tends to be well tolerated by most pts as long as ventricular rate is sufficient to maintain cardiac output.

59
Q

Where do ventricular abnormalities originate?

A

in the ventricles or His-purkinje

60
Q

What is a bundle branch block?

A

Occurs in either of the branches of the Purkinje system of the intraventricular septum and is often d/t MI.

61
Q

What does a bundle branch block look like on an ECG?

A

widening of the QRS, because ventricular depolarization is less synchrous in half the heart

62
Q

What is the direct physiological effect of a bundle branch block?

A

Inconsequential

63
Q

What causes premature ventricular contractions (PVCs)?

A

APs initiated by and propagated away from an ectopic focus in the ventricle, caused by the ventricle depolarizing early.

64
Q

Why are PVCs often followed by a missed beat?

A

BEcause ventricular cells are still refractory at the next normal SA impulse.

65
Q

What do PVCs look like on ECG?

A

Large amplitude, long duration QRS. Shapes are variable and depend on ectopic site of origin and depolarization pathway involved.

66
Q

When do PVCs usually occur and when should you be worried about them?

A

PVCs occur occasionally in most people. Frequent occurence is concern for myocardial damage/perfusion problems.

67
Q

What is ventricular tachycardia?

A

When ventricles are drive at high frequency rates (rapid depolarization) usually be ectopic focus.

68
Q

What are the different types of V tac?

A
  1. Generally ventricular contraction is less synchronous
  2. Rapid rate of QRS
  3. Widening rate of QRS
69
Q

Is V tac serious? Why?

A

VERy SERious

It often precedes ventricular fibrillation

70
Q

What is prolonged QT?

A

Delayed ventricular myocyte repolarization that may be d/t an inappropriate opening of Na channels or prolonged closure of K channels during phase 2 of the AP.

71
Q

What is a normal QT interval?

A

Less than 40% of cardiac cell length

72
Q

What is a long QT?

A

greater than 50% cycle duration

73
Q

What is the mechanism of a prolonged QT?

A

The prolonged refractory period extends the vulnerable period when extra stimuli can evoke tachycardia or fibrillation

74
Q

What is ventricular fibrillation?

A

Various areas of the ventricle are excited and contract asynchronously

75
Q

What is the mechanism for v. fib and what does it look like on ECG?

A

Similar to A. fib

ECG shows no discernible waves, rate, rhythm

76
Q

When is the ventricle particularly susceptible to fibrillation?

A

When premature excitation at the end of T wave (when the T wave is hyperexcitable)

77
Q

How do you correct v-fib?

A

It’s fatal unless quickly corrected by cardiac conversion. Attempts to depolarize ALL heart cells simultaneously allows for normal excitation pathways to re-establish.

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