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CCRN > Cardiovascular > Flashcards

Cardiovascular Flashcards

1
Q
  • Caused by closure of AV valves and marks the end of diastole & beginning of systole.
  • Loudest at the apex of the heart.
A

S1 “Lub”

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2
Q
  • Caused by closure of semilunar valves and marks the end of systole & beginning of diastole.
  • Loudest at the base.
  • Splits on inspiration but wide/fixed splitting is caused by RBBB.
  • Loudest with pulmonary embolism.
A

S2 “Dub”

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3
Q
  • Caused by rapid rush of blood into a dilated ventricle
  • Occurs early in diastole, after S2
  • Heard best at the apex with the bell of the stethoscope
  • Associated with heart failure but also caused by pulmonary hypertension, mitral, aortic, or tricuspid insufficiency.
  • “Kentucky”
A

S3

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4
Q
  • Caused by atrial contraction of blood into a noncompliant ventricle
  • Occurs right before S1
  • Best heard at the apex with the bell of the stethoscope
  • Associated with myocardial ischemia, infarction, hypertension, ventricular hypertrophy. and aortic stenosis
  • Not heard with atrial fibrillation because no atrial contraction
  • “Tennessee”
A

S4

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5
Q

Due to pericarditis, associated with pain on deep inspiration, may be positional.

A

Pericardial friction rub

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6
Q

Normal pulse pressure?

A

40-60 mmHg

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7
Q

Indirect measurement of cardiac output and stroke volume.

A

Systolic blood pressure

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8
Q

Seen most often with severe hypovolemia or sever drop in cardiac output. Usually from drop in systolic pressure.

A

Narrowing or pulse pressure

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9
Q

An indirect measurement of the systemic vascular resistance (SVR)

A

Diastolic blood pressure

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10
Q

May indicate vasodilation, drop in SVR, and is often seen in sever sepsis/septic shock. Usually from drop in diastolic blood pressure.

A

Widened pulse pressure

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11
Q

When are coronary arteries perfused?

A

During diastole

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12
Q

Which is longer - diastole or systole?

A

Diastole is 1/3 longer than systole

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13
Q

Are murmurs of stenosis acute or chronic?

A

Chronic problem that develops overtime

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14
Q

Will cause large, giant V-waves on the PA catheter.

A

Mitral insufficiency

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15
Q

Most common with acute MI, may result in systolic murmur, heard at the left sternal border, 5th intercostal space.

A

Ventricular septal defect (VSD)

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16
Q

Associated with atrial fibrillation due to atrial enlargement that occurs over time.

A

Mitral stenosis

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17
Q

AV valves closed, semi-lunar valves open.

A

Diastolic murmur

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18
Q

AV valves open, semi-lunar valve closed.

A

Systolic murmur

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19
Q

When does mitral insufficiency occur?

A

Systole

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20
Q

When does mitral stenosis occur?

A

Diastole

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21
Q

When does aortic insufficiency occur?

A

Diastole

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22
Q

When does aortic stenosis occur?

A

Systole

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23
Q

Chest pain with activity, predictable, lesions usually fixed and calcified lesions.

A

Stable angina

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24
Q

Chest pain at rest, unpredictable, may be relieved with nitro, troponin negative, ST depression, or T-wave inversion on ECG.

A

Unstable angina

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25
Q

Troponin positive, ST depression, T-wave inversion on ECG, unrelenting chest pain.

A

NSTEMI

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26
Q

Troponin positive, ST elevation in 2 or more contiguous leads, unrelenting chest pain.

A

STEMI

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27
Q
  • A type of unstable angina associated with transient ST segment elevation.
  • Due to coronary artery spasm with or without atherosclerotic lesions.
  • Occurs at rest, may be cyclic (same time each day)
  • May be precipitated by nicotine, ETOH, cocaine ingestion.
  • Troponin negative
  • Nitro administration results in relief of chest pain and ST returns to normal.
A

Variant or Prinzmetal’s Angina

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28
Q

When may patients not experience chest pain with MI?

A

Women and diabetics

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29
Q

Improves morbidity/mortality of ACS

A

Aspirin

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30
Q

When are beta blockers contraindicated in ACS?

A

When caused by cocaine use, hypotension, bradycardia, or Viagra was taken.

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31
Q

ECG changes in II, III, aVF, reciprocal changes in lateral wall (I, aVL)

A

Right coronary artery (RCA), inferior LV.

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32
Q

ECG changes in V1, V2, V3, V4, reciprocal changes (ST depression) in inferior wall (II, III, aVF).

A

Left anterior descending (LAD), anterior LV.

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33
Q

ECG changes (ST elevation) in V5, V6 & (ST elevation) in I, aVL

A

Circumflex, lateral LV.

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34
Q

ECG changes in V1, V2

A

RCA, posterior LV.

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35
Q

ECG changes in V3R, V4R

A

RCA, right ventricular (RV) infarct.

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36
Q

What is the eligibility criteria for treatment of STEMI?

A
  • ST elevation in 2 or > contiguous leads, or new onset LBBB.
  • Onset of CP <12 hours
  • CP of 30 min in duration
  • CP unresponsive to sublingual nitro
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37
Q

How long do you hold pressure at sheath site?

A

20 min (30 min if still on GP IIb/IIIa inhibitors)

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38
Q

Signs and symptoms of retroperitoneal bleeding?

A

Sudden hypotension and severe low back pain.

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39
Q

Due to myocardial “stunning” when vessel opens.

A

Reperfusion arrhythmias

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40
Q

Treatment for NSTEMI

A

No emergent treatment. If high risk score or continues CP, s/s of instability - start GP IIb/IIIa inhibitors and prepare for diagnostic cath within 24h.

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41
Q

Associated with AV conduction disturbances: 2nd degree type 1, 3rd degree HB, sick sinus syndrome, sinus brady (if tachycardia=higher mortality), RV infarct & posterior MI.

A

Inferior MI

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42
Q

30% of inferior wall MI patients also have a?

A

Right ventricular (RV) infarct

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43
Q

Signs and symptoms of right ventricular (RV) infarct?

A

JVD at 45 degrees, high CVP, hypotension, usually clear lungs, brady arrhythmias, & ECG with ST elevation in V4R.

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44
Q

Treatment for right ventricular (RV) infarct?

A

Fluids & inotropes

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45
Q

What do you want to avoid with right ventricular (RV) infarct?

A

Preload reducers -> nitro, diuretics. Caution with beta blockers, often cannot given initially due to hypotension.

46
Q

Ominous sign of anterior MI?

A

Development of 2nd degree type 2 HB or RBBB. This has a higher mortality than inferior due to HF.

47
Q

Most common complication of acute MI?

A

Arrhythmias

48
Q

When does stent thrombosis occur?

A

Most incidents occur acutely within 24 hours of stent placement or subacutely within 30 days.

49
Q

Vasovagal management?

A

Give Atropine 0.5 mg IV (even in absence of bradycardia if other s/s occur) then fluids

50
Q

Elevated BP with evidence of end-organ damage (brain, heart, kidney, retina) that can be related to acute hypertension.

A

Hypertensive emergency or crisis.

51
Q

Elevated BP without evidence of acute end-organ damage.

A

Hypertensive urgency

52
Q

What medication do you need to assess for cyanide toxicity?

A

Nitroprusside

53
Q

What are the 6 Ps of peripheral arterial disease?

A
  1. Pain
  2. Pallor
  3. Pulse absent or diminished
  4. Parethesia
  5. Paralysis
  6. Poikilothermia (loss of hair on toes or lower legs; glossy, thin, cool, dry skin)
    * Additionally minimal edema
54
Q
  • Test to assess for PAD.
  • Used to assess adequacy of lower extremity perfusion.
  • Determined by dividing the ankle pressure by the brachial pressure on the same side.
  • Normal is >1.
A

Ankle-brachial index (ABI)

55
Q

Best position for someone with PAD?

A

Bed in reverse trendelenburg. DO NOT elevate the extremity because it will decrease perfusion.

56
Q

First initial in pacemaker code =

A

Chamber being paced (A, V, or D).

57
Q

Second initial in pacemaker code =

A

Chamber being sensed (A, V, or D).

58
Q

Third initial in pacemaker code =

A

Response to sensing.

59
Q

Pacer detects intrinsic cardiac activity and withholds its pacing stimuli. In other words, inhibits pacing in response to sensing.

A

“I” = inhibits

60
Q

Pacer detects intrinsic cardiac activity and fires a pacing stimulus in response.

A

“D” = inhibits and triggers

61
Q

No spike at all when expected

A

Failure to pace

62
Q

Spikes without a QRS for ventricular pacing.

A

Failure to capture

63
Q

Pacing in native beats

A

Failure to sense

64
Q

Sense tachyarrhythmias, provide a series of beats faster than the tachyarrythmias, then stop suddenly with hopefully the SA node recovering.

A

Burst pace

65
Q

Heart failure with EF <40%, problem with ejection.

A

Systolic dysfunction

66
Q

Heart failure with EF >50%, problem with filling, ejection is OK.

A

Diastolic dysfunction

67
Q

Often associated with a shift of the point of maximal impulse (PMI) from midclavicular to the left.

A

Enlarged heart (on xray) which is associated with systolic HF

68
Q

Presents with normal heart size on xray but 12-lead may show changes of left ventricular hypertrophy, especially when the patient has history of uncontrolled hypertension.

A

Diastolic HF

69
Q

How is heart failure classified?

A

It is based on patient report of symptoms, not objective findings. And should only be classified after optimal drug therapy has been achieved, not during acute exacerbation.

70
Q

Ordinary activity does not cause fatigue, dyspnea, palpitations, or anginal pain. There is no limitation of physical activity. EXTRAORDINARY ACTIVITY results in heart failure symptoms.

A

Class 1 of NYHA

71
Q

Comfortable at rest, but ordinary physical activity results in heart failure symptoms. There is some limitations of physical activity. ORDINARY ACTIVITY results in heart failure symptoms.

A

Class 2 of NYHA

72
Q

Comfortable at rest but less than ordinary activity causes heart failure symptoms. There is marked limitations of physical activity. MINIMAL ACTIVITY results in heart failure symptoms.

A

Class 3 of NYHA

73
Q

Symptoms of heart failure occur at rest. If any physical activity is attempted, discomfort is increased. There is severe limitations of physical activity. Remaining AT REST results in heart failure symptoms.

A

Class 4 of NYHA

74
Q

What is the main cause of death in heart failure patients?

A

Sudden arrhythmias. Patient’s with class 2-4 of NYHA qualify for an ICD.

75
Q
  • Systolic dysfunction (problem ejecting).
  • Classical signs: Thinning, dilation, enlargement of LV chamber, MVR.
  • Symptoms: Similar to systolic HF
A

Dilated cardiomyopathy

76
Q
  • Diastolic dysfunction (problem filling)
  • Classical signs: Increased thickening of the heart muscle & septum inwardly at the expense of the LV chamber.
  • Symptoms: fatigue, dyspnea, CP, palpitations, S3, S4, presynope/syncope.
  • Increased risk for sudden death.
A

Hypertrophic cardiomyopathy

77
Q

What is cardiogenic shock most commonly caused by?

A

Extreme drop in stroke volume secondary to systolic dysfunction.

78
Q

What is the main purpose of IABP?

A

It inflates (increased coronary artery perfusion) and dilates (decrease afterload)

79
Q

When does the IABP inflate?

A

Inflated at dicrotic notch or the arterial waveform, beginning of diastole.

80
Q

When does the IABP deflate?

A

Deflated right before systole begins, R-wave of ECG or upstroke of the arterial pressure wave.

81
Q

What are the most common cannulations sites for bypass sugery?

A

Aorta & right atrium

82
Q

The longer the bypass time…?

A

The more bleeding and more complications post-operatively.

83
Q

What are the FOUR steps to bypass procedure?

A
  1. Priming with isotonic crystalloids (enhances oxygenation by improving blood flow)
  2. Hypothermia (28-36 degrees C)
  3. Anticoagulation with large heparin doses
  4. Circulatory arrest - rapid, during diastole with K cardioplegic agent, reinfused at intervals, may be warm or cold.
84
Q

Remove serosanguinous fluid from the operative site.

A

Mediastinal chest tubes

85
Q

Remove air, blood, or serous fluid from pleural space.

A

Pleural chest tubes

86
Q

Abnormal chest tube output?

A

100 ml/hr for 2 consecutive hours

87
Q

Advantages: Easy to insert, very reliable, last longer.
Disadvantages: High risk for thrombosis (permanent anticoagulation therapy)

A

Mechanical valve

88
Q

Advantages: Anticoagulation required short term (maybe only ASA)
Disadvantages: Wears down, especially in high pressure systems

A

Biological valves

89
Q

THREE things to remember with valves repairs

A
  1. Avoid drop in preload (patient is use to elevated end-diastolic volumes.
  2. Anticoagulation (aspirin & plavix)
  3. Antipate conduction disturbances (TPM of PPM)
90
Q

Signs & symptoms of cardiac tamponade?

A

Restlessness/agitation, HoTN, increase JVD, CVP = PA diastolic pressure, muffled heart tones, enlarging cardiac silhouette & mediastinum on CXR, narrow pulse pressure.

91
Q

Excessive drop in SBP (>12 mmHg) during inspiration. Cardiac muscle restriction due to tamponade, with inspiration, intrathoracic pressure increases, decreased venous return. Best seen on aline.

A

Pulses paradoxus

92
Q

Which valve is at most risk for rupture due to trauma?

A

Aortic valve

93
Q

Pericarditis due to immune response after a MI, surgery, or traumatic injury.

A

Dressler’s syndrome

94
Q

Distinguishing s/s of pericarditis

A

Pain worsens with inspiration, ST elevation in all leads (medical) or at the area of injury (trauma), low-grade temp.

95
Q

Signs & symptoms of thoracic aortic aneurysms?

A
  • Sudden tearing, ripping pain in chest radiating to shoulders, neck, and back.
  • Cough
  • Hoarseness
  • Dysphagia
  • Dizziness, difficulty walking & speaking
  • Widening of mediastinum on CXR
  • 25% of all CV-related aneurysms
96
Q

Signs & symptoms of abdominal aortic aneurysm

A
  • Asymptomatic if small
  • Pulsations in abdominal area
  • Abdominal or low back pain
  • Nausea, vomiting
  • Shock
  • 75% of all CV-related aneurysms
97
Q

What is the treatment for aneurysms <5 cm in diameter & no symptoms?

A
  • Monitor regularly (US or CT)
  • Treat HTN (beta blockers because they may slow growth)
  • People with Marfan’s are usually treated sooner
98
Q

What is the treatment for thoracic aneurysm causing symptoms or >6 cm?

A
  • Surgical repair
  • Dissection: SURGERY
  • Aggressive treatment of HTN & heart rate control (labetalol)
99
Q

What is normal cardiac output?

A

4-8L

100
Q

What is normal cardiac index?

A

2.5-4.0 L/min/m2

101
Q

What is normal stroke volume?

A

50-100 ml per beat

102
Q

What is normal stroke index?

A

25-45 ml/beat/m2

103
Q

What is normal CVP?

A

2-6 mmHg or 3-8 cm H2O

104
Q

What is normal PAP?

A

20-30/8-15 (mean <20)

105
Q

What is normal wedge pressure?

A

8-12 mmHg

106
Q

What is normal SVR?

A

800-1200

107
Q

What is a normal mixed venous?

A

60-75% and is the most sensitive indicator of cellular oxygenation.

108
Q

What is a normal venous O2M?

A

> 70%

109
Q

How could SvO2 be increased?

A

In the presence of severe sepsis, septic shock, hypothermia, or paralysis.

110
Q

Causes giant V waves on PA catheter wave form.

A

Acute mitral valve insufficiency (regurgitation)

111
Q

Results in a falsely decreased systolic pressure and false high diastolic pressure and poorly defined components (i.e., dicrotic notch).

A

Overdamped

  • Can be caused by air or blood clot in the system, loose connections, loss of air in pressure bag, or kinking or the catheter tubing.
  • More common
112
Q

Results in a false high systolic pressure , possibly low diastolic pressure, and “ringing” artifacts on the waveform.

A

Underdamped

-Maybe be causes by pinpoint bubbles in the system, add-on tubing, or defective transducer.

CCRN (8 decks)

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