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Board Review CRNA (Memory Master) > Cardiac > Flashcards

Cardiac Flashcards

1
Q

What causes the first (S1) and second (S2) heart sound?

A

1st: closure of the mitral and tricuspid valves at the beginning of systole.
2nd: closure of the aortic and pulmonic valves (semilunar valves) at the beginning of diastole

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2
Q

An S3 heart sound is an indicator of what condition?

A

An S3 heart sound (gallop rhythm) during mid-diastole is most often heard in the context of CHF.

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3
Q

What is the postulated mechanism (s) that produces an S3 heart sound?

A
  • S3 is thought to reflect a flaccid and inelastic condition of the heart during diastole (Stoelting)
  • Guyton says: a logical but unproven explanation of this sound (S3) is oscillation of blood back and forth between the walls of the ventricles initiated by inrushing blood from the atria
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4
Q

*Describe the murmurs heard, and specify the stethoscope location where they are best heard, if the patient has mitral stenosis. If the patient has mitral regurgitation.

A
  • mitral stenosis is recognized by the characteristic opening snap that occurs early in diastole and by a rumbling diastolic murmur, best heard with the chest piece placed over the cardiac apex.
  • cardinal feature of mitral regurgitation is a blowing pansystolic (heard throughout systole) murmur, best heard with the chest piece placed over the cardiac apex.
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5
Q

*Describe the murmurs heard, and specify the stethoscope location where they are best heard, if the patient has aortic stenosis. If the patient has aortic regurgitation.

A
  • aortic stenosis is recognized by its characteristic systolic murmur, best heard in the second right intercostal space with transmission into the neck
  • aortic regurgitation is recognized by its diastolic murmur, best heard in the second right intercostal space
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6
Q

How is aortic valvular regurgitation graded?

A

severity is graded angiographically after contrast injection into the aortic root as follows:
1+= small amount of contrast material enters left ventricle during diastole, but is cleared from left ventricle during systole
2+= left ventricle is faintly opacified by contrast media during diastole and not cleared during systole
3+= left ventricle is progressively opacified
4+= left ventricle is completely opacified during the first diastole and remains so for several beats
NOTE: there are 4 grades for aortic valvular regurgitation reflecting the severity of the problem

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7
Q

What left heart valve problems cause diastolic murmurs?

What left heart valve problems cause systolic murmurs?

A
  • aortic regurgitation and mitral stenosis are associated with diastolic murmurs
  • aortic stenosis and mitral regurgitation are associated with systolic murmurs
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8
Q

Which left heart valve problems can best be auscultated to the right of the sternum in the second intercostal space?
Which valve problems can best be auscultated at the cardiac apex?

A
  • aortic stenosis or aortic regurgitation can best be auscultated in the second intercostal space
  • mitral stenosis and mitral regurgitation are best auscultated at the apex of the heart
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9
Q

What is the problem if the newborn has a systolic and a diastolic murmur?

A

The patient with patent ductus arteriosus has both systolic and diastolic murmur

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10
Q

A patient is in CHF, and you are listening to the heart sounds. What should be heard? Where on the chest should this be heard?

A

An S3 gallop should be heard if the patient is in CHF. Left sided S3 is best heard with the bell piece of the stethoscope at the left ventricular apex during expiration and with the patient in the lateral position. Right sided S3 is best heard at the left sternal border or just beneath the xiphoid and is increased with inspiration.

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11
Q

What dysrhythmia is most commonly observed in the patient with mitral stenosis?

A

Atrial fibrillation

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12
Q

What dysrhythmia in the patient is most likely to occur with mitral valve regurgitation?

A

Premature ventricular beats

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13
Q

*With atrial flutter, atrial fibrillation, or junctional rhythms a portion of left ventricular filling is lost; what percent of left ventricular end diastolic volume is normally contributed by atrial contraction (atrial kick or atrial priming)?

A

passive diastolic filling usually accounts for 75% of LV filling, with atrial contraction causing an additional 25% filling of ventricles
- Stoelting states: during the latter portion of diastole, the atria contract to deliver about 30% of the blood that normally enters the ventricle during each cardiac cycle

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14
Q

What is the normal range for stroke volume in ml in a 70kg male? Write the formula for stroke index (SI). What is the normal range for stroke volume index?

A
  • normal range for SV is 60-90ml
  • stroke index is stroke volume (SV) divided by body surface area (BSA) in meters squared; so, SI= (SV) (BSA)
  • normal range for SV index is 40-60 ml/beat/m2
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15
Q

Define ejection fraction, and state its normal range.

A

EF is the ratio of SV (end-diastolic volume minus end-systolic volume) to end-diastolic volume

  • EF= SV/EDV= (EDV-ESV)/EDV
  • normal range is 0.6-0.8, or 60-80%
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16
Q

What are the two determinants of cardiac output? If stroke volume is 70ml and HR is 70bpm what is the CO?

A
  • SV and HR are the two determinants of CO
  • CO= SV x HR
  • with a stroke volume of 70ml and a HR of 70bpm, CO is 70ml/beat x 70bpm= 4900ml/min-4.9liters/min
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17
Q

What is the cardiac output in liters/min for a healthy 70kg person? In mL/kg/min?

A

CO is normally 5L/min
-CO in mL/kg/min is calculated as follows:
5L/min= 5,000ml/min= 5,000ml/70kg/min (assume 70kg person)= 71.43ml/kg/min
Remember you may be asked to convert a normal value to a per kg.

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18
Q

What is cardiac index? What is the normal range for cardiac index?

A

CI is CO divided by body surface area in meters squared. CI= CO/BSA
-normal CI ranges from 2.5-4.0 l/min/m2

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19
Q

Starlings law of the heart relates ventricular filling during diastole to what?

A

Starlings law of the heart relates ventricular filling during diastole to the amount of blood ejected during systole.
-the greater the ventricular filling during diastole (> the preload), the greater the quantity go blood pumped into the aorta during systole.

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20
Q

Describe the process at causes ventricular myocyte relaxation (lusitropy).

A

Ventricular myocyte contraction requires increased intracellular calcium.
Thus, for the ventricular myocyte to relax, intracellular calcium must be reduced back to resting levels.
-calcium is sequestered in the sarcoplasmic reticulum (SR) through energy-dependent processes.

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21
Q

Name the five organs in the vessel rich group. What percent of cardiac output goes to each of these organs?

A 
1- brain (15%)
2- kidney (20%)
3- liver (25%)
4- lungs (100%)
5- heart (4-5%, 225ml/min)
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22
Q

What percent of the right hearts CO traverses the pulmonary circulation? Bronchial circulation?

A

100% of blood pumped by the right heart traverses pulmonary circulation and 0% traverses the bronchial circulation

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23
Q

What percent of the left hearts output traverses the bronchial circulation? Vessels delivering blood to the bronchial circulation arise from what arteries?

A

1-2% of the left hearts output traverses the bronchial circulation.
The bronchial circulation arises from the thoracic aorta and intercostal arteries.

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24
Q

In words, describe where isovolumetric relaxation occurs on the left ventricular pressure volume loop.

A

Isovolumetric relaxation occurs from the closure of the aortic valve to the opening of the mitral valve on the left ventricular pressure volume loop.

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25
Q

In words, describe where isovolumetric contraction occurs on the left ventricular pressure volume loop.

A

Isovolumetric contraction occurs from closure of the mitral valve to opening of the aortic valve on the left ventricular pressure volume loop

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26
Q

What is the range of normal pressures in each chamber of the heart?

A

RA: 1-8mmHg
RV: 15-30/0-8mmHg
LA: 2-12mmHg
LV: 100-140/0-12mmHg

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27
Q

What is the normal range of values for pulmonary capillary wedge pressure?

A

normally, PCWP= 5-15mmHg

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28
Q

What is the normal value for mean pulmonary artery pressure? For pulmonary artery systolic and diastolic pressures?

A

mean pulmonary artery pressure normally is about 16mmHg; systolic/diastolic pressures average 25/8mmHg

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29
Q

What is the normal value for mean systemic arterial pressure?

A

80-120mmHg

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30
Q

What are the two determinants of arterial blood pressure?

A

2 determinants of systemic arterial BP are SVR and CO; this is called Ohm’s law.

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31
Q

What most determines SVR?

A

SVR is determined by the tone (degree of constriction) of arterioles and small arteries.

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32
Q

What is the normal range of values for SVR?

A

1200-1500 dynes-sec-cm-5 is the normal range for SVR

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33
Q

How do you calculate SVR?

A

SVR= [(MAP-CVP)/CO] x 80, where MAP is mean arterial pressure, CVP is central venous pressure, and CO is cardiac output. The units for SVR are the dynes-sec-cm-5

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34
Q

If MAP is 80mmHg, CO is 9 L/min, and CVP is 8mmHg, calculate SVR.

A

SVR= [(MAP-CVP)/CO] x 80 = [(80-8)/9] x 80= 640 dynes/sec/cm-5

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35
Q

In what segment of the systemic circulation is resistance greatest? The greatest decrease in BP in the arterial tree occurs where?

A

The resistance to blood flow is greatest in the arterioles, accounting for about half the resistance in the entire systemic circulation. The greatest decrease in BP in the arterial tree occurs in the arterioles.

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36
Q

What maintains systemic arterial BP during diastole?

A

Elastic recoil of arterial blood vessels during diastole keeps systemic arterial BP from falling precipitously during diastole.

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37
Q

What is pulse pressure? The patient’s arterial BP is 160/90mmHg. What is the patient’s pulse pressure?

A
  • pulse pressure is the difference between the systolic and diastolic arterial pressures during the cardiac cycle
  • the patient with a BP of 160/90 has a pulse pressure of 160-90= 70mmHg
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38
Q

What are two determinants of pulse pressure? What changes can increase pulse pressure? Decrease pulse pressure?

A
  • two determinants are CO and SVR
  • pulse pressure increases when either CO or SVR increases
  • pulse pressure decreases when either CO or SVR decreases
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39
Q

Define compliance. When peripheral vessels become less compliant (as would occur in the patient with atherosclerosis), does the pulse pressure increase or decrease?

A
  • compliance is defined as a change in volume for a given change in pressure
  • when compliance of arterial vessels decreases, pulse pressure increases
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40
Q

Where are arterial baroreceptors located? To what do the baroreceptors respond?

A
  • baroreceptors are located in the aortic arch and carotid sinus
  • respond to stretching caused by MAP > 90mmHg
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41
Q

When BP increases and the baroreceptors are stimulated, what happens reflexly (baroreceptor reflex) to myocardial contractility, venous tone, HR, SVR, and BP?

A
  • when stretched, baroreceptors fire and reflexly inhibit the sympathetic nervous system outflow resulting in a decrease in myocardial contractility, a decrease in HR, a decrease in venous tone, decrease in SVR, and a decrease in BP.
  • parasympathetic outflow is simultaneously increased, which also decreases HR
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42
Q

Where are venous baroreceptors located, how do they work, and what is the reflex called?

A
  • venous baroreceptors are located in the right atrium and great veins
  • they produce increase in HR when the right atrium or great veins are stretched by increased vascular volume
  • this is called the Bainbridge reflex
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43
Q

What happens to HR during inspiration and during expiration in the spontaneously breathing individual? Explain.

A
  • HR increases with inspiration and decreases with expiration
  • during inspiration, the pressure within the thorax decreases (becomes more negative) and venous return increases; the increased venous return stretches the right atrium leading to a reflex increase in HR
  • the opposite occurs during expiration
  • this is the Bainbridge reflex
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44
Q

*What nerves carry the afferent and efferent signals of the Bainbridge reflex? What does the Bainbridge reflex help prevent?

A
  • when the great veins and RA are stretched by increased vascular volume, stretch receptors send afferent signals to the medulla via the vagus nerve
  • the medulla then transmits efferent signals via the sympathetic nerves to increase HR (by as much as 75%) and myocardial contractility
  • Bainbridge reflex helps prevent the pooling of blood in veins, the atria, and the pulmonary circulation
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45
Q

What happens to arterial BP during inspiration in the spontaneously breathing individual? Why?

A
  • arterial BP normally decreases several mmHg during inspiration
  • with inspiration, pulmonary venous capacitance increases and venous return to the left heart decreases
  • according to Starling’s law, with a decrease in venous return (preload) to the left ventricle, SV, CO, and arterial BP all decrease (even though HR may increase b\c of the Bainbridge reflex)
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46
Q

How does a normal dorsalis pedis arterial waveform differ from the waveform found in the aorta in the supine or prone patient?

A
  • pulse pressure undergoes a natural amplification during transit through the arterial tree
  • compared with the aortic pressure waveform, systolic pressure is greater and diastolic pressure is lower in the dorsalis pedis
  • pulse pressure is, therefore, greater in the dorsalis pedis than in the aorta
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47
Q

Angiotensin I is converted to angiotensin II in what organ?

A

-angiotensin I is converted to angiotensin II in the pulmonary vasculature of the lung

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48
Q

*Which is the more potent vasoconstrictor, angiotensin II or antidiuretic hormone (ADH)?

A

ADH–also called vasopressin–is even more powerful than angiotensin II as a vasoconstrictor
-has been a controversial topic

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49
Q

How do you estimate MAP?

A

Use the 1, 2, 3 rule.
MAP= (1 x SBP + 2 x DBP)/3
Alternatively, MAP can be calculated as follows: MAP= DBP + (1/3) (pulse pressure) = DBP + (1/3) (SBP-DBP)

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50
Q

If arterial BP is 150/90, what is the MAP?

A

MAP = [1 x 150 + (2 x 90)]/3 = [150+180]/3= 330/3 = 110mmHg

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51
Q

What causes a change in BP when changing the patient’s position?

A

-altered preload (altered venous return) is most responsible for a change in BP when the patient is repositioned

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52
Q

The arterial system contains what percent of the total blood volume? The capillary system contains what percent? What percent is found in the venous segment of the circulation?

A
  • arterial blood vessels contain 13% TBV
  • capillaries contain 7% TBV
  • venous side contains 64% TBV
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53
Q

What is the function of the capillaries?

A

-capillaries allow exchange of oxygen, fluid, nutrients, electrolytes, hormones, and other substances between the blood and the interstitial space

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54
Q

How are the oxygen and nutrients delivered from capillary blood to the tissues? What law applies?

A
  • oxygen and nutrients are delivered from the capillary to the cell by diffusion
  • diffusion supplies all oxygen required for metabolism
  • Fick’s law of diffusion applies
55
Q

Changes in any of what four factors may promote peripheral edema?

A

-peripheral edema may result from one or more of the following:
1- decreased plasma colloid osmotic pressure (hypoalbuminemia, liver disease)
2- increased capillary hydrostatic pressure (usually secondary to increased CVP, sometimes secondary to heart failure)
3-increased interstitial protein (lymphatic obstruction)
4- increased permeability in the capillary wall

56
Q

What is the colloidal osmotic pressure in mmHg of albumin? How much does albumin contribute to the total colloid osmotic pressure of the plasma?

A
  • colloid osmotic pressure of albumin is 22mmHg

- albumin is responsible for approx 75% of the total colloid osmotic pressure in the plasma

57
Q

What determines blood flow through an organ or tissue? This is an application of what law?

A
  • two determinants of blood flow are (P) pressure gradient and (R) resistance
  • blood flow= (Pinflow-Poutflow)/R
  • blood flow to any tissue is directly proportional to the hydrostatic pressure gradient (Pinflow-Poutflow) and inversely proportional to vascular resistance (R)
  • (Pinflow-Poutflow) is usually (Parterial-Pvenous)
  • This is an application of Ohm’s law
58
Q

In general, blood flow to a tissue or organ is most directly related to what? Explain.

A
  • blood flow to a tissue or organ is generally directly related to tissue metabolism
  • metabolites (local factors) dilate the vasculature, and blood flow to the tissue increases
59
Q

What are the two most important determinants of oxygen delivery to the tissues?

A
  • CO and arterial blood O2 content

- arterial blood oxygen content is determined by the blood Hgb concentration and percent saturation

60
Q

*Describe the effect of hypercapnia on the cerebral vasculature and on the systemic vasculature.

A
  • hypercapnia causes dilation of both the cerebral vasculature and systemic vasculature
  • an increase in CO2 concentration in the arterial blood perfusing the brain decreases cerebral vascular resistance and increases cerebral blood flow
  • hypercapnia also relaxes systemic vascular smooth muscle causing decreased systemic vascular resistance (SVR)
61
Q

How does hypercarbia affect pulmonary vascular resistance?

A
  • pulmonary vascular resistance increases in response to hypercarbia
  • the pulmonary vasoconstrictor response to hypercarbia is opposite that observed in the systemic and cerebral vasculature
62
Q

With hypercapnia is there HYPERtension or HYPOtension?

A
  • both hypertension and hypotension may occur with hypercapnia
  • hypercapnia appears to cause direct depression of both cardiac muscle and vascular smooth muscle, but at the same time it causes reflex stimulation of the sympathoadrenal system; thus, hypercapnia, like hypoxemia, may cause increased myocardial O2 demand (tachycardia, early HTN) and decreased myocardial O2 supply (tachycardia, late hypotension)
63
Q

How does severe acidosis alter pulmonary vascular resistance (PVR) and systemic vascular resistance (SVR)?

A

-acidosis increases PVR and decreases SVR

64
Q

When during the cardiac cycle is blood flow through the coronary arteries greatest? Explain.

A
  • coronary flow is greatest during diastole
  • during diastole, ventricular muscle relaxes completely, and blood flow through the ventricular capillaries is not obstructed
65
Q

Describe the flow pattern in the left and right coronary arteries during systole and diastole.

A
  • during early systole, the compression of the vasculature in the left ventricle causes a brief cessation of flow in the left ventricle
  • on the other hand, flow through the right ventricle is sustained during both systole and diastole
66
Q

State the resting coronary blood flow in: (1) ml/minute, (2) as a percent of cardiac output.

A

-coronary blood flow is 225-250ml/minute, or about 4-5% of cardiac output

67
Q

*What is the venous saturation of coronary blood? In other words, what is the oxygen extraction level of coronary blood?

A
  • the venous saturation of coronary blood is 30% (PO2= 18-20mmHg).
  • therefore, the oxygen extraction level of coronary blood is 70% (100% - 30%, assuming 100% saturation for coronary arterial blood)
68
Q

What is the normal range for coronary perfusion pressure?

A
  • coronary blood flow is autoregulated when coronary perfusion pressure ranges between 60mmHg and 160mmHg
  • we assume 60-160mmHg is the normal range for coronary perfusion pressure
69
Q

How is coronary perfusion pressure (CorPP) calculated?

A
  • coronary perfusion pressure (CorPP) is the difference between the aortic diastolic pressure (AoDP) and the left ventricular end-diastolic pressure (LVEDP)
  • CorPP=AoDP - LVEDP
  • usually, PCWP is used to estimate LVEDP, so CorPP= AoDP - PCWP
70
Q

A patient has a blood pressure of 130/80mmHg, HR of 120, and PCWP of 30mmHg. What is his coronary perfusion pressure?

A

CorPP= AoDP - LVEDP

-since PCWP reflects LVEDP, AoDP= 80 - 30= 50mmHg

71
Q

Changes in either of what two parameters will decrease coronary perfusion pressure?

A

-since coronary perfusion pressure (CorPP) equals aortic diastolic pressure (AoDP) minus left ventricular end-diastolic pressure (LVEDP), a decrease in AoDP or an increase in LVEDP will decrease coronary perfusion pressure (PCWP), so CorPP will DECREASE when PCWP increases

72
Q

What most determines coronary blood flow?

A

-myocardial metabolism is the major determinant of coronary blood flow; normally, coronary blood flow and myocardial metabolism are closely matched

73
Q

Explain how an increase in coronary blood flow is achieved when the work of the heart increases.

A

-usually changes in coronary blood flow are entirely due to changes in metabolism; local factors are produced when metabolism increases, and these local factors decrease coronary vascular resistance; hence, coronary dilation in response to increased metabolic demand produces the increase in myocardial flow when work load increases.

74
Q

What theory relates to the metabolic control of the coronary circulation?

A

The vasodilation theory of blood flow regulation states that the greater the rate of metabolism or the lower the availability of oxygen, the greater becomes the rate of accumulation of vasodilator substances such as adenosine, carbon dioxide, lactic acid, histamine, potassium ions, and hydrogen ions.

With vasodilation, blood flow is increased to meet the metabolic demands of the myocardium.

75
Q

What is the most potent local vasodilator substance released by cardiac cells?

A

ADENOSINE
-in general, the most important regulators of coronary vascular tone are metabolic and involve multiple pathways; most if not all references list adenosine first in the metabolites that control coronary vascular tone

76
Q

State the oxygen consumption rate of the heart.

A

The oxygen consumption rate of the heart ranges from 8-10ml O2/100g/minute

77
Q

What four factors determine myocardial oxygen demand?

A

(1) HR
(2) diastolic wall tension (preload)
(3) systolic wall tension (afterload)
(4) contractility, determined by chemical environment
- -An increase in each of these parameters will increase myocardial oxygen consumption. Conversely, a decrease in each of these parameters will decrease myocardial oxygen consumption

78
Q

Arrange afterload, preload, and HR in an order that shows greatest to least effect on myocardial oxygen consumption?

A

HR>afterload>preload

  • increases in HR are likely to increase oxygen consumption more than increases in BP (afterload)
  • increasing venous return (increasing preload) increases oxygen consumption less than either increases in HR or afterload
  • increasing preload is the least costly means of increasing cardiac output
79
Q

What cardiovascular parameter correlates best with myocardial oxygen consumption?

A

HR

80
Q

What 5 factors determine myocardial oxygen supply?

A

1- aortic diastolic pressure (perfusion pressure)
2- left ventricular end diastolic pressure (high LVEDPs compress the subendocardium and decrease flow)
3- HR (high HRs may decrease perfusion because the time in diastole, the time when coronary flow occurs, is decreased)
4- oxygen content of arterial blood (% saturation)
5- oxygen extraction

81
Q

Describe the distribution of alpha-1 and beta-2 receptors in the coronary vasculature. What responses do these receptors mediate?

A
  • both are found throughout the coronary vasculature
  • epicardial blood vessels have mostly alpha receptors, which promote vasoconstriction
  • intramuscular and subendocardial blood vessels have mostly beta-2 receptors, which promote vasodilation
82
Q

In the left ventricle, where is the density of capillaries greatest: base, apex, subepicardium, or subendocardium? What is the significance of this?

A

The subendocardium (the muscle just inside the endocardial lining of the left ventricle) has the densest network of capillaries. This capillary network is referred to as the subendocardial plexus. During diastole, blood flow in the subendocardium is considerably greater than blood flow to the mid-wall or subepicardial regions. This higher blood flow reflects the greater oxygen requirements of the subendocardium. During systole, the subendocardium of the left ventricle is compressed and subendocardial blood flow is zero.

83
Q

What layer of ventricle, the subendocardium (inner layer) of the subepicardium (outer layer), is most vulnerable to ischemia? Why?

A

The subendocardium is most vulnerable to ischemia because it has the greatest metabolic demands and is most compressed (no blood flow) during systole

84
Q

Define excitability.

A

Excitability is the ability of a cell (cardiac, nerve, or muscle cell) to respond to a stimulus by depolarizing and firing an action potential.

85
Q

Define depolarization.

A

Occurs when there is a decrease in polarity across the cell membrane (a reduction in both the number of positive charges on the outside surface of the membrane and the number of negative charges on the inside surface of the membrane)

86
Q

Define hyperpolarization.

A

Hyperpolarization occurs when here is an increase in the polarity across the cell membrane (an increase in both the number of positive charges on the outside surface of the membrane and the number of negative charges on the inside surface of the membrane)

87
Q

Define conductivity.

A

Conductivity is the ability to transmit action potentials from cell to adjacent cell.

88
Q

Does a change in membrane potential from -70mV to -60mV represent depolarization or hyperpolarization?

A

Depolarization…. The membrane potential decreases

89
Q

If the membrane potential becomes more negative (-70 to -80 mV) has depolarization or hyperpolarization occurred?

A

Hyperpolarization….. Membrane potential increased

90
Q

Define rhythmicity.

A

Is the ability of cells to generate action potentials automatically on a rhythmic, or regular, basis.

91
Q

Identify the only site through which cardiac impulses can be transmitted from atria to the ventricles. Normally, the pause is how long at this site?

A

The impulse must traverse the atrioventricular (AV) node to pass from atria to ventricles.
-normally, the pause at the AV node is 100 milliseconds

92
Q

In what segment of the cardiac conduction system is the action potential conducted slowest? Fastest?

A

Conduction is slowest through the AV node and fastest in the Purkinje fibers.

93
Q

Compared with cardiac muscle cells and junctional tissue (sinoatrial and atrioventricular nodes), how fast do Purkinje fibers conduct impulses?

A

Purkinje fibers are large diameter fibers that transmit impulses at a velocity 6 times that of cardiac muscle cells and 150 times that of nodal tissue (SA and AV nodes)

94
Q

What is the function of the Purkinje system? How is this function accomplished?

A
  • it synchronizes right and left ventricular contractions
  • this occurs because the Purkinje fibers allow very rapid transmission of the cardiac impulses from the atrioventricular node (AV node) to the ventricles
95
Q

Tissues in the conduction system of the heart depolarize spontaneously in phase 4. What tissue in the heart’s conduction system has the fastest phase 4 depolarization? Intermediate? Slowest? What is the importance of a fast phase 4 depolarization?

A
  • phase 4 depolarization is the fastest in the SA node, somewhat slower in the AV node and slowest in the terminal Purkinje fibers
  • because phase 4 depolarization is fastest in the SA node, the SA node is the dominant pacemaker of the heart
96
Q

What are the intrinsic firing rates of the SA node, AV node, and the Purkinje fiber network?

A 
SA= 60-100
AV= 40-60
Purkinje= 15-40
97
Q

What peripheral nerves innervate the heart’s SA node, AV node, and the Purkinje network?

A

These tissues are innervated by both the sympathetic and parasympathetic nervous systems.

98
Q

Compare and contrast the the parasympathetic and sympathetic innervation of the heart. Is the heart equally innervated by both autonomic divisions?

A
  • the heart is NOT equally innervated by the sympathetic and parasympathetic divisions of the ANS.
  • in general, the sympathetic system innervates both the atria and ventricles and the conduction system (SA and AV nodes), whereas parasympathetic innervation is mainly to the SA and AV nodes and atria, with minor input to the ventricles.
99
Q

Where does the parasympathetic innervation of the heart arise?

A

The parasympathetic innervation of the heart arises from the dorsal motor nucleus of the vagus nerve in the medulla of the brain
++ remember: the parasympathetic division is also known as the craniosacral division

100
Q

What cardiac electrical event is represented by the P wave? The T wave?

A
  • P wave occurs when the atria depolarize

- T wave occurs when the ventricles repolarize

101
Q

What cardiac electrical event is represented by the PR interval?

A

The action potential is passing through the atrioventricular (AV) node

102
Q

What cardiac electrical event is represented by the QT segment?

A

The ventricular action potential is in phase 2, the plateau phase.

  • the duration of the QT segment is determined by the duration of the plateau
  • ventricular contraction is occurring during this time
103
Q

What ion controls the resting membrane potential, and what ion controls threshold?

A

Potassium ions control the resting potential, and calcium ions control threshold

104
Q

Does acute hypokalemia increase or decrease the excitability of nerve and cardiac muscle? Explain.

A

hypokalemia decreases excitability (increases stability); the resting membrane becomes more polarized (hyperpolarized); the difference between the resting and threshold potentials increases thereby making the tissue less excitable

105
Q

Does acute hyperkalemia increase or decrease the excitability of nerve and cardiac muscle? Explain.

A

-hyperkalemia increases excitability (decreases stability); the resting membrane becomes less polarized (depolarized); the difference between the resting potential and threshold potential decreases, thereby making the tissue more excitable

106
Q

Does hypocalcemia increase or decrease the excitability of nerve and cardiac muscle? Explain.

A

-hypocalcemia increases membrane excitablity (decreases stability); the threshold potential increases (becomes more negative); thus, the resting and threshold potentials approach each other, and nerves and cardiac cells become more excitable; recognize that the excitability of nerve and muscle is increased when hypocalcemia is present

107
Q

Does hypercalcemia increase or decrease the excitability of nerve and cardiac muscle? Explain.

A

-hypercalcemia decreases excitability (increases stability); the threshold potential decreases (becomes less negative); thus, the resting and threshold potentials diverge from each other, and nerves and cardiac cells become less excitable

108
Q

An increase in calcium concentration decreases excitability, or stabilizes, the cardiac cell. An increase in concentration of what other ion decreases excitability of, or stabilizes, the cardiac cell?

A

-an increase in concentration of magnesium (Mg2+) decreases excitability (increases stability) of cardiac cells; calcium ions and magnesium ions are membrane potential stabilizers

109
Q

What are the characteristics of sick sinus syndrome?

A

-bradycardia, punctuated by episodes of SVT, most often observed in the elderly patient

110
Q

Why is atrial fibrillation particularly dangerous in a patient with Wolff-Parkinson-White (WPW) syndrome?

A

-the refractory period of an accessory pathway determines the ventricular rate, which may exceed 300 bpm in a patient in AFIB with WPW syndrome; syncope or CHF, or both, could result from the rapid ventricular rate

111
Q

The patient has WPW syndrome. Atrial fibrillation develops. How should the AFIB be treated? What drugs should be avoided in this situation?

A

-if rapid ventricular response during AFIB results in life threatening hypotension, electrical cardioversion is necessary; if the AFIB is tolerated, give procainamide or quinidine, either of which prolong the refractory period of accessory fibers; AVOID verapamil or digitalis because either may decrease the refractory period of the accessory pathway!!

112
Q

Is it necessary to treat any of the following before surgery: First degree heart block; Mobitz type I (Wenkebach) second degree HB; Mobitz type II second degree HB?

A

-first degree HB and Mobitz type I second degree HB ordinarily DO NOT require treatment; Mobitz type II second degree HB has a serious prognosis and may require pacemaker insertion prior to major surgical procedures

113
Q

What are two signs of POOR right ventricular function?

A

(1) venous congestion (2) neck vein distention; pulsating neck veins indicate venous congestion secondary to right sided heart failure

114
Q

What Swan-Ganz catheter data suggests left ventricular failure?

A

-decreased CO and increased preload are signs of left heart failure; the Swan Ganz catheter data for the patient in heart failure would show cardiac index 15mmHg

115
Q

**What pulmonary capillary wedge pressure (PCWP) is indicative of heart failure?

A

PCWP > 18mmHg is indicative of HF

116
Q

What is the hallmark of decreased cardiac reserve (poor ventricular function)? What is the best indicator of a persons cardiac reserve?

A

-the hallmark of decreased cardiac reserve and low cardiac output is fatigue at rest with minimal reserve; cardiac reserve should be estimated through questioning the patient about their usual physical activities and exertional tolerance; both perioperative and long-term cardiac risks are increased in a patient who is unable to achieve a level of expenditure of about 4 METs (metabolic equivalents); A level of 4 METs corresponds to: taking a flight of stairs without fatigue, walking at a 4mph pace, ability to run a short distance, or participation in recreational sports such as bowling, golf, tennis, or dancing

117
Q

**List 4 compensatory responses in the patient with cardiac failure.

A

(1) increased left ventricular preload, (2) increased sympathetic tone, (3) activation of the renin-angiotensin-aldosterone system, (4) release of AVP (arginine vasopressin, antidiuretic hormone), and (5) ventricular hypertrophy; these mechanisms initially compensate for cardiac failure, but with increasing severity of the disease, they may actually contribute to the cardiac impairment

118
Q

With chronic CHF what hormonal system is activated as a compensatory mechanism? What compensatory changes are brought about by activation of this hormonal system?

A

-in response to chronic CHF, the renin-angiotensin-aldosterone system (RAA) and sympathetic nervous system are activated; the RAA and SNS contribute to the progressive structural changes in the peripheral vasculature and in the remodeling of the left ventricle

119
Q

What is the problem if cardiac output is low, central venous pressure (CVP) is increased and PCWP is normal?

A

-CVP is used to assess blood volume and right heart function; elevated CVP suggests hypervolemia or right heart failure; CO, however, increases with hypervolemia and decreases with heart failure; the data suggest that right ventricular failure is probably the problem

120
Q

How does CVP compare with PCWP if pulmonary hypertension is present?

A

-with severe pulmonary HTN, right ventricular output will decrease–> right atrial pressure and CVP will increase; hence, CVP will be greater than PCWP

121
Q

What promotes concentric hypertrophy? Identify two condition that cause concentric left ventricular hypertrophy. Identify two conditions that cause concentric right ventricular hypertrophy.

A

-concentric hypertrophy develops in response to a chronically elevated afterload (referred to as a pressure overload); two conditions that cause concentric left ventricular hypertrophy are (1) systemic arterial hypertension, and (2) aortic valve stenosis; two consitions that cause concentric right ventricular hypertrophy are (1) pulmonary artery hypertension and (2) pulmonic valve stenosis

122
Q

What happens to the ventricular wall with a chronically elevated afterload? What is the advantage of this adaptation? What happens to chamber size?

A

-the ventricular wall and septum thicken, which permits the ventricle to develop more tension and eject blood more effectively against an increased afterload; the chamber size remains unchanged with a chronically elevated afterload; this is concentric hypertrophy

123
Q

Does concentric hypertrophy decrease wall tension?

A

Yes. According to the version of the law of Laplace that assumes a structure with a finite wall thickness (T= Pr/2h), the tension (T) in the wall decreases with wall thickness (h); you can see from the equation that as thickness (h) increases, tension (T) decreases (an inverse, or reciprocal, relationship); the thickening of the ventricular wall associated with concentric hypertrophy produces a substantial decrease in wall tension, at rest; concentric hypertrophy may be one of the best ways to decrease wall tension; NOTE: r= radius of ventricular chamber

124
Q

What changes occur in the left ventricle in the patient with chronic aortic stenosis?

A

-concentric ventricular hypertrophy develops. In concentric hypertrophy, the left ventricular wall thickens but the chamber size remains unchanged; this change preserves ejection fraction until late in the disease

125
Q

Is left ventricular hypertrophy associated with mitral stenosis? Is right ventricular hypertrophy associated with mitral stenosis?

A
  • In mitral stenosis, the left ventricle is subjected to neither a pressure nor a volume overload. The increase in left atrial pressure, however, is reflected back through the pulmonary circulation leading to right ventricular pressure overload and right ventricular concentric hypertrophy
126
Q

What promotes eccentric hypertrophy? What happens to the size of the left ventricular chamber when there is eccentric hypertrophy? Identify three factors that will promote left ventricular eccentric hypertrophy.

A

-volume overload (chronically increased preload) stimulates the ventricular free wall to dilate; the chamber enlarges and can accommodate a larger volume of blood; three factors that promote left ventricular eccentric hypertrophy are (1) excessive intravascular volume, (2) aortic regurgitation, and (3) mitral regurgitation

127
Q

What changes occur in the left ventricle in the patient with aortic regurgitation or insufficiency?

A

-eccentric hypertrophy, in which there is a chamber enlargement (dilation), develops. There are enormous increases in end-diastolic volume. Cardiac output may increase 3-4 times

128
Q

In general, what causes left ventricular diastolic dysfunction? What specific events can cause left ventricular diastolic dysfunction during anesthesia and surgery?

A

-A decrease in left ventricular compliance is the general cause of left ventricular diastolic dysfunction. Reductions in left ventricular compliance can be seen with myocardial ischemia, shock, or pericardial effusion

129
Q

How is the diastolic function of the left ventricle assessed? What is the BEST indicator of left ventricular diastolic dysfunction?

A

-diastolic funciton of the left ventricle is assessed by examining left ventricular compliance; the BEST indicator of diastolic dysfunction is a decrease in left ventricular compliance

130
Q

**What monitoring is indicated for managing the patient with a history of congestive heart failure secondary to diastolic dysfunction?

A

-the use of invasive monitoring such as CVP or pulmonary artery catheter may be indicated in managing the patient with a history of CHF secondary to diastolic dysfunction

131
Q

How is left ventricular compliance assessed?

A

-LV compliance, the BEST indicator of diastolic function, can be assessed clinically by Doppler electrocardiography; Doppler electrocardiography assesses LV compliance

132
Q

What valve problem (aortic stenosis, aortic regurgitation, mitral stenosis, mitral regurgitation) may be associated with both a systolic and a diastolic murmur?

A

-aortic stenosis; with AS, there is a midsystolic ejection murmur that peaks in late systole. There is often a faint diastolic murmur of minimal aortic regurgitation.

133
Q

What valve problem (aortic stenosis, aortic regurgitation, mitral stenosis, mitral regurgitation) may be associated with both a systolic and a diastolic murmur if the patient has a HR of 100 and a BP of 135/45?

A

-aortic regurgitation; The very low diastolic pressure and wide pulse pressure suggest aortic regurgitation as the primary problem; with severe and prolonged aortic regurgitation, the dilation of the ventricle (eccentric hypertrophy) may be assocaited with a secondary mitral regurgitation; hence, there is a diastolic murmur (aortic regurgitation) and a systolic murmur (mitral regurgitation)

Board Review CRNA (Memory Master) (10 decks)

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