Cardio - Physio (Cardiac Output & related concepts) Flashcards

Pg. 266-268 in First Aid 2014 or Pg. 253-254 in First Aid 2013 Sections include: -Cardiac output -Cardiac output variables -Starling curve

1
Q

What is the equation that defines cardiac output?

A

CO = stroke volume (SV) x heart rate (HR)

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2
Q

What is the equation for the fick principle?

A

CO = rate of O2 consumption / (arterial O2 content - venous O2 content)

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3
Q

What is the equation that defines mean arterial pressure? How does MAP relate to diastolic and systolic pressures?

A

MAP = CO x total peripheral resistance; MAP = 2/3(diastolic pressure) x 1/3(systolic pressure);

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4
Q

What is the equation that defines the pulse pressure? What is pulse pressure’s relationship to stroke volume versus arterial compliance?

A

Pulse pressure = systolic pressure - diastolic pressure; Pulse pressure is directly proportional to stroke volume (i.e., as one goes one way, the other follows in the same direction), inversely proportional to arterial compliance

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5
Q

What is/are the equation(s) that define stroke volume?

A

SV = EDV - ESV (also, SV = CO/HR)

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6
Q

Characterize the early and late stages of exercise in terms of changes to heart physiology.

A

During the early stages of exercise, CO is maintained by the increased HR and increased SV; During the late stages of exercise, CO is maintained by increased HR only (SV plateaus)

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7
Q

What happens in heart physiology if HR is too high? Give an example of a clinical condition that exemplifies this.

A

Diastole is preferentially shortened with high HR; less filling time –> decreased CO (e.g., ventricular tachycardia)

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8
Q

What approximates preload versus afterload?

A

Preload = ventricular EDV; Afterload = mean arterial pressure (proportional to peripheral resistance)

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9
Q

What general effect do venodilators have? What is an example of a venodilator? What is a good way to remember this?

A

vEnodilators decrease prEload; e.g., nitroglycErinE; (see E mnemonic in answer)

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10
Q

What general effect do vasodilators have? What is an example of a vasodilator?What is a good way to remember this?

A

vAsodilators decrease Afterload (Arterial); e.g., hydAlAzine; (see A mnemonic in answer)

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11
Q

Again, what approximates preload? What are three things that can increase preload?

A

ventricular EDV; (1) Exercise (slightly) (2) Increased blood volume (e.g., overtransfusion) (3) Excitement (increased sympathetic activity)

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12
Q

What 3 key factors affect stroke volume (and thus affect cardiac output)? What changes in these factors leads to an increase in stroke volume (and thus increase in cardiac output)?

A

(1) Contractility - increased (2) Afterload - decreased (3) Preload - increased

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13
Q

What are 4 examples (including names and mechanisms) of increased contractility? Again, what effect do these have on SV and CO?

A

(1) Catecholamines (increased activity of Ca2+ in sarcoplasmic reticulum) (2) Increased intracellular Ca2+ (3) Decreased extracellular Na+ (decreased activity of Na+/Ca2+ exchanger) (4) Digitalis (blocks Na+/K+ pump –> increase intracellular Na+ –> decrease Na+/Ca2+ exchanger activity –> increase intracellular Ca2+) ; Increase

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14
Q

What effect does digitalis have on contractility, and to which factor impacting contractility does this relate? What is the mechanism behind this effect?

A

Increase, because increased intracellular Ca2+ by following mechanism: block Na+/K+ pump –> Increase intracellular Na+ –> decrease Na+/Ca2+ exchanger (normally puts calcium out and brings sodium in) activity –> Increase intracellular Ca2+

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15
Q

What are 5 examples (including names and mechanisms) of decreased contractility? Again, what effect do these have on SV and CO?

A

(1) Beta1-blockade (decreased cAMP) (2) Heart Failure (systolic dysfunction) (3) Acidosis (4) Hypoxia/Hypercapnea (decreased PO2/increased PCO2) (5) Non-dihydropyridine Ca2+ channel blockers ; DECREASE

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16
Q

In what (non-pathologic) situations might a patient’s SV increase?

A

(1) Anxiety (2) Exercise (3) Pregnancy

17
Q

What effect does a failing heart have on SV, and why?

A

A failing heart has decreased SV (both systolic and diastolic dysfunction)

18
Q

What increases myocardial O2 demand?

A

(1) Increased afterload (directly proportional to arterial pressure) (2) Increased contractility (3) Increased heart rate (4) Increased heart size (increased wall tension)

19
Q

To what is the force of contraction proportional?

A

End-diastolic length of cardiac muscle fiber (preload)

20
Q

What 3 factors/conditions increase contractility?

A

(1) Sympathetic stimulation (2) Catecholamines (3) Digoxin;

21
Q

What 4 factors/conditions decrease contractility?

A

(1) Loss of myocardium (MI) (2) Beta-blockers (3) Calcium channel blockers (4) Dilated cardiomyopathy

22
Q

Draw the Starling graph/curve, labeling its axes and creating curves for the following scenarios: (1) Exercise (2) Normal (3) CHF+digoxin (4) CHF.

A

Axes: y = CO or stroke volume, x = Ventricular EDV (preload); See FA p. 254 for Starling curve visual

23
Q

What is/are the equation(s) that characterizes/defines ejection fraction?

A

EF = SV / EDV = (EDV - ESV) / EDV

24
Q

Of what is left ventricular ejection fraction an index?

A

Ventricular contractility

25
Q

What is a normal EF?

A

Greater than or equal to 55%

26
Q

What effects do systolic versus diastolic heart failure have on EF?

A

EF decreases in systolic heart failure; EF is normal in diastolic heart failure

27
Q

Name 5 conditions in which there is high pulse pressure.

A

High pulse pressure in (1) hyperthyroidism (2) aortic regurgitation (3) arteriosclerosis (4) obstructive sleep apnea (increased sympathetic tone) (5) exercise (transient)

28
Q

Name 4 conditions in which there is low pulse pressure.

A

Low pulse pressure in (1) aortic stenosis (2) cardiogenic shock (3) cardiac tamponade (4) advanced heart failure

29
Q

On what 2 factors does preload depend?

A

Depends on venous tone and circulating blood volume

30
Q

What does Laplace’s law tell us about afterload? Give the equation. Relate this equation to LV compensation for increased afterload.

A

Relation of LV size and afterload –> Laplace’s law; Wall tension = (pressure x radius) / (2 x wall thickness); LV compensates for increased afterload by thickening (hypertrophy) to decrease wall tension

31
Q

What effect do ACE inhibitors have on preload and/or afterload? What other substance has this same effect?

A

ACE inhibitors and ARBs decrease both preload and afterload

32
Q

What physiological change occurs with chronic hypertension? What effect does this have on the heart?

A

Chronic hypertension (increased MAP) –> LV hypertrophy