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
What is the equation that defines cardiac output?
CO = stroke volume (SV) x heart rate (HR)
What is the equation for the fick principle?
CO = rate of O2 consumption / (arterial O2 content - venous O2 content)
What is the equation that defines mean arterial pressure? How does MAP relate to diastolic and systolic pressures?
MAP = CO x total peripheral resistance; MAP = 2/3(diastolic pressure) x 1/3(systolic pressure);
What is the equation that defines the pulse pressure? What is pulse pressure’s relationship to stroke volume versus arterial compliance?
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
What is/are the equation(s) that define stroke volume?
SV = EDV - ESV (also, SV = CO/HR)
Characterize the early and late stages of exercise in terms of changes to heart physiology.
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)
What happens in heart physiology if HR is too high? Give an example of a clinical condition that exemplifies this.
Diastole is preferentially shortened with high HR; less filling time –> decreased CO (e.g., ventricular tachycardia)
What approximates preload versus afterload?
Preload = ventricular EDV; Afterload = mean arterial pressure (proportional to peripheral resistance)
What general effect do venodilators have? What is an example of a venodilator? What is a good way to remember this?
vEnodilators decrease prEload; e.g., nitroglycErinE; (see E mnemonic in answer)
What general effect do vasodilators have? What is an example of a vasodilator?What is a good way to remember this?
vAsodilators decrease Afterload (Arterial); e.g., hydAlAzine; (see A mnemonic in answer)
Again, what approximates preload? What are three things that can increase preload?
ventricular EDV; (1) Exercise (slightly) (2) Increased blood volume (e.g., overtransfusion) (3) Excitement (increased sympathetic activity)
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)?
(1) Contractility - increased (2) Afterload - decreased (3) Preload - increased
What are 4 examples (including names and mechanisms) of increased contractility? Again, what effect do these have on SV and CO?
(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
What effect does digitalis have on contractility, and to which factor impacting contractility does this relate? What is the mechanism behind this effect?
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+
What are 5 examples (including names and mechanisms) of decreased contractility? Again, what effect do these have on SV and CO?
(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
In what (non-pathologic) situations might a patient’s SV increase?
(1) Anxiety (2) Exercise (3) Pregnancy
What effect does a failing heart have on SV, and why?
A failing heart has decreased SV (both systolic and diastolic dysfunction)
What increases myocardial O2 demand?
(1) Increased afterload (directly proportional to arterial pressure) (2) Increased contractility (3) Increased heart rate (4) Increased heart size (increased wall tension)
To what is the force of contraction proportional?
End-diastolic length of cardiac muscle fiber (preload)
What 3 factors/conditions increase contractility?
(1) Sympathetic stimulation (2) Catecholamines (3) Digoxin;
What 4 factors/conditions decrease contractility?
(1) Loss of myocardium (MI) (2) Beta-blockers (3) Calcium channel blockers (4) Dilated cardiomyopathy
Draw the Starling graph/curve, labeling its axes and creating curves for the following scenarios: (1) Exercise (2) Normal (3) CHF+digoxin (4) CHF.
Axes: y = CO or stroke volume, x = Ventricular EDV (preload); See FA p. 254 for Starling curve visual
What is/are the equation(s) that characterizes/defines ejection fraction?
EF = SV / EDV = (EDV - ESV) / EDV
Of what is left ventricular ejection fraction an index?
Ventricular contractility
What is a normal EF?
Greater than or equal to 55%
What effects do systolic versus diastolic heart failure have on EF?
EF decreases in systolic heart failure; EF is normal in diastolic heart failure
Name 5 conditions in which there is high pulse pressure.
High pulse pressure in (1) hyperthyroidism (2) aortic regurgitation (3) arteriosclerosis (4) obstructive sleep apnea (increased sympathetic tone) (5) exercise (transient)
Name 4 conditions in which there is low pulse pressure.
Low pulse pressure in (1) aortic stenosis (2) cardiogenic shock (3) cardiac tamponade (4) advanced heart failure
On what 2 factors does preload depend?
Depends on venous tone and circulating blood volume
What does Laplace’s law tell us about afterload? Give the equation. Relate this equation to LV compensation for increased afterload.
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
What effect do ACE inhibitors have on preload and/or afterload? What other substance has this same effect?
ACE inhibitors and ARBs decrease both preload and afterload
What physiological change occurs with chronic hypertension? What effect does this have on the heart?
Chronic hypertension (increased MAP) –> LV hypertrophy