Front | Back |
Cardiac Output equation
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=(stroke volume) x (heart rate)
During exercise, CO increases initially as a result of an increase in HR. If HR is too high, diastolic filling is incomplete and CO decreases (e.g. ventricular tachycardia). During the early stages of exercise, CO is maintained by SV; during the late stages of exercise, CO is maintained by HR. |
Fick Principle
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CO=(rate of O2 consumption) / (arterial O2 content-venous O2 content)
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Pulse Pressure
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=systolic pressure-diastolic pressure
proportional to SV |
Stroke Volume equation
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=CO/HR
=(end diastolic volume)-(end stroke volume) |
Mean Arterial Pressure
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=(CO)x(Total Peripheral Resistance--TPR)
=(2/3)Diastolic Pressure + (1/3)Systolic Pressure |
Cardiac Output variables
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1. Stroke Volume
2. Contractility 3. Afterload 4. Preload Note: Increase SV by increasing preload, decreasing afterload, and/or increasing contractility |
Contractility (and SV) increase with (list the components):
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1. Catecholamines
2. Increased intracellular Calcium 3. Decreased extracellular Na+ (decrease the activity of the Na+/Ca2+ exchanger, which pumps 3 Na in for every 1 Ca out 4. Digitalis 5. Anxiety, exercise, and pregnancy |
Contractility (and SV) with Catecholamines:
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Think: Flight or Fight response; includes:
1. Epi/NE neuromodulators in the CNS, which act as hormones 2. Dopamine Effects=increased HR, increased BP, and increased blood glucose -Catecholamines increase the activity of the Ca2+ pump in the sarcoplasmic reticulum, enabling more frequent generated action potentials and, therefore, increased contractility. Increased catecholamines are associated with stress; extremely high levels are associated with neuroendocrine tumors in the adrenal medulla (i.e. pheochromocytoma) Increased catecholamines also assocated with monoamine oxidase-A (MAO-A) deficiency. MAO-A is an enzyme in which, under normal conditions, degradess neurotransmitters. |
Contractility (and SV) with Digitalis:
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Digitalis is a positive ionotrope (meaning it increases contractility) and is also an anti-arrhythmic to control HR in atrial fibrillation.
Mxn of Action: digitalis inhibits the Na+/K+ ATPase: 1. in doing do, this increases the intracellular [Na] and therefore a decreased concentration gradient across the membrane (i.e. Na is less likely to come into the cell if there is increased concentration in the cell already) 2. The increase in intracellular Na makes the actions of the Na/Ca exchanger less effective, since entry of Na into the cell in exchange for Ca out of the cell is less favorable. 3. As a result, Ca efflux is reduced, and Ca remains inside the cell and creates a higher cytoplasmic calcium concentration-->this leads to increased Ca storage in the sarcoplasmic reticulum. 4. Upon an action potential, more Ca is released from the SR, resulting in higher contractility. |
Contractiliy (and SV) decreased with (list the components):
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1. B1-Blockade (decreased cAMP)
2. Heart Failure (systolic dysfunction--under normal conditions, Ca2+ enters the cell during ventricular systole, and Ca leaves the cell during diastole) 3. Acidosis 4. Hypoxia/hypercapnea (decreased PO2/increased PCO2) 5. Non-dihydropyridine Ca2+ channel blockers |
Contractility (and SV) with Acidosis
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Acidosis is when the extracellular H+ is increased. If so, H+ will enter the cell in order to normalize the pH. As H+ enters, H+ pushes K+ outside the cell (to maintain electrical neutrality).
As K+ leaves the cell, the transmembrane potential decreases (becoming more negative) and therefore excitability (and contractility) decreases) |
Myocardial demand is increased by:
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1. increased afterload (proportional to arterial pressure)
2. increased contractility 3. increased heart rate 4. increased heart size (increased wall tension) |
Preload and Afterload:
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1. Preload=ventricular end diastolic volume (EDV); increased with exercise (slightly), increased with blood volume (overtransfusion), and excitment (sympathetics). Preload pumps the heart
Venodilators (e.g. nitroglycerin) work on veins DECREASE preload 2. Afterload=mean arterial pressure (proportional to peripheral resistance) Vasodilators (e.g. hydralazine) work on arteries to DECREASE afterload |
Starling Curve
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Look at Image: y-axis: remember, the y-axis can be labeled as either SV or CO x-axis: remember, the x-axis can be labled as either Ventricular EDV or Preload Increasing Contractile State of myocardium: =shifting the curve to up and to the left 1. circulating catecholamines 2. digitalis 3. sympathetic stimulation Decreasing Contractile State of myocardium: =shifting the curve down and to the right 1. heart failure and/or loss of myocardium 2. pharmachologic depressants Bottom line: force of contraction is proportional to end-diastolic length of cardiac muscle fiber (preload). |
Ejection Fraction equation
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=SV / EDV
=(EDV-ESV) / EDV 1. ejection fraction is an index of ventricular contracility 2. ejection fraction is normall >55% 3. ejection fraction decreased in systolic heart failure |