Principles of Cardiac Output Flashcards

1
Q

cardiac output (CO)

A

the amount of blood pumped by each ventricle per minute

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2
Q

stroke volume (sv)

A

the amount of blood pumped by each ventricle per beat
- correlates with strength of ventricular contraction
- typically about 70mL

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3
Q

solving for co

A

heart rate (HR) x stroke volume (SV)
- the entire human blood supply passes each side of the heart per minute
- co will increase if either HR or SV increases (and vice versa)

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4
Q

cardiac reserve

A

the difference in resting CO and maximal CO
- typically 4-5x resting CO (20-25L/min)
- in a highly trained athlete, maximal CO can be as much as 7x resting CO (35L/min)

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5
Q

solving for sv

A

edv - esv

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6
Q

EDV

A

typically ~120mL
- depends on how long ventricular diastole lasts and what venous pressure is

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7
Q

ESV

A

typically ~50mL
- depends on arterial pressure and the force of ventricular contraction

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8
Q

ejection fraction

A

each ventricle pumps about 60% of its blood with each contraction

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9
Q

factors regulating stroke volume

A
  • preload
  • frank-starling law
  • contractility
  • after load
  • hypertension
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10
Q

preload

A

the degree to which muscle cells are stretched before contraction
- higher preload = higher SV

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11
Q

frank-starling law

A

a length tension relationship - cardiac muscle cells are stretched to their optimal length for maximal contraction
- a higher EDV will breed higher SV
- increased venous return - such as through exercise, with activity of the SNS, or increased filling time, will increase preload
- a low venous return might occur after blood loss or with tachycardia (fast heart rate)

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12
Q

contractility

A

the contractile strength achieved at a given muscle length
- will increase with rises in ca2+ - either from extracellular fluid or the sarcoplasmic reticulum

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13
Q

increased contractility

A

will increase SV and decrease ESV

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14
Q

increased SNS activity

A

increases contractility

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15
Q

epinephrine and norepinephrine’s effect on contractility

A

increase ca2+ entry and increase cross bridge cycling

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16
Q

positive ionotropic agents

A

increase contractility
- epinephrine, norepinephrine, thyroxine, glucagon, high levels of extracellular ca2+, and the drug Digitalis

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17
Q

negative ionotropic agents

A

decrease contractility
- acidosis, rising extracellular k+ levels, and the ca2+ channel blocker class of drugs (AmIodipine, cardizem)

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18
Q

afterload

A

the pressure the ventricles must overcome to eject blood
- “back pressure” on the aortic and pulmonary valves
- typically ~80 mmHg in the aorta and ~10 mmHg in the pulmonary trunk

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19
Q

hypertension (HTN)

A

(high blood pressure) increases afterload - the ventricles will have to work harder to eject blood
- ESV increases, SV decreases

20
Q

regulation of heart rate

A

when blood volume decreases or the heart is weakened, heart rate must increase to maintain cardiac output

21
Q

positive chronotropic agents

A

things that increase heart rate

22
Q

negative chronotropic agents

A

things that decrease heart rate

23
Q

regulation of heart rate by SNS

A
  • Emotional and physical stressors activate the SNS – epinephrine is released, the SA Node depolarizes more rapidly
  • SNS also increases heart contractility and speeds heart relaxation via enhanced Ca2+ movement
  • Enhanced contractility lowers ESV so SV doesn’t decline as it typically does with an increased HR
24
Q

regulation of the heart rate by PNS

A
  • Reduces heart rate, mediated by Acetylcholine
  • Acetylcholine hyperpolarizes the membranes of its effector cells by opening K+ channels
25
regulation of heart rate by ANS
- both the SNS and PNS are continuously sending signals to the heart - typically the PNS predominates - 'vagal tone' - when either the SNS or PNS is activated more strongly, the other is inhibited
26
vagal tone
an impairment of the vagus nerve will increase HR by ~25 bpm (75bpm-100bpm)
27
atrial (bainbridge) reflex
- an autonomic reflex initiated by increased venous return and increased atrial filling - stretching of the atrial walls increases heart rate by stimulating the SA node and the atrial stretch receptors - stretch receptor activation triggers reflexive adjustments of autonomic output to the SA node - increased HR
28
regulation of heart rate by chemicals
hormones and ions
29
regulation of heart rate by hormones
- Epinephrine: increases both heart rate and contractility - Thyroxine: increases heart rate, enhances the effects of epinephrine and norepinephrine
30
regulation of heart rate by ions
normal heart function depends on normal levels of intra and extracellular ions - electrolyte imbalances can be very dangerous - hypo/hyper calcemia (ca2+) - hypo/hyper kalemia (k+)
31
hypocalcemia
too little calcium - depresses heart function
32
hypercalcemia
too much calcium - stimulates heart function and can increase risk of arrythmia
33
hypokalemia
too little potassium - weakens heart contraction
34
hyperkalemia
too much potassium - alters the heart's electrical activity, can increase risk of heart block and cardiac arrest
35
other factors regulating heart rate
- Age: HR is 140-160 bpm in fetuses then declines - Gender: HR is typically faster in females - Exercise: HR increases secondary to activation of the SNS * BP also increases * BUT Resting HR will be lower in highly trained athletes – why? - Temperature: heat increases HR, cold decreases HR
36
tachycardia
HR 100+ bpm
37
bradycardia
HR < 60 bpm
38
imbalances in cardiac output
typically, co and venous return are balanced - congestive heart failure
39
congestive heart failure
- secondary to a weakened myocardium, the heart becomes an inefficient pump; circulation is not adequate to meet the tissues' needs
40
causes of a weakened myocardium
- coronary atherosclerosis - HTN - Multiple MIs - Dilated cardiomyopathy
41
coronary atherosclerosis
fat build up clogs coronary arteries, and myocardial cells are starved
42
HTN
an aortic diastolic BP < 90 mmHg forces the myocardium to work harder to open the aortic valve; chronically elevated afterload and ESV leads to myocardial hypertrophy
43
multiple MIs
dead myocytes are replaced by noncontractile scar tissue; the pumping efficiency of the heart is reduced
44
dilated Cardiomyopathy
the ventricles become stretched and flabby, and the myocardium becomes less effective
45
pulmonary congestion
- Failure of the left side of the heart - Fluid leaks from pulmonary blood vessels into lung tissue - Symptom: shortness of breath/dyspnea on exertion - “Pulmonary Edema”
46
peripheral congestion
- Failure of the right side of the heart - Blood stagnates in the organs and tissues - Symptom: swelling in the distal extremities - “Peripheral Edema”
47