Principles of Cardiac Output

Question 1

cardiac output (CO)

Answer 1

the amount of blood pumped by each ventricle per minute

Question 2

stroke volume (sv)

Answer 2

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

Question 3

solving for co

Answer 3

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)

Question 4

cardiac reserve

Answer 4

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)

Question 5

solving for sv

Answer 5

edv - esv

Question 6

EDV

Answer 6

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

Question 7

ESV

Answer 7

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

Question 8

ejection fraction

Answer 8

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

Question 9

factors regulating stroke volume

Answer 9

• preload
• frank-starling law
• contractility
• after load
• hypertension

Question 10

preload

Answer 10

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

Question 11

frank-starling law

Answer 11

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)

Question 12

contractility

Answer 12

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

Question 13

increased contractility

Answer 13

will increase SV and decrease ESV

Question 14

increased SNS activity

Answer 14

increases contractility

Question 15

epinephrine and norepinephrine’s effect on contractility

Answer 15

increase ca2+ entry and increase cross bridge cycling

Question 16

positive ionotropic agents

Answer 16

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

Question 17

negative ionotropic agents

Answer 17

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

Question 18

afterload

Answer 18

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

Question 19

hypertension (HTN)

Answer 19

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

Question 20

regulation of heart rate

Answer 20

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

Question 21

positive chronotropic agents

Answer 21

things that increase heart rate

Question 22

negative chronotropic agents

Answer 22

things that decrease heart rate

Question 23

regulation of heart rate by SNS

Answer 23

• 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

Question 24

regulation of the heart rate by PNS

Answer 24

• Reduces heart rate, mediated by Acetylcholine
• Acetylcholine hyperpolarizes the membranes of its effector cells by opening K+ channels

Question 25

regulation of heart rate by ANS

Answer 25

• 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

Question 26

vagal tone

Answer 26

an impairment of the vagus nerve will increase HR by ~25 bpm (75bpm-100bpm)

Question 27

atrial (bainbridge) reflex

Answer 27

• 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

Question 28

regulation of heart rate by chemicals

Answer 28

hormones and ions

Question 29

regulation of heart rate by hormones

Answer 29

• Epinephrine: increases both heart rate and contractility
• Thyroxine: increases heart rate, enhances the effects of epinephrine and norepinephrine

Question 30

regulation of heart rate by ions

Answer 30

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+)

Question 31

hypocalcemia

Answer 31

too little calcium
- depresses heart function

Question 32

hypercalcemia

Answer 32

too much calcium
- stimulates heart function and can increase risk of arrythmia

Question 33

hypokalemia

Answer 33

too little potassium
- weakens heart contraction

Question 34

hyperkalemia

Answer 34

too much potassium
- alters the heart’s electrical activity, can increase risk of heart block and cardiac arrest

Question 35

other factors regulating heart rate

Answer 35

• 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

Question 36

tachycardia

Answer 36

HR 100+ bpm

Question 37

bradycardia

Answer 37

HR < 60 bpm

Question 38

imbalances in cardiac output

Answer 38

typically, co and venous return are balanced
- congestive heart failure

Question 39

congestive heart failure

Answer 39

• secondary to a weakened myocardium, the heart becomes an inefficient pump; circulation is not adequate to meet the tissues’ needs

Question 40

causes of a weakened myocardium

Answer 40

• coronary atherosclerosis
• HTN
• Multiple MIs
• Dilated cardiomyopathy

Question 41

coronary atherosclerosis

Answer 41

fat build up clogs coronary arteries, and myocardial cells are starved

Question 42

HTN

Answer 42

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

Question 43

multiple MIs

Answer 43

dead myocytes are replaced by noncontractile scar tissue; the pumping efficiency of the heart is reduced

Question 44

dilated Cardiomyopathy

Answer 44

the ventricles become stretched and flabby, and the myocardium becomes less effective

Question 45

pulmonary congestion

Answer 45

• 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”

Question 46

peripheral congestion

Answer 46

• Failure of the right side of the heart
• Blood stagnates in the organs and tissues
• Symptom: swelling in the distal extremities
• “Peripheral Edema”