Principles of Cardiac Output Study Guide

Question 1

Cardiac Output (CO)

Answer 1

the amount of blood pumped by each ventricle per minute 5-6L/min

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

equation for CO.

Answer 3

CO = Heart Rate (HR) x Stroke Volume (SV)
- ex: CO = 75 bpm x 70mL/min = 5250mL/min = 5.25L/min

Question 4

cardiac reserve

Answer 4

the difference in resting CO and maximal CO (typically 4-5x resting CO, but in athletes can be as much as 7x CO)

Question 5

How do EDV and ESV relate to SV and therefore CO?

Answer 5

EDV - ESV = SV
Bigger SV = bigger CO

Question 6

typical ejection fraction for a healthy heart

Answer 6

Each ventricle pumps abt 60% of its blood w each contraction 70mL/120mL x 100 = 60%

Question 7

3 factors that regulate stroke volume

Answer 7

preload, afterload, contractility

Question 8

Preload

Answer 8

the degree to which muscle cells are stretched before contracting
- Higher Preload = Higher SV
- Preload increases with increased venous return – through exercise w increased SNS activity, and increased filling time

Question 9

Afterload

Answer 9

the pressure the ventricles must overcome to eject blood, ‘back pressure’ on the aortic and pulmonary valves 80 mmHg in aorta and 10 mmHg in pulmonary trunk
- Hypertension increases afterload - ventricles have to work harder to eject blood

Question 10

Contractility

Answer 10

the contractile strength achieved at a given muscle length, increases with rises in ca2+ and increased SNS activity

Question 11

Frank-Starling Law

Answer 11

A length tension relationship – cardiac muscle cells are stretched to their optimal length for maximal contraction

Question 12

Ionotropic agents

Answer 12

increase contractility

Question 13

Positive ionotropic agents

Answer 13

Epinephrine, norepinephrine, thyroxine, glucagon, high levels of extracellular ca2+, and the drug digitalis

Question 14

negative ionotropic agents.

Answer 14

acidosis, rising extracellular K+ levels, and Ca2+ channel blocker class of drugs (amlodipine, cardizem)

Question 15

Chronotropic agents

Answer 15

increase/decrease heart rate

Question 16

positive chronotropic agents

Answer 16

epinephrine, thyroxine, hypercalcemia

Question 17

negative chronotropic agents

Answer 17

hypocalcemia

Question 18

How to calculate your maximal heart rate

Answer 18

Age - 220

Question 19

How does maximal heart rate guide your exercise routines?

Answer 19

You want to be in the 50-85% range for exercise, so for example, a 20 year old would subtract 220 from their age (=200) and then aim to have the heart rate be 100-170 bpm

Question 20

how SNS regulates heart rate

Answer 20

• 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 21

how PNS regulates heart rate

Answer 21

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

Question 22

vagal tone

Answer 22

Both the SNS and PNS are continuously sending signals to the heart – typically, the PNS predominates (lowers heart rate)
- An impairment of the vagus nerve will increase resting HR by ~25 bpm (75 bpm to 100 bpm)
* When either the SNS or PNS is activated more strongly, the other is inhibited

Question 23

Define the atrial or Bainbridge reflex.

Answer 23

• 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 atrial stretch receptors
• Stretch receptor activation triggers reflexive adjustments of autonomic output to the SA node – increased HR

Question 24

Epinephrine

Answer 24

increases both heart rate and contractility

Question 25

Thyroxine

Answer 25

increases heart rate, enhances the effects of epinephrine and norepinephrine

Question 26

Hypocalcemia

Answer 26

depresses heart function

Question 27

Hypercalcemia

Answer 27

stimulates heart function and can increase risk of arrythmia

Question 28

Hypokalemia

Answer 28

weakens heart contraction

Question 29

Hyperkalemia

Answer 29

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

Question 30

age & heart rate

Answer 30

HR is 140-160 bpm in fetuses then declines

Question 31

gender & heart rate

Answer 31

HR is typically faster in females

Question 32

exercise & heart rate

Answer 32

HR increases secondary to activation of the SNS
- BP also increases
- BUT Resting HR will be lower in highly trained athletes

Question 33

temperature & heart rate

Answer 33

heat increases HR, cold decreases HR

Question 34

Congestive Heart Failure

Answer 34

weakened myocardium causes the heart tp become an inefficient pump; circulation is not adequate to meet the tissues’ needs

Question 35

4 ways myocardium can weaken

Answer 35

• Coronary Atherosclerosis: fat clogs coronary arteries
• HTN: an aortic diastolic BP < 90mmHg forces the myocardium to work harder to open the aortic valve; chronically elevated afterload and ESV leads to myocardial hypertrophy
• Multiple MIs: dead myocytes are replaced by noncontractile scar tissue; the pumping efficiency of the heart is reduced
• Dilated Cardiomyopathy: the ventricles become stretched and flabby, and the myocardium becomes less effective

Question 36

side of the heart that is failing when peripheral congestion is seen

Answer 36

failure of right side of heart

Question 37

side of the heart that is failing when pulmonary congestion is seen

Answer 37

failure of left side of heart

Question 38

Diuretics

Answer 38

increase excretion of Na+,H2O by the kidneys (used to manage heart failure)

Question 39

Digitalis

Answer 39

increases heart contractility (used to manage heart failure)

Question 40

4 primitive chambers of the heart and what they become as the heart matures

Answer 40

• Sinus Venosus: receives all venous blood from the embryo – becomes the smooth-walled portions of the atria, the coronary sinus, and the SA node
• Atrium: becomes the pectinate muscle-ridged parts of the atria
• Ventricle: the strongest part of the embryonic heart – becomes the left ventricle
• Bulbus Cordis: has a cranial extension – the truncus arteriosus – becomes the pulmonary trunk, part of the aorta, and most of the right ventricle

Question 41

gestational age that the fetal heart contracts

Answer 41

22 days

Question 42

two ways nonfunctional fetal lungs are bypassedand what they become after birth

Answer 42

• Foramen Ovale: a hole in the interatrial septum, a bypass for the lungs – becomes the Fossa Ovalis in adults
• Ductus Arteriosus: a shunt between the pulmonary trunk and the aorta, another bypass for the lungs – becomes the Ligamentum Arteriosum in adults

Question 43

two classes of congenital heart defects

Answer 43

• Mixing of O2 rich and O2 poor blood – inadequately oxygenated blood reaches the body’s tissues
  *Ex: septal defects, patent ductus arteriosus
• Narrowed valves/vessels increase the heart’s workload
  *Ex: Coarctation of the Aorta - really narrow aorta (heart has to work harder to push blood through)

Question 44

Tetralogy of Fallot (4)

Answer 44

a serious condition in which cyanosis appears within minutes of birth - encompasses both types of defects

Question 45

4 features of Tetralogy of Fallot

Answer 45

• narrowed pulmonary trunk/pulmonary valve stenosed
• hypertrophied right ventricle
• ventricular septal defect
• aorta receiving blood from both chambers

Question 46

Explain how a highly trained aerobic athlete could have a resting HR as low as 30-40 bpm.

Answer 46

The heart becomes more powerful, efficient, and enlarged with vigorous exercise, which means it can pump more blood, and when CO increases, HR increases