Integration of Cardiac Function Flashcards

1
Q

2 mechanisms to control CO

A

intrinsic - local to heart

  • mechanical/muscular (Starling’s law related to contractility)
  • electrical/ionic (membrane potential; ionic concentrations)

extrinsic - extra-cardiac neuronal and hormonal signaling pathways
-baroreceptors and chemoreceptors related to sympathetic stimulation and parasympathetic inhibition

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2
Q

neurotransmitter, receptors, second messenger, and functional “results” for sympathetic stimulation of the heart

A

NE to beta1 (pacemakers and myocetes) that increase cAMP

-cause tachycardia and increased contractility

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3
Q

neurotransmitter, receptors, second messenger, and functional “results” for parasympathetic stimulation of the heart

A

ACh to M2 (pacemakers, minor myocete effect) that decrease cAMP
-cause bradycardia and decreased contractility

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4
Q

how does CO compare in the aorta and pulmonary artery?

A

CO is the same in both, b/c they are in series

-it is NOT the sum of flows into aorta and pulmonary arteries

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5
Q

how low does CO go to be defined as hypoxia?

A

falls below 1/3 normal

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6
Q

what is the relationship between CO, work, and O2 consumption during exercise?

A

positive linear relationship

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7
Q

how does mild inspiratory hypoxia change CO?

A

increases CO

-decreased O2 concentration in environment (like at high altitude)

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8
Q

how does chronic anemia change CO?

A

increases CO

-decreased O2 content in blood when RBC concentration is reduced

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9
Q

how does histotoxic hypoxia change CO?

A

increases CO

-tissue poisoning involves decreased ability of tissues to utilize O2 as occurs after cyanide ingestion

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10
Q

how does pulmonary disease change CO?

A

increases CO

-in general, resulting in hypoxemia (lowered O2 concentration in blood)

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11
Q

what are 4 compensatory diseases that increase CO?

A
  • chronic anemia
  • histotoxic hypoxia
  • pulmonary disease with hypoxemia
  • mild inspiratory hypoxia
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12
Q

how does hyperthyroidism change CO?

A

increases CO b/c increased metabolic rate

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13
Q

how does pregnancy change CO?

A

increases CO (by 8%) corresponding to increased metabolism

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14
Q

difference between mild anoxia and severe anoxia

A

mild anoxia: increases CO b/c decrease peripheral resistance

severe anoxia: decreases CO b/c O2 deprivation in heart

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15
Q

how does HTN change CO?

A

unaltered in most forms

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16
Q

what happens to CO during hemorrhage?

A

CO is less than 1/2 normal for a significant period of time

-can cause severe shock

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17
Q

what 3 heart diseases decrease CO?

A

acute myocardial infarction
rheumatic fever
congestive heart failure

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18
Q

effect of body size on CO

A

CO increases in proportion to size

-CO = k * W^(3/4)

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19
Q

cardiac index and equation

A

CI = CO/body surface area

-attempt to normalize CO to individuals of different sizes

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20
Q

how does CO change with age?

A

body metabolism slows with increasing age, as does CO, by about 30% between 20 to 45 years old
-drops from 6 to 5.25 L/min

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21
Q

effect of anxiety on CO

A

emotional factors increase CO

22
Q

effect on posture on CO

A

if laying down to sitting up: CO decreases by 23%

if laying/sitting to standing up, CO increases b/c tensing muscles

23
Q

effect of temperature on CO

A

during fever, CO rises due to effects of temperature on metabolic rates of tissue

24
Q

4 phases of cardiac cycle

A
  1. filling phase
  2. isovolumetric contraction phase
  3. ejection phase
  4. isovolumetric relaxation phase
25
Q

what does the P wave correspond to

A

atrial depolarization
-while the AV node, bundle of his, bundle branches, and Purkinje network are depolarized as well, they don’t generate voltages large enough to be measured

26
Q

what does the QRS complex correspond to?

A

ventricular depolarization (upstrokes)

27
Q

what does the T-wave correspond to?

A

ventricular repolarization

28
Q

what does the ST segment correspond to?

A

plateau phase (phase 2)

29
Q

what does the TP segment correspond to?

A

ventricular diastole

30
Q

ventricular volume changes in cardiac cycle

A
  1. ejection: falls from 120 to 50 mL, corresponding to stroke volume of 70 mL, and EJ of 58%
  2. filling: occurs during early diastole as mitral and tricuspid valves open
    - atrial systole occurs at the end of diastole, with only a small rise in pressure for both right and left hearts, so responsible for only a small increase in ventricular volume
31
Q

atrial diastole

A

occurs during ventricular systole

-atrial pressure rises, then falls when mitral valve opens

32
Q

when does diastole begin?

A

at the dichrotic notch when aortic valve closes

33
Q

what happens to ventricular pressure when mitral valve opens?

A

this is shortly after the beginning of diastole: left ventricular pressure is falling when ventricular volume is increasing
-forward momentum of blood entering ventricles expands them and drops pressure, even though ventricular blood volume is increasing

34
Q

what happens to dynamic pressure during systole?

A

ventricular pressure is greater than aortic pressure during rapid ejection phase

  • during slow ejection phase, pressure falls so rapidly in LV that LV pressure falls below aortic pressure
  • blood continues to flow forward due to forward momentum, but decelerated by reversed pressure gradient
35
Q

filling phase

  • ventricular pressure?
  • which valves are open
  • how much do ventricles fill?
  • how does the ECG count?
A

ventricles are at low pressure, and tricuspid and mitral valves are open

  • ventricles fill from 50 mL to 120 mL blood
  • P wave of ECG precedes atrial contraction, and corresponds to atrial depolarization
36
Q

jugular pulse and it’s A, C, and V waves

A

follows right atrial pressure

  • A = atrial contraction
  • C = closure of tricuspid valve
  • V = atrial filling and emptying
37
Q

what do the first and second heart sounds correspond to?

A

1st: closure of AV valves
2nd: closure of aortic and pulmonic valves

38
Q

isovolumetric contraction phase

  • how does it relate to ECG?
  • what happens to ventricular pressure?
  • what happens to the valves?
A
  • QRS complex occurs (ventricular depolarization)
  • -ventricular muscles contract, so no immediate volume change
  • ventricular pressure rapidly increases b/c AV valves rapidly close (first sound)
  • pulmonary and aortic valves then open, even though destination pressures initially higher
39
Q

ejection phase

  • what is it the dominant event of?
  • how does it correspond to ECG?
A

once the ventricular pressure exceeds “destination” vasculature

  • blood ejected from ventricles in dominant event of systole
  • T wave occurs during end half of outflow phase
  • at end of outflow phase, ventricular pressure decreases
40
Q

isovolumetric relaxation phase

  • what happens to pressure?
  • what sound does it make?
  • when does a new cardiac cycle begin?
A

pressure rapidly drops in both ventricles (little blood flow in or out)

  • pulmonic and aortic valves close (beginning of diastole)
  • when ventricular pressure drops below atria, mitral and tricuspid valves open, and new cardiac cycle begins
41
Q

how do increased contractility and pre-load effect stroke volume?

A

both increase SV

  • increased contractility = decreased ESV
  • increased pre-load = increased EDV
42
Q

when and how would you want to increase contractility?

A

treat CHF or infarction via positive inotropic drugs

43
Q

what can increased preload be an adaptive response to?

A

aortic stenosis, ventricular hypertrophy, anemias, hyperthyroidism

44
Q

what does increased afterload do to SV?

A

increased afterload will decrease stroke volume b/c needs more pressure than normal to eject blood
-can be due to aortic valve defects or HTN

45
Q

how does atrial filling pressure, ventricular filling time, and HR effect SV?

A

AFP: increasing will impede venous return, thus decreasing EDV to decrease SV
VFT: increased time causes increased EDV, so increased SV
HR: increased will decrease diastole time, which decreases EDV to decrease SV

46
Q

how is rhythmicity provided?

A

provided by intrinsic mechanisms of SA node

47
Q

which chambers of heart contract first, second, third, and fourth

A
  1. RA
  2. LA (both only contribute a little)
  3. LV (like squeezing toothpaste tube)
  4. RV (like a bellows, and both eject about same volume)
48
Q

how do mitral/tricuspid valves open/close in succession?

A

mitral valve closes before tricuspid, but tricuspid opens before mitral
-this is because LV contraction is before RV contraction, but drop in pressure in LV is larger and takes longer than in right ventricle

49
Q

how do aortic and pulmonary valves open/close in succession?

A

pulmonary valve opens before aortic valve, but aortic closes before pulmonary valve
-this is because pulmonary artery pressure is less than aortic pressure

50
Q

what are the 4 heart sounds?

A
  1. closure of AV valves (lub)
  2. closure of aortic and pulmonary valves (dub)
  3. particularly evident in kids; diastolic filling “gallop” from recoil of ventricles that have limited distensibility/compliance
  4. atrial contraction “gallop” that is usually pathologic