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Physio > The Regulation of Cardiac Output > Flashcards

The Regulation of Cardiac Output Flashcards

1
Q

cardiac output

A

the volume of blood pumped by the ventricle per unit of time (ml/min)

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2
Q

stroke volume

A

the volume of blood pumped in one cardiac cycle

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3
Q

heart rate

A

the total number of cycles (beats) per minute

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4
Q

change in pressure

A

the pressure difference across the network (driving pressure)

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5
Q

total peripheral resistance

A
  • resistance to flow in the vascular regions (arteries and veins)
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6
Q

what factors regulate cardiac output?

A
  • preload
  • afterload
  • heart rate
  • contractility
    (divided into coupling factors and cardiac factors)
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7
Q

what are the coupling factors?

A
  • they involve the functional coupling of the heart and blood vessels
  • preload
  • afterload
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8
Q

what is preload?

A

the initial stretching of a single cardiac myocyte PRIOR TO CONTRACTION
- the passive stretch of the LV at the end of filling (EDV)

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9
Q

what is afterload?

A

= the pressure that the chambers of the heart are “working against”
- ventricles must generate enough pressure to open the aortic or pulmonary valves
- is a consequence of the aortic pressure (LV) and/or pulmonary artery pressure (RV)
- factors that impede ejection of blood from the ventricles

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10
Q

cardiac factors

A

= intrinsic to the heart and are modulated by neural and hormonal stimulation
- heart rate
- contractility
- determined by Ca level in cardiomyocyte cytoplasm

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11
Q

what is heart rate?

A

the number of APs or cardiac cycles per unit of time

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12
Q

what is contractility?

A

the intrinsic ability of the heart to contract, independent of preload and afterload

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13
Q

what is inotropy?

A

= contractility

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14
Q

how is cardiac output controlled by these factors?

A
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15
Q

what is the pressure-volume loop?

A

it depicts the changes in ventricular pressure and volume during one cardiac cycle

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16
Q

how can we understand the changes in preload, afterload, and contractility and how it affects the cardiac cycle?

A

the pressure-volume loop

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17
Q

factors that affect preload include:

A
  • vascular resistance = arteriolar and capillary bed resistance to flow and venous vascular resistance
  • venous capacitance = volume of blood stored in the venous circulation
  • ventricular filling time
18
Q

what happens when you increase preload?

A
19
Q

how can you measure preload clinically?

A

determine:
- RA pressure
- RV preload
- central venous pressure

20
Q

what must be maintained for ventricular contraction?

A

venous return = cardiac output

21
Q

what is the Frank Starling relationship?

A
  • based on the length-tension relationship of single cardiac cells
  • the volume of blood ejected by the ventricle depends on the volume of the ventricle at the end of diastole
22
Q

why is it important to understand the frank-starling relationship?

A
  • if the degree of overlap is too low, you cannot generate enough force to contract
  • if there is too much overlap, you generate poor contraction
  • helps our understanding of the heart function and what could be going wrong clinically
  • if the heart is not generating enough force –> increase preload –> increase stretch –> increase to optimum length –> increase contractility
  • adaptive mechanism
  • if venous return increases –> EDV increases –> SV increases (relationship will remain linear until very high levels of EDV are reached
23
Q

what factors affect afterload?

A
  • the volume of blood in the arterial circulation
  • the pressure in the aorta at the onset of ejection
  • the compliance of the aorta
  • the size of the aortic valve
24
Q

what happens when afterload (AoP) increases?

A
  • the pressure against which the ventricle contracts is much greater
  • the larger pressure increases the resistance to the ejection of blood (more blood left in ventricle and higher ESV)
25
Q

what happens with persistent increased afterload?

A

the heart compensates by increasing the EDV to maintain normal SV

26
Q

what influences contractility changes?

A
  • contractile proteins –> alter cardiac performance
  • intracellular Ca concentration during excitation-contraction coupling
27
Q

how does sympathetic stimulation alter contractility?

A
  • release of epinephrine and norepinephrine
  • isoproterenol (act on beta-1 receptors)
  • stimulation
28
Q

how does positive inotropic drugs alter contractility?

A
  • digitalis (Na-K ATPase blocker)
  • increase Ca and increases contractility
29
Q

how does negative inotropic drugs alter contractility?

A
  • toxins
  • general anesthetics
  • ACh
  • beta adrenergic receptor blockers (propanolol)
  • decrease Ca and decrease contractility
30
Q

what happens when contractility is enhanced?

A
  • the heart is able to increase the force and pressure generated during systole
  • leads to ejection of a larger blood volume from the ventricles
  • there is a shift in the active tension curve to the left
31
Q

how does contractility affect the frank-starling relationship?

A
  • positive inotropic drugs enhance contractility
  • negative inotropic drugs reduces contractility
  • the SV and CO is altered
32
Q

what happens when there is an increased heart rate?

A

SV increase
CO increases
similar effect to increasing contractility

33
Q

how does sympathetic activation alter heart rate? parasympathetic?

A
  • higher rate of AP firing
  • decreased rated of AP firing
34
Q

autonomic influences of cardiac function

A
35
Q

about hypertension:

A

= high blood pressure
- usually asymptomatic until damaging effects occur

36
Q

how is hypertension diagnosed?

A
  • when BP readings are taken at least 2-3 times at 2 or more separate appts
  • abnormally high BP
37
Q

what is essential hypertension?

A
  • 90-95% of patients
  • unknown cause
  • spontaneous onset
38
Q

what is secondary hypertension?

A
  • 5-10% of patients
  • caused by an underlying/secondary condition
  • like: renal disease, endocrine disorders, or other identifiable causes
39
Q

what causes hypertension (anatomically)?

A
  • an increase in systemic vascular resistance (SVR) or total peripheral resistance (TPR)
  • due to changes in vascular tone (state of constriction) of systemic resistance vessels
  • an increase in CO due to changes in HR and SV
40
Q

categories of hypertension

A

see more about dealing with it on slide 94

Physio (15 decks)

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