Module 2: Cardiovascular Ax Flashcards

1
Q

cardiac output assessment

A
  • determined by stroke volume and heart rate
  • stroke volume is determined by preload, afterload, and contractility
  • each of these components exert influence over the others, impacting overall cardiac output
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2
Q

cardiac output

A

volume of blood ejected from the heart in one minute (L/min)

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3
Q

what will heart rate do as a compensatory mechanism for low CO and low PaO2

A

increase

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4
Q

what are the effects of an excessively increased HR?

A
  • reduced ventricular filling time (leading to decreased preload and decreased contractility)
  • increased cardiac demand
  • reduced coronary artery filling time (coronary arteries fill and supply cardiac muscle with oxygen during diastole)
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5
Q

stroke volume

A

amount of blood ejected from the heart with each contraction (mL/beat)

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6
Q

how is stroke volume determined?

A

by the volume of blood in the heart at the end of diastole (the period of relaxation between beats) and the amount of blood that is expelled during systole (the period of contraction when the heart pumps blood)

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7
Q

what is stroke volume influenced by?

A
  • preload
  • afterload
  • ventricular contractility
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8
Q

preload

A

the amount of stretch or tension in the ventricular wall of the heart at the end of diastole just before the contraction or systolic phase begins

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9
Q

what is preload influenced by?

A
  • venous return (circulating blood volume and its ability to return to the heart)
  • cardiac rhythm (which impacts atrial kick and filling time)
  • ventricular ability (related to ventricular compliance as well as ability to contract).
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10
Q

assessments that provide info about preload

A
  • S3 heart sounds (caused by the “sloshing” of excessive blood flowing from the left atrium into the left ventricle)
  • fluid balance (ins/outs, daily weights, mucous membranes, skin turgor)
  • crackles on lung auscultation**
  • edema**
  • POCUS
  • echo
  • fluid volume responsiveness
  • pulse pressure variation
  • stroke volume variation
  • CVP
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11
Q

can you rely on crackles and edema as evidence of preload status?

A

NO:
- Crackles can result from pulmonary congestion caused by fluid overload and poor contractility but can also signify consolidation from pneumonia.
- peripheral edema can take time to both accumulate and reabsorb. Fluid collected in the interstitial spaces is not a direct reflection of fluid currently circulating intravascularly

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12
Q

afterload

A

force, or the resistance, against which the ventricles must pump in order to eject blood

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13
Q

what is afterload determined by?

A

the tension or pressure that the ventricles must generate to overcome the resistance in the blood vessels and pump blood forward

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14
Q

what happens if increased resistance is encountered?

A

ventricles must contract more forcefully in order to maintain a normal stroke volume, increasing myocardial workload and oxygen demand

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15
Q

what if a ventricle is not able to generate sufficient force?

A

stroke volume will decrease, and the amount of blood leaving the heart will be reduced

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16
Q

what factors influence afterload?

A

vessel diameter, aortic impedance, blood viscosity

17
Q

what is the primary determinant of afterload?

A

vessel diameter

18
Q

what is dBP an indicator of and why?

A

arterial tone because it is a measurement of pressure within the body’s vasculature between heartbeats. A vasoconstricted system will have a higher DBP and a vasodilated system will have a lower DBP

19
Q

what is the difference between sBP and dBP?

A

pulse pressure

20
Q

what is normal pulse pressure?

A

40mm Hg

21
Q

what would a narrow pulse pressure indicate? a wider pulse pressure?

A

narrow = increased vascular tone
widened = decreased vascular tone

22
Q

what does increase in arterial tone mean and what are examples?

A

vasoconstriction, will decrease the diameter of the vessels and increase afterload.

  • circulating catecholamines (epinephrine, norepinephrine released from the adrenal glands)
  • compensatory mechanisms such as the RAAS and SNS stimulation
  • hypothermia
  • vasoconstrictive drugs (e.g., norepinephrine, vasopressin, epinephrine)
23
Q

what does decrease in arterial tone mean and what are examples?

A

vasodilation, will increase the diameter of the vessels and decrease afterload

  • hyperthermia
  • inflammatory responses
  • vasodilating drugs (e.g., nitroglycerin)
24
Q

what can aortic impedance cause?

A

increased resistance of blood flow out of the left ventricle

25
Q

viscosity

A

measure of a fluid’s resistance to flow

26
Q

what plays a major role in determining fluid viscosity?

A

RBCs - viscosity of an individual’s blood can be determined by evaluating their hematocrit

27
Q

Hematocrit

A

measurement of the percentage of RBCs in a sample of blood

28
Q

what will hematocrit and viscosity be for higher % of RBCs in a given volume of blood?

A

high Hct, thicker/more viscous blood

29
Q

assessment cues that provide info about afterload

A
  • pulse pressure
  • DBP as evidence of vascular tone
  • aortic stenosis
  • cardiac history
  • signs of vasoconstriction or vasodilation:

Peripheral vasoconstriction reduces blood flow to the extremities. This can result in cool skin temperature, pallid extremities, delayed capillary refill, and weak peripheral pulses.

Peripheral vasodilation increases blood flow to the extremities. This results in warm extremities, brisk capillary refill, and full or bounding peripheral pulses.

30
Q

contractility

A

ability of the heart’s myofibrils to change their strength of contraction

31
Q

what factors influence contractility?

A
  • presence of hormones
  • neurotransmitters
  • cardiac history
  • other chemical substances
  • availability of oxygen and nutrients to the heart muscle
32
Q

what can contractility be decreased by?

A
  • Decreased preload (not stretching myofibrils enough)
  • Increased preload (overstretches the myofibrils)
  • Increased afterload (increases the pressure the heart must pump against)
  • Inadequate oxygen supply to myocardial tissue.
  • Negative inotropic drugs (e.g., beta blockers, calcium channel blockers)
  • Some electrolyte imbalances, particularly hypocalcemia
  • Extreme tachycardia
  • Pre-existing medical conditions
33
Q

what can contractility be increased by?

A
  • stimulatory effect of the SNS
  • circulating catecholamines
  • inotropic drugs (e.g., digoxin, dopamine, dobutamine)
  • balanced electrolytes, particularly calcium
  • obtaining adequate preload
  • decreased afterload
34
Q

starling’s law

A

describes the relationship between the amount of stretch experienced by the myocardial fibers caused by preload during diastole, and the resulting force they can contract with in systole

35
Q

assessments that can provide evidence for contractility

A
  • preload and afterload status
  • heart rate
  • medical history
  • echocardiogram
  • blood work, including lytes, trops, CK
  • end-organ perfusion, including global markers