Module 2: Cardiovascular Ax

Question 1

cardiac output assessment

Answer 1

• 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

Question 2

cardiac output

Answer 2

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

Question 3

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

Answer 3

increase

Question 4

what are the effects of an excessively increased HR?

Answer 4

• 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)

Question 5

stroke volume

Answer 5

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

Question 6

how is stroke volume determined?

Answer 6

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)

Question 7

what is stroke volume influenced by?

Answer 7

• preload
• afterload
• ventricular contractility

Question 8

preload

Answer 8

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

Question 9

what is preload influenced by?

Answer 9

• 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).

Question 10

assessments that provide info about preload

Answer 10

• 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

Question 11

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

Answer 11

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

Question 12

afterload

Answer 12

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

Question 13

what is afterload determined by?

Answer 13

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

Question 14

what happens if increased resistance is encountered?

Answer 14

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

Question 15

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

Answer 15

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

Question 16

what factors influence afterload?

Answer 16

vessel diameter, aortic impedance, blood viscosity

Question 17

what is the primary determinant of afterload?

Answer 17

vessel diameter

Question 18

what is dBP an indicator of and why?

Answer 18

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

Question 19

what is the difference between sBP and dBP?

Answer 19

pulse pressure

Question 20

what is normal pulse pressure?

Answer 20

40mm Hg

Question 21

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

Answer 21

narrow = increased vascular tone
widened = decreased vascular tone

Question 22

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

Answer 22

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)

Question 23

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

Answer 23

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

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

Question 24

what can aortic impedance cause?

Answer 24

increased resistance of blood flow out of the left ventricle

Question 25

viscosity

Answer 25

measure of a fluid’s resistance to flow

Question 26

what plays a major role in determining fluid viscosity?

Answer 26

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

Question 27

Hematocrit

Answer 27

measurement of the percentage of RBCs in a sample of blood

Question 28

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

Answer 28

high Hct, thicker/more viscous blood

Question 29

assessment cues that provide info about afterload

Answer 29

- 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.

Question 30

contractility

Answer 30

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

Question 31

what factors influence contractility?

Answer 31

- presence of hormones - neurotransmitters - cardiac history - other chemical substances - availability of oxygen and nutrients to the heart muscle

Question 32

what can contractility be decreased by?

Answer 32

- 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

Question 33

what can contractility be increased by?

Answer 33

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

Question 34

starling's law

Answer 34

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

Question 35

assessments that can provide evidence for contractility

Answer 35

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