Cardio Physiology Review Flashcards
What changes in blood volume distribution normally occur immediately when moving from supine to standing?
Blood volume transfers from central reservoirs and pools in highly compliant large veins of the lower extremity
Why does walking decrease venous pressure in the foot?
Role of muscle pump & one-way venous valves to facilitate venous return
What effect does the venous pooling in our patient’s lower extremity upon standing (prior to compensation) have on her cardiac output and arterial blood pressure?
↓ CO and MAP
Why?
VR ↓ CVP ↓ EDV ↓ SV ↓ CO ↓ (CO = HR x SV) MAP ↓ (MAP = CO x TPR)
If our patient’s BP dropped to 95/65 when she fainted, what was her MAP?
75mmhg
Calculation to approximate Mean Arterial Pressure at Rest
MAP = DBP + 1/3 (SBP – DBP)
What is the integration center where baroreceptor firing rate information is processed?
Medullary Cardiovascular Center
Cerebral circulation is capable of autoregulation in order to meet tissue O2 demand, so why did this patient lose consciousness?
Even though resistance to flow can be decreased via autoregulation/vasodilation, a sufficient driving force (MAP) must be maintained for adequate flow.
Her sudden, severe drop in MAP was below the autoregulatory limit of her cerebral circulation and thus blood flow (and O2 supply) was compromised.
Ohm’s Law Applied
Flow = Pressure Gradient/ Resistance
What happened?
Decreased Flow = Decreased Pressure Gradient/ decreased Resistance to Flow
Systemic application
MAP = CO x TPR
Effect of nitroglycerin on arterioles and veins?
Promotes vascular smooth m. relaxation (veins > arterioles) > dilation of venous and arterial beds
Opposes reflex response which promotes vasoconstriction of arterioles and veins > Result?
Further promoted pooling within L.E. veins and ↓ VR
Effect of nitroglycerin on cardiac tissue?
No direct effect of nitroglycerin on cardiac tissue
Reflex response which ↑ in HR and ↑ contractility is unopposed > Result?
Tachycardia experienced by the patient upon standing
During which phase of the cardiac cycle does the left ventricular myocardium receive the majority of blood flow?
Diastole
Why did the patient only experience angina during physical exertion?
Insufficient O2 supply to meet increased demand during exertion
Stenotic LAD → ischemia
Which specific factors contributed to our patient’s increased myocardial O2 demand?
At rest?
Hypertension: BP 160/95
↑ Afterload
Which specific factors contributed to our patient’s increased myocardial O2 demand?
How does ↑ afterload affect O2 demand?
increase wall stress
Which specific factors contributed to our patient’s increased myocardial O2 demand?
Working on the lawn or during the exercise stress test?
increase heart rate
According to the relationship of Laplace, which would most likely promote a decrease in ventricular wall stress? Aortic regurgitation Aortic stenosis Concentric ventricular hypertrophy Dilated ventricular chamber Systemic hypertension
Concentric Ventricular Hypertrophy
Wall stress is related to ?
Wall stress (σ) is related to transmural pressure (P), radius (r), and wall thickness (η)
Wall stress is directly proportional to?
Systolic ventricular pressure (P)
Radius of ventricular chamber (r)
wall stress is inversely proportional to?
Ventricular wall thickness (η)
What is the normal mechanism by which O2 supply is increased in order to meet the demand of the exercising heart?
Autoregulation
When O2 demand exceeds O2 supply: vasodilation promoted
Active hyperemia:
Adenosine
Increased Pco2
NO
H+
Prostaglandins
Myocardial O2 Consumption: Fick Calculation
Myocardial O2 consumption can be calculated by the Fick Principle if coronary blood flow (CBF) is known and arterial/venous O2 content is known.
Fick calculation also be used to determine cardiac output (CO) if whole-body oxygen consumption (VO2) and arterial/venous O2 content is known
Practice Calculation:Myocardial O2 Consumption & Fick Principle
What is this patient’s myocardial O2 consumption (MVO2)?
Coronary Blood flow = 100 ml/min
Arterial O2 = .2 ml O2/ml blood
Venous O2 = .1 ml O2/ml blood
Q=(VO2)/(A-VO2 difference)
Note: Q is used to indicate CO or blood flow (CBF in this case)
MVO2 = 10 ml O2/min
Rearrange Fick Eq: MVO2 = CBF x (AO2 - VO2)
= 100 x (.1)
= 10 ml O2/min
Why was autoregulation of the patient’s coronary circulation during exertion insufficient to meet myocardial O2 demand when doing yard work and during the stress test?
A portion of his arteriolar dilating capacity (coronary reserve) was already utilized at rest in order to compensate for the resistance to flow caused by his stenotic LAD
If a patient with a LAD stenosis were prescribed a vasodilator, would blood flow to ischemic tissue downstream of the stenosis likely increase or decrease?
May actually decrease, why?
“Coronary Steal”
If arterioles are already maximally dilated in response to ischemia, vasodilator action likely to only affect vessels in nonischemic vascular beds
An additional reduction in perfusion pressure can further compromise blood flow to ischemic tissue downstream of stenosis
Which effects of a vasodilator could be beneficial for our patient with angina upon exertion?
↓ peripheral resistance
↓ afterload
↓ wall tension
↓ myocardial oxygen demand
Which cardiac layer is generally first to be compromised during ischemic conditions?
subendocardium
Imagine if our patient’s exercise stress test had not been stopped quickly enough, or if the LAD stenosis had not been identified and he continued to exert himself at home until he suffered a M.I.
Shift of the mean QRS vector toward the right: Right Axis Deviation
What causes this shift?
Decreased depolarization of the LV due to loss of electrical activity from infarcted cells
“Shift towards hypertrophy and away from infarction”
Our patient’s resting BP is 160/95 and HR is 85 bpm. If his cardiac output is 5 L/min, what is his total peripheral resistance? (assume RAP = 0 mmHg)
TPR = ~23 mmHg x min/L
MAP = DBP + 1/3 PP
= 95 + 1/3(65) = ~117 mmHg
MAP = CO x TPR
117 mmHg = 5 L/min x TPR
TPR = 117 mmHg / 5 L/min
= ~23 mmHg x min/L
What changes occur to CO as you exercise?
↑, Why? CO = HR x SV ↑ HR ↑ sympathetic input ↑ SV ↑ contractility (sympathetic input) ↑ EDV (Muscle pump, cardio-thoracic pump, venoconstriction)
what chanes occur to tpr as you exercise?
↓ overall, Why?
Balance of sympathetic-mediated vasoconstriction of non-active tissue beds and autoregulation resulting in vasodilation to exercising skeletal m.
What changes occur to MAP as you exercise?
MAP = CO x TPR
↑ MAP is relatively moderate considering the large ↑ in CO (due to ↓ TPR)
Review: CV Changes During Exercise
↑ HR and VR: ↑ CO
↓ TPR
MAP: General Increase
SBP > DBP
↑ PP
MAP increase is due to increased CO, but somewhat offset by decrease in TPR
Vasoconstriction in inactive vascular beds contributes to maintain MAP to allow for adequate perfusion of active tissues
Which cyclic change is primarily responsible for the “pacemaker potential” (slow depolarization phase 4) of the SA node?
increased na+ current
Which other currents also contribute to the SA nodal pacemaker function? (i.e. phase 4)
ICa: Ca2+ influx
increasing
IK: K+ efflux
decreasing
Slow diastolic depolarization (phase 4) is mediated by 3 major currents:
- If: inward current (mainly Na+ via non-specific cation channels) activated during hyperpolarization
- ICa: Ca2+ influx
- IK: K+ efflux
Which ion has the greatest contribution to the change in membrane potential during the fast depolarization phase (phase 0) of the ventricular myocardial AP?
na+ influx
Which valve is primarily auscultated at the apex?
mitral
What does a low-frequency, rumbling diastolic murmur indicate about the mitral valve?
Stenosis
Auscultatory finding of a loud S1 also support dx of mitral stenosis
