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
a soft, blowing systolic murmur was also auscultated at the cardiac apex.
What does this murmur indicate about the mitral valve?
Mitral regurgitation/insufficiency
How does stenosis alter the properties of the mitral valve, and how does this affect blood flow across the valve causing a murmur?
:
Hemodynamic consequences
What effect does stenosis have on valve “radius” and resistance to flow?
Resistance to flow 1/r4 : Radius ↓; Resistance ↑
What is the effect of increased resistance on the pressure gradient across the valve?
↑ (i.e., greater pressure difference, P1 – P2)
What is the effect on velocity of flow across the narrowed valve?
↑
Causes of increased turbulence:
↑ Velocity
Sudden, local decrease in diameter (↑ Velocity)
Atherosclerosis
Cardiac valve lesions
Application to Sphygmomanometry
↑ Diameter
↓ Viscosity
Anemia
There is no evidence that her tachycardia is due to a pathology of the pacemaker function. What is the likely cause?
↑Sympathetic
↓Parasympathetic
Sinoatrial Node: Depolarization Rate
Sympathetic input:
Norepinephrine → Adrenergic (b1-adrenoceptors)
Positive chronotropy: ↑ HR
Parasympathetic (vagal) input:
Acetylcholine → Cholinergic (M2-Muscarinic receptors)
Negative chronotropy: ↓ HR
intrinsic rate is 100-110 beats per minutes
How Does Activation of β1-adrenergic receptors ↑ HR?
Increased If in nodal cells
↑ rate of depolarization (phase 4)
Increased ICa in all myocardial cells
↑ rate of depolarization (phase 4)
Muscarinic receptors mediate their effect on cardiac pacemaker cells by increasing which ion current?
Ik
Effects via M2-muscarinic receptors:
Increased IK in nodal cells
Hyperpolarizes phase 4
Decreased If in nodal cells
↓ rate of depolarization (phase 4)
Decreased ICa in all myocardial cells
↓ rate of depolarization (phase 4)
Threshold more positive, takes longer to reach
Pulmonary wedge pressure provides information about the pressure of which cardiac chamber?
left atrium
If a patient had a tricuspid valve stenosis (vs. Ms. Davis’ mitral stenosis), what change would you expect to observe on a jugular-venous pulse wave?
Large a waves
a wave
RA contraction
av minimum:
RA relaxation (tricuspid closure)
c wave:
RV pressure in early systole (bulging of tricuspid valve into RA)
x minimum:
elongation of veins during ejection phase with ventricle contraction
v wave:
RA filling (tricuspid closed)
y minimum:
fall in RA pressure (tricuspid open; rapid ventricular filling
Increase pressure subsequent to y minimum
occurs as VR continues with reduced ventricular filling
Large a waves:
Tricuspid Stenosis, Right Heart Failure
Cannon a waves:
3 °, Complete Heart Block (AV dissociation)
No a waves:
atrial fibrillation
c wave:
RV pressure in early systole (tricuspid bulging)
large v wave:
Tricuspid regurgitation
What effect do you expect Ms. Davis’ increased LA pressure and volume to have on her pulmonary circulation blood pressure?
Increased
Pulmonary hypertension >Pulmonary edema
Factors Influencing Net Filtration Pressure
(1) Capillary BP (Pc )
Hydrostatic pressure: Out (Favors filtration)
(2) Interstitial Fluid-Colloid Osmotic Pressure (πIF ) Osmotic pressure (leaked proteins): Out (Favors filtration)
(3) Plasma-Colloid Osmotic Pressure (πc ) Osmotic pressure (plasma proteins): In (Favors reabsorption)
(4) Interstitial Fluid Hydrostatic Pressure (PIF )
Hydrostatic pressure: In (Favors reabsorption)
What is the net filtration pressure for this individual?
Capillary hydrostatic pressure (Pc) = 19 mmHg
Capillary osmotic pressure (πP) = 23 mmHg
Interstitial fluid hydrostatic pressure (PIF) = 2 mmHg
Interstitial fluid osmotic pressure (πIF) = 1 mmHg
- 5
Outward pressure (Pc + πIF) - Inward pressure (πP + PIF) = (19 + 1) - (23 + 2) = - 5
Is filtration or reabsorption promoted?
Net inward pressure of 5, favors reabsorption
Splitting of the S2 heart sound can normally be auscultated during inspiration because inspiration results in delayed:
pulmonary valve closing
Cardiac Cycle & Heart Sounds
Right ventricular ejection longer vs. left ventricular ejection (tan)
Aortic valve closes before pulmonary valve
Greater afterload (systemic pressure)
Pulmonary valve: opens first and closes last (lower afterload pressure)
Normal physiological splitting of S2 heart sound (A2, P2)
Inspiration: Splitting of
S2 (A2 before P2)
Expiration: S2
normally heard as one sound
Effect of Respiratory Cycle on S2
Effect on Right Heart
Relatively negative intrathoracic pressure > greater VR to RA/RV> increased EDV> greater RV ejection volume
Additional time for RV ejection delays pulmonary valve closure (P2) more
Enhances physiological splitting of S2
Effect of Respiratory Cycle on S2
Effect on Left Heart
Relatively negative intrathoracic pressure> retention of blood in dilated pulmonary v.v> reduced VR to LA/LV> decreased LV EDV & ejection
Less time for LV ejection accelerates aortic valve closure (A2) more
Enhances physiological splitting of S2
P2 corresponds to pulmonary valve closure
Following RV relaxation, elevated pulmonary pressure due to pulmonary hypertension results in
more forceful closing of the pulmonary valve
Why did right ventricular hypertrophy develop in this patient with mitral stenosis and insufficiency?
Response of cardiac m. to increased afterload
Right ventricle must generate a greater systolic pressure in order to eject blood through pulmonary valve into hypertensive pulmonary circulation
Pulmonary circulation has become hypertensive due to back-up from LA
How Can the Mean QRS Vector be Determined in the Frontal Plane?
Perpendicular to the axis of a limb lead, there will be an isoelectric voltage recorded for that lead.
Parallel and in the same direction as the axis of a limb lead, there will be a large positive voltage recorded for that lead.
Parallel and in the opposite direction as the axis of a limb lead, there will be a large negative voltage recorded for that lead.
On follow-up exam, if Ms. Davis’ CO is 3.6 L/min, and her HR is 90 bpm. What is her stroke volume?
40 ml/beat
CO = HR x SV
3,600 ml/min = 90 bpm x SV
SV = 3,600 ml/min / 90 bpm
= 40 ml/beatStroke volume
(SV = EDV − ESV)
Left ventricular ejection fraction
(EF = SV/EDV)
End diastolic volume = 120 ml End systolic volume = 60 ml Stroke volume (ejection volume) = 60 ml What is the Ejection Fraction?
Ejection fraction= 60 ml/120 ml = .50 (50%)
normal ejection fraction
> .55 - .60
Fick Principle
another method to determine CO if you don’t know SV (or EDV, ESV)?
If you know whole-body oxygen consumption (VO2) and if arterial and venous blood gasses are measured, you can determine CO.
CO=(oxygen consumption)/(arterial -venous oxygen difference)
A 70-kg male:
Resting VO2 = 250 ml/min
Peripheral arterial O2 content = .2 ml O2/ml
Mixed venous O2 content = .15 ml O2/ml
What is his cardiac output?
5,000 ml/min (5 L/min)
CO = 250 ml O2/min / (.2 - .15 ml O2/ml blood)
In addition to CO, Cardiac Index is another measure used clinically to determine effectiveness of heart function
Cardiac Index = CO relative to body surface area
For example Ms. Davis’:
CO = 3.6 L/min
m2 = 1.8
Cardiac Index = 2.0 (normal range: 2.8 - 4.2)
CO (Q) =
HR X SV
CO=
MAP/TPR
Q=
VO2/(A-VO2 Difference)
MAP=
DBP + 1/3 (SBP – DBP)
PP=
SBP-DBP
EF=
SV/EDV
Net Filtration Pressure=
(Pc – PIF) – (πc – πIF)
Although her jugular veins are not distended, Ms. Davis is showing some symptoms of elevated central venous pressure (CVP; pulmonary and pedal edema). What is the effect of her pulmonary hypertension on her right heart and venous pressure?
RV pressure ↑ RA pressure ↑ VR ↓ Venous pressure ↑ Capillary hydrostatic pressure ↑ Pedal edema ↑
What effect would a cardiac glycoside such as digoxin have on the function of Ms. Davis’ ventricular cells?
How?
↑ contractility (increased inotropy)
↑ [Ca2+]i
Digitalis slows the Na+-K+ pump in the cell membrane of cardiac cells
Results in accumulation of intracellular Na+
Slows Na+- Ca2+ antiporter
Increases intracellular Ca2+
Positive inotropy
Removal of Ca2+ to the ECF from Cardiac Cells
Sarcolemmal 3Na+- 1Ca2+ antiporter
Ca2+ removal against large chemical gradient
[Na+] higher in ECF, uses the Na+ gradient to power Ca2+ removal
Ms. Davis asks if she can donate a pint of blood to a nephew with the same blood type who is going to have a major surgery. If she were to do this, what changes would occur in her cardiovascular system immediately after the procedure?
Immediate Neural Reflex Response
↓ MSFP ↓ VR ↓ EDV ↓ SV ↓ CO ↓ MAP ↓ Baroreceptor firing rate ↑ Sympathetic output
then
↑ HR and contractility ↑ TPR (vasoconstriction) ↑ Venoconstriction ↓ Venous capacitance ↑ VR ↑ EDV ↑SV ↑ CO ↑ MAP (Restored)
What other compensatory changes would occur in the intermediate- to long-term time frame following blood donation?
Endocrine/Humoral response to volume depletion
↑ RAAS
What are 6 important actions of Angiotensin II that work to restore MAP and effective circulating volume?
Vasoconstriction
Stimulates adrenal gland aldosterone production
Stimulates ADH/AVP
Stimulates thirst
Stimulates renal Na+ reabsorption
Stimulates SNS activity
