Cardiovascular phys Review Flashcards
What changes in blood volume distribution normally occur immediately when moving from supine to standing?
Blood volume transfers from central reservoirs → pools in highly compliant large veins of the lower extremity
A-V difference in pressure is 85 approximately and this stays the same when you go to standing from laying. but what does change/increases is the actual pressure the further you are from the heart b/c of the hydrostatic pressure, but at the head its lower
why does walking decrease venous pressure in the foot?
one way valves and muscles pumping
what effect does the venous pooling in a patients lower extremity upon standing prior to compensation have on her cardio output and arterial blood pressure
CO decreases
arterial blood pressure decreases
b/c VR decreases–> decrease CVP –> decreased EDV–> decreased SV–> decreased CO
MAP= COxTPR so decrease CO and decrease MAP
MAP = what?
CO x TPR
or
MAP = DB + 1/3 PP
considering cerebral circulation and its ability to autoregulate, why would a patient lose consciousness ?
what is the driving force for blood flow?
the driving force for blood flow is a pressure gradient
even though resistance to flow can be decreased via autoregulation/vasodilation, a sufficient driving for (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
what is Ohm’s law?
flow = pressure gradient/resistance
CO = what?
MAP/TPR
if a patient’s BP dropped to 95/65 when she fainted what is her MAP?
MAP = CO x TPR
MAP = DB + 1/3(PP)
65 + 1/3 (95-65)
= 75
when someone goes from laying to standing, what is the firing rate of their high pressure aortic and carotid baroreceptors
what is the integration center where the baroreceptor firing rate information is processed
firing decreases
integration center is? –> medulla
what are the effects of a normal reflexive response to hypotension
standing–> blood pools in veins –> decrease in MAP–> decrease in baroreceptor firing–> baroreceptor reflex –> increase sympathetic output and decrease parasympathetic output
- Heart –> increase HR, contractility –> increase CO
- arterioles–> TPR increase b/c of constriction
- veins –> Constriciton of veins–> increased VR –> increase SV –> increase CO
what are some factors that influence the degree of orthostatic response?
total blood volume
vascular distensibility
skeletal muscle tone ; strength and rate of intermittent contraction of sk. musc.
temperature
initial HR
initial myocardial contractility
how does a double dose of nitroglycerin affect the ability of baroreceptor response to correct for postural hypotension?
arterioles and veins–> antagonized sympathetic vasoconstrictor effects on arterioles and veins –> results in further pooling of blood within LE when a patient goes from supine to standing
effect on cardiac tissue? no direct effect on cardiac tissue
reflexive increase in HR and contractility remain intact
during which phase of the cardiac cycle does the left ventricular myocardium receive majority of blood flow ?
diastole
left coronary artery is filled most during this time
what is the cause of the angina in a patient doing yardwork/exercise that has a stenotic LAD?
he had decreased oxygen delivery from a stenotic LAD –> ischemia
which specific factors increase O2 demand in a patient at rest?
exercise?
rest–> HR, force of contraction, afterload increased, HTN
exercise?
–> increase in HR
how does increased afterload affect O2 demand?
increased wall stress
what is ventricular wall stress/tension ?
force acting on myocardial fibers, tends to pull fibers apart
energy must be expended to oppose wall stress
what is Laplace law?
wall stress is related to transmural pressure, radius and wall thickness
wall stress is directly proportional to…
pressure (systolic ventricular pressure)
radius (radius of ventricular chamber)
wall stress is indirectly proportional to ….
wall thickness of ventricle
so aortic regurg–> increases ventricualr wall stress
aortic stenosis increases wall stress
dilated ventricular chamber increases wall stress
systemic HTN increases wall stress
what is the normal mechanism by which O2 supply is increased in order to meet demand of the exercising heart?
with increased tissue metabolism–> increased release of metabolic vasodilators/autoregulation (adenosine, PCO2, NO, H+, prostaglandins) –> dilation of arterioles –> decreased resistance creates increased blood flow–> Increase O2 and nutrient supply to tissue as long as metabolism is increased
what is the 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
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
MVO2 = CBF x (AO2 - VO2)
100 x (.2 - .1)
=10 mL o2/min
Q = VO2 / A - VO2 difference Q = CO or flow
why was autoregulation of a patient’s coronary circulation (who has an occlusion of his LAD) during exertion insufficient to meet his myocardial oxygen demand when doing yard work or stress test?
even at rest this patient is maximally vasodilated
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
“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 vasodilator effects could be beneficial for a patient with angina upon exertion
decrease peripheral resistance –> decrease afterload–> decrease wall tension –> decrease myocardial oxygen demand
which cardiac layer is generally compromised first during ischemic conditions
subendocardium
myocardial contraction effectively compresses vascular supply
-pressure especially compress subendocardial aa.
CBF restriction–> subendocardium is generally first to be damaged
druing a stress test in a patient with an LAD occlusion, what did the patients ST segment depression likely indicate?
subendocardial ischemia
following a left ventricular infarction, in which quadrant would we expect a mean QRS vector to be?
right axis deviation
this is b/c the left heart cells are dead and not contributing to the heart electrical activity
away from infarction, toward hypertrophy
in addition to increased blood flow to supply of cardiac muscle, what are other shifts in blood distribution that normally occur in response to exercise?
skeletal muscle
brain stays the same
decrease supply to GI, kidneys
Michael Jordan’s resting BP is 110/80. His resting HR is 60 bpm, and his cardiac output is 6 L/min. What is his total peripheral resistance? (assume RAP = 0 mmHg)
MAP = TPR x CO
MAP = 80 + 1/3 (110-80) = 90
CO = 6 L
So TPR = MAP/CO
TPR = 90/6 = 15
what changes occur to CO, TPR and MAP during exercise
CO increases
CO = HR x SV
HR increases b/c of sympathetic input
SV increases b/c increased contractictility (sympathetic input) and EDV increases (Muscle pump, cardio-thoracic pump, venoconstriction, rate of relaxation)
TPR decreases why?
balance of symp-mediated vasoconstriction of non-active tissue beds and autoregulation resulting in vasodilation to exercising skeletal m.
MAP
increases b/c there is an increase in CO (more increase than there is decrease in TPR) q
what are the CV changes during exercise?
HR SV CO Arterial pressure TPR O2Consumption Arteriovenous difference
HR increases steadily
SV increases to a point and then slightly decreases
CO increases steadilty
MAP steadily/shallow increase (b/c increase in CO offset by decrease in TPR)
TPR decreases
O2 consumption increases
Arteriovenous O2 diff–> increases
at rest, what is the response to an increased rate of firing of the high pressure baroreceptors located in the aortic arch?
vasodilation and bradycardia
this is sensed as an increase in BP
increased firing of baroreceptors causes a decrease in sympathetic output and increase in parasympathetic output
decreased sympathetc =
-decreased NE release on alpha 1 receptors –> vasodilation of arteriolars smooth muscle –> decreased peripheral resistance –> decrease in BP
decrease in NE release on B1 receptors in heart
1) decrease ventricular myocardium–> decrease force of contraction –> decrease CO
2) decrease SA node –> decrease HR –> decrease CO –> decrease BP
increased ACh on muscarinic receptors on SA node–> decrease HR
what does sinus rhythm mean?
SA node is setting the pace
this is normal
no ectopic pacemakers
which cyclic change is primarily responsible for the pacemaker potential? slow depolarization phase of the SA node (phase 4)
increased Na current (funny current) b/c these open with hyperpolarization allowing sodium influx
increase in Ica (Ca influx increases)
decrease in K+ efflux
which ion has the greatest constribution to the change in membrane potential occurring during the fast depolarization phase (phase 0) of the ventricular myocardial AP?
what ion is responsible for the plateau phase?
Sodium (Na)
slow Ca influx is responsible for the plateau phase
ausculation of heart reveals a low-freq rumbling DIASTOLIC murmur at the cardiac apex…. ECG also showed evidence of LA enlargement…
which valve is involved ?
what does a low frequency rumbling diastolic murmur indicated about the mitral valve?
mitral valve
atria are contracting against a stenotic valve
mitral valve stenosis
auscultation revealed a soft, blowing murmur throughout systole at the cardiac apex….
what does this indicate about the mitral valve
mitral regurgitation/insufficiency
how does stenosis alter the properties of the mitral valve and how does this affect flow across it causing a murmur?
what effect does stenosis have on valve radius and resistance to flow?
if you increase resistance, what is the effect on the pressure gradient across the valve?
reistance to flow 1/r^4 : radius decreases and resistance increases
with increased resistance, there is an increase in pressure gradient across the valve, and therefore there is a greater velocity of flow across the narrowed valve
this results in turbulent flow responsible for the murmur…
what are causes of increased turbulence?
increased velocity
decreased viscosity - anemia
larger diameter OR
sudden local decrease in diameter (resulting in increased velocity)
-atherosclerosis
-cardiac valve lesions (insufficiency)
mitral stenosis
heard during diastole (B/w S2 and first S1 sound)
greater left atrial pressure
decreased EDV
aortic pressure is decreased due to decreased CO
decreased (slightly) ESV
SV is reduced
Mitral insufficiency/regurg
heard during systole
left ventricle ejects blood back into the left atrium as well as into the aorta-> left atrial pressure increases
aortic pressure and left ventricular pressure may fall in response to a reduction in net volume of blood ejected into the aorta
end systolic volume is reduced b/c of decreased outflow resistance (afterload)
EDV is increased b/c increased left atrial pressure increases ventricular filling
SV is enhanced
aortic stenosis
heard during systole
Left ventricular pressure exceeds aortic pressure
ESV is increased
increase in EDV (compensatory)
SV decreased
aortic insufficiency/regurg
heard during diastole
blood flows backward from the aorta into the ventricle (left)
more rapid fall in aortic pressure
this increases diastolic pressure and increases aortic pulse pressure
left ventricular pressure and left EDV increase
increased SV b/c of increased filling
no true isovolumetric phases
what can rheumatic fever as a child cause?
valve dysfunction…
how does activation of B1 adrenergic receptors increase HR
Increased I-f in nodal cells (increase rate of depolarization = phase 4)
increase I-ca in all myocardial cells (increase rate of depolarization phase 4)
muscarinic receptors mediate their effect on cardiac pacemaker cells by increasing which ion current?
K efflux (hyperpolarizes)
moving membrane potential further from threshold
decreases I f in nodal cells (decreases rate of depolarization phase 4)
decreased I ca in all myocardial cells (decreases rate of depolarization phase 4) moves threshold more positive, takes longer to reach threshold
what are chronotropy
inotropy
dromotropy
and what are the effects of parasympathetic and sympathetic input
chronotropy–> rate
increases with symp
decrease with para
inotropy–> contractility
increased and decreased
parasympa–> more effect on atria than ventricles
Dromotropy –> conduction velocity
increased with symp
decreased with parasym
what are the sympathetic influences on capacitance of veins and venules
increases capacitance
what is the cause of an increased pulmonary wedge pressure (normal range is 4-12 mmHG)
this is giving information about left atrium
Stenosis and regurgitant mitral valve –> increases LA volume
if a patient had a tricuspid valve stenosis what change would you expect to observe on a jugular venous pulse wave ?
atrial pressure will go up with stenosis so you will expect large A waves
JVP pulse wave
a ?
C?
v?
a-> right atrial contraction
C –> RV pressure in early systole. all valves are closed and there is bulging in isovolumetric contraction. there is bulging of the tricuspid valve into the RA)
V wave–> RA filling (tricuspid is closed)
large a waves ? what could this indicate
tricuspid stenosis
right heart failure
cannon a waves (very large a waves)
complete heart block (AV dissociation)
atria could be contracting against a closed valve
no a waves?
atrial fibrillation
large v wave?
tricuspid regurgitation
what effect will increased LA pressure and volume have on pulmonary circulation blood pressure?
increased
pulmonary HTN will lead to pulmonary edema
if a patient complains of propping their head up on 3 pillows to breathe at night this may indicate pulmonary edema
pulmonary edema is also indicated by crackles
which starling force is most likely responsible for pulmonary edema observed in our patient
capillary hydrostatic pressure
promoting net filtration and edema
as you move to one end of capillary bed to another, the main thing that changes is capillary hydrostatic pressure so there is net reabsorption
causes of edema?
increased capillary pressure -increased venous pressure: heart failure increased blood volume venous obstruction incompetent venous valves gravity
-increased arterial pressure
HTN
-decreased arterial resistance
vasodilation
-increased capillary permeability vascular damage (burns, inflammation)
-decreased plasma oncotic pressure
reduced plasma proteins (Malnutritions, burns, liver dysfunction)
-lymphatic blockage
tissue injury
inflammation of lymphatics
practice calculation
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
19 + 1- outward
23 + 2- inward
outward pressure - inward pressure = -5
net inward pressure of 5 favors reabsorption
NOT likely to produce edema
what the heck is splitting of S2 heart sound?
delayed pulmonary valve closing
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 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
if a patient has an ECG that indicates ventricular hypertrophy, and the patient has pulmonary HTN, what is the most likely shift in the axis?
right axis deviation
b/c there is increased afterload the right ventricle must work against
CO = 3.6 L/min
HR is 90 Bpm
SV?
CO = SV x HR
SV = CO/HR
3.6–> 3600 ml/mn
3600/ 90 = 40 ml/beat
SV = ?
EDV-ESV
can find on 2D electrocardiography
Left ventricular ejection fraction = ?
EF= SV/EDV
this is an indicator of cardiac function
how much of what you had (EDV) did you eject (SV)
normal = .55 - .6
what is another method to determine CO if you don’t know SV (or EDV, ESV) ?
use the Fick Principle
CO = Oxygen consumption / Arterial - Venous Oxygen Difference
CO = VO2 / A-VO2 difference
A 70-kg male has a resting VO2 of 250 ml/min, a peripheral arterial O2 content of .2 ml O2/ml of blood, and a mixed venous O2 content of .15 ml O2/ml of blood. What is his cardiac output?
5,000 ml/min (5 L/min)
CO = 250 ml O2/min / (.2 - .15 ml O2/ml blood)
what is the cardiac index?
this is anther measure used clinically to determine effectiveness of heart function
just use surface area
Cardiac INdex = CO relative to body surface area
CO = 3.6 m^2 = 2.1 CI = 1.7 (normal is 2.8 - 4.2)
PP =
SBP - DBP
SV = ?
EDV - ESV
EF =?
SV / EDV
net filtration pressure =
(Pc- Pif) - (oncotic capillary-oncotic IF)
CO =
MAP /TPR
CO =
HR x SV
increased contractility of the heart has what outcomes in terms of volume and pressure?
it generates higher pressure in the left ventricle but at the same time it lowers ESV which is GOOD unlike aortic stenosis which increases LV pressure at the same time increasing ESV BAD
what factors influence SV ?
how can you increase SV ?
EDV
ESV
you can increase SV by
1) increase EDV by increasing preload
2) decrease ESV by decreasing the afterload and increasing contractility
what is the effect of pulmonary HTN on right heart and venous pressure?
RV pressure RA pressure VR Venous pressure Capillary hydrostatic pressure Pedal edema
RV pressure- increase RA pressure- increase VR - decrease Venous pressure- increase Capillary hydrostatic pressure- increase Pedal edema--INCREASE
what effect would a cardiac glycoside such as digoxin have on function of ventricular cells?
↑ contractility (increased inotropy)
↑ [Ca2+]i
How?
Digitalis slows the Na+-K+ pump in the cell membrane of cardiac cells
Results in accumulation of intracellular Na+
Slows Na+- Ca2+ antiporter (3Na - 1Ca antiporter)
(usually this pumps Na into the cell and Ca out)
Increases intracellular Ca2+ (retaining calcium longer)
Positive inotropy
if someone lost a pint of blood what effect does this have on cardiovascualr system?
decreases Blood volume decreases VR decreases EDV decrease SV decrease CO decrease MAP baroreceptor firing decreased increased symp output increase HR and contractility increase TPR increase venoconstriction (decreases venous capacitance)
this is the short term neural reflex
the long term response would be RAAS system
what are the 6 major effects of ANG II
1 Vasoconstriction 2Stimulates adrenal gland aldosterone production 3 Stimulates ADH/AVP 4. Stimulates thirst 5. Stimulates renal Na+ reabsorption 6. Stimulates SNS activity
what is the bainbridge reflex?
when there is volume loading there is an increase in HR
stretching of low pressure atrial receptors causes tachycardia
