Physiology Flashcards
Cardiac output equation
CO=SV x HR
Fick principle
CO=rate of O2 consumption/ arterial O2 content - venous O2 content
Mean Arterial Pressure (MAP) equation
MAP = CO x TPR (total peripheral resistance)
MAP= 2/3 diastolic pressure + 1/3 systolic pressure
pulse pressure equation
PP=systolic pressure -diastolic pressure
pulse pressure is proportion to
Stroke Volume
pulse pressure is inversely proportional to
arterial compliance
what are examples of pulse pressure being proportional to SV
increase PP in hyperthyroidism, aortic regard, aortic stiffening (isolated systolic hypertension in elderly), obstructive sleep apnea (increase sympathetic tone), exercise (transient)
what are examples of pulse pressure being inversely proportional to aortic compliance
decrease PP in aortic stenosis,, cardiogenic shock, cardiac tamponade, advanced heart failure
Stroke volume equation
SV = EDV - ESV
how is CO maintained in the early stages of exercise?
by increase in HR and increase in SV
how is CO maintained in the late stage of exercise?
increase in HR ONLY (SV plateaus)
Diastole is preferentially shortened with
increase HR; less filling time –> decrease CO (ex: V tach)
stroke volume is affected by what variables
Contractility, after load and preload
an increase in SV is seen with:
an increase in contractility and preload, but a decrease in afterload
what are examples of increased contractility
exercise pregnancy anxiety
a failing heart has an increase or decreased SV
decreased
Contractility (and SV) increases with:
Catecholamines, increase intracellular Ca2+, decrease extracellular Na+, digitalis
contractility (and SV) decrease with:
B1 blockade, HF with systolic dysfunction, acidosis, hypoxia/hypercapnia, Non-dihydropyridine Ca2+ channel blockers
and increase in myocardial oxygen demand is increased by:
increase in contractility, increase in after load, increase in hr, increase in diameter of ventricle (increase in wall tension)
what law does wall tension follow?
Laplaces law
What is laplace’s law
wall tension: Pressure x Radius / 2 x thickness
preload is approximated by what variable?
ventricular EDV
after load is approximated by what variable?
MAP
preload depends on:
venous tone and circulating blood volume
what drugs will decrease preload?
Venodilators (ex: nitroglycerin)
what drugs will decrease after load?
Vasodilators (ex: hydralazine)
if you have an increase in after load you will see and increase in what else?
increase after load–> increase pressure –> increase wall tension
how does the LV compensate for an increase after load
lv compensates for an increase afterlaod by thickening (hypertrophy) in order to decrease wall tension
what drugs will decrease both after load and preload?
ACEi and ARBs
if you have chronic hypertension (increase MAP)
increase LV hypertrophy
Ejection Fraction
EF= SV/EDV= EDV-ESV/EDV
what is a normal ejection fraction?
> 55%
Left ventricular EF is an index of
ventricular contractility
does ejection fraction increase or decrease in systolic HF?
decreases
does ejection fraction increase or decrease in diastolic HF?
normal
Force of contraction is proportional to end diastolic length of cardiac muscle fiber (preload)
True
how can you increase contractility?
digoxin, catecholamines
how can you decrease contractility?
mi, b blockers, nondihydropyrdinine Ca channel blockers, dilate cardiomyopathy
resistance presssure flow equation
change in P = Q x R
Ohm’s law
change in V = IR
volumteric flow rate equation
change in Q= V (flow velocity) x A (cross-sectional area)
resistance equation
change in P / Q = 8n x Length / (pi)r^4
Total resistance of vessels in series
TR= R1 +R2 +R3…
Total resistance of vessels in parallel
1/TR=1/R1+1/R2+1/R3….
viscosity depends on
hematocrit
when do you see an increase in viscosity
hyperproteinemic states (multiple myeloma) or polycythemia
when do you see a decrease in viscosity?
anemia
Capillaries have the highest total cross-sectional area and lowest flow velocity
TRUE
what changes will you see in TPR and CO when removing an organ, for example in nephrectomy
increase in TPR, decrease in CO
who accounts for most of TPR
arterioles
who provides most of blood storage capacity?
veins
who provides most of blood storage capacity?
veins
isometric contraction
period between mitral valve closing and aortic valve opening
period of highest O2 consumption
systolic ejection
period between aortic valve opening and closing
isovolumetric relaxation
period between aortic valve closing and mitral valve opening
rapid filling
period just after mitral valve opening
reduced filling
period just before mitral valve closing
S1
mitral and tricuspid valve closure
loudest at mitral area
S2
aortic and pulmonary valve closure
loudest at left upper sternal border
S3
in early diastole during rapid ventricular filling phase
Which S sound is associated with increase filling pressured more common in dilated ventricles?
S3
S4
in late diastole (“atrial kick”
which S sound is best heard at apex with patient in left lateral decubitus position?
S4
Which S sound is associated with a high atrial pressure, ventricular hypertrophy ( left atrium must push against LV wall)?
S4
a wave
atrial contraction
when do you see an absent a wave?
afib
c wave
RV contraction (closed tricuspid valve bulging into atrium)
x descent
atrial relaxation and downward displacement of closed tricuspid valve during ventricular contraction
when is X descent absent
in tricuspid regurg
v wave
increase right atrial pressure due to filling against closed tricuspid valve
y descent
RA emptying in RV
R to L shunt description
early cyanosis; “blue babies”, diagnosed prenatally or immediately after birth
usually require surgery/correction and/or maintenance of a PDA
examples of a R to L shunt
THE 5 T’s:
- Truncus Arteriosus
- Transposition
- Tricupsid Atresia
- Tetralogy of Fallot
- TAPVR
Persistent Truncus Arteriosus
failure of the Truncus Arterioles to divide into Ascending aorta and pulmonary trunk due to failure of Aorticopulmonary septum to form
most puts have accompanying VSD
D-Transposition of great vessels
Due to failure of the aorticopulmonary septum to spiral, causing the Aorta to leave from the Right ventricle and the Pulmonary trunk to leave from the left ventricle, in turn this causes a separationg of the pulmonary and systemic circulations
this is not compatible with life unless a shunt is created to allow the mixing of blood (ex: VSD, patent foramen ovale or PDA)
without surgical intervention most infants die within a few months of life!
Tricuspid atresia
absence of a tricuspid valve and hypoplastic RV
requires both ASD and VSD for survival!
Tetralogy of fallot
caused by anterosuperior displacement of the infundibular septum
which congenital heart disease is the most common cause of early childhood cyanosis?
TOF
what are the 4 defects seen in TOF?
PROV
- Pulmonary infundibular stenosis (most important determinant factor for diagnosis)
- Right ventircualr hypertrophy- boot shaped heart on CXR
- Overriding aorta
- VSD
what causes the early cyanotic get spells and RVH in TOF?
pulmonary stenosis forces R to L flow across VSD
What improves cyanosis in TOF?
squatting
how does squatting improve cyanosis in TOF?
increase in SVR , decrease in R to L shunt†
how does squatting improve cyanosis in TOF?
increase in SVR , decrease in R to L shunt
how does squatting improve cyanosis in TOF?
increase in SVR , decrease in R to L shunt
TAPVR
Pulmonary veins drain into right heart circulation (SVC, coronary sinus, etc)
associated with ASD and sometimes PDA to allow for R to L shunting to maintain CO
