Cardio Equations * Flashcards
CO =
SV x HR
- also: (MAP - Right atrial P) / TPR
- R atrial P = preload
Ficke equation; CO =
rate of O2 consumption/ (arterial O2 cont. - venous O2 cont)
MAP = (#1)
CO x TPR
MAP = (#2)
2/3 diastolic pressure + 1/3 systolic pressure
what does MAP give a measure of
afterload!
pulse pressure =
systolic pressure - diastolic pressure
what is pulse pressure proportional to?
stroke volume
SV = (2 equations)
CO/ HR = EDV - ESV
what two factors maintain HR in early exercise? Late exercise?
HR and SV increase initially, but SV can only increase so much, so eventually only HR is increasing to ↑ HR
what happens to CO if HR gets too high
as HR ↑ diastolic filling is incomplete, so CO ↓
two conditions that ↑ HR leads to ↓ CO
Ventricular tachycardia and atrial fibrillation
What three variables affect SV
- Contractility
- Preload
- Afterload
- ” SV CAP”
Contractility (and SV) increase in what 3 changes?
- Catecholamines (β1 agonism = ↑[Ca] intracell by stimulating SR release)
- ↓ extracell Na+
- Digitalis⇒ (blocks Na/K pump, leading to ↑ [Na] intracell; this ↓ action of Ca/Na pump that pumps Ca out of cell = ↑ intracell Ca
Contractility (and SV) decrease in what 5 ways
- β1 blockade (↓cAMP)
- Heart failure (systolic dysfunction)
- Acidosis
- Hypoxemia/ Hypercapnia
- Non-DHP CCB (verapamil)
* also MI ( loss of myocardium)
mycocardial O2 demand is increased when what 4 variables increase?
- ↑ afterload (proportional to arterial pressure)
- ↑ contractility
- ↑ HR
- ↑ heart size (↑ wall tension)
Preload is roughly equal to what 3 other measures?
- ventricular EDV
- Right atrial pressure
- Central venous pressure
Afterload is equal to what
MAP (proportional to TPR)
Venodilators decrease what? example of one
Preload (vEno = prEload)
- nitroglycerin is venodilator
vasodilators (arterial) decrease what? example
afterload (vAso = Afterload)
- hydralazine is vasodilator
preload increases in what 3 conditions
- exercise (slightly)
- ↑ blood volume (pregnancy, overtransfusion over hydration)
- excitement (↑ sympathetic activity)
what usually happens to CO or SV as preload (ventricular EDV) increases? (Starling curve)
usually increases in healthy individuals⇒ force of contraction is proportional to end-diastolic length of cardiac muscle fiber
why can CO or SV increase even more during exercise with increasing preload than under normal conditions
sympathetic nerve stimulation⇒ β1 stimulation, which increase contractility and thus SV, leading to increased CO
why does the CO or SV actually fall in CHF once preload gets past a certain point (starling curve rises, then begins to dip)
fluid overload⇒ overloads capacity of SV to increase anymore and past a certain point is actually counter-productive (drop in CO)
*CHF already have high preload to begin with (starling curve shifted to the right)
what drug can be helpful in maintaining CO in CHF
digoxin ⇒ ↑ contractility, increasing SV
EF = (2 forms of the equation)
(SV) / (EDF, or preload, RAP) = (EDV - ESV) / EDV
what is EF an index of
ventricular contractility or function
what is normal EF?
usually 55%- 75% (2/3 or 66% is a good approx.)
when does EF decrease
systolic HF⇒ a failing heart has ↓ SV (numerator decreases)
what 3 factors determine resistance
- viscosity
- length of vessel
- radius of vessel
what two factors are directly proportional to resistance
- viscosity
- length of vessel
- resistance increases when these do
what factor is inversely proportional to resistance?
Radius⇒ 1/ R^4
- any decrease in vessel radius GREATLY increases resistance
what are three conditions viscosity is increased (and therefore resistance)
- polycythemia
- hyperproteinemic states (multiple myeloma)
- hereditary spherocytosis
what does viscosity mostly depend on
hematocrit
where does most of the regulation of resistance in vessels take place
arterioles
vessels in an organ are arranged in series what does this mean for blood flow (Q) and pressure
blood flow is constant, from the aorta to the arteries to the veins–> what decreases is the pressure
