Cardiovascular Questions Flashcards
CO equation
HR * SV
Ficks Principle of CO
CO= rate of consumption /
/arterial O2 content - venous O2 Content
“ROS” / (a O2)- (v O2)
MAP (mean arterial Pressure)
CO * TPR (total resistance)
2/3 diastolic pressure + 1/3 systolic pressure
Pulse pressure=
Systolic Pressure- Diastolic Pressure
PP (pulse pressure) proportional to:
SV
PP (pulse pressure) inversely proportional to:
Arterial Compliance
SV=
EDV - ESV
How is CO maintained during Early & Late stages of exercise?
Early= ^HR, ^SV Late= ^ HR only (SV plateaus)
What happens typically to Diastole with ^ HR
Shortened, less filling time –> decreased CO (e.g. ventricular tachycardia)
Increased PP
- Hyperthyroidism
- Aortic Regurgitation
- Aortic Stiffening (isolated systolic hypertension in elderly)
- Obstructive sleep apnea (^ sympathetic tone)
- Exercise (transient)
Decreased PP
- Aortic Stenosis
- Cardiogenic Shock
- Cardiac Temponade
- Advanced HF
SV affected by which 3 factors?
SV ( CAP)
- Contractility. ^
- Afterload (decrease)
- Preload ^
Catecholamine stimulation via B1 Receptors
- pathway
- affect of Contractility
- Ca2+ channels phosphorylated
- ^ Ca2+ entry, Ca2+ induced release of Ca2+
- ^ storage of Ca2+ in Sarcoplasmic Reticulum
Increase Intracellular Ca2+
Decrease Extracellular Na+ ( dec activity of Na+/Ca2+ exchanger)
effect on contractility?
Increase Contractility (SV)
Digitalis is used to treat:
congestive heart failure (CHF) and heart rhythm problems (atrial arrhythmias)
can increase blood flow throughout your body
reduce swelling in your hands and ankles
Digitalis
- pathway
- effect of Contractility
- blocks Na+/K+ pump
^ Intracellular Na+
dec Na+/Ca2+ exchanger activity
^ intracellular Ca2+ - Increase Contractility
Acidosis affect on contractility
Decrease
HF w. Systolic dysfunction affect on contractility
Decrease
B1- Blockage (decrease cAMP) affect on contractility
Decrease
Hypoxia/ hypercapnia (dec Po2/ inc PCo2 affect on contractility
Decrease
Non-dihydropyridine Ca 2+ Channel Blockers affect on contractility
Decrease
myoCARDial o2 demand in increase by?
increased:
Contractility
Afterload (proportional to arterial pressure)
HR
Diameter of Ventricule (increased wall tension)
Wall Tension follows Laplace’s Law:
Wall tension= pressure x radius
Wall stress= (pr)/ (2wall thickness)
vEnous vasodilators (e.g. nitroglycerin) effect on Preload
decrease preload
Approximated by EDV
PRELOAD
Approximated by MAP
AFTERLOAD
Preload depends
- venous tone
2. circulating blood volume
Increased Afterload leads to?
Increased Pressure
Increased wall tension per Laplace’s law
LV compensates for increased after load by
thickening (Hypertrophy) in order to decrease wall tension
Arterial vasodilators (e.g. hydrAlAzine) effect on Afterload
Decrease afterload
decrease both preload & afterload
ACE inhibitors ( inhibit angiotensin converting enzyme)
(Hypertension, CHF; decrease BP, bv)
ARBS (angiotensin II antagonists)
Chronic Hypertension (increase MAP) results in
LV Hypertrophy
Index of ventricular contractility
Left ventricular EF
EF=
sv/edv
(edv-esv)/edv
Preserved ejection fraction
EF normal HFpEF
Systolic HF (EF?)
Decreased EF
dilated cardiomyopathy affect on Contracility
Decrease contracility
Catecholamines, Positive inotropes (digoxin) affect on contracility
Increase contracility
? highest total cross sectional area
capillaries
? lowest flow velocity
capillaries
? accounts for TPR
Arterioles
? provide most of blood storage capacity
Veins
Viscosity depends mostly on
hematocrit
hyperproteinemic states (e.g. multiple myeloma) polycythemia affect on viscocity
Increase Viscosity
Anemia affect of viscosity
decrease viscosity
Preload 3 variables inc/dec
- volume
- heart rate (filling time)
- veins. constrict or dilate (storage)
Other than Stress & Drugs
Contractility is stimulated by
SNS
- B1 receptors
- Release of Epinephrine/ Norepinephrine
Heart Pressure > Resistance
leads to:
push blood out of Aortic Valve
After load depends on:
- Blood Pressure (resistance)
2. Obstruction (stenosis; abnormal narrowing of Lumen)
Average pressure in Aorta during Cardiac Cycle
MAP
Increase CO ? blood concentration in aorta
Increase
Vasoconstriction of Arterioles ? TPR
TPR
How do you Maintain MAP
control Hormonal & Neural
Short term regulation of MAP (seconds to minutes)
Baroreceptors & Chemoreptors (respect to respiration)
Long term regulation of MAP (minutes to days)
Kidneys , which regulate Blood Volume
Where are Baroreceptors located?
Carotid Sinuses
Aortic Arch
Baroreceptors are ? type of Receptors?
Stretch Receptors
Stretch Receptors (baroreceptors) are able to detect “stretch” and send
Action Potentials to the Medulla Oblangata
Cardiovascular Control Center
Medulla Oblangata
The “stretch” (baroreceptors detect) is altered by
Pressure
Myosin- Actin proteins in the heart require
Ca2+
Ca2+ binds to
Troponin C
if you are “scared” which ion floods the cell from the SNS
Ca2+
Myosin head binding can depend on :
correct polarity of Actin
for any given Volume, pressure Increase
more vertical slope ESPVR
“How many Myosin Heads are working, at End of Systole”
Contractility
Contractility altered by:
- Ca 2+ (Sympathetic Nerves)
- pH
- Temperature
End Diastolic Volume
Volume of Blood in VENTRICLES before Contraction
Preload
End Diastolic Pressure, stretching walls of ventricles to greatest dimensions
Volume of Blood Ejected from blood per Heart Beat
Stroke Volume
SV directly proportional to:
Preload
at a greater EDV
- -> ? strength of contractility of ventricles
- ->? SV
Increase Contractility of Ventricles
Increase SV
Increase in Myocardium stretch
- -> ? sacromere length
- -> ? sensitivity to Ca2+
increase sarcomere length
increase sensitivity to Ca2+
Increase contractility
