2 - cardiac phys HR and contractility Flashcards
diastole
cardiac muscle at rest
systole
cardiac muscle during contraction
isovolumic ventricular contraction
first phase of ventricular contraction when AV valves are pushed closed by pressure within ventricles; semilunar valves remain open
ventricular ejection
pressure within ventricles increases forcing semilunar valves open (leaving the heart), allows ejection of blood into the pulmonary or aortic circuit
s1 sound
sound due to closure of the AV valves
s2 sound
second heart sound due to the closure of the semilunar valves
late diastole
both chambers are relaxed and ventricles fill passively
atrial systole
atrial contraction forces a small amount of additional blood into the ventricles
isovolumic ventricular relaxation
a ventricles relax, pressure in ventricles falls, blood flows back into the cusps of semilunar valves and snaps them closed
Preload
myocardial stretch before contraction, preload is a volume = EDV
afterload
a pressure, pressure in the aorta or pulmonary artery + EDP
contractility
cardiac muscle fibers contract at given fiber length
increase in stretch
increase in stretch exposes additional sites for Ca2+ binding and for actin-myosin interaction, increased stretch also effects greater release of Ca2+ from the SR
normal SV number
55-100mL
normal ESV number
50 mL
normal EDV number
120 mL
SV =
ESV - EDV
ESV
volume of blood in a ventricle at the end of contraction, or systole, and the beginning of filling, or diastole. ESV is the lowest volume of blood in the ventricle at any point in the cardiac cycle
EDV
volume of blood in the right and/or left ventricle at end load or filling in (diastole) or the amount of blood in the ventricles just before systole
varies with venous return aided by skeletal muscle and respiratory pump and increases with sympathetic innervation and epinephrine
SV
volume of blood in millilitres ejected from the each ventricle due to the contraction of the heart muscle
Factors affecting EDV (4)
- skeletal muscle pump - goes against gravity
- respiratory pump- helps blood return to the heart - makes pressure gradient less so draws air in and increases the abdominal pressure
- sympathetic nervous system innervation of veins - increases sympathetic nerve firing on veins - contracts - goes back to the heart
how does diuretic affect blood volume
causes blood volume to decrease
force of contraction in ventricular myocardium is influenced by
contractility and EDV
how does SNS increase contractility (NE and EPI)
increases the ability of the heart to contract at any EDV
NE is a positive inotropic agent
binds to b1 receptors and activates cAMP - phosphorylating VGCC so calcium entry increases as open time increases
phosphorylating phospholamban reducing inhibiting on Ca-ATPase on SR - increasing stores of Ca in SR which makes a more forceful contraction and removing Ca2+ from the cytosol faster so that Ca and troponin binding time shortens which causes a shorter duration of contraction
phospholamban
inhibits ca2+ atpase (SERCA - delivers Ca2+ into the ER. Inhibited by PKA to cause an increase in heart rate. Epi is an inhibitor of PKA
elevation of cAMP in cardiac myocytes results in
PKA activation and phosphorylation of
- VGCC that increase Ca2+ induced Ca2+ release from the SR
- phospholamban, removes inhibitory effect on SR Ca2+ ATPase (SRCA)
verapamil
negative ionotropic agent and negative chronotropic agent. inhibits VGCC
mirlinone is a phosphodiesterase inhibitor - phosphodiesterase breaks down cAMP
makes a more forceful contraction - positive ionotrope- this will increase cAMP which will increase
how does afterload affect CO
L heart: pulmonary pressure
R heart: aortic pressure
Afterload effects on the Frank-Starling Curve
Vasoconstriction increases: makes the curve go down, as SV will decrease
relaxes smooth muscle: curve will increase as the SV will also increase but the EDV will decrease
signs/symptoms of low cardiac output - heart failure
fatigue, weakness
rapid or irregular heart beat ( body is trying to compensate for not enough oxygen getting to the blood)
reduced ability to exercise
difficulty concentrating or decreased alertness
chest pain if your heart failure is caused by a heart attack
signs/symptoms of high end diastolic pressure
(left ventricle is stiff and impaired relaxation)
shortness of breath (dyspnea) when you exert yourself when you lie down
swelling (edema) in your legs, ankles and feet
persistent cough or wheezing with white or pink blood-tinged phlegm
increased need to urinate at night (antidiuretic - releasing pressure)
swelling of your abdomen (ascites)
very rapid weight gain from fluid retention
sudden, severe shortness of breath and coughing up pink, foamy mucus
diuretic effect on the Frank-Starling curve
lowers the edv down and to the left - moves pt to a lower cardiac filling pressure along the same ventricular curve- not as much preload to increase SV
positive inotropic effect on the frank-starling curve
digoxin or dobutamine - straight up - moves patients to a higher ventricular function curve
negative inotropic effect on the frank-starling curve
straight down
vasodilator effect on the frank-starling curve
Angiotensin converting enzymes (ACE) inhibitors or nitroprusside - up and left - reduces cardiac filling pressures - decreases afterload, increases sv, decreases edv
how does digoxin affect contractility
Na/K Atpase provides a conc gradient so that Ca levels can be maintained - maintains a conc gradient - no RMP - narrow TI - more Ca can get pumped into the SR
