CV Physiology 1-3 Flashcards
what is the preferred ATP production pathway for cardiac muscle? how does this change under stress?
basal: beta-oxidation of free fatty acids (FFA)
under stress: shift towards glucose oxidation (glycolysis) - yields more ATP
how does the phosphocreatine system produce ATP in skeletal and cardiac muscle?
phosphotransferase creatine kinase transfers phosphate onto ADP to yield ATP
isoform of creatine kinase in cardiomyocytes is CK-MB
which of these is a better diagnostic marker for cardiac injury, CK-MB or troponin I/T? why?
following myocardial injury, levels of CK-MB (cardiac isoform of creatine kinase) and cardiac troponin I/troponin T rise in the blood
however, serum levels of CK-MB can increase even during vigorous exercise, so it is less specific to cardiac damage
on the other hand, cTnI and cTnT should not be found in blood during normal circumstances, so these are more specific diagnostic markers of cardiac injury
describe how serum levels of cardiac troponin I (cTnI) and troponin T (cTnT) rise following myocardial injury
should not be detectable in blood during normal circumstances
following myocardial injury, rise within 3-4 hours, peak by 18-36 hours, gradually return to normal over 10-14 days
specific to cardiac injury, thus are important diagnostic markers
cardiac output =
CO = SV x HR
SV (stroke volume) = EDV - ESV
= end diastolic volume - end systolic volume
HR = beats/min
mean arterial pressure =
what is normal?
MAP = CO x TPR
where CO = cardiac output, TPR = total peripheral resistance
MAP is a measure of tissue perfusion pressure - important to measure to determine that there is adequate BP to maintain tissue perfusion
typically 80-100mmHg
central venous pressure =
what is normal?
central venous pressure = right atrial pressure (RAP)
effectively the lowest blood pressure we have, typically ~2mmHg
how is ejection fraction measured? what is normal?
EF = SV/EDV
measurement of what fraction of blood is actually ejected during ventricular systole
recall SV = EDV - ESV
normal = 55-75%
what afterload does the left ventricle have to overcome with preload in order to contract?
preload (isovolumetric contraction) of left ventricle must overcome aortic pressure (afterload) in order for systolic ejection to occur
remember cardiac muscle works against pressure to displace blood volume
In cardiomyocytes, activated Gs proteins simulate adenyl cyclase, which increase cAMP, which simulates PKA (protein kinase A). PKA phosphorylates the following proteins:
a. Type L Ca2+ channels
b. Troponin I
c. Phospholamban
What is the role of each of these in regulating cardiomyocyte contractibility?
a. Type L Ca2+ channels: in sarcolemma, activated by both mechanical stretch (as blood fills during diastole) and membrane depolarization - cause calcium-induced calcium release from SR —> contraction
b. Troponin I: dissociates Ca2+ from troponin C —> relaxation
c. Phospholamban: activates SERCA in SR —> re-uptake of Ca2+ into SR —> relaxation
how does the NCX transporter contribute to cardiomyocyte relaxation?
NCX = Na+-Ca2+ ATPase, exchanges intracellular Ca2+ for extracellular Na+ (secondary active transport)
recall that changes in [Ca2+] are directly proportional to changes in contractility of cardiac muscle
so NCX helps decrease [Ca2+] in order to induce cardiomyocyte relaxation
how does the drug digitalis (digoxin) work and what is it used for?
digitalis (digoxin) blocks Na+/K+ ATPase in ventricular myocytes, thereby elevating intracellular [Na+]…
… this reduces the electrochemical driving force for the NCX (Na+-Ca2+ ATPase - secondary transport of intracellular Ca2+ for extracellular Na+)…
… therefore, intracellular [Ca2+] remains elevated, increasing contractibility of the cardiac muscle (force of contraction is proportional to concentration of calcium) —> greater cardiac output
used to increase force of heart contractions (and CO) inpatients with heart failure
explain why a person with atrial arrhythmia might still have a normal cardiac output
most of ventricular filling (~80%) is passive due to pressure gradient
atrial systole only contributes ~20%
CO may not be affected by loss of atrial function
Describe how the left ventricle pressure-volume relationship would be affected by increased afterload without an increase in inotropy
increased afterload (resistance to ejection) will increase peak- and end-systolic LV pressures
resistance will also make systolic ejection harder such that LV won’t be able to empty as effectively —> decreased stroke volume
what does end-systolic pressure-volume relationship (ESPVR) represent?
end-systolic pressure-volume relationship refers to the inotropic state of the left ventricle, as a result of the max pressure in the LV
remember inotropy refers to contractile force of cardiac muscle
