Cardiac Physiology Flashcards
Describe the cardiac conduction system.
the cardiac conduction system consists of spontaneously depolarizing pacemaker cells located along the conduction pathway: SA node (70-80/min), AV node (40 - 60/min), bundle of His, and Purkinje fibers (15-40/min). The fastest pacemaker usually determines the HR, but when it fails, the next fastest pacemaker assumes its role.
What physiologic events define the cardiac cycle?
A complete cycle of ventricular contraction (systole) and relaxation (diastole).
What intracellular events cause myocardial contraction?
Increase in the intracellular Ca2+ from 10 ^-7 to 10^-5 mol/L), which binds to troponin (troponin-tropomyosin complex), exposes active sites on actin, which interacts with myosin via a ATPase.
Stroke volume is dependent on what cardiac physiology parameters?
Stroke volume depends on preload, afterload, and contractility and thus, so does BP.
What is the definition of preload?
Preload is best defined as the end-diastolic fiber length or end-diastolic volume. According to the Frank-Starling relationship, increases in LVEDV produces increases in CO until excessive LV filling leads to failure.
What is the definition of afterload?
Afterload is the stress (force/unit area) encountered by the myocardial fibers throughout systole. It can be described by the LaPlace equation: Stress = Pressure x Radius/2H (where H = wall thickness). Afterload has also been described as the external forces opposing ejection (also known as impedence) and often approximated by SVR. Because afterload continually changes throughout ejection, afterload is difficult to measure.
What is the definition of cardiac contractility?
State of cardiac performance independent of preload and afterload. It can be determined by the end-systolic pressure volume relationship (the slope of the line connecting end systolic volumes of pressure volume loops.)
Define cardiac relaxation.
An energy-dependent process that occurs when calcium is sequestered by the sarcoplasmic reticulum. Ischemic diastolic dysfunction resulting from diminished distensibility or compliance often precedes systolic dysfunction, leading to pulmonary congestion.
What factors determine cardiac output?
CO = HR x SV and SV depends on preload, afterload, and contractility.
What factors affect preload?
Rhythm: atrial kick normally contributes 15 - 20% of CO.
HR: HR >120 decreases diastolic filling time
Venous return: most important; impaired by hypovolemia, decreases in venous sympathetic tone, cardiac tamponade, increases in intrathoracic pressure, and decreased myocardial compliance.
What factors affect SVR?
SVR is primarily determined by the tone of the arteries, but is also affected by the viscosity of the blood. The lower the viscosity, the lower the SVR.
Is SVR a good measure of afterload?
Only the nonpulsatile component of afterload is determined by SVR. There is a pulsatile component which is affected by the aortic elastance, reflected arteriolar waves, and blood viscosity.
What happens to stroke volume when afterload increases?
Initially, it is preserved due to an increase in both LVESV and LVEDV (preload reserve). Eventually however, the sarcomeres are stretched to their maximum diastolic length and further increases in afterload actually decrease SV (afterload mismatch).
What factors affect myocardial contractility?
Sympathetic tone (beta-1 in the atria, ventricles, and nodal tissues; alpha effects less), inotropic agents (e.g. digoxin, amrinone, glucagon), and increases in HR increase contractility (by increasing intracellular Ca2+). Calcium channel or beta-blockers, negative inotropes, hypoxia, ischemia, intrinsic cardiac disease, and parasympathetic stimulation (by decreasing HR) all decrease contracility.
What is the Frank-Starling relationship?
It describes the ability of the heart to increase its CO in response to increases in preload. We construct a rough FS curve every time we administer a fluid bolus and look for the CO or BP to increase. When the heart no longer increases its CO in response to fluid boluses, the myocardial fibers have been stretched beyond their functional limits.
