Cardiac Study Guide PHA 404.docx

Study guide for exam 2 Please remember that this is just a guide and not a comprehensive list. In preparation for your exam, please be familiar with the following terms, topics, and concepts. The process of cardiac conduction/action potential generation in the heart. Cardiac conduction – electrical...

Study guide for exam 2 Please remember that this is just a guide and not a comprehensive list. In preparation for your exam, please be familiar with the following terms, topics, and concepts. The process of cardiac conduction/action potential generation in the heart. Cardiac conduction – electrical activation is communicated between myocytes triggering their synchronous contraction Generation of action potential – Sodium channels open and potassium channels close It takes time for sodium to come in Transient calcium channels (T-Type) open and that pushes the membrane potential to threshold Absolute refractory period = time it takes to move calcium Long lasting calcium channels (L-type) channels open and that lets action potentials rise Potassium channels open and the L-type calcium channel closes and hyperpolarizes the cell When repolarizing the cell, the pacemaker brings in more ions to help the pacemaker potential hit threshold Cardiac muscle fiber – gets rapid change in membrane potential, does not have summation. **has a STRICT LONG refractory period of how fast blood fills left ventricle Contraction sequence – i.e., what parts of the heart contract first, middle, and last Sinoatrial node (SA) – pacemaker, initiates heartbeat and sets the rate of the heart Atrioventricular node (AV)- electrical gateway to ventricles. Could act as a secondary pacemaker, is autorhythmic at about 55 bpm has a brief delay so the atria can contract before the ventricles bundle of histamine (AV bundle) – pathway for signals from AV node right and left bundle branches – divisions of AV bundle that enter interventricular septum Purkinje Fibers – upward from apex spread throughout ventricular myocardium to maximize ventricular ejection (45bpm) Phases of the cardiac cycle and what happens at each phase Right atria, right ventricle – pumps blood to the lungs Left atria, left ventricle – pumps blood back into body Aorta- carries oxygenated blood to the body Superior/inferior vena cava – carries deoxygenated blood to the heart Phases Blood enters heart. Late diastole – both sets of chambers relaxed and there is passive ventricular filling Atrial systole – atrial contraction forces a small amount of additional blood into vessels End diastolic volume – the maximum amount of blood in ventricles occurs at the end of ventricular relaxation (EDV = 135 ml) EDV – ESV = Stroke Volume Isovolumic ventricular contraction – first phase of ventricular contraction pushes AV valves closed but does not create enough pressure to open semilunar valves (no movement of blood outside of LV) Ventricular ejection- as ventricular pressure rises and exceeds pressure in the arteries, the semilunar valves open and the blood is ejected End systolic volume – minimum amount of blood is in the ventricles (ESV=65 ml) Isovolumic ventricular relaxation – as ventricles relax, pressure in ventricles drops, blood flows back into cups of semilunar valves and snaps them closed PV loop Cardiac output and all factors involved Cardiac output = HR * SV Diastole – relaxation phase Chambers fill with blood and it is twice as long as systole (2/3) Relaxation begins, ventricular pressure drops, semilunar valves close, “dub”, atrioventricular valves open, fills 70% passively and 30% by atrial contraction, EDV Systole – contraction phase 1/3 of cardiac cycle Contraction begins, ventricular pressure rises, atrioventricular valves close “lub”, semilunar valves open, blood ejected, ESV Frank-Starling mechanism defined As EDV increases, SV increases This increases preload and contractility The more the heart is stretched (increases preload) the harder they contract Venous return (preload) The flow of blood from veins into the heart Increases with Skeletal muscle pump Respiratory pump Blood volume Posture Blood pooling or in muscles/skin post exercise Afterload how hard the heart must work to eject blood the greater the afterload, the less contracting muscle fibers can shorten at a given contractility function of total peripheral resistance Preload volume of blood in ventricle prior to contraction = venous return EDV end diastolic volume ESV end systolic volume SV stroke volume governed by preload, contractility, and afterload ↑Preload↑EDV↑ SV ↑Contractility ↓ESV ↑ SV ↑Afterload↑ESV↓ SV Normal values for cardiac output Ejection fraction EF% = Stroke Volume / End-Diastolic Volume In a healthy heart, it is maintained at 60% During exercise, EDV goes up but EF remains at 60%. Thus, contractility must increase to pump higher volume Regulation of osmotic pressures and movement of fluid Blood flow changes Effects of gravity on blood flow when going from sitting to standing- venous return is reduced, which leads to a decrease in cardiac stroke volume, a decline in arterial blood pressure, and an immediate decrease in blood flow to the brain Effects of exercise on stroke volume and heart rate Brain, heart, skeletal muscle cardiac output increases. skin, kidneys, abdominal organs, etc decrease cardiac output SV is easiest to increase bc its cheapest to change increases venous return, breathing hard Regulation of SV and Heart rate once you max out SV only HR can increase Q so people who exercise have lower HR and increased SV at rest bc LV holds more blood Changes in cardiovascular function with exercise systole increases, diastole stays the same (afterload increases, preload stays the same) Mechanics of breathing (i.e., pressure changes) External respiration - exchange of gasses (oxygen and CO2) Parasympathetic and sympathetic effects on the cardiovascular system Sympathetic Nervous System Raises Heart Rate Sympathetic chain ganglia increases norepi release onto pacemaker cells. That goes to beta adrenergic receptors and it increases cAMP. That opens HCN channels and opens calcium channels Increases rate of SA node depolarization, increasing HR, increasing contractility, increasing BP Parasympathetic Nervous system slows Heart Rate The vagus nerve is activated and Ach released onto pacemaker cells. That activates muscarinic receptors and decreases cAMP. It closes HCN channels and opens potassium channels Decreases SA node depolarization, decreasing HR< decreasing contractility, decreasing BP Sensitivity to hormones is a function of ___________ a cell's sensitivity to any hormone is determined by the presence or absence of the receptor molecule specific to that hormone. Left and right sided heart failure CHF - decreased contractility increased ESV, decreasing SV left sided CHF - if the blood backs up into the lungs because the left ventricle contractility is impaired pulmonary edema (congestion in the lungs) right sided CHF - blood backs up into the body because right ventricle’s contractility is impaired (feet) pitting edema, ascites ALL LECTURE OBJECTIVES