Cardiac Cycle: the mechanical events of the heart The depolarization causes the atria to contract (systole) and fill the ventricles and AV valves then close. The pressure in the ventricles will increase because it’s filled with blood. When they then contract will increase the tones but no measurement of myocardiac cell volume (isometric). The aortic pressure varies from 80-120mmHg (diastole and systole of the heart) When the heart is diastole, the ventricles fill with blood passively (no contraction needed) thru the atria. The relaxation is in the interval of T-P segment. Isometric contraction: When the ventricle contract, there’s no increase in the ventricle volume but increased pressure Cardiac output: how much being pumped from the heart HR= Heart rate, SV= stroke volume Without the ANS, we’ll have intrinsic control-SA firing- which is higher than parasympathetic control. HR can be changed as long as two control systems of ANS have different balances; athletics during exercise have bradicardia due to the imbalance between the sympathetic and parasympathetic systems; their bradicardia cases resulted from diminished of sympathetic system (adaptation). SV= amount of blood ejected in each systole. Intrinsic= related to the heart (depending on its function); Spacemaker Extrinsic= other control upon the heart; Para/sympathetic control More blood will be pumped if the heart contracted/ pumped forcefully and less blood left at the end of the systole. The rapid filling into the ventricles is passive filling The higher heart rate is the shorter the time of filling out the ventricles. The heart failure causes more blood left in the ventricle at the end of systole. Hypertrophy in athletics that increase the blood volume pumped. Hypertrophy in heart failure is compensation; also the same in Chagas disease and the pumping is not efficient. In aging, the heart grows and this normal physiological process (compensation). Inotropic: a drug that induces the stimulation the contractility. Afterload: the pressure necessary in the ventricle to exceed the aortic pressure. Preload: the time before the heart beat The only way to improve the stroke volume is by increasing the heart rate (HR is the first in any activity that increases the cardiac output). (Ef) tells how good the heart pumps; how much blood ejected in a fraction of the EDV BSA= depends on the height and weight More stroke volume because the increase in the EDV (intrinsic), the sympathetic (extrinsic) the final result is increase of SV. It matters because in each beat we have more blood ejected. The Frank-Starling curve With the same EDV and sympathetic stimulation, we’ll see more Stroke volume. If there’s heart failure, will have lower SV, it has more blood stays after the beat and heart less efficient to pump. Compensated heart failure The failure heart tries to compensate and build more muscle, but still hypertrophy not efficient during systole, and the sympathetic system tries to pump even more by increasing the heart rate. There are valves in the veins that prevent the backflow of blood. NE> Tachycardia Modulation of HR NE/E (adrenal medulla) increases the flow thru the funny channels. Tachycardia (more force of the heart) stimulate the pacemaker and conduction Ach increases the flow thru K channels, and decrease the flow thru Ca2+ channels. Hyperpolarize: induce bradicardia Autonomic Regulation Positive chronotrope= increase the rate Thyroid hormone increase the metabolism in the cells Exercise at 25 watts Propranolol= blocks the beta receptors and HR decreases, (blocks the sympathetic system); like parasympathetic effect. Blocks the adrenergic receptors, NE, and diminishes the HR. the rapid increase is because the parasympathetic isn’t blocked, it’s the sympathetic that’s blocked. The fast increase of the heart rate is because the parasympathetic response. Atropine= antagonist of Ach at the muscarinic, and blocks the Ach receptors (blocking the parasympathetic intervention; inhibition) so the heart rate goes up. Ach on the heart diminishes the heart rate, and during rest the rate is high (no increase) because the inhibition of the parasympathetic system. Here there is no rapid increase because the parasympathetic is blocked or inhibited. Exercise at 150 watts The slow increase is because the sympathetic response. Nourishing the heart During exercise, the coronary flow increases during diastole because the increase of demand of oxygen. Cardiac myopathies Necrosis: no repair can be done. If the cardiac muscle injured, it can’t contract. The site of the ischemia is close to the conduction system it’s more complicated. That area of the muscle will die (Necrosis) Silent ischemia: ischemia sometimes doesn’t give any signals, and suddenly the patient experience a heart attack. The problem was there and no signal or abnormality. It gets blocked again due to the adipose tissue and scar tissues form. The best thing is prevent the cardiac disease (the heart and vessels) Coronary Artery Diseases (CAD) Acute myocardial infarction (heart attack) Profound vascular spasm of coronary arteries (sudden vasoconstriction) Formation of atherosclerotic plaques: accumulation/aggregation of platelets or lipids. The flow will be turbulent (more noise) no more laminar flow (which is silent). Same analogy when measuring the blood rate; by turbulent flow. The lipids can move anywhere in the vessels. Thromboembolism… the blood blocked because of the globulin and can move inside the vessels to different parts. Blood vessel pathologies: aneurysms Atherosclerosis After the heart attack, there’s weak chance to get the heart as strong as before the attack and the patient needs rehabilitation.