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Cardiovascular Physiology Blood Pressure =force exerted by the blood against the walls of the blood vessel; Changes throughout cardiac cycle – Systolic Blood pressure=maximal pressure achieved by ventricular contraction – Diastolic Blood pressure=lowest pressure remaining in blood vessels after ventricle contracts Blood Pressure Blood flow - amount of blood flowing at any given time. Dependent on Cardiac output (CO). Blood pressure - force per unit area exerted on wall of blood vessel Autonomic Nervous System – Sympathetic – causes vasoconstriction of arterioles Increases blood pressure – Parasympathetic – causes vasodilation Decreases blood pressure Blood Pressure Systolic pressure Diastolic pressure Pulse pressure = systolic - diastolic MAP = Diastolic + (Pulse pressure/3) Hypotension - Low blood pressure (Nutritional, anesthesia) Hypertension - High blood pressure (increased peripheral resistance, high blood viscosity) Pressure Systemic circulation-high hydraulic pressure required to overcome gravitational forces and resistance Arteriole-vessels with high resistance to reduce pressure before reaching capillary beds Pulmonary Circulation-low pressure, due to low resistance to blood flow Effects of High Blood Pressure Abnormally high blood pressure within veins-can cause leaking of fluid from blood vessels – Result-edema – Congestive heart failure Right cava heart failure-leaking of fluid from vena – Pleural effusion Left heart failure-leaking of fluid within lungs – Pulmonary edema Distribution of Blood Flow Pulmonary Circulation – 15% Systemic Circulation – 80% – 65% in veins – 10% in arteries and arterioles – 5% in capillary beds Heart – 5% Functions of the CV System Maintain blood pressure within the arteries Maintain blood flow to the tissues Maintain normal blood pressures within the capillaries and veins =Perfusion Perfusion Allows delivery of oxygen and nutrients (i.e. glucose) Removal of waste products – Carbon dioxide Transport of hormonal messages from one part of the body to another Forces Heart must adjust contractility (inotropic state) based on forces working on the heart. – Preload – Afterload Afterload =Sum of forces the ventricles must contract against to make blood flow forward Increased systemic blood pressure – Increases or Decreases Afterload???? – Chronic blood pressure-increases the work of the heart-heart enlarges! Preload =Amount of blood in the heart just prior to contraction of the ventricle =Venous Return or amount of blood returning to the heart – Leaky valves-regurgitate blood back into the atrium Increases or Decreases Preload?? Inotropic State Adjustments in contractility based on Calcium and contractile protein interactions – Sympathetic tone (norepinephrineneurotransmitter) – Increases heart rate and contractility by increasing Calcium availability – Starling’s law-increased contractility with stretching of sarcomere The Cardiac Cycle “Pacemakers” of the heart-send electrical signal through heart – Systole-ventricular contraction – Diastole-Heart is relaxed allowing filling of the heart **Based on Ventricle, although atria also contract and relax The Cardiac Cycle End of Diastole-maximal ventricular filling Electrical signal-triggers ventricular contraction. Pressure in Ventricle > Atria = closes AV valves; semilunar valves not open yet The Cardiac Cycle First Heart Sound =closure of AV valves Semilunar Valves open once pressure in ventricle is greater than aorta or pulmonary artery Stroke Volume = amount of blood ejected (end diastolic volume-end systolic volume) Second Heart Sound= Closure of the Semilunar valves The Cardiac Cycle Semilunar Valve-open AV valves-closed Ventricle Relaxes Once pressure in the ventricle is less than the atrium-AV valves open allowing filling of ventricle Third heart sound =passive filling of the ventricle – Normal to hear in horses and ruminants-not carnivores Ventricular Filling Initial, rapid filling phase-passive Slow-filling phase-atrial contraction Fourth heart sound =atrial contraction – Normal in ruminants and equine, not in carnivores Cardiac Muscle Striated muscle Impulse from cell to cell Automaticity-cells can become selfexcitable – Small portion of the muscle cells Activation of cell Depolarization=Opening of fast sodium channels Wave of depolarizations travels down myocardium-Ca++ channels open in sarcoplasmic reticulum – Crosslink of myocardium Refractory Period-resting between depolarization, unable to contract Cardiac Impulse Propagation Automatic Tissues-generate action potentials Sequence of activation – Sinoatrial (SA) node-fastest rate! Atrial Contraction – AV node – Bundle of His – Rt. And Lt. Bundle Branch to v. apex – Purkinje fibers to myocardium Conduction Propagation Action Potential THE WHOLE PICTURE Na + influx creates (+) internal charge 1 + CHARGE INSIDE 0 CELL - 2 Repolarization 3 0 Depolarization K+ leaves cell and cell returns to it’s resting or repolarized 4 state Resting cell TIME **Purple numbers indicate phase numbers Action Potential 0-Sodium enters cell via fast channels 1-fast sodium channels close 2-Ca and Na enter cell via slow channels 3-K exits cells 4- Na and K equilibrium Intrinsic Rate SA node-fastest AV note-40-60 bpm Sympathetic and Parasympathetic Nervous System-alter the intrinsic rate – SNS-increase rate of depolarization – PNS-decrease rate of depolarization Heart Rate Regulation Baroreceptors-in heart chamber blood vessels and – If blood pressure decreases Brain>>Increased Sympathetic nervous system Increases Heart rate and vasoconstricts to increase blood pressure – If blood pressure increases? Excitation-Contraction Coupling See muscle physiology!! Ca++ influx Myofibrils couple via troponin/tropomysin complex The Electrocardiogram (ECG) Recording of electrical activity of the heart Waves-positive vs. negative depending on the direction the impulse is traveling ECG P wave- – Atrial depolarization QRS complex – Ventricular depolarization T wave-ventricular repolarization Conduction This workforce solution was funded by a grant awarded under the Workforce Innovation in Regional Development (WIRED) as implemented by the U.S. Department of Labor’s Employment and Training Administration working in partnership with the Colorado Department of Labor and Employment, the Metro Denver Economic Development Corporation, and the City and County of Denver's Office of Economic Development. The solution was created by the grantee and does not necessarily reflect the official position of the U.S. Department of Labor. 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