Cardiac Muscle Myocytes Individual cells with a nucleus and plasma membrane sarcolemma joined end to end to form a long fiber Each individual muscle fiber comprises a group of multiple parallel myofibrils Myofibrils consist of two kinds of proteins actin and myosin o Various bands in each sarcomere o A Band myosin o Z Band actin overlapping During cardiac contraction myosin actin interaction leads to the formation of cross bridges As myofibrils slide past one another force is generated Ca triggers and releases this activity Ca comes from action potential Anatomy of a Heartbeat Channel Openings During an Action Potential Phase 0 Fast upstroke o Triggers reach the threshold of Na channels o Na channels open causing rapid depolarization o Depolarization stops when the sodium channels inactivate o Sodium current is slowed by class IA and IC antiarrhythmic drugs Phase 1 Partial Repolarization o Na channels close o K channels open and start repolarization Phase 2 Plateau Phase o Ca channels open depolarization balances K channel repolarization o Class IV antiarrhythmic drugs shorten this phase o Currents balance each other Phase 3 Repolarization o Calcium channels close o K channels are still open and repolarize fiber making it more negative o Class IB drugs shorten this phase class III drugs lengthen it Phase 4 Forward Current o In pacemaker cells cells slowly depolarize source of automaticity o In pacemaker cells an increase in threshold lengthens this phase o This phrase corresponds to a quiet period diastole o In non pacemaker cells phase 4 is flat no repolarization o Ca that enters in Phase 2 is removed by mitochondria and by a protein that causes Na Ca exchange Pumps out Ca in exchange for bringing Na in o Na that enters in all other phases is removed by Na K ATP ase Contraction Terms and Definitions Systole a period of cardiac muscle contraction Diastole a period of cardiac muscle relaxation Frank Starling Law states that within physiological range the farther the muscle is stretched the greater the force of contraction Electrophysiological Properties Automaticity Pacemaker Cells the property of some cells to spontaneously depolarize phase 4 and to fire action potentials if threshold is reached Conductivity the property of cells to conduct action potentials in either direction also the rate at which action potentials propagate Refractoriness a period after an action potential that a cell cannot fire another a major reason why colliding action potentials cancel each other reset themselves so the channel can open again when depolarized Normal Conduction Path in the Heart SA Node fires action potentials causing atria to contract Atrial wall AV node Bundle of his AV bundle Purkinje fibers modified muscle cells that carry action potentials very quickly Ventricle myocardium squeeze blood out major pumping action A Normal Electrocardiogram P Wave depolarization of atria after there is a period of quiet where neither the atria or ventricles are contracting interval determines heart rate ARS Complex depolarization of ventricles and repolarization of atria T Wave repolarization of ventricles QT Interval ventricular contraction systole Autonomic Nervous System Control Parasympathetic stimulation vagal o Acetylcholine muscarinic receptors o Decreases depolarization rates in SA node and AV node o Decreases heart rate 60 min bradycardia Sympathetic o Norepinephrine B1 receptors o Epinephrine from adrenal medulla B1 receptors o Stimulates SA node AV node atrial and ventricular muscle o Increase in heart rate 100 min tachycardia o Increase force of myocardial contraction o Increase conduction velocity Heart Problems Inadequate oxygen delivery leads to myocardial ischemia angina heart attack myocardial infarction Cardiac failure congestive heart failure cardiac arrhythmia Hypertension Stage Prehypertension Mild Moderate Crisis Diastolic BP 80 mmHg 90 100 120 Systolic BP 120 mmHg 140 160 210 Effects a silent killer that exacerbates Atherosclerosis Coronary artery disease causes myocardial infarction Congestive heart failure Diabetes Leads to stroke cerebrovascular accidents Renal and retinal disease Causes of Hypertension Etiology Only 10 of hypertensive have increase BP due to identifiable disease o Patient usually feels okay 90 have essential hypertension cause unknown Mechanisms of Controlling Blood Pressure Arterial Blood Pressure CO x peripheral resistance Cardiac Output stroke volume x heart rate Stroke volume is dependent on filling pressure combination of blood volume and venous tone and heart contractility o Amount of blood squeezed out every beat Left ventricle pumps against diastolic pressure to get the blood out Higher number pressure it reaches when the ventricle is doing all the contraction Blood Pressure Heart Rate x Stroke Volume Cardiac Output Cardiac output heart rate contractility filling pressure Baroreceptor Reflex Rapidly acting in seconds Increase in blood pressure which stretches baroreceptor in carotid and aorta arch Sensory information processed by brainstem changing ANS system output o Increase in parasympathetic and or decrease in sympathetic o Decrease in heart rate o Increase in vasodilation However continued high blood pressure has less effect Decrease in blood pressure causes an increase in sympathetic nervous system releasing epinephrine adrenal medulla and NE sympathetic postganglionics NE increases A receptor activity vasoconstriction and peripheral resistance Epinephrine increases heart rate contractility and cardiac output Renin Angiotensin System Slower Renin angiotensin aldosterone Decrease in blood pressure and B adrenergic stimulation in kidney causing an increase in renin release Renin converts angiotensinogen to angiotensin I Angiotensin I is converted to angiotensin II by angiotensin converting enzyme ACE Angiotensin II causes o Increase in vasoconstriction increase peripheral resistance increase blood pressure o Increase in aldosterone secretion increase in Na and water retention increase blood volume cardiac output increase blood pressure Reflex Increase in Blood Pressure Regulation of blood pressure is abnormal in hypertension Treatment Strategies mild For hypertension changes in lifestyle may o Lower Na in diet increase exercise decrease alc and nicotine suffice consumption Drug classes used for hypertension o Diuretics o B blockers and A B blockers o ACE inhibitors o Angiotensin II receptor blockers o Ca channel blockers o A adrenergic blockers o