Flashcards
Heart and Circulation C
Flashcards do conjunto (169)
- 1nodal/ conducting cellscontract very weakly because they contain very few contractile elements (myofibrils).
- 2nodal/conducting cells are special cells that are able tospontaneously generate action potentials without the help of nervous input; also rapidly conduct the action potentials to atrial and ventricular muscle.
- 3where is the SA node locatedis located in the upper posterior wall of the right atrium
- 4What is the first area to spontaneously depolarize, producing an action potentialSA node
- 5pacemaker of the heartSA Node
- 6The action potentials travel through the_______ to the _____ ______atria;atrial-ventricular node (AV node)
- 7from the atrial-ventricular node (AV node) it travels to the bundle ___ ______Bundle of His.
- 8From the Bundle of His, the action potential travels through the __________ ______Purkinje Fibers
- 9from the Purkinje Fibers the action potential finally reaches the __________ _________ and leads to contractionthe ventricular muscle.
- 10Chronotropic effectsproduce changes in heart rate.
- 11A negative chronotropic effectdecreases heart rate by decreasing the firing rate of the SA node.
- 12A positive chronotropic effectincreases heart rate by increasing the firing rate of the SA node.
- 13Dromotropic effectsproduce changes in conduction velocity, primarily in the AV node.
- 14A negative dromotropic effect decreases conduction velocity through theAV node, slowing the conduction of action potentials from the atria to the ventricles and increasing the PR interval.
- 15A positive dromotropic effect increases conduction velocity through theAV node, speeding the conduction of action potentials from the atria to the ventricles and decreasing the PR interval.
- 16A negative inotropic decreasesforce of contraction, a positive inotropic effect increases force of contraction.
- 17At rest, a normal heart beats around 50 to 99 times a minute. T or FTrue
- 18ArrhythmiasIt results from abnormalities in impulse formation or in impulse conduction, Disturbances in the formation of impulses lead to change in the sinus rhythm.
- 19sinus tachycardiaIf sinus frequency rises above 100/min (exercise, psychic excitation, fever, rise of 10 beats/min.
- 20Sinus bradycardiaIf it drops below 50-60/min.
- 21Supraventricular arrhythmiadue to atrial or nodal extrasystole (ES); Abnormal or ectopic (heterotopic) impulses may arise in the atria (atrial), in the AV node (nodal) or in the ventricle (ventricular). The impulses from an atrial (or nodal) ectopic focus are transmitted to the ventricle, which thus thrown out of its sinus rhythm
- 22In atrial ES the_ ______ is deformed but the QRS complex is normal.P wave
- 23In nodal extrasystole, stimulation of the atria is retrograde;the P wave is thus negative and is either masked by the QRS wave or appears shortly after it T or FTrue
- 24in supraventricular extrasystole the sinus nodes often also depolarized or repolarizeddepolarized
- 25AutomaticityThis is the development of a new site of depolarization in nonnodal ventricular tissue, which can lead to a VPC
- 26Increased automaticity could be due toelectrolyte abnormalities or ischemic myocardium.
- 27Reentry circuitReentry typically occurs when slow-conducting tissue (eg, infarcted myocardium) is present adjacent to normal tissue.
- 28slow-conducting tissue could be due todamaged myocardium, as in the case of a healed MI.
- 29Ventricular premature complexes (VPCsectopic impulses originating from an area distal to the His Purkinje system.
- 30VPCs are the most common ventricular arrhythmia In this case the QRS complex of the extrasystole is deformed T or FTrue
- 31Premature ventricular contraction possible causesIschemia
Certain medicines such as digoxin, which increases heart contraction
Myocarditis
Cardiomyopathy hypertrophic or dilated
Hypoxia
Hypercapnia (CO2 poisoning)
Mitral valve prolapse
Smoking
Alcohol
Drugs such as cocaine
Caffeine
Magnesium and potassium deficiency
Calcium excess
Thyroid problems
Heart attack - 32ischemiaan inadequate blood supply to an organ or part of the body, especially the heart muscles.
- 33MyocarditisMyocarditis is an inflammation of the myocardium, the middle layer of the heart wall. Myocarditis is usually caused by a viral infection. Signs and symptoms of myocarditis include chest pain, heart failure and abnormal heart rhythms.
- 34hypertrophic Cardiomyopathyin which a portion of the myocardium is hypertrophied (thickened) without any obvious cause, creating functional impairment of the cardiac muscle
- 35Hypoxiadeficiency in the amount of oxygen reaching the tissues.
- 36Hypercapniaexcessive carbon dioxide in the bloodstream, typically caused by inadequate respiration.
- 37Mitral valve prolapseMitral valve prolapse (MVP) occurs when the valve between your heart's left upper chamber (left atrium) and the left lower chamber (left ventricle) doesn't close properly; the leaflets of the mitral valve bulge (prolapse) upward or back into the left atrium as the heart contracts.
- 38Premature ventricular contraction symptomsChest pain ; faint feeling ; fatigue; Hyperventilation (after exercise)
- 39Frequent episodes of continuous PVCs (Premature ventricular contractions) becomes a form ofof ventricular tachycardia
- 40ventricular tachycardiawhich is a rapid heartbeat, because there is an extra electrical impulse, causing an extra ventricular contraction.
- 41Treatment of Ventricular extrasystole (premature Ventricular Contraction (PVC)restoring the balance of magnesium, calcium and potassium within the body
- 42What are the Pharmacological Treatment of Ventricular extrasystoleClass 1 Agents Class 2 Agents Class 3 and Class 4
- 43Class 1 AgentsSodium channel blockers . Class I agents are grouped by what effect they have on the Na+ channel, and what effect they have on cardiac action potentials. Lidocaine, Phenytoin.
- 44lidocainemedication used to numb tissue in a specific area and to treat ventricular tachycardia
- 45Class 2 AgentsBeta blockers.
- 46how do Beta blockers workerThey act by blocking the effects of catecholamines at the β1-adrenergic receptors, thereby decreasing sympathetic activity on the heart. They decrease conduction through the AV node.
- 47Class II agents includeatenolol, propranolol, and metoprolol
- 48Class 3 AgentsBlock the potassium channels, thereby prolonging repolarization. Since these agents do not affect the sodium channel, conduction velocity is not decreased.
- 49an example of a class 3 agent issotalol
- 50Class IV agentsCalcium channel blockers.
- 51Calcium channel blockers.decrease conduction through the AV node, and shorten phase two (the plateau) of the cardiac action potential. They thus reduce the contractility of the heart, so may be inappropriate in heart failure.
- 52This class of pharmacological agents allow the body to retain adrenergic control of heart rate and contractility.Class IV agents Calcium channel blockers
- 53Class IV agents includeverapamil and diltiazem.
- 54Atrial tachycardiarhythm disturbance that arises in the atria. Heart rates during atrial tachycardia are highly variable, with a range of 100-250 beats per minute (bpm). The atrial rhythm is usually regular.
- 55Ventricular Tachycardiaresults from a rapid sequence of ectopic ventricular impulses. Beginning with ES;
- 56What is the bpm range for ventricular tachycardiarate between 120 and 250 beats per minute
- 57in ventricular tachycardia the Ventricular filling and cardiac outputdecrease and ventricular fibrillation can even ensue, that is a high frequency uncoordinated twitching of the myocardium. Unless treated the failure to eject blood can be just as dangerous as cardiac arrest.
- 58PR interval in the normal heart,0.12 to 0.20 second in duration
- 59damage to AV node causes slowing of impulse conduction and is reflected by changes in the PR interval. This is considered aAV node block.
- 60First degree AV node blockPR interval exceeds 0.20 second
- 61Second degree AV node blockwhen the AV node is damaged so severely that only one out of every two, three, or four atrial electrical waves can pass through to the ventricles.
- 62Third-degree, or complete, AV node blocknon of the atrial waves can pass through the AV node to the ventricles. Result is bradycardia.
- 63What are the are two principal types of myocardial cellscontractile cells conducting cells
- 64conducting cellsfeatures similar to nerve cells.
- 65contractile cellssimilar features to skeletal muscle cells
- 66The contractile cells of the heart containsame contractile proteins actin and myosin arranged in bundles of myofibrils surrounded by a sarcoplasmic reticulum.
- 67Contractile Cells differ from skeletal muscle byhaving only one nucleus but far
more ; one-third of
their volume is taken up by mitochondria. - 68Contractile Cells are extremely efficient at extractingoxygen
- 69contractile cells are joined byintercalated discs
- 70intercalated discs containcontain tight junctions that bind the cells together, while gap junctions allow for the movement of ions and ion currents between the myocardial cells.
- 71gap junctions allow myocardial cells of the heartto conduct action potentials from cell to cell without the need for nerves.
- 72Contractilityis the intrinsic ability of the cardiac muscle to develop force at a given muscle length
- 73inotropism is estimated bythe ejection fraction (stroke volume/end-diastolic volume), which is normally 0.55 (55%)
- 74Positive inotropic agents produce anincrease in contractility
- 75Negative inotropic agents producedecrease in contractility.
- 76Factors that increase contractility (positive inotropismIncreased heart rate
Sympathetic stimulation
Cardiac glycoides (digitalis) - 77what happens when the heart rate increasesmore action potentials occur at a time more Ca2+ enters the myocardial cells during the AP plateaus, more Ca2+ is released from the SR, and greater tension is produced during contraction.
- 78Sympathetic stimulation Increases the inwardCa2+ current during the plateau of each cardiac action potential; the Ca2+ pump of the SR as a result more Ca2+ is accumulated by the SR and thus more Ca2+ is available for release in subsequent beats.
- 79Factors that decrease contractility (negative inotropism)Parasympathetic (Ach) via muscarinic receptors
decrease the force of concentration in the atria by decreasing the inward Ca2+ current during the plateau of the cardiac action potential. - 80Heart murmursare generated by turbulent flow of blood, which may occur inside or outside the heart.
- 81physiological Murmursbenign
- 82pathological Murmurs(abnormal
- 83Abnormal murmurs can be caused byStenosis or Valve insufficiency
- 84Stenosisrestricting the opening of a heart valve, causing turbulence as blood flows through it.
- 85Valve insufficiencyallows backflow of blood when the incompetent valve is supposed to be closed.
- 86Causes and symptoms of atrial fluttermany types of heart disease
stress and anxiety
caffeine
alcohol
tobacco
diet pills
open heart surgery - 87Atrial fibrillation and flutterheart rhythms in which the atria are out of sync with the ventricles.
- 88atrial flutteratria beat regularly and faster than the ventricles.
- 89atrial fibrillationheart beat is completely irregular. The atrial muscles contract very quickly and irregularly; the ventricles beat irregularly but not as fast as the atria.
- 90When the atria fibrillates what happens with the bloodblood that is not completely pumped out can pool and form a clot.
- 91Atrial fibrillation may also result from anan inflammation of the heart's covering (pericarditis), chest trauma or surgery, pulmonary disease, and certain medications
- 92atherosclerosisplaque build up in medium and large arteries
- 93what is the plaque buildup in atherosclerosis made up ofcontain lipids, inflammatory cells, smooth muscle cells, and connective tissue.
- 94Which arteries are affected by atherosclerosiscoronary, carotid, and cerebral arteries, the aorta, its branches, and major arteries of the extremities
- 95what are the causes of atherosclerosisDyslipidemia, diabetes, cigarette smoking, family history, sedentary lifestyle, obesity, and hypertension Smoking
- 96symptoms of atherosclerosisShortness of breath Tightening pain in the chest
- 97complications of atherosclerosisStrokes Damage of muscles, body organs and blood vessels Deficiency of blood supply due to obstruction (angina)
- 98The hallmark of atherosclerosis isatherosclerotic plaque,
- 99atherosclerotic plaque containslipids (intracellular and extracellular cholesterol and phospholipids) inflammatory cells (eg, macrophages, T cells) smooth muscle cells connective tissue (eg, collagen, elastic fibers) thrombi Ca++ deposits.
- 100All stages of atherosclerosis—from initiation and growth to complication of the plaque—are considered aninflammatory response to . Endothelial injury is thought to have a primary role.
- 101Endothelial dysfunctioninhibits endothelial production of nitric oxide, a potent vasodilator and anti-inflammatory molecule.
- 102how are the plaques built in atherosclerosisis endothelial binding of monocytes and T cells, migration of these cells to the subendothelial space, and initiation and perpetuation of a local vascular inflammatory response. Monocytes in the subendothelium transform into macrophages.
- 103Preloadequivalent to end-diastolic volume, which is related to right atrial pressure
- 104When venous return increases, end-diastolic volume_________ and stretches or lengthens the ventricular muscle fibersincreases
- 105Afterloadfor the left ventricle is equivalent to aortic pressure
- 106For the left ventricle: Increases in aortic pressure cause an increase in afterload on the____ ventricle.left
- 107Afterload for the right ventricle is equivalent topulmonary artery pressure
- 108Increases in pulmonary artery pressure cause an increase in afterload on the ______ ventricleright
- 109Saromere lengthdetermines the maximum number of cross-bridges that can form between actin and myosin.
- 110Sarcomere length determines the maximum tension, or force of contraction
- 111Velocity of contraction is maximal when the afterload iszero.
- 112Velocity of contraction is decreased by increasesafterload
- 113Frank-Starling relationshipDescribes the increases in stroke volume and cardiac output that occur in response to an increase in venous return or end-diastolic volume.
- 114Frank-Starling relationship is based on thelength-tension relationship in the ventricle. Increases in end-diastolic volume cause an increase in ventricular fiber length, which produces an increase in developed tension.
- 115the mechanism that matches cardiac output to venous return. The greater the venous return, the greater the cardiac output.Frank-Starling relationship
- 116Increases in contractility cause an increase incardiac output for any level of right atrial pressure or end-diastolic volume.
- 117Decreases in contractility cause adecrease in cardiac output for any level of right atrial pressure or end-diastolic volume.
- 118Isovolumetric ventricular contraction is also known asventricular systole
- 119Isovolumetric ventricular contraction begins withthe ventricles depolarizing (QRS complex) then contracting.
- 120How are the ventricles filled during isovolumetric ventricular contractionThe left ventricle is filled with blood from the left atrium and its volume is about 140 ml (end-diastolic volume).
- 121The mitral valve closes when left ventricular pressure isis greater than left atrial pressure.
- 122What makes Step 1-2 Isovolumetricall valves are closed, no blood can be ejected from the ventricle
- 123Step 2-3 Ventricular Systoleejection period
- 124When does the aortic valve open during the cardiac cyclepoint 2 when pressure in the left ventricle exceeds pressure in the aorta
- 125Step 2-3 Blood is ejected into _____ and ventricular volume decreasesaorta
- 126. The volume that is ejected in ventricular systole isstroke volume
- 127The volume remaining in the left ventricle at point 3 isend-systolic volume.
- 128Step (3-4) is known asventricular diastole or isovolumetric relaxation phase
- 129At what point does the ventricle relaxAt point 3
- 130When ventricular pressure decreases to less than aortic pressure, the_____ valve closes.aortic
- 131Late ventricular diastole is known asventricular filling
- 132left ventricular pressure decreases to less than left atrial pressure, the valve opens and filling of the ventricle beginsmitral (AV)
- 133During what phase, ventricular volume increases to about 140 ml (the end-diastolic volume).Ventricular filling
- 134Increased preload refers toan increase in end-diastolic volume and is the result of increased venous return.
- 135Increased preload causes an increase in________ ________ base on the Frank-Starling relationshipstroke volume
- 136The increase in stroke volume is reflected in increasedwidth of the pressure-volume loop.
- 137Increased afterload refers to an increase inaortic pressure.
- 138in Increased after load The ventricle must eject blood against a higher pressure, resulting in adecrease in stroke volume.
- 139The decrease in stroke volume is reflected in _______ _______ of the pressure-volume loopdecreased width
- 140The decrease in stroke volume results in an _________ in end-systolic volume.increase
- 141. Increased contractilityventricle develops greater tension than usual during systole, causing an increase in stroke volume.
- 142The increase in SV results in a_____in end-systolic volume.decrease
- 143Stroke volumeis the volume ejected from the ventricle on each beat.
- 144How do you find the stroke volumeend diastole - end systolic volume
- 145How do you find the cardiac outputstroke volume times heart rate
- 146Ejection fraction is normally what percentage55 percent
- 147ejection fractionstroke volume/ end-diastolic volume
- 148Cardiac Oxygen consumption is directly relatedto the amount of tension developed by the ventricles.
- 149Cardiac oxygen consumption is increase byincreased afterload
increased size of the heart
increased contractility
increased heart rate - 150In order for blood to be ejected from the heart, the pressure in the ventricles must begreater than the pressure in the aorta
- 151When the pressure in the left ventricle rises above 80 mmHg, the aortic valve opens.
- 152What is the pressure in the aorta80mmhg
- 153When the aortic valve open and receives blood the pressure increases to120 mmHg
- 154ejection periodThe period during which the ventricles empty blood into the aorta i
- 155The first heart sound is produced by the closure of theAV valve
- 156The second heart sound is produced by the closing ofaortic and pulmonary semilunar valves;
- 157third heart sound sometimes occurs in the middle of diastole T or FTrue
- 158What is the third heart sound caused byThis is caused by blood flowing with rumbling motion into the almost filled ventricles
- 159What is cardiac outputthe amount of blood each ventricle can pump in one minute
- 160At rest the cardiac output is5 liters a min
- 161during vigorous exercise it can increase up to20 liters a min
- 162stroke volume (SV) is the amount of blood pumped byone ventricle during one contraction/heartbeat.
- 163resting heart rate is70 beats per minute
- 164Which nervous system controls the heart rate and the force of contractionautonomic nervous system
- 165the heart is innervated byparasympathetic nervous system (PSYN) and the sympathetic nervous system (SYN).
- 166parasympathetic nerves are distributed mainly toSA and AV nodes and to a lesser extent to atrial and ventricular muscles.
- 167Sympathetic nerves are distributedSA and AV nodes, atrial muscle but with a stronger innervation to the ventricular muscle.
- 168parasympathetic nervous system will decrease heart rate byaffecting both the SA node and AV node and will (to a lesser extent) decrease the force of contraction of the heart.
- 169sympathetic nervous system ________ heart rate and force of contraction.increase