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Flashcards by tiwariashley, updated more than 1 year ago
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Created by tiwariashley
over 8 years ago
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| Question | Answer |
| nodal/ conducting cells | contract very weakly because they contain very few contractile elements (myofibrils). |
| nodal/conducting cells are special cells that are able to | spontaneously generate action potentials without the help of nervous input; also rapidly conduct the action potentials to atrial and ventricular muscle. |
| where is the SA node located | is located in the upper posterior wall of the right atrium |
| What is the first area to spontaneously depolarize, producing an action potential | SA node |
| pacemaker of the heart | SA Node |
| The action potentials travel through the_______ to the _____ ______ | atria;atrial-ventricular node (AV node) |
| from the atrial-ventricular node (AV node) it travels to the bundle ___ ______ | Bundle of His. |
| From the Bundle of His, the action potential travels through the __________ ______ | Purkinje Fibers |
| from the Purkinje Fibers the action potential finally reaches the __________ _________ and leads to contraction | the ventricular muscle. |
| Chronotropic effects | produce changes in heart rate. |
| A negative chronotropic effect | decreases heart rate by decreasing the firing rate of the SA node. |
| A positive chronotropic effect | increases heart rate by increasing the firing rate of the SA node. |
| Dromotropic effects | produce changes in conduction velocity, primarily in the AV node. |
| A negative dromotropic effect decreases conduction velocity through the | AV node, slowing the conduction of action potentials from the atria to the ventricles and increasing the PR interval. |
| A positive dromotropic effect increases conduction velocity through the | AV node, speeding the conduction of action potentials from the atria to the ventricles and decreasing the PR interval. |
| A negative inotropic decreases | force of contraction, a positive inotropic effect increases force of contraction. |
| At rest, a normal heart beats around 50 to 99 times a minute. T or F | True |
| Arrhythmias | It results from abnormalities in impulse formation or in impulse conduction, Disturbances in the formation of impulses lead to change in the sinus rhythm. |
| sinus tachycardia | If sinus frequency rises above 100/min (exercise, psychic excitation, fever, rise of 10 beats/min. |
| Sinus bradycardia | If it drops below 50-60/min. |
| Supraventricular arrhythmia | due 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 |
| In atrial ES the_ ______ is deformed but the QRS complex is normal. | P wave |
| In 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 F | True |
| in supraventricular extrasystole the sinus nodes often also depolarized or repolarized | depolarized |
| Automaticity | This is the development of a new site of depolarization in nonnodal ventricular tissue, which can lead to a VPC |
| Increased automaticity could be due to | electrolyte abnormalities or ischemic myocardium. |
| Reentry circuit | Reentry typically occurs when slow-conducting tissue (eg, infarcted myocardium) is present adjacent to normal tissue. |
| slow-conducting tissue could be due to | damaged myocardium, as in the case of a healed MI. |
| Ventricular premature complexes (VPCs | ectopic impulses originating from an area distal to the His Purkinje system. |
| VPCs are the most common ventricular arrhythmia In this case the QRS complex of the extrasystole is deformed T or F | True |
| Premature ventricular contraction possible causes | Ischemia 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 |
| ischemia | an inadequate blood supply to an organ or part of the body, especially the heart muscles. |
| Myocarditis | Myocarditis 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. |
| hypertrophic Cardiomyopathy | in which a portion of the myocardium is hypertrophied (thickened) without any obvious cause, creating functional impairment of the cardiac muscle |
| Hypoxia | deficiency in the amount of oxygen reaching the tissues. |
| Hypercapnia | excessive carbon dioxide in the bloodstream, typically caused by inadequate respiration. |
| Mitral valve prolapse | Mitral 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. |
| Premature ventricular contraction symptoms | Chest pain ; faint feeling ; fatigue; Hyperventilation (after exercise) |
| Frequent episodes of continuous PVCs (Premature ventricular contractions) becomes a form of | of ventricular tachycardia |
| ventricular tachycardia | which is a rapid heartbeat, because there is an extra electrical impulse, causing an extra ventricular contraction. |
| Treatment of Ventricular extrasystole (premature Ventricular Contraction (PVC) | restoring the balance of magnesium, calcium and potassium within the body |
| What are the Pharmacological Treatment of Ventricular extrasystole | Class 1 Agents Class 2 Agents Class 3 and Class 4 |
| Class 1 Agents | Sodium 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. |
| lidocaine | medication used to numb tissue in a specific area and to treat ventricular tachycardia |
| Class 2 Agents | Beta blockers. |
| how do Beta blockers worker | They 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. |
| Class II agents include | atenolol, propranolol, and metoprolol |
| Class 3 Agents | Block the potassium channels, thereby prolonging repolarization. Since these agents do not affect the sodium channel, conduction velocity is not decreased. |
| an example of a class 3 agent is | sotalol |
| Class IV agents | Calcium channel blockers. |
| Calcium 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. |
| This class of pharmacological agents allow the body to retain adrenergic control of heart rate and contractility. | Class IV agents Calcium channel blockers |
| Class IV agents include | verapamil and diltiazem. |
| Atrial tachycardia | rhythm 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. |
| Ventricular Tachycardia | results from a rapid sequence of ectopic ventricular impulses. Beginning with ES; |
| What is the bpm range for ventricular tachycardia | rate between 120 and 250 beats per minute |
| in ventricular tachycardia the Ventricular filling and cardiac output | decrease 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. |
| PR interval in the normal heart, | 0.12 to 0.20 second in duration |
| damage to AV node causes slowing of impulse conduction and is reflected by changes in the PR interval. This is considered a | AV node block. |
| First degree AV node block | PR interval exceeds 0.20 second |
| Second degree AV node block | when 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. |
| Third-degree, or complete, AV node block | non of the atrial waves can pass through the AV node to the ventricles. Result is bradycardia. |
| What are the are two principal types of myocardial cells | contractile cells conducting cells |
| conducting cells | features similar to nerve cells. |
| contractile cells | similar features to skeletal muscle cells |
| The contractile cells of the heart contain | same contractile proteins actin and myosin arranged in bundles of myofibrils surrounded by a sarcoplasmic reticulum. |
| Contractile Cells differ from skeletal muscle by | having only one nucleus but far more ; one-third of their volume is taken up by mitochondria. |
| Contractile Cells are extremely efficient at extracting | oxygen |
| contractile cells are joined by | intercalated discs |
| intercalated discs contain | contain tight junctions that bind the cells together, while gap junctions allow for the movement of ions and ion currents between the myocardial cells. |
| gap junctions allow myocardial cells of the heart | to conduct action potentials from cell to cell without the need for nerves. |
| Contractility | is the intrinsic ability of the cardiac muscle to develop force at a given muscle length |
| inotropism is estimated by | the ejection fraction (stroke volume/end-diastolic volume), which is normally 0.55 (55%) |
| Positive inotropic agents produce an | increase in contractility |
| Negative inotropic agents produce | decrease in contractility. |
| Factors that increase contractility (positive inotropism | Increased heart rate Sympathetic stimulation Cardiac glycoides (digitalis) |
| what happens when the heart rate increases | more 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. |
| Sympathetic stimulation Increases the inward | Ca2+ 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. |
| Factors 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. |
| Heart murmurs | are generated by turbulent flow of blood, which may occur inside or outside the heart. |
| physiological Murmurs | benign |
| pathological Murmurs | (abnormal |
| Abnormal murmurs can be caused by | Stenosis or Valve insufficiency |
| Stenosis | restricting the opening of a heart valve, causing turbulence as blood flows through it. |
| Valve insufficiency | allows backflow of blood when the incompetent valve is supposed to be closed. |
| Causes and symptoms of atrial flutter | many types of heart disease stress and anxiety caffeine alcohol tobacco diet pills open heart surgery |
| Atrial fibrillation and flutter | heart rhythms in which the atria are out of sync with the ventricles. |
| atrial flutter | atria beat regularly and faster than the ventricles. |
| atrial fibrillation | heart beat is completely irregular. The atrial muscles contract very quickly and irregularly; the ventricles beat irregularly but not as fast as the atria. |
| When the atria fibrillates what happens with the blood | blood that is not completely pumped out can pool and form a clot. |
| Atrial fibrillation may also result from an | an inflammation of the heart's covering (pericarditis), chest trauma or surgery, pulmonary disease, and certain medications |
| atherosclerosis | plaque build up in medium and large arteries |
| what is the plaque buildup in atherosclerosis made up of | contain lipids, inflammatory cells, smooth muscle cells, and connective tissue. |
| Which arteries are affected by atherosclerosis | coronary, carotid, and cerebral arteries, the aorta, its branches, and major arteries of the extremities |
| what are the causes of atherosclerosis | Dyslipidemia, diabetes, cigarette smoking, family history, sedentary lifestyle, obesity, and hypertension Smoking |
| symptoms of atherosclerosis | Shortness of breath Tightening pain in the chest |
| complications of atherosclerosis | Strokes Damage of muscles, body organs and blood vessels Deficiency of blood supply due to obstruction (angina) |
| The hallmark of atherosclerosis is | atherosclerotic plaque, |
| atherosclerotic plaque contains | lipids (intracellular and extracellular cholesterol and phospholipids) inflammatory cells (eg, macrophages, T cells) smooth muscle cells connective tissue (eg, collagen, elastic fibers) thrombi Ca++ deposits. |
| All stages of atherosclerosis—from initiation and growth to complication of the plaque—are considered an | inflammatory response to . Endothelial injury is thought to have a primary role. |
| Endothelial dysfunction | inhibits endothelial production of nitric oxide, a potent vasodilator and anti-inflammatory molecule. |
| how are the plaques built in atherosclerosis | is 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. |
| Preload | equivalent to end-diastolic volume, which is related to right atrial pressure |
| When venous return increases, end-diastolic volume_________ and stretches or lengthens the ventricular muscle fibers | increases |
| Afterload | for the left ventricle is equivalent to aortic pressure |
| For the left ventricle: Increases in aortic pressure cause an increase in afterload on the____ ventricle. | left |
| Afterload for the right ventricle is equivalent to | pulmonary artery pressure |
| Increases in pulmonary artery pressure cause an increase in afterload on the ______ ventricle | right |
| Saromere length | determines the maximum number of cross-bridges that can form between actin and myosin. |
| Sarcomere length determines the maximum t | ension, or force of contraction |
| Velocity of contraction is maximal when the afterload is | zero. |
| Velocity of contraction is decreased by increases | afterload |
| Frank-Starling relationship | Describes the increases in stroke volume and cardiac output that occur in response to an increase in venous return or end-diastolic volume. |
| Frank-Starling relationship is based on the | length-tension relationship in the ventricle. Increases in end-diastolic volume cause an increase in ventricular fiber length, which produces an increase in developed tension. |
| the mechanism that matches cardiac output to venous return. The greater the venous return, the greater the cardiac output. | Frank-Starling relationship |
| Increases in contractility cause an increase in | cardiac output for any level of right atrial pressure or end-diastolic volume. |
| Decreases in contractility cause a | decrease in cardiac output for any level of right atrial pressure or end-diastolic volume. |
| Isovolumetric ventricular contraction is also known as | ventricular systole |
| Isovolumetric ventricular contraction begins with | the ventricles depolarizing (QRS complex) then contracting. |
| How are the ventricles filled during isovolumetric ventricular contraction | The left ventricle is filled with blood from the left atrium and its volume is about 140 ml (end-diastolic volume). |
| The mitral valve closes when left ventricular pressure is | is greater than left atrial pressure. |
| What makes Step 1-2 Isovolumetric | all valves are closed, no blood can be ejected from the ventricle |
| Step 2-3 Ventricular Systole | ejection period |
| When does the aortic valve open during the cardiac cycle | point 2 when pressure in the left ventricle exceeds pressure in the aorta |
| Step 2-3 Blood is ejected into _____ and ventricular volume decreases | aorta |
| . The volume that is ejected in ventricular systole is | stroke volume |
| The volume remaining in the left ventricle at point 3 is | end-systolic volume. |
| Step (3-4) is known as | ventricular diastole or isovolumetric relaxation phase |
| At what point does the ventricle relax | At point 3 |
| When ventricular pressure decreases to less than aortic pressure, the_____ valve closes. | aortic |
| Late ventricular diastole is known as | ventricular filling |
| left ventricular pressure decreases to less than left atrial pressure, the valve opens and filling of the ventricle begins | mitral (AV) |
| During what phase, ventricular volume increases to about 140 ml (the end-diastolic volume). | Ventricular filling |
| Increased preload refers to | an increase in end-diastolic volume and is the result of increased venous return. |
| Increased preload causes an increase in________ ________ base on the Frank-Starling relationship | stroke volume |
| The increase in stroke volume is reflected in increased | width of the pressure-volume loop. |
| Increased afterload refers to an increase in | aortic pressure. |
| in Increased after load The ventricle must eject blood against a higher pressure, resulting in a | decrease in stroke volume. |
| The decrease in stroke volume is reflected in _______ _______ of the pressure-volume loop | decreased width |
| The decrease in stroke volume results in an _________ in end-systolic volume. | increase |
| . Increased contractility | ventricle develops greater tension than usual during systole, causing an increase in stroke volume. |
| The increase in SV results in a_____in end-systolic volume. | decrease |
| Stroke volume | is the volume ejected from the ventricle on each beat. |
| How do you find the stroke volume | end diastole - end systolic volume |
| How do you find the cardiac output | stroke volume times heart rate |
| Ejection fraction is normally what percentage | 55 percent |
| ejection fraction | stroke volume/ end-diastolic volume |
| Cardiac Oxygen consumption is directly related | to the amount of tension developed by the ventricles. |
| Cardiac oxygen consumption is increase by | increased afterload increased size of the heart increased contractility increased heart rate |
| In order for blood to be ejected from the heart, the pressure in the ventricles must be | greater than the pressure in the aorta |
| When the pressure in the left ventricle rises above 80 mmHg | , the aortic valve opens. |
| What is the pressure in the aorta | 80mmhg |
| When the aortic valve open and receives blood the pressure increases to | 120 mmHg |
| ejection period | The period during which the ventricles empty blood into the aorta i |
| The first heart sound is produced by the closure of the | AV valve |
| The second heart sound is produced by the closing of | aortic and pulmonary semilunar valves; |
| third heart sound sometimes occurs in the middle of diastole T or F | True |
| What is the third heart sound caused by | This is caused by blood flowing with rumbling motion into the almost filled ventricles |
| What is cardiac output | the amount of blood each ventricle can pump in one minute |
| At rest the cardiac output is | 5 liters a min |
| during vigorous exercise it can increase up to | 20 liters a min |
| stroke volume (SV) is the amount of blood pumped by | one ventricle during one contraction/heartbeat. |
| resting heart rate is | 70 beats per minute |
| Which nervous system controls the heart rate and the force of contraction | autonomic nervous system |
| the heart is innervated by | parasympathetic nervous system (PSYN) and the sympathetic nervous system (SYN). |
| parasympathetic nerves are distributed mainly to | SA and AV nodes and to a lesser extent to atrial and ventricular muscles. |
| Sympathetic nerves are distributed | SA and AV nodes, atrial muscle but with a stronger innervation to the ventricular muscle. |
| parasympathetic nervous system will decrease heart rate by | affecting both the SA node and AV node and will (to a lesser extent) decrease the force of contraction of the heart. |
| sympathetic nervous system ________ heart rate and force of contraction. | increase |
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