Heart and Circulation C

Frage	Antworten
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 cellsconnective tissue (eg, collagen, elastic fibers)thrombiCa++ 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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Heart and Circulation C

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