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80 Cards in this Set

  • Front
  • Back
Vm = membrane potential.(gNa)
is the symbol for Na+ conductance (the higher the conductance, the easier an ion moves across the cell membrane)
Heart-Electrical Activity
The ionic basis of the resting membrane potential of the heart is the____ as that for nerve or skeletal muscle.
resting state, K+ is _____ permeable than Na+ or Ca++.
Calcium is necessary for contraction of which types of muscle:
skeletal, smooth and cardiac
In cardiac and smooth muscle Ca+ must come for what source, intracellular or extra?
Ca++ in part must be supplied from extracellular sources.
Ca++ moves into the cell through ______ channels
calcium channels.
Some calcium channels are opened by which neurotransmitter?
channels are opened by neurotransmitters such as norepinephrine.
Drugs that cause vasodilation (relaxation) of blood vessels are called
afterload reducing drugs
afterload is the ______ blood pressure that the heart must overcome to pump blood.
drug that drops diastolic blood pressure will then reduce the _____ on the heart.
the afterload on the heart.
heart has specialized tissue that generates its own action potential. True or False
Sick Sinus Syndrome:
The cells of the SA node will stop firing for a number of seconds. It may take a few seconds before an ectopic site develops. The patients may lose consciousness.
Wolff-Parkinson White-Syndrome:
The syndrome is caused when a secondary conduction tract develops in the heart: the ventricles are depolarized sooner than normal (pre-excited)
Wolff-Parkinson White-Syndrome:
accessory fibers not only conduct the action potential or wave of conduction from the atrium to ventricle antigrade, but also from ventricle back to atrium (retrograde), thus setting up a loop conduction. This can cause a severe tachycardia
In order to get a contraction:
a wave of depolarization must spread through the muscle to initiate the process of contraction. Under normal conditions,
Under normal conditions depolarization wave is started by the:
SA node
normal electrocardiogram consists of a P wave: What depolarizies
caused by depolarization of the atria),
QRS complex: What depolarizies
(caused by depolarization of the ventricles)
T wave generated as a result of
the repolarization of the ventricles
QT interval is closely correlated with the
mean action potential and contraction of the ventricles
Why is Long QT dangerous during ventricular repolarization?
May cause eddies of current which can cause areas of depolarization leading to fibrillation and death
LQTS can be caused by
drugs, alcoholism and genetic mutations
Describe the mutations of ion channels that may lead to Long QT. 
potassium channels in heart muscle (outward movement of K+ to repolarize). a mutation of sodium channels causing them to stay open long after the cell is depolarized. Sodium continues to leak into the cell, delaying the end of the action potential. 
How does the Heart contract as an entire unit?
with gap junctions between each cell, the action potential moves over the entire muscle, thus the muscle functions as a syncytium. The action potential is coupled to the muscle contraction.
Metabolism of cardiac muscle (Basal)
Aerobic under basal condition and uses free fatty acids and lactate as primary substrates
What are the affects of Hypoxia on aerobic metabolism ?
metabolism is reduced and may approach 10%. metabolic energy is insufficient to sustain adequate function.
velocity and force of contraction are functions of free ____.
Ca++ ions.
Force and velocity are ______related.
So with no load, velocity is maximal but force is negligible.
Chemicals that affect and change contractility are called
inotropic agents
A change in end diastolic volume will lead to a change in muscle fiber length. This, in turn, will lead to a change in force of contraction
Frank-Starling's Law
Starling's Law of the heart. 
blood enters the right or left ventricle, muscle fibers are stretched. This increase will increase the force of contraction. More blood will be pumped, thus matching the amount of blood leaving the heart with that entering. This is Starling's Law of the heart. 
EDV increases more pressure is generated and more blood is pumped. What is represented in addition to EDV?
Fiber length can also be represented as end diastole volume (EDV)
SNS stimulation on the heart realeases more ____ -> binds to beta adrenergic recptors -> increased release of trigger the release of intracellular _______which increases contractility. 
ionized Ca++
isovolumic contraction
the ventricle is contracting with no volume change (pressure is increasing)
Stroke Volume
(End diastolic volume) - (end systolic volume) or the volume ejected for each heart beat (ml)
End Diastolic Volume
The volume of blood in the heart before ejection
End Systolic Volume
The volume remaining right after a contraction
Cardiac Output
The stroke volume X heart rate (ml/min)
Ejection Fraction
Stroke volume (SV)
End-diastolic volume (EDV)
· Pericarditis
(inflammation of pericardium) - causes - infections, trauma, neoplasm, metabolic, immunologic or vascular.
Hypertropic cardiomyopathy
is a disproportionate thickening of the interventricular septum. This thickening lends to a hyperdyamic state-increased contactiliy and ejection fraction. In severe cases this can lead to a decreased cardiac output.
Mitral Stenosis
A narrowing of the opening of valves between atrium and ventricle - Leaflets of valves fibrosis - incomplete emptying of atrium - Thus elevated atrial pressure - lends to a decreased cardiac output - can lend to pulmonary hypertension 
Aortic stenosis
- the opening of the valve narrows causing reduced blood flow to the aorta (this type problem develops slowly) - Decreased stroke volume causes reduced systolic blood pressure
(insufficiency) the valve leaflets fail to shut completely permitting blood to continue to back flow.
Mitral Regurgitation
- back flow from left ventricle - to atrium, the left ventricle becomes dilated and hypertrophies to maintain C.O
· Left ventricular failure - in general is caused by:
o Inappropriate work loads placed on the heart volume or pressure overload.
o Tissue damage, causing decreased contractility (possible cause myocardial infarction)
o Diastolic Dysfunction. Contractility is normal, however there is an increase in left ventricular end-diastolic pressure. Hypertension can change all or any of the three conditions leading to congestive failure: (1)decreased relaxation, (2)decreased elastic recoil, (3)increased stiffness of the ventricle
Right ventricular failure - in general is caused by:
Left failure can cause right heart failure because of increased afterload. In right heart failure both systolic and diastolic abnormalities can occur - causes are similar to left ventricular failure.
1.List and explain the four phases of the cardiac action potential.
Phase 0- rapid upstroke of the action potential (depolarization, before force develops)
Phase 1- early repolarization immediately following the upstroke
Phase 2- plateau following repolarization that last approx. 0.1-0.2 seconds
Phase 3- final repolarization
Phase 4- resting state of polarization (relaxation of the muscle)
2. What is the cause of over shock of the cardiac action potentials?
When the membrane potential reaches zero, an electrostatic force no longer exists to pull sodium into the cell, but it continues to move into the cell because of the high concentration gradient. The inside of the cell becomes more positive. The resulting change in membrane polarity is the overshoot.
3. How would Phase O be affected in a person that ate a puffer fish and was poisoned by tetrodotoxins? (Tetrodotoxins blocks Na+ channels)
TTX binds to the extracellular side of the sodium channel thus blocking the fast Na+ channels that exists in the cell membrane. This will in turn prevent influx of Na+ into the cardiac cell during phase 0. The result is a failure to neutralize the neg. charge inside the cell or in other words an inability to bring the cell to a threshold (make the cell less negative) that would generate an action potential.
4. What are the effects of the sympathetic nervous system on the generation of action potentials in the heart?
Sympathetic activation will increase HR and contractility. The sympathetic system (norepinephrine) works through β1-adrenergic receptors. β1-adrenergic stimulation works through a second messenger system (raises cAMP) to increase available Ca2+ in the cell.
What are the effects of the parasympathetic nervous system on the generation of action potentials in the heart?
Parasympathetic activation (via the Vagus nerve) will decrease HR. The parasympathetic system (ACh) uses muscarinic receptors to inhibit the cardiac pacemaker, and atrial conduction (it has very little effect on the ventricular system). This too is a second messenger system (decreases cAMP) and decreases intracellular Ca2+ concentration.
Which receptors are responsible for these changes in the SNS?
β1-adrenergic receptors
Which receptors are responsible for these changes in the PNS?
muscarinic receptors to inhibit the cardiac pacemaker
5. Explain the effect of catecholamines on the strength of contraction and heart rate in terms of changes in ionic currents.
Catecholamines increase the movement of Ca2+ into the cell by phosphorylation of the channels via cAMP-dependent protein kinase. In addition, catecholamines, like other agonists, enhance myocardial contractile force by increasing the sensitivity of the contractile machinery to Ca2+ or decreasing the Na+ gradient across the sarcolemma also results in an increase in the cytosolic concentrations of Ca2+.
How do Ca++ channel antagonists nifedipine and diltiazen affect cardiac contraction and firing frequency of the SA nodes?
The Ca2+ channel antagonists block Ca2+. These drugs decrease conductance of calcium and thereby impede the influx of Ca2+ into myocardial cells. The antagonists decrease the duration of the action potential plateau and diminish the strength of the cardiac contraction.
Lead I.
Right arm to left armThe right arm is connected to the negative terminal of the electrocardiograph, and the left arm to the positive terminal. When the right arm is negative to the left arm, the record shows an upward deflection. Thus, lead I measures the potential difference between the electrodes on the left and right arms, or across the base of the heart.
Lead II.
Right arm to left legThe right arm is connected to the negative terminal, and the left leg to the positive terminal. Thus, lead II measures the potential difference between the left leg and the right arm, or along the long axis of the heart from base to apex.
Lead III.
Left arm to left leg The left arm is connected to the negative terminal, and the left leg to the positive terminal. This combination allows lead III to measure the potential difference between the left leg and the left arm, or along the left side of the heart.The sinoatrial (SA) node initiates the cardiac impulse (epicardium in this area becomes negative first), and this wave of negativity sweeps over the heart
three unipolar leads known as the augmented leads. These three leads are referred to as
aVR (right arm), aVL (left arm) and aVF (left leg) and also record a change in electric potential in the frontal plane
What is meant by the terms preload and afterload?
Preload – end diastolic volume (resistance from the venous side of blood flow)
Afterload – increased aortic pressure on the ventricular cycle (arterial side)
List a pathological state in which preload would be above normal and one which afterload would be high.
Increased preload could be induced by Right ventricular failure; and an increased afterload could be induced by hypertension.
How would a change in fiber length (Frank-Starling's Law) affect cardiac output
The Frank Starling mechanism means that the greater the heart muscle is stretched during filling, the greater the force of contraction and the greater the quantity of blood pumped into the aorta.
Constrictive pericarditis can restrict ventricular filling. How could this effect CO?
Constrictive pericarditis (CP) is a reduction in compliance, or stiffening, of the sack surrounding the heart that results in impaired filling. Symptoms appear insidiously.
How would a change in contractility affect output (inotropic effect)?
Contractility defines the performance of the heart at a given preload and afterload. Contractility can be augmented by certain drugs, such as norepinephrine or digitalis, or by an increase in contraction frequency.
Dilated (congestive) cardiomyopathy - What would happen to contractility? stroke volumes? If stroke volume is decreased how would you plot this using the Frank-Starling Relationship?
As a result of extensive damage to myocardial muscle fibers, the ventricles become weak and dilated. Muscle contraction is impaired (decreased contractility) and the heart ejects blood less efficiently (decreased stroke volume).
The curve of the Frank-Starling graph will be dampened.
Hypertropic cardiomyopathy - If contractility and ejection fraction are increased, why is cardiac output decreased?
This disease is characterized by thickening of the myocardium, especially the interventricular septum and the free wall of the left ventricle. It causes impaired diastolic relaxation, which produces symptoms of heart failure even in the presence of a normal/high ejection fraction (caused by high filling pressures). Cardiac output is low when the thickening of the interventricular septum obstructs outflow from the mitral valve, worsening the outflow from the already narrowed left ventricular chamber.
Aortic stenosis - What would happen to cardiac output?
Cardiac output is comprised of heart rate and stroke volume. With a reduced stroke volume, the heart would try to compensate by increasing the heart rate; however, the ultimate effect would be a reduction in cardiac output.
Aortic Regurgitation - What is the mechanism that the heart uses to compensate for the increased volume and to maintain cardiac output?
The heart attempts to compensate for the decreased cardiac output by increasing both the rate and force of contraction. However, the incompetent aortic valve allows blood from the aorta to reenter the left ventricle during diastole, which increases the workload of the heart and can lead to CHF
Isometric relaxation:
Decrease in tension of a muscle while the length remains constant due to fixation of the ends.
Isotonic relaxation:
Relaxation (lengthening) of a muscle, the tension remaining constant. (Not sure if this is right)
Isovolumetric contraction:
Occurs where the muscle is prevented from shortening (increase in tension without change in length). Examining such preparations we find that when we "preload" the muscle (stretch it by adding weight before stimulation) then there is an increase in the tension that the muscle develops when stimulated. The time to development of peak tension remains the same, implying that the rate of tension development also increases as does the preload.
Action Potentials Spread from cell membrane into the
During Plateau of the AP, Ca+ conductance is increased and Ca+ enters the cell from the extracellular fluid (Inward Ca+ Current). Opening of the Ca+ channels is initiated by the phosphorylation of the channel proteins by .
camp dependent protein kinase
C. The Ca+ entry triggers the release of even more Ca+ from the SR (Ca+ induced Ca+ release)
-The amount of Ca+ released from the SR depends______ and on the size of the Inward current during the plateau of the AP
on the amount of Ca+ previously stored
As a result of this Ca+ release, Intracellular (Ca+) (increases or decreases)
E. Ca+ binds to Troponin C, and Tropomyosin is moved out of the way, removing the inhibition of the_________ binding
actin and myosin
F. Actin and Myosin bind, the thick and thin filimants slide past each other and the myocardial cells contract. The magnitude of the tension that develops is proportional to the
intracellular Ca+
Relaxation occurs when Ca+ is reaccumulated by the SR by an active Ca+-ATPase pump.
• If we have too little calcium available for the cardiac cycle then a decrease in force will exist and may lead to
to arrest of diastole
Increase in the amount of calcium will cause increase the force of contraction and may induce
cardiac arrest in systole