Download Functions of the Heart

Functions of the Heart
The Heart
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The heart functions as a pump supplying blood
to every cell in the body. The heart is an
adaptable pump. The heart alters its pumping
activity to meet the demands of physiologic
functions; eating, exercise, and responding to
changes n environmental temperature; it also
adapts for disease.
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How does the heart know when to beat faster,
slower, weaker or stronger?
Cardiac Cycle
Cardiac cycle is a sequence of events that occurs during one
heart beat. Coordinated contraction and relaxation of the
chambers of the heart
Systole - coordinated contraction of the myocardium - when
blood is pumped out of the chamber
Diastole - relaxation of the myocardium, when blood is
filling the chambers
The relationship between the atria and the ventricle is
coordinated - when the atria contract (systole) the ventricles
are relaxed (diastole) allowing blood to fill the ventricular
chambers...note the stages to cardiac cycle...
Stages to cardiac Cycle
Atrial systole:
atria contract and pump blood into the ventricles
AV valves are open and the ventricles are relaxed
Ventricular systole: at the end of atrial systole
ventricles contract - pump blood... forcing AV valve closure, pushes open
semilunar valve...blood flows into the aorta and pulmonary artery
Diastole: atria and ventricles are relaxed (diastole), “period of filling”
blood flows into the atria
AV valves are open allowing much of the blood to flow passively into the
ventricles
Atrial systole follows...
With heart rate of 70 beats per minute, the duration of the cardiac cycle is 0.8
seconds
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all chambers rest for 0.4 seconds
Increase in heart rate, cardiac cycle shortens...
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period of rest shortens...may compromise cardiac function...
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decreased filling time, less blood enters the chambers...less blood is
pumped out
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coronary blood flow to the myocardium is decreased because coronary
blood flow happens during diastole...diminished diastole=diminished
coronary blood flow
Autonomic control of the
heart
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ANS (autonomic nervous system) plays an important role in
coordinating and adapting cardiac function
We know:
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cardiac tissue displays automaticity and rhythmicity - electrical
signal arises within the cardiac cells and spreads throughout the
heart
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ANS does not cause the cardiac impulse...it affects the rate in which
the impulse is fired and the speed it travels throughout the heart
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ANS can make the heart muscle contract more forcefully
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EX the ANS kicks in when a person suddenly starts to sprint
down the street - heart rate increases and force of contraction
increases in order to meet the demands for more oxygen
ANS wiring
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We know:
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ANS has two branches; sympathetic (fight or flight) and parasympathetic
(breed and feed)
Sympathetic nerves supply:
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SA node
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AV node
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Ventricular myocardium
Parasympathetic nerves (vagus nerve) supply:
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SA node
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AV node
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Does not supply the ventricular myocardium
Autonomic firing
Sympathetic nervous system
Sympathetic stimulation:
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increases SA node activity - increases heart rate
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increases speed of cardiac impulse travel from SA node throughout His-purkinje system
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increases force of myocardial contraction
Excess sympathetic stimulation - clinically important:
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produces fight or flight response in which a person will feel a racing, pounding heart - usually associated
with panic or anxiety
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play a key role in some disease states...s/s of cardiogenic shock are due to excessive sympathetic firing
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EX - pt with heart failure deteriorate quickly with excess sympathetic firing and usually receive
medications aimed at minimizing the effects
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produces tachydysrhythmias - fast, irregular heart rhythms
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treatment:
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sympathomimetic - medication that mimic the effects of sympathetic stimulus (adrenalin,
dopamine) - increase heart rate an myocardial contractile force
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sympatholytic - medication that produce effects that are similar to an inhibition of the sympathetic
nervous system (clonidine)
Autonomic firing
parasympathetic nervous system
Parasympathetic (vagus nerve) stimulation:
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Decreases SA node activity - decreases heart rate
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Decreases speed of cardiac impulse from SA node to the AV node
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Exerts n effect on the strength of myocardial contraction (no parasympathetic innervation)
Clinical importance:
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in the resting heart - vagal tone is more intense than sympathetic activity... SA node wants to fire at 90
beats per minute...however the parasympathetic inhibiting effect of the vagus nerve slows SA node firing to
a rate of 72 beats per minute..if the vagus nerve was interrupted...the heart rate would jump to 90 beats per
minute
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Certain drugs (digoxin) and certain conditions (MI) can cause excess vagal (parasympathetic)
discharge...causes bradycardia (slow heart rate) which increases the tendency for life-threatening electrical
rhythm disturbance. There can also be an effect on the travel time, conduction of the cardiac impulse
through the heart causing a block.
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treatment:
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vagomimetic (parasympathomimetic) - medications that mimic the effects of vagal stimulation
(digoxin) - slows the heart rate and slows the conduction of the cardiac impulse through the heart
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vagolytic (parasympatholytic) - medications that produce effects that are similar to an inhibition of
vagal discharge (atropine) - blocks the effects of the vagus nerve and increases heart rate
Cardiac Output
CO = HR X SV
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Cardiac output is the amount of blood pumped
by each ventricle in 1 minute
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normal cardiac output is 5 L per minute
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total blood volume is 5 L = entire blood volume
is pumped through the heart each minute
2 factors determine cardiac output...
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Heart rate
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Stroke volume
Heart rate...
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Heart rate is the number of times the
heart beats each minute
Heart rate is due to the rhythmic
firing of the SA node
Normal adult resting heart rate is
(60-100) beats per minute, average =
72 bpm
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Age - younger the person, faster the heart rate
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Adult - 60-100 bpm
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Child - 100 bpm
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Infant - 120 bpm
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Fetal - 140 bpm Exercise -
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Stimulation of ANS – stimulation of sympathetic
nerve increases HR, stimulation of the parasympathetic
nerve decreases HR.
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Hormonal influence - Epinephrine,norepinephrine
(adrenal gland), thyroid hormones increase heart rate
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Pathology - fever, MI
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Mediations - digoxin (slows), epinephrine,
Heart rates differ for many reasons:
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Size - larger the size, slower the
rate
Gender - women have faster heart
rates than men
dopamine(increase), caffeine (increase),
Stroke Volume
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Stroke volume is the amount of blood pumped by the
ventricle per beat
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Average stroke volume is 60-80 ml per beat
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At rest, ventricles pump out only 67% of blood in the
ventricles...
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If the ventricles were made to pump more
forcefully...stroke volume could be increased.
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CO = HR X SV
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Cardiac output = heart rate X stroke volume
Changes to Stroke
Volume
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Stroke volume can be changed in 2 ways:
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Starling’s Law of the heart - depends on the degree of stretch!
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the greater the stretch, the stronger the force of contraction
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increase in the amount of blood entering the ventricles causes the ventricle to
stretch...stretch increases force of contraction...increases stroke volume
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decrease in the amount of blood entering the ventricles causes less
stretch...force of contraction decreases...decreasing stroke volume
Inotropic Effect - changing myocardial contraction w/o stretching the
myocardial fibers
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stimulation of the sympathetic nerves causes a (+) inotropic effect
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decreasing the force of contraction, weaker myocardial contraction
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Medications can cause either a (+) inotropic effect (digoxin,epinephrine) or a
(-) inotropic effect
Heart Talk...
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End diastolic volume (EDV) - amount of blood in the ventricle at the end of its resting phase (diastole)
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Preload - amount of blood in the ventricles at the end of diastole (same as EDV)
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increase in preload...stretches the ventricles...stronger force of contraction...increases stroke volume...increases cardiac
output
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Medications: vasodilators...decreases amount of blood returning to heart...decreases amount of blood filling
ventricles...decreases preload(EDV), stroke volume and cardiac output
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Medications: vasoconstrictors...increase amount of blood returning to heart...increases preload (EDV) increases stroke
volume and cardiac output
Ejection Fraction - the percentage of EDV that is pumped out of the ventricle...we know that the ventricle pumps about 67%
of the EDV
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EF (ejection fraction) is an indicator of cardiac health
Afterload - refers to resistance or opposition
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in order for the ventricle to pump out the blood it needs to push against blood that is already in the aorta/pulmonary artery
- the aortic/pulmonary arterial blood pressure is the afterload (resistance)
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Conditions: HTN, aortic stenosis - indicative of an increase in afterload demanding the left ventricle to work harder to
overcome resistance ---untreated... left ventricle is working too hard...ventricular hypertrophy will occur...pump failure!
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Conditions: pulmonary arterial hypertension(emphysema, COPD, asthma) - indicative of an increase in afterload of the
right ventricle demanding the right ventricle to work against increased resistance ...causing right ventricular
hypertrophy...right pump failure
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Cor Pulmonale - condition of pulmonary hypertension and right ventricular hypertrophy
Heart Talk...
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Inotropic effect - change in myocardial contraction that is not due to stretch
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(+)inotropic effect - increases force of contraction EX digoxin
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(-) inotropic effect - decreases force of contraction
Chronotropic effect - change in heart rate
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(+) chronotropic effect - heart rate is increased EX sympathetic nerve stimulus
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(-) chronotropic effect - hear rate is decreased EX parasympathetic nerve stimulus
Dromotropic effect - change in the speed that the cardiac impulse travels from the
SA node through the AV node and the His-purkinje system
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(+) dromotropic effect - increased the speed of the impulse
sympathetic nerve stimulation
EX
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(-) dromotropic effect - decreased the speed of the impulse
vagal stimuation
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Heart Talk: Receptor Language
Beta 1 - adrenergic receptors
Beta 1- adrenergic receptor activation
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Sympathomimetic effect...
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We know... that sympathetic nerves innervate the SA node, AV node, His-purkinje system and
ventricular myocardium...
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Neurotransmitter of the adrenergic neuron is norepinephrine (NE) Adrenergic neuron of the
heart is called beta 1- adrenergic receptors
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Activation of the beta 1 - adrenergic receptor causes a (+) chronotropic effect, (+) dromotropic
effect, and (+) inotropic effect
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Medications that activate the beta 1 - adrenergic receptors are called beta 1- adrenergic agonist (
dopamine, epinephrine)
Beta 1 - adrenergic receptor blockade - prevents cardiac beta 1- adrenergic receptor
activation
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sympatholytic effect...
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heart rate will not increase despite firing of the sympathetic nerves
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Medications such as propanolol can decrease heart rate and force of contraction resulting in
decreased cardiac output
Heart Talk: Receptor language
Muscarinic (cholinergic) receptor activation
Muscarinic (cholinergic) receptor activation:
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Parasympathomimetic effect...
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We know...that parasympathetic (vagus) nerves supply only the SA node and the AV node
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Neurotransmitter for the cholinergic receptor is acetylcholine (ACh)
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Cholinergic receptors of the heart are called muscarinic receptors
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Activation of the muscarinic receptors causes a (-) chronotropic effect and (-) dromotropic
effect only! There is no effect on contractility because there is no parasympathetic
innervation to the ventricular myocardium
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Medications that activate the muscarinic receptors are called cholinergic (muscarinic)
agonist which cause a (-) dromotropic effect and a (-) chronotropic effect
Muscarinic (cholinergic) receptor blockade:
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Parasympatholytic effect...
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Medications act by by blocking the effects of ACh at the muscarinic receptor, increasing
heart rate and increasing the speed of cardiac impulse from the atria to the ventricles
EX atropine is a drug often used to treat bradycardia
The Failing Heart
Left heart failure
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Left Heart Failure - when the left ventricle fails to pump blood into the aorta
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Blood backs up in the lungs
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Heart is unable to pump a sufficient amount of blood to the systemic circulation
Backward Failure - when blood backs up into the structure behind the left
ventricle...left atrium, pulmonary veins, pulmonary capillaries
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pulmonary edema - presence of fluid in the lungs which impairs oxygenation of
blood
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S/S of pulmonary edema - exertional SOB, dyspnea (shortness of breath),
cyanosis (bluish appearance), blood-tinged sputum, cough, orthopnea (inability
to breathe lying down), tachycardia
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Treatment: (+) inotropic agents (digoxin, dopamine) NO MUD
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Nitroglycerin, oxygen,morphine, upright position, diuretic
Forward Failure - inadequate amount of blood pumped to the systemic circulation,
all organs of the body are being deprived of oxygenated blood
The Failing Heart
right heart failure
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Blood backs up behind the failed right ventricle,
causing jugular vein distention, hepatomegaly,
splenomegaly, digestive problems, and ankle
edema.
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Heart failure is also described as backward heart
failure and forward heart failure.
Goals of Treatment of
heart failure
Disorders of the Heart
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Angina Pectoris
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Cardiac dysrhythmias
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Congenital heart defects
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CAD (coronary artery disease)
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MI (myocardial infarction)
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Inflammation of the heart
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Valvular heart disease