Chapter 17

Functions of the Heart

The Heart• 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.

• How does the heart know when to beat faster, slower, weaker or stronger?

Cardiac CycleCardiac 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 CycleAtrial 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

• all chambers rest for 0.4 seconds

• Increase in heart rate, cardiac cycle shortens...

• period of rest shortens...may compromise cardiac function...

• decreased filling time, less blood enters the chambers...less blood is pumped out

• 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

• ANS (autonomic nervous system) plays an important role in coordinating and adapting cardiac function

• We know:

• cardiac tissue displays automaticity and rhythmicity - electrical signal arises within the cardiac cells and spreads throughout the heart

• 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

• ANS can make the heart muscle contract more forcefully

• 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• We know:

• ANS has two branches; sympathetic (fight or flight) and parasympathetic (breed and feed)

• Sympathetic nerves supply:

• SA node

• AV node

• Ventricular myocardium

• Parasympathetic nerves (vagus nerve) supply:

• SA node

• AV node

• Does not supply the ventricular myocardium

Autonomic firingSympathetic nervous system

• Sympathetic stimulation:

• increases SA node activity - increases heart rate

• increases speed of cardiac impulse travel from SA node throughout His-purkinje system

• increases force of myocardial contraction

• Excess sympathetic stimulation - clinically important:

• produces fight or flight response in which a person will feel a racing, pounding heart - usually associated with panic or anxiety

• play a key role in some disease states...s/s of cardiogenic shock are due to excessive sympathetic firing

• EX - pt with heart failure deteriorate quickly with excess sympathetic firing and usually receive medications aimed at minimizing the effects

• produces tachydysrhythmias - fast, irregular heart rhythms

• treatment:

• sympathomimetic - medication that mimic the effects of sympathetic stimulus (adrenalin, dopamine) - increase heart rate an myocardial contractile force

• sympatholytic - medication that produce effects that are similar to an inhibition of the sympathetic nervous system (clonidine)

Autonomic firingparasympathetic nervous system

• Parasympathetic (vagus nerve) stimulation:

• Decreases SA node activity - decreases heart rate

• Decreases speed of cardiac impulse from SA node to the AV node

• Exerts n effect on the strength of myocardial contraction (no parasympathetic innervation)

• Clinical importance:

• 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

• 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.

• treatment:

• 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

• 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 OutputCO = HR X SV

• Cardiac output is the amount of blood pumped by each ventricle in 1 minute

• normal cardiac output is 5 L per minute

• total blood volume is 5 L = entire blood volume is pumped through the heart each minute

• 2 factors determine cardiac output...

• Heart rate

• Stroke volume

Heart rate...

• 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

• Heart rates differ for many reasons:

• Size - larger the size, slower the rate

• Gender - women have faster heart rates than men

• Age - younger the person, faster the heart rate

• Adult - 60-100 bpm

• Child - 100 bpm

• Infant - 120 bpm

• Fetal - 140 bpm Exercise -

• Stimulation of ANS – stimulation of sympathetic nerve increases HR, stimulation of the parasympathetic nerve decreases HR.

• Hormonal influence - Epinephrine,norepinephrine (adrenal gland), thyroid hormones increase heart rate

• Pathology - fever, MI

• Mediations - digoxin (slows), epinephrine,

dopamine(increase), caffeine (increase),

Stroke Volume• Stroke volume is the amount of blood pumped

by the ventricle per beat

• Average stroke volume is 60-80 ml per beat

• At rest, ventricles pump out only 67% of blood in the ventricles...

• If the ventricles were made to pump more forcefully...stroke volume could be increased.

• CO = HR X SV

• Cardiac output = heart rate X stroke volume

Changes to Stroke Volume

• Stroke volume can be changed in 2 ways:

• Starling’s Law of the heart - depends on the degree of stretch!

• the greater the stretch, the stronger the force of contraction

• increase in the amount of blood entering the ventricles causes the ventricle to stretch...stretch increases force of contraction...increases stroke volume

• 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

• stimulation of the sympathetic nerves causes a (+) inotropic effect

• decreasing the force of contraction, weaker myocardial contraction

• Medications can cause either a (+) inotropic effect (digoxin,epinephrine) or a (-) inotropic effect

Heart Talk...• End diastolic volume (EDV) - amount of blood in the ventricle at the end of its resting phase (diastole)

• Preload - amount of blood in the ventricles at the end of diastole (same as EDV)

• increase in preload...stretches the ventricles...stronger force of contraction...increases stroke volume...increases cardiac output

• Medications: vasodilators...decreases amount of blood returning to heart...decreases amount of blood filling ventricles...decreases preload(EDV), stroke volume and cardiac output

• 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

• EF (ejection fraction) is an indicator of cardiac health

• Afterload - refers to resistance or opposition

• 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)

• 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!

• 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

• Cor Pulmonale - condition of pulmonary hypertension and right ventricular hypertrophy

Heart Talk...• Inotropic effect - change in myocardial contraction that is not due to stretch

• (+)inotropic effect - increases force of contraction EX digoxin

• (-) inotropic effect - decreases force of contraction

• Chronotropic effect - change in heart rate

• (+) chronotropic effect - heart rate is increased EX sympathetic nerve stimulus

• (-) 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

• (+) dromotropic effect - increased the speed of the impulse EX sympathetic nerve stimulation

• (-) dromotropic effect - decreased the speed of the impulse EX vagal stimuation

Heart Talk: Receptor Language

Beta 1 - adrenergic receptors• Beta 1- adrenergic receptor activation

• Sympathomimetic effect...

• We know... that sympathetic nerves innervate the SA node, AV node, His-purkinje system and ventricular myocardium...

• Neurotransmitter of the adrenergic neuron is norepinephrine (NE) Adrenergic neuron of the heart is called beta 1- adrenergic receptors

• Activation of the beta 1 - adrenergic receptor causes a (+) chronotropic effect, (+) dromotropic effect, and (+) inotropic effect

• 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

• sympatholytic effect...

• heart rate will not increase despite firing of the sympathetic nerves

• 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:

• Parasympathomimetic effect...

• We know...that parasympathetic (vagus) nerves supply only the SA node and the AV node

• Neurotransmitter for the cholinergic receptor is acetylcholine (ACh)

• Cholinergic receptors of the heart are called muscarinic receptors

• 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

• Medications that activate the muscarinic receptors are called cholinergic (muscarinic) agonist which cause a (-) dromotropic effect and a (-) chronotropic effect

• Muscarinic (cholinergic) receptor blockade:

• Parasympatholytic effect...

• 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 HeartLeft heart failure

• Left Heart Failure - when the left ventricle fails to pump blood into the aorta

• Blood backs up in the lungs

• 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

• pulmonary edema - presence of fluid in the lungs which impairs oxygenation of blood

• 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

• Treatment: (+) inotropic agents (digoxin, dopamine) NO MUD

• 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 Heartright heart failure

• Blood backs up behind the failed right ventricle, causing jugular vein distention, hepatomegaly, splenomegaly, digestive problems, and ankle edema.

• Heart failure is also described as backward heart failure and forward heart failure.

Goals of Treatment of

heart failure

Disorders of the Heart• Angina Pectoris

• Cardiac dysrhythmias

• Congenital heart defects

• CAD (coronary artery disease)

• MI (myocardial infarction)

• Inflammation of the heart

• Valvular heart disease