1. Functions of the Heart
Chapter 17

2. 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?

3. 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...

4. 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...

5. 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

6. 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

7. 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:
Does not supply the ventricular myocardium

8. Autonomic firing Sympathetic 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)

9. Autonomic firing parasympathetic 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

10. Cardiac Output CO = 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

11. Heart rate...
Age - younger the person, faster the heart rate
Adult bpm
Child bpm
Infant bpm
Fetal 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),
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

12. Stroke Volume
Stroke volume is the amount of blood pumped by the ventricle per beat
Average stroke volume is 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

13. 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

14. 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

15. 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

16. 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

17. Heart Talk: Receptor language 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

18. The Failing Heart Left 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

21. The Failing Heart right 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.

22. Goals of Treatment of heart failure

23. 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