Function of the heart

Function of the heart

Chapter 17

1

Cardiac Cycle

• Sequence of events that occurs during one heartbeat

• Coordinated contraction and relaxation of the chambers of the heart

• Systole- contraction of myocardium• Diastole- relaxation of myocardium

2

Systole & Diastole

• Systole– Contraction of heart muscle forces blood

out of the chamber• Diastole

– Relaxation of heart muscle allows the chamber to fill with blood

• Atrial and ventricular activity are closely coordinated: atrial systole = ventricular diastole

3

Three Stages of Cardiac Cycle

• Atrial Systole– Atria contract; pump blood into ventricles– AV valves open, ventricles relaxed

Ventricular SystoleVentricles contract; pushes AV valves closed; pushes semilunar valves openBlood pumped to pulmonary artery & aorta

4

Three Stages of Cardiac Cycle

• Diastole– Brief time when both atria and ventricles are

relaxed– Blood flows into atria; some blood flows

passively into ventricles– Diastole is a “filling” period

Cycle repeats itself starting with atrial contraction again

5

Position of valves during systole & diastole 7

Which of the following occurs during ventricular

diastole?1. The ventricles fill with blood.2. The atrioventricular valves close.3. The ventricles pump blood into the

great vessels.4. The semilunar valves open.

8

Cardiac Cycle

• Cardiac cycle is repeated with every heartbeat; if heart rate is 70 bpm, then cardiac cycle lasts approx. 0.8 sec; diastole lasts approx. 0.4 sec

• If heart rate increases, diastole shortens- can impact cardiac function. How?

• Decreased filling time reduces the amount of blood that enters the ventricles; and coronary blood flow occurs during diastole

9

Autonomic Control of the Heart

• If cardiac cells can initiate cardiac impulses, why are autonomic nerves needed?

• Affect the rate at which cardiac impulses are fired

• Affects how fast the impulses travel through the heart

• Affects how forcefully the heart contracts

10

ANS

• The autonomic nervous system allows the heart to respond to increased oxygen demand by increasing the rate and force of cardiac contraction.

11

Autonomic Wiring

• Sympathetic– Supply the SA node, AV node and ventricular

myocardium• Parasympathetic

– Vagus nerve– SA node and AV node (does not innervate the

ventricles)

12

Autonomic Firing

• Sympathetic stimulation– Increases SA node activity ( HR)– Increases speed of impulse (from SA node to

His-Purkinje)– Increases strength of contraction

13

Important points to remember

• Excessive sympathetic activity leads to “fight or flight” response (panic causes racing and pounding heart)

• May be involved in certain illnesses- shock, heart failure (need to treat with drugs that reduce excessive sympathetic firing)

15


• Causes tachydysrhythmias• Nurses often give drugs that mimic or

block sympathetic activity– Drugs that mimic sympathetic activity

increase HR and force of contraction (epinepherine & dopamine); called sympathomimetic drugs

– Drugs that inhibit SNS effects are called sympatholytic drugs (clonidine)

16

Autonomic Firing

• Paraympathetic stimulation– Decreases SA node activity ( HR)– Decreases the speed of cardiac

impulses from SA to AV node– Does not affect strength of myocardial

contraction (no innervation of ventricles)

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• Parasympathetic effects are exerted by the vagus nerve

• In the resting heart, the vagus nerves slows the firing of the SA node (SA node wants to fire at 90 bpm, vagus nerve keeps it around 70)

• Excessive vagal discharge can be caused by different things, including certain drugs(digoxin) and conditions (MI)

19


• Excessive vagal discharge causes bradycardia (<60 bpm); it also increases the likelyhood of lethal dysrhythmias

• Vagal stimulation can also slow conduction through the heart, leading to potentially lethal heart blocks

20


• Drugs that mimic the effects of vagal activity (slow HR or conduction) are called vagomimetic (or, parasympathomimetic) drugs (digoxin)

• Drugs that inhibit vagal discharge (like atropine) are called vagolytic (or, parasympatholytic) drugs

21

Cardiac Output

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

• Normal cardiac output is 5 liters per minute (an average adults entire blood volume)

• Cardiac output is determined by heart rate and stroke volume

• CO = HR x SV

22

Heart Rate

• The number of times the heart beats in one minute (avg 72 bpm for adult)

• Resting HRs differ because of size, age and gender– Larger size- slower HR– Women tend to have faster HR than men– Age- generally, younger hearts beat faster

(fetal HR avgerages 140’s)

23

Heart Rate

• Other factors that affect HR– Exercise- increases HR (response to

increased oxygen demand)– Stimulation of ANS (sympathetic stim causes

increased HR, parasympathetic (vagus) stim causes decreased HR

– Hormone secretion- epi, norepi and thyroid hormones increase HR

24

Heart Rate

• Pathology- certain diseases or conditions can affect HR (sick sinus syndrome, MI, fever)

• Medications- many drugs can affect the heart rate (digoxin, epi/ norepi, caffeine); important to know effects of drugs and the patients HR before giving them

25

Stroke Volume

• The amount of blood pumped by the ventricles per beat

• Average is 60-80 ml per beat• Normally, ventricles pump out about 65%

of the blood they contain; if force of contraction is increased, more blood will be forced out

26

Changing Stroke Volume

• Stroke volume can be changed though Starling’s Law or through an inotropic effect (strength of contraction)

27

Starling’s Law

• Depends on the degree of stretch of the myocardial fibers

• Greater the stretch, greater the force of contraction

• If more blood enters the ventricle, the fibers are stretched more, the ventricle contracts more forcefully (conversely, less blood = less stretch, decreased force of contraction)

• So, stroke volume can be increased by increasing venous return to the heart

28

Starling’s Law29

An increase in end diastolic volume

1. elicits Starling’s law of the heart.2. decreases stroke volume.3. decreases cardiac output.4. All of the above

30

Inotropic Effect• Increasing the force of myocardial

contraction without stretching the myocardial fibers; called (+) inotropic effect

• Stimulation of the heart by sympathetic nerves causes +inotropic effect; epi and digoxin are +inotropes

• (-)Inotropic effects decrease the force of contraction (excessive depression can lead to heart failure)

31

Cardiac Output

• Since cardiac output is determined by heart rate and stroke volume, changing one or both can affect output

• Cardiac reserve refers to the capacity to increase cardiac output above normal resting state

• Diseased hearts often have little reserve, so the person may become easily tired with minimal exertion

32

Clinical Terminology

• Special vocabulary related to the heart

33

End Diastolic Volume

• The amount of blood in the ventricle at the end of diastole (resting phase)

• Determines the amount of stretch in the muscle fibers; basis for Starling’s Law

34

Preload

• Same as EDV; amount of blood in the ventricles after diastole; increased preload stretches the ventricles, causing stronger force of contraction (which increases stroke volume, and therefore cardiac output)

• Drugs can affect preload- dilate veins to decrease preload, constrict veins to increase preload

35

Ejection Fraction

• Remember ventricles pump about 65-67% of their volume; this is referred to as the ejection fraction

• Indicated cardiac health- a healthy heart can increase EF to 90% with exercise; diseased or weakened heart are much lower, may be less than 30%

36

Afterload

• Refers to resistance against blood as it is pumped out of the heart

• From the LV, blood must push against blood already in the aorta; increased resistance (stenosis, high pressure) causes the heart to work harder

• Continued increased resistance (hypertension, especially) can cause LV hypertrophy

37

Afterload

• Afterload in the right ventricle is determined by the pulmonary artery; high pressure can be caused by chronic lung diseases (asthma, emphysema)

• RV hypertrophy and increased pulmonary artery pressure is referred to as cor pulmonale (often causes RV failure)

38

Afterload

• Drugs can alter afterload by relaxing or dilating blood vessels in the periphery; decreases workload of the heart

• Drugs that constrict blood vessels will increase afterload and increase the workload of the heart

39

Which of the following is most related to preload?

1. Blood pH2. End-diastolic volume3. Cyanosis4. Coronary blood flow

41

Inotropic Effect

• Refers to change in myocardial contraction not due to stretching of fibers

• + inotrope increases contractile force• - inotrope decreases contractile force• Sympathetic nerve stimulation causes a

positive inotropic effect

42

Chronotropic Effect

• Refers to a change in heart rate• + chronotropic effect increases HR• - chronotropic effect decreases HR• Sympathetic nerve stimulation causes a +

chronotropic effect• Parasympathetic (vagal) stimulation

causes a – chronotropic effect

43

Dromotropic Effect

• Refers to a change in the speed at which the cardiac impulse travels through the conduction system

• + dromotropic effect increases speed of conduction

• - dromotropic effect decreases speed of conduction

• Pronounced (-) dromotropic effects may lead to heart block

44

A (+) inotropic effect increases cardiac output because it

1. decreases afterload.2. increases stroke volume.3. intensifies vagal discharge.4. expands blood volume.

45

Autonomic Receptors

46

Beta1 adrenergic receptors

• The adrenergic neurotransmitter is norepinepherine (NE)

• The cardiac receptors for NE are beta1-adrenergic receptors

• Activation of beta1 receptors cause– +chronotropic effects– +dromotropic effects– +inotropic effects

47

Beta1 adrenergic receptors

• Drugs that activate beta1-adrenergic receptors increase HR, stroke volume and overall cardiac output

• These drugs are called beta1-adrenergic agonists (or simply “beta agonists”)

• Include dopamine and epinephrine

• Note: beta1 receptor activation is the same as a sympathomimetic effect

48

Beta1 Receptor Blockade

• Blockade of the beta1-adrenergic receptors prevents receptor activation

• People taking beta1-adrenergic blockers (or, “beta blockers”) will not increase their heart rate when sympathetic nerves fire (stress or exercise)

49

Beta1 Receptor Blockade

• May be administered to tachycardic patients or patients having an MI; reduces HR and force of contraction… reduces workload of heart and therefore oxygen demand of the heart

• Beta1-adrenergic blockade is the same as a sympatholytic effect

50

Cholinergic (muscarinic) Receptors

• The cholinergic neurotransmitter is acetylcholine (ACh) (vagus nerve)

• The cardiac cholinergic receptors are called muscarinic receptors

• Activation of muscarinic receptors causes– (-)chronotropic effect– (-) dromotropic effect– No inotropic effect (vagus does not innervate

ventricles)– Same as parasympathomimetic effect 51

Cholinergic (muscarinic) Blockade

• Muscarinic/ cholinergic blockers act by blocking the effects of ACh at the muscarinic receptors

• Therefore, HR and speed of conduction is increased (atropine)

• Muscarinic (cholinergic)-receptor blockade is the same as parasympatholytic effect

52

Tricky terminology…

• Muscarinic agonist = cholinergic agonist• Muscarinic blocker = antimuscarinic agent

= cholinergic blocker = anticholinergic agent

• Beta1 receptor activation = sympathomimetic effect

• Beta1-adrenergic blockade = sympatholytic effect

53

Tricky terminology…

• Muscarinic (cholinergic) receptor activation = parasympathomimetic effect

• Muscarinic (cholinergic) receptor blockade = parasympatholytic effect

54

Which of the following is least apt to slow heart rate?

1. Activation of the muscarinic receptors2. Firing of the vagus nerve3. A sympathomimetic effect4. Binding of ACh to its receptor on the SA

node

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The Failing Heart

• When the heart can’t pump

56

The heart as a double pump…

• Remember the heart functions as two pumps

• The right side of the heart pumps blood to the lungs for oxygenation

• The left side of the heart pumps blood to the aorta and to the systemic circulation

57

Left-Heart Failure

• Two main components– Blood backs up in the lungs– Insufficient amount of blood is pumped out to

the systemic circulation• Can be described in terms of forward

failure of backward failure

58

Backward Failure

• Blood backs up in structures behind the left ventricle- left atrium, pulmonary veins and pulmonary capillaries

• Increased pressure in the pulmonary capillaries forces fluid into the lungs

• Called pulmonary edema• Fluid in the lungs impairs the lungs’ ability

to oxygenate blood59

Backward Failure

• Pulmonary Edema– Signs & symptoms (S&S) include: exertional

dyspnea (-pnea means breathing)– Cyanosis– Blood tinged sputum and cough– Orthopnea (pillows?)– Tachycardia and restlessness

60

Backward Failure

• Most symptoms are respiratory• Treatment includes:

– +inotropic agent (increase force of myocardial contraction to push excess blood out)

– Nitroglycerine (NTG) (decreases preload)– Oxygen (increase oxygenation)– Morphine (decrease workload, anxiety)– Upright position (ease work of breathing)– Diuretic (relieve edema)

61

Left-sided heart failure 63

Forward Failure

• The damaged ventricle cannot pump adequate blood to the systemic circulation

• S&S include: – kidneys filter less water and reabsorb excess

salt and water, increases blood volume and edema

– Decreased cardiac output stimulates sympathetic activity- temporarily improves C.O. but eventually the heart wears out

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Left-Heart Failure

• Commonly caused by myocardial infarction and chronic, uncontrolled hypertension (HTN)

• In MI, if the damaged tissue is in the left ventricle, the heart may fail as a pump (LAD- the “widow maker”)

• In HTN, the LV has to continuously pump against resistance- LV hypertrophies and eventually fails

65

Right-Heart Failure

• Blood backs up in the veins that return blood to the heart

• Superior vena cava receives blood from the jugular veins; congestion in the jugular veins is known as jugular vein distention (JVD)

• Blood also backs up into major viscera, causing enlargement- hepatomegaly and splenomegaly (-megaly means enlargement)

66

Right-Heart Failure

• Edema also found in the feet and ankles- pedal edema; pitting edema is severe edema that will indent when pressed

• Right-heart failure is usually a result of left heart failure; can also be caused by chronic lung disease (emphysema)

67

Marked pitting edema of leg (arrow) as a result of chronic heart failure.

68

Right-sided heart failure

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Treatment of Heart Failure

• Goals of treatment– Strengthen myocardial contraction– Remove excess edema– Decrease workload of heart– Protect the heart from excess sympathetic

activity

71

NCLEX Question

• After an anterior wall myocardial infarction (MI), which problem is indicated by auscultation of crackles in the lungs?

1.left sided heart failure2.right sided heart failure3.pulmonic valve dysfunction4.tricuspid valve malformation

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Rationale

• 1. Anterior wall MIs usually cause extensive damage to the left ventricle, resulting in left sided heart failure. The symptoms of left sided failure are predominantly pulmonary in nature- usually resulting in pulmonary edema

73

NCLEX Question

• Which drug class protects the ischemic myocardium by decreasing catecholamines and sympathetic nerve stimulation?

1.opiods2.beta-adrenergic blockers3.nitrates4.calcium channel blockers

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Rationale

• 2. Beta-adrenergic blockers work by blocking receptors activated by norepinepherine, thereby decreasing the sympathetic stimulation to the heart

75

NCLEX Question

• With which disorder is jugular vein distention (JVD) most prominent?

1.abdominal aortic aneurysm2.anterior wall myocardial infarction3.right sided heart failure4.pneumothorax

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Rationale

• 3. Right sided heart failure results in congestion of the superior vena cava, which drains the jugular veins

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NCLEX Question• Stool softeners would be given to a client

after a myocardial infarction for which reason?

1.to stimulate the bowel because of loss of nerve innervation

2.to prevent the Valsalva maneuver, which may lead to bradycardia

3.to prevent straining, which increases intracranial pressure (ICP)

4.to prevent constipation when osmotic diuretics are used

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Rationale

• 2. Straining to have a bowel movement may stimulate the vagus nerve, resulting in bradycardia. This can be potentially life-threatening in a patient with damage to the myocardium

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NCLEX Question• A nurse is collecting data from a client with

left-sided heart failure. The client states that it is necessary to use three pillows under the head and chest at night to be able to breathe comfortably while sleeping. The nurse documents that the patient is experiencing:

1.orthopnea2.dyspnea on exertion3.dyspnea at rest4.paroxysmal nocturnal dyspnea

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Rationale

• 1. Left sided heart failure results in pulmonary edema. This is exacerbated by lying flat. The patient will find it easier to breath while sitting up, called orthopnea

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NCLEX Question

• A nurse is performing a cardiovascular assessment on a client. Which of the following items should the nurse check to obtain the best information about the client’s left-sided heart function.

1.status of breath sounds2.presence of hepatojugular reflex3.presence of peripheral edema4.presence of jugular vein distention

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Rationale

• Left sided heart failure will result in pulmonary edema, so a client’s lung sounds need to be assessed frequently

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THE END

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Function of the heart

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