Function of the heart

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Function of the heart

• Chapter 17

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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

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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

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Three Stages of Cardiac Cycle

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

• Ventricular Systole
• Ventricles contract pushes AV valves closed
  pushes semilunar valves open
• Blood pumped to pulmonary artery aorta

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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

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Position of valves during systole diastole
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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.

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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

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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

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ANS

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

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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)

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Autonomic Firing

• Sympathetic stimulation
• Increases SA node activity ( HR)
• Increases speed of impulse (from SA node to
  His-Purkinje)
• Increases strength of contraction

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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)

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Important points to remember

• 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)

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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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Important points to remember

• 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)

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Important points to remember

• Excessive vagal discharge causes bradycardia (lt60
  bpm) it also increases the likelyhood of lethal
  dysrhythmias
• Vagal stimulation can also slow conduction
  through the heart, leading to potentially lethal
  heart blocks

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Important points to remember

• 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

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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

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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 140s)

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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

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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

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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

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Changing Stroke Volume

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

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Starlings 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

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Starlings Law
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An increase in end diastolic volume

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

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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)

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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

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Clinical Terminology

• Special vocabulary related to the heart

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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 Starlings Law

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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

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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

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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

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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)

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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

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Which of the following is most related to
preload?

1. Blood pH
2. End-diastolic volume
3. Cyanosis
4. Coronary blood flow

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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

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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

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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

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A () inotropic effect increases cardiac output
because it

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

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Autonomic Receptors
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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

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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

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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)

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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

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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

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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

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Tricky terminology

• Muscarinic agonist cholinergic agonist
• Muscarinic blocker antimuscarinic agent
  cholinergic blocker anticholinergic agent
• Beta1 receptor activation sympathomimetic
  effect
• Beta1-adrenergic blockade sympatholytic effect

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Tricky terminology

• Muscarinic (cholinergic) receptor activation
  parasympathomimetic effect
• Muscarinic (cholinergic) receptor blockade
  parasympatholytic effect

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

1. Activation of the muscarinic receptors
2. Firing of the vagus nerve
3. A sympathomimetic effect
4. Binding of ACh to its receptor on the SA node

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The Failing Heart

• When the heart cant pump

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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

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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

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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 blood

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Backward Failure

• Pulmonary Edema
• Signs symptoms (SS) include exertional
  dyspnea (-pnea means breathing)
• Cyanosis
• Blood tinged sputum and cough
• Orthopnea (pillows?)
• Tachycardia and restlessness

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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)

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Left-sided heart failure
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Forward Failure

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

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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)

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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)

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

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NCLEX Question

• After an anterior wall myocardial infarction
  (MI), which problem is indicated by auscultation
  of crackles in the lungs?
• left sided heart failure
• right sided heart failure
• pulmonic valve dysfunction
• 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

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NCLEX Question

• Which drug class protects the ischemic myocardium
  by decreasing catecholamines and sympathetic
  nerve stimulation?
• opiods
• beta-adrenergic blockers
• nitrates
• 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

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NCLEX Question

• With which disorder is jugular vein distention
  (JVD) most prominent?
• abdominal aortic aneurysm
• anterior wall myocardial infarction
• right sided heart failure
• 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?
• to stimulate the bowel because of loss of nerve
  innervation
• to prevent the Valsalva maneuver, which may lead
  to bradycardia
• to prevent straining, which increases
  intracranial pressure (ICP)
• 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
• orthopnea
• dyspnea on exertion
• dyspnea at rest
• 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 clients left-sided heart function.
• status of breath sounds
• presence of hepatojugular reflex
• presence of peripheral edema
• presence of jugular vein distention

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Rationale

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

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THE END