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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
Systole
Ventricles
contract; pushes AV valves
closed; pushes semilunar valves open
Blood 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
6
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 shortenscan 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
14
Important points to remember
• Excessive sympathetic activity leads to
“fight or flight” response (panic causes
racing and pounding heart)
• May be involved in certain illnessesshock, heart failure (need to treat with
drugs that reduce excessive sympathetic
firing)
15
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)
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)
17
18
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)
19
Important points to remember
• 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
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
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 Law
29
An increase in end diastolic
volume
1.
2.
3.
4.
elicits Starling’s law of the heart.
decreases stroke volume.
decreases cardiac output.
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
40
Which of the following
is most related to preload?
1.
2.
3.
4.
Blood pH
End-diastolic volume
Cyanosis
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.
2.
3.
4.
decreases afterload.
increases stroke volume.
intensifies vagal discharge.
expands blood volume.
45
Autonomic Receptors
46
Beta1 adrenergic receptors
• The adrenergic neurotransmitter is
norepinepherine (NE)
• The cardiac receptors for NE are beta1adrenergic 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.
2.
3.
4.
Activation of the muscarinic receptors
Firing of the vagus nerve
A sympathomimetic effect
Binding of ACh to its receptor on the SA
node
55
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 blood
59
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
62
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
64
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 anklespedal 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
69
Right-sided
heart
failure
70
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 failure
2.right sided heart failure
3.pulmonic valve dysfunction
4.tricuspid valve malformation
72
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 natureusually resulting in pulmonary edema
73
NCLEX Question
• Which drug class protects the ischemic
myocardium by decreasing
catecholamines and sympathetic nerve
stimulation?
1.opiods
2.beta-adrenergic blockers
3.nitrates
4.calcium channel blockers
74
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 aneurysm
2.anterior wall myocardial infarction
3.right sided heart failure
4.pneumothorax
76
Rationale
• 3. Right sided heart failure results in
congestion of the superior vena cava,
which drains the jugular veins
77
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
78
Rationale
• 2. Straining to have a bowel movement
may stimulate the vagus nerve, resulting in
bradycardia. This can be potentially lifethreatening in a patient with damage to the
myocardium
79
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.orthopnea
2.dyspnea on exertion
3.dyspnea at rest
4.paroxysmal nocturnal dyspnea
80
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
81
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 sounds
2.presence of hepatojugular reflex
3.presence of peripheral edema
4.presence of jugular vein distention
82
Rationale
• Left sided heart failure will result in
pulmonary edema, so a client’s lung
sounds need to be assessed frequently
83
THE END
84