Lecture Mosby''s paramedic textbook (4th ed) - Chapter 22: Cardiology
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9/10/2012
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Chapter 22
Cardiology
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Lesson 22.1
Cardiovascular Disease
Risk
Factors, Heart Anatomy,
and
Physiology
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Learning Objectives
• Identify risk factors and prevention strategies
associated with cardiovascular disease.
• Describe the normal anatomy and physiology
of
the heart.
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Morbidity Rates
• MI death rates have declined over past several
decades due to
– Heightened public awareness
– Increased availability of automated external
defibrillators
– Improved cardiovascular diagnosis and therapy
– Use of cardiovascular drugs by persons at high risk
– Improved revascularization techniques
– Improved, more aggressive risk factor modification
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Risk Factors/Modifications
• Risks for cardiovascular disease
– Advanced age
– Male sex
– Diabetes
– Hypertension
– Hypercholesterolemia
– Hyperlipidemia
– Family history of premature cardiovascular disease
– Known coronary artery disease
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Risk Factors/Modifications
• Risks increased with
– Obesity
– Smoking
– Sedentary lifestyle
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Risk Factors/Modifications
• Modifiable risk factors
– Cessation of smoking
– Medical management and control of blood
pressure, diabetes, cholesterol, and lipid disorders
– Exercise
– Weight loss
– Diet
– Stress reduction
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Risk Factors/Modifications
• Modifying risk factors can slow arterial disease
development and reduce rate of
– MI
– Sudden death
– Renal failure
– Stroke
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Prevention Strategies
• Paramedics can support and practice
prevention strategies
– Educational programs about nutrition in
their communities
– Cessation of smoking
• Smoking prevention for children
– Early recognition and management of hypertension
and cardiac symptoms
– Prompt intervention
• CPR
• Early use of automated external defibrillator
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Heart Anatomy
•
•
•
•
Muscular organ with four chambers
Cone shaped
Size of man's closed fist
Lies just to left of midline of thorax
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Heart Anatomy
• Enclosed in pericardial sac lined with parietal
layers of serous membrane that form wall of
heart
– Outer layer (epicardium)
– Middle layer (myocardium)
– Inner layer (endocardium)
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Heart Anatomy
• Chambers
– Right atrium
• Receives deoxygenated blood from systemic veins
– Right ventricle
– Left atrium
• Receives oxygenated blood from pulmonary veins
– Left ventricle
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Heart Anatomy
• Valves
– Keep blood flowing in right direction
– Atrioventricular (cuspid) valves
• Located between atria and ventricles
– Semilunar valves
• Located at large vessels leaving ventricles
– Right atrioventricular valve
• Tricuspid valve
– Left atrioventricular valve
• Bicuspid or mitral valve
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Heart Anatomy
• Valves
– Pulmonary semilunar valve
• Between right ventricle and pulmonary trunk
– Aortic semilunar valve
• Between left ventricle and aorta
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Heart Anatomy
• When ventricles contract, atrioventricular
valves close to prevent blood from flowing
back into atria
• When ventricles relax, semilunar valves close
to prevent blood from flowing back into
ventricles
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Blood Supply to Heart
• Coronary arteries
– Sole suppliers of arterial blood to heart
– Deliver 200 to 250 mL of blood to myocardium
each minute during rest
– Left coronary artery carries about 85 percent of
blood supply to myocardium
– Right coronary artery carries rest
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Blood Supply to Heart
• Coronary arteries
– Begin just above aortic valve where aorta exits
heart
– Run along epicardial surface
– Divide into smaller vessels as they penetrate
myocardium and endocardial (inner) surface
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Blood Supply to Heart
• Left main coronary artery supplies
– Left ventricle
– Interventricular septum
– Part of right ventricle
– Two main branches
• Left anterior descending
• Circumflex artery
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Blood Supply to Heart
• Right coronary artery supplies
– Right atrium and ventricle
– Part of left ventricle
– Conduction system
– Two major branches
• Right anterior descending
• Marginal branch
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Blood Supply to Heart
• Connections (anastomoses) exist between
arterioles to provide backup (collateral)
circulation
– Play key role in providing alternative routes of
blood flow in event of blockage in one or more of
coronary vessels
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Blood Supply to Heart
• Coronary capillaries
– Allow for exchange of nutrients and metabolic
wastes
– Merge to form coronary veins
• Veins deliver most of blood to coronary sinus
• Coronary sinus empties directly into right atrium
• Coronary sinus is major vein draining myocardium
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Physiology
• Heart is two pumps in one
– Low pressure
• Right ventricle
• Right atrium
• Supplies blood to lungs
– High pressure
• Left ventricle
• Left atrium
• Supplies blood to body
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Physiology
• Right atrium
– Receives venous blood from systemic circulation
and from coronary veins
– Then passes to right ventricle as ventricle relaxes
from previous contraction
– Once right ventricle receives about 70 percent of
its volume, right atrium contracts
– Blood remaining is pushed into ventricle
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Physiology
• Right ventricle contraction pushes blood
against tricuspid valve (forcing it closed) and
through pulmonic valve (forcing it open)
– Allows blood to enter lungs via pulmonary arteries
• Blood enters capillaries in the lungs where gas
exchange takes place
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Physiology
• Atrial kick
– From lungs, blood travels through four pulmonary
veins back to left atrium
– Mitral valve opens, and blood flows to left
ventricle
– Once left ventricle receives about 70 percent of its
volume, left atrium contracts
– Remaining blood 20 to 30 percent is pushed into
ventricles during atrial contract
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Physiology
• Blood passing from left atrium to left ventricle
opens bicuspid valve when ventricle relaxes to
complete left ventricular filling
• As left ventricle contracts, blood is pushed
against bicuspid valve (closing it) and against
aortic valve (opening it)
– Allows blood to enter the aorta
• From aorta, blood is distributed first to heart itself and
then throughout systemic arterial circulation
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Cardiac Cycle
• Heart pumping
– Rhythmic, alternate contraction and relaxation
– Systole
• Contraction
– Diastole
• Relaxation
– Beats about 70 times/min in resting adults
– Responsible for blood movement
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Heart Pumping
• As ventricles begin to contract, ventricular
pressure exceeds atrial pressure
– Causes atrioventricular valves to close
– As contraction proceeds, ventricular pressure
continues to rise
– Pressure rises until it exceeds that in pulmonary
artery on right side of heart and in aorta on left
side
• At that time, pulmonary and aortic valves open
• Then blood flows from ventricles into those arteries
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Heart Pumping
• After ventricular contraction, ventricular
relaxation begins
– Ventricular pressure falls rapidly
– When pressure falls below pressure in aorta or
pulmonary trunk, blood is forced back toward
ventricles
– This closes pulmonic and aortic valves
– As ventricular pressure drops below atrial pressure,
tricuspid and mitral valves open
– Then blood flows from atria into ventricles
– Atrial systole occurs during ventricular diastole
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Stroke Volume
• Amount of blood ejected from heart with each
ventricular contraction
• Depends on
– Preload
• Volume of blood returning to heart
– Afterload
• Resistance against which heart muscles must pump
– Myocardial contractility
• Performance of cardiac muscle
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Preload
• During diastole, blood flows from atria into
ventricles
• End‐diastolic volume
– Volume of blood returning to each ventricle
– Normally reaches 120 to 130 mL
– As ventricles empty during systole, their volume
decreases to 50 to 60 mL (end‐systolic volume)
• Amount of blood ejected during each cardiac cycle
(stroke volume) in average adult is about 70 mL
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Preload
• Healthy heart capacity to increase stroke
volume is great
– If large amounts of blood flow into ventricles
during diastole, their end‐diastolic volume can be
as much as 200 to 250 mL
– In this way, stroke volume can increase to more
than double that of normal
– Ability of heart to pump more strongly when it has
larger preload is explained by Starling’s law of the
heart
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Preload
• Starling's law
– Myocardial fibers contract more forcefully when
they are stretched
– When ventricles are filled with larger‐than‐normal
volumes of blood (increased preload), they
contract with greater‐than‐normal force to deliver
all blood to systemic circulation
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How does the behavior of a
latex balloon resemble
myocardial fibers?
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Preload
• Most important feature of heart's ability to
handle changes in venous blood return
– Changes in arterial pressure have minimal effect
on cardiac output
– Heart can pump small or large amount of blood
– Heart adapts as long as total quantity of blood
does not exceed limit that heart can pump
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Preload
• Venous return is most important factor in
stroke volume, with arterial pressure causing a
lesser effect in form of afterload
– Starling’s law and its effect on stroke volume
can be applied only up to certain limit of muscle
fiber stretching
• Beyond that limit, muscle fiber stretch actually
diminishes strength of contraction
• At that point, heart begins to fail
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Afterload
• Pressure within aorta prior to ventricular
contraction
• Result of peripheral vascular resistance
– Total resistance against which blood must be
pumped
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Afterload
• The more afterload, the more difficult it is for
left ventricle to pump blood to body
• Amount of blood ejected with ventricular
contraction (stroke volume) also is reduced
• As afterload is decreased, stroke volume
increases, provided there is enough blood in
system
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Myocardial Contractility
• Unique function of myocardial muscle fibers
and influence of autonomic nervous system
play major role in function of the heart
– Ischemia or various drugs can decrease myocardial
contractility
– Ischemia can decrease total number of working
myocardial cells
• This occurs in myocardial infarction
– Hypoxia or administration of beta‐blockers can
decrease ability of myocardial cells to contract
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Cardiac Output
• Amount of blood pumped by ventricles per
minute
– Cardiac output can increase by increasing heart
rate, stroke volume, or both
– Cardiac output is calculated as follows
• Cardiac output = stroke volume × heart rate
– Peripheral vascular resistance changes cardiac
output by affecting stroke volume
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Cardiac Output
• Body responds to decreased afterload by
constricting venous circulation
– Increases amount of blood returning to heart and
causes heart to contract more forcefully (Starling’s
law)
• Helps to maintain or increase cardiac output
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Nervous System
Control of Heart
• Autonomic nervous system also controls
behavior of heart
– Influences heart rate, conductivity, and
contractility
– Innervates atria and ventricles
• Atria are supplied with large numbers of sympathetic
and parasympathetic nerve fibers
• Ventricles mainly are supplied by sympathetic nerves
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Nervous System
Control of Heart
• Parasympathetic nervous system mainly is
concerned with vegetative functions
• Sympathetic nervous system helps prepare
body to respond to stress
• These control systems work in check‐and‐
balance manner
– Stimulate heart to increase or decrease cardiac
output according to metabolic demands of body
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How is the behavior of the
autonomic nervous system
similar to how you would
regulate the hot and cold taps in
your shower?
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Parasympathetic Control
• Through vegus nerve
– Control by these nerve fibers has continuous
restraining influence on heart
• Decreases heart rate and contractility
– May be stimulated in several ways
•
•
•
•
Valsalva maneuver
Carotid sinus massage
Pain
Distention of the urinary bladder
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Parasympathetic Control
• Strong parasympathetic stimulation can
decrease heart rate to 20 to 30 beats/minute
– Such stimulation generally has little effect on
stroke volume
– Stroke volume may increase with decreased heart
rate
• Occurs because longer time interval between
heartbeats allows heart to fill with larger amount of
blood and thus contract more forcefully
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Sympathetic Control
• Sympathetic nerve fibers originate in thoracic
region of spinal cord
– Form ganglia
• Groups of nerve fibers
– Their postganglionic fibers release chemical
norepinephrine
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Sympathetic Control
• Norepinephrine
– Positive chronotropic effect
• Stimulates an increase in heart rate
– Positive inotropic effect
• Stimulates increase in force of muscle contraction
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Sympathetic Control
• Sympathetic stimulation of heart
– Causes coronary arteries to dilate
– Causes constriction of peripheral vessels
– Effects help to increase blood and O2 supply to
heart
– Cardiac effects of norepinephrine result from
stimulation of alpha‐ and beta‐adrenergic
receptors
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Sympathetic Control
• Strong sympathetic stimulation of heart may
increase heart rate notably
– When rates are significantly high (greater than 150
beats/minute), time available for heart to fill is
decreased
• Produces decrease in stroke volume
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Hormonal Regulation of Heart
• Impulses from sympathetic nerves are sent to
adrenal medulla at same time that they are
sent to all
blood vessels
– Adrenal medulla secretes hormones epinephrine
and norepinephrine into circulating blood in
response to increased physical activity, emotional
excitement, or stress
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Hormonal Regulation of Heart
• Epinephrine
– Has basically same effect on cardiac muscles as
norepinephrine
– Increases rate and force of contraction
– Causes blood vessels to constrict in skin, kidneys,
gastrointestinal tract, and other organs (viscera)
– Causes dilation of skeletal and coronary blood vessels
– From adrenal glands takes longer to act on heart than
direct sympathetic innervation does
• Effect lasts longer
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Hormonal Regulation of Heart
• Norepinephrine
– Causes constriction of peripheral blood vessels in
most areas of body
– Stimulates cardiac muscle
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Role of Electrolytes
• Myocardial cells are bathed in an electrolyte
solution
• Major electrolytes that affect cardiac function
– Calcium
– Potassium
– Sodium
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Role of Electrolytes
• Magnesium is major intracellular cation
• Changes in electrolytes can affect
depolarization, repolarization, and myocardial
contractility
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Lesson 22.2
Electrophysiology and the
Electrical Conduction
System
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Learning Objectives
• Discuss electrophysiology as it relates to the
normal electrical and mechanical events in the
cardiac cycle.
• Outline the activity of each component of the
electrical conduction system of the heart.
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Heart Electrophysiology
• Paramedic must understand
– Mechanical and electrical functions of heart
– Why and how electrical conduction system
can malfunction
– Effect that lack of O2 to cells (myocardial ischemia)
has on cardiac rhythms
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Heart Electrophysiology
• Two basic groups of cells within myocardium
are vital for cardiac function
– One group is specialized cells of electrical
conduction system
• Responsible for formation and conduction of electrical
current
– Second group is the working myocardial cells
• These cells possess the property of contractility
• They do the actual pumping of the blood
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Cardiac Cell Electrical Activity
• Ions are charged particles
– Positive or negative
– Charge depends on ability of ion to accept or to
donate electrons
• In solutions containing electrolytes, particles with
unlike (opposite) charges attract each other, and
particles with like charges push away from each other
• Results in tendency to produce ion pairs, which keep
solution neutral
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Cardiac Cell Electrical Activity
• Electrically charged particles
– Can be thought of as small magnets
• Require energy to pull them apart if they have
opposite charges
• Require energy to push them together if they have like
electrical charges
• Separated particles with opposite charges have
electrical magnetic‐like force of attraction
• This gives them potential energy
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Cardiac Cell Electrical Activity
• Electrical charge creates membrane potential
between inside and outside of cell
– Electrical charge (potential difference) between
inside and outside of cells is expressed in millivolts
(1 mV = 0.001 volt)
– This potential energy is released when cell
membrane separating ions becomes permeable
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Resting Membrane Potential
• When cell is in its resting state, electrical
charge difference
– Potential is synonym for voltage
– Inside of cell is negative compared with outside of
cell membrane
• Recorded from inside of cell
• Reported as negative number (about –70 to –90 mV)
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Resting Membrane Potential
• Result of balance between two opposing
forces
– Factors
• Concentration gradient of ions (mainly potassium)
across a permeable cell membrane
• Electrical forces produced by separation of positively
charged ions from their negative ion pair
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Resting Membrane Potential
• Established by difference between
intracellular potassium ion level and
extracellular potassium ion level
– Ratio of 148:5 produces large chemical gradient
for potassium ions to leave cell
– Negative intracellular charge relative to
extracellular charge tends to keep potassium ions
in cell
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Resting Membrane Potential
• Sodium ions
– Positively charged ions on outside of cell
– Have chemical and electrical gradient
• Tend to cause sodium ions to move intracellularly,
making cell more positive on inside compared with
outside
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Diffusion Through Ion Channels
• Cell membrane
– Relatively permeable to potassium
– Somewhat less permeable to calcium chloride
– Minimally permeable to sodium
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