Transcript Physiology of the Cardiovascular System

Physiology of the
Cardiovascular System
Chapter 19
Heart’s Role in Maintaining
Homeostatis
• Circulation (pumping action) varies
based on needs of the body
• Hemodynamics - Describes a collection
of mechanisms that influence the active
and changing circulation of blood
throughout the body
– Increase activity = increased blood flow
Heart as a Pump
• 4 Chambers of the heart create two
pumps
– Right side  pulmonary circulation
– Left side  systemic circulation
Conduction System of the Heart
• 4 structures composed of specialized
cardiac muscle make up the conduction
system of the heart:
– SA Node, AV Node, AV bundle (Bundle of
His), Purkinje Fibers
– Non contractile
– Permit generation or rapid conduction of an
action potential
SA Node
• Pacemaker of the heart
• R atrium at base of superior vena cava
• Specialized cells within the node
produce an intrinsic rhythm
– Produce impulses without stimulation from
any other body system
• Fires or discharges 70-75
times/minutes
Conduction Route
Impulse generated in SA node 
interatrial bundle allows conduction of
impulse to L atrium  internodal
bundles carry impulse to AV node
**conduction slows through AV node to allow complete
contraction of atria**
Conduction increases after passing though
AV node  R/L branches of AV bundle
 purkinje fibers  ventricular muscles
 simultaneous ventricular contraction
Conduction Route
• Ectopic pacemakers
– If SA node loses ability to generate
impulses, the AV node or Purkinje fibers
will take over
– HR will be slower
Artificial Pacemakers
• Surgically inserted device which
stimulates the heart at a set rhythm
• Stimulate a set rhythm or fire when HR
drops below a set minimum
• Transvenous approach
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Incision above R clavicle
Electrode threaded into jugular vein
Advanced to apex of R ventricle
Power pack is attached to subcutaneous
tissue
Artificial Pacemakers
Electrocardiogram (ECG)
• Conduction through the heart creates
electrical currents that spread to the
surface of the body
• ECG is a graphic record of the electrical
activity of the heart
• Electrodes of a electrocardiograph
attached to a person’s skin can record
changes in the heart’s electrical activity
– Observed as deflections
Cardiac muscle @ rest – no difference in
charge btwn electrodes
Action potential reaches first electrode.
External surface becomes relatively
negative. Upward deflection on ECG.
AP reaches 2nd electrode. No difference in
charge. Deflection returns to zero.
End of AP reaches the 1st electrode.
Sarcolemma is slightly positive creating a
downward deflection.
End of AP reaches the 2nd electrode. No
difference in charges. Deflection returns to
zero.
Summary
• Depolarization – deflection representing
cardiac muscle moving away from
resting membrane potential
• Repolarization – deflection in the
opposite direction; cardiac muscle
moving back towards resting membrane
potential
Analyzing ECGs
• Series of deflection
waves and intervals
• Represents net
change in polarity
– Ex: ventricles are
depolarizing while
atria are repolarizing
Analyzing ECGs
• P wave
– Depolarization of the atria
– Electrical impulse passes from SA node to
R/L atria
• QRS complex
– Depolarization of the ventricles
– Repolarization of the atria
• Voltage fluctuation overshadowed by the
depolarization of the ventricles
• First to depolarize, first to repolarize
Analyzing ECGs
• T wave
– Repolarization of the ventricles
• First to depolarize, last to repolarize
**ECG is a record of the electrical activity of
the heart, NOT of the heart’s contraction.
Contraction occurs after depolarization**
Cardiac Dysrhythmias
• Abnormal rhythm of the heart
• Heart Block
– Conducted blocked after AV node
– Ventricles contract slowly
– Wide spaces between P waves and QRS
complex
– Complete Heart Block – multiple P wave per
QRS complex
Cardiac Dysrhythmias
• Bradycardia
– Slow HR (< 60bpm)
– ECG will show spread out waves
– Causes:
• Damaged SA node
• Abnormal autonomic nervous control
• Tachycardia
– Increased HR (>100bpm)
– ECG will show condensed waves
– Causes:
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Abnormal autonomic nervous control
Blood loss/shock
Drugs
Fever
Cardiac Dysrhythmias
• Atrial fibrillation (“A-fib”)
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Premature contractions
Absence of P waves
Chambers do not pump efficiently
Treated with digoxin (digitalis) or defibrilation
Causes:
• Mitral stenosis
• Rheumatic heart disease
• Myocardial infarction
Cardiac Dysrhythmias
• Ventricular fibrillation (“v-fib”)
– Ventricular contraction/pumping stops
– Life threatening situation
– Treated with defibrillation
Cardiac Cycle
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One complete heart beat
Consists of one contraction (systole)
and one relaxation (diastole) of both
the atria and ventricles
1. Atria contract simultaneously
2. Ventricles contract; atria relax
3. Ventricles relax; atria remain relaxed
Atrial Systole
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Atria contracted
AV valves open
Ventricles filling with blood
Semilunar valves closed
Begins with P wave of the ECG
Isometric Ventricular Contraction
• “having the same measured volume”
• Time between ventricular systole and
opening of SL valves
• Volume is constant; pressure increases
• Ventricular systole coincides with the R
wave & the first heart sound
Ejection
• Ejection occurs when pressure in the
ventricles exceeds pulmonary artery &
aorta
• Rapid ejection – initial, shorter phase
• Reduced ejection – coincides with T
wave
• Residual volume – blood that remains in
the ventricles after ejection
– Increases in ppl with heart failure
– Ejection fraction
Isovolumetric Ventricular
Relaxation
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Begins with ventricular diastole
SL valves close; AV valves remain closed
Volume is constant; pressure decreases
Second heart sound
Passive Ventricular Filling
• Atria filling increases intraatrial
pressure
• AV valves are forced open
Heart Sounds
• “Lubb-Dubb”
• “Lubb” – systolic sound
– contraction of the ventricules and closing of the AV
valves
– Longer, lower
• “Dubb” – diastolic sound
– Closure of the SL valves
– Shorter, sharper
• Heart murmur – abnormal heart sounds
– Incomplete closing of the valves
• Valvular insufficiency or stenosis
Primary Principle of Circulation
Arterial Blood Pressure
• Maintaining arterial pressure is
necessary to maintain circulation
• Arterial blood pressure is directly
proportional to arterial blood volume
• Cardiac output and peripheral
resistance influence arterial volume
Cardiac Output
• Stroke volume x Heart Rate = Cardiac
output
(SV x HR = CO)
• Stroke volume: volume of blood pumped
out of the ventricles by each heart beat
• Increase speed or strength of
contraction = increase arterial volume =
increase arterial pressure
Factors Affecting Stroke Volume
• Starling’s Law of the
Heart
– Longer muscle fibers
prior to contraction =
stronger contraction
• Increased blood return
to the heart per
minute = longer muscle
fibers
Factors Affecting Heart Rate
• Aortic baroreceptors and carotid
barorecetors are located near the heart
and are sensitive to changes in pressure
– Carry sensory information to cardiac center
in medulla oblongata
– If HR above a set point, a signal is sent to
the SA node via efferent parasympathetic
pathways of the vagal nerve
– Achtylcholine is released to decrease firing
of SA node
– Negative feedback loop
Factors Affecting Heart Rate
• Sympathetic nervous system can
increase heart rate
– Release of epinephrine and norepinephrine
– Exercise, fight or flight response, pain,
fever
Peripheral Resistance
• Resistance to blood flow due to friction
between blood and arterial walls
• Friction due to:
– 1) viscosity
• Red blood cell count
• Blood protein concentration
– 2) diameter of arterioles and capillaries
• “arteriole runoff” = amount of blood that runs out
of the arteries into the arterioles
• Greater resistance = less runoff = increased
blood volume in arteries = increased arterial
pressure
Peripheral Resistance
• Aortic and carotid baroreceptors also
exhibit vasomotor control
– Increase in arterial pressure inhibits
vasoconstrictor center in medulla oblongata
• Impulses sent via parasympathetic fibers to slow
HR and dilate arterioles
– Decrease in arterial pressure stimulates
vasoconstrictor center in medulla oblongata
• Impulses send via sympathetic fibers to increase
vasoconstriction
Venous Return to the Heart
• Venous Pumps
– Inspiration increases pressure gradient
between peripheral and central veins (vena
cava)
• Contraction of the diaphragm increases thoracic
cavity therefore decreasing pressure within
those blood vessels (vena cava and atria)
Venous Return to the Heart
• Venous pumps
– Skeletal muscle contractions squeeze
surrounding veins and help “milk” blood back
to heart
Venous Return to the Heart
• Total Blood Volume
– Increase blood volume = increased blood
return to the heart
– Capillary Exchange: exchange of material
between plasma and interstitial fluid in
tissues
• Osmotic and hydrostatic pressure create inward
and outward directed forces at arterial and
venous ends
• No net loss of blood volume
• Fig 19-18, page 614
Capillary Exchange
Venous Return to the Heart
• Changes in Total Blood Volume
– Antidiuretic Hormone (ADH)
• Secreted from posterior pituitary
• Increases water absorption in kidneys
• Increase water absorption = increase blood plasma
volume
– Renin-angiotensin mechanism
• Renin is secreted from kidneys when blood
pressure is low
• Triggers series of events leading to secretion of
aldosterone from adrenal glands
• Aldosterone causes sodium retention in kidneys;
water follows Na+ = blood volume increases
Venous Return to the Heart
• Changes in Total Blood Volume
– ANH mechanism (atrial natriuretic
hormone)
• Released from cells of the atrial wall in
response to overstretching (abnormally high
venous return)
• Increases sodium loss in urine; water follows
Measuring Arterial Blood
Pressure
• Measured using a sphygmomanometer
• Measured in mmHg
– How high (in mm) air pressure raises a
column of mercury (Hg)
• Procedure:
– Cuff wrapped around brachial artery (upper
arm)
– Pump cuff full of air until the air pressure
exceeds blood pressure (compresses the
artery)
Measuring Arterial Blood
Pressure
– Place stethoscope of brachial artery at
bend of elbow
– Slowly release air from cuff and listen for
Korotkoff sounds
– First sound will be heard when air pressure
= blood pressure  Systolic Blood Pressure
• Force against arterial wall when ventricles are
contracting
– Second sound  Diastolic Blood Pressure
• Force against arterial wall when ventricles are
relaxed
Measuring Arterial Blood Pressure
• Difference between systolic and diastolic
blood pressure = pulse pressure
SBP – DBP = PP
– Increased in patients with arteriosclerosis and
aortic valve insufficiency
– Bruits (“vascular murmur”): abnormal blowing
sounds heard in the carotid arteries
• Present in patients with increased pulse pressure
and/or arteriosclerosis
Measuring Arterial Blood
Pressure
• Continuous Blood Pressure Monitoring –
Arterial blood pressure
Pulse
• Expansion and recoil of an artery
• Based on 2 factors:
– 1) Intermittent ejections of blood from the
ventricles into the aorta
– 2) Elasticity of the arterial walls allows for
stretch and recoil
Hypertension
• High blood pressure exceeding 140/90
• Causes:
– Idiopathic, kidney disease, oral
contraceptives, pregnancy
• S/S:
– Headache, fainting, dizziness
• Complications:
– Ischemic heart disease, heart failure,
kidney failure, stroke
Circulatory Shock
• Failure of circulatory system to deliver
oxygen to tissues
– Cardiogenic shock: results from heart
failure
• MI, heart infection, etc
• Heart can no long act as efficient pump
– Hypovolemic shock: loss of blood volume
• Hemorrhage is common cause
• Loss of interstitial fluid (ex: diarrhea, vomiting,
dehydration, extensive burns)
Circulatory Shock
– Neurogenic shock: systemic dilation of blood
vessels
• Results from abnormal autonomic control
• Decreased blood pressure = decreased blood flow
– Anaphylactic shock: acute allergic reaction
called anaphylaxis
• Causes systemic vasodilation
– Septic shock: complication of septicemia
• Toxins in bloodstream cause vasodilation
• Toxins also damage tissues
• Ex: toxic shock syndrome (TSS) results from
staphylococcal infection