Download Nerve activates contraction

PowerPoint® Lecture Slide Presentation
by Patty Bostwick-Taylor,
Florence-Darlington Technical College
The
Cardiovascular
System
11
PART B
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The Heart: Conduction System
 Intrinsic conduction system (nodal system)
 Heart muscle cells contract, without nerve
impulses, in a regular, continuous way
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The Heart: Conduction System
 Special tissue sets the pace
 Sinoatrial node = SA node (“pacemaker”),
is in the right atrium
 Atrioventricular node = AV node, is at the
junction of the atria and ventricles
 Atrioventricular bundle = AV bundle
(bundle of His), is in the interventricular
septum
 Bundle branches are in the interventricular
septum
 Purkinje fibers spread within the ventricle
wall muscles
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Heart Contractions
Figure 11.6
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Heart Contractions
 Contraction is initiated by the sinoatrial node (SA
node)
 About 75 beats per minute
 AV node can initiate pulse if needed, but at a
much slower pace
 Force cardiac muscle depolarization in one
direction—from atria to ventricles
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Heart Contractions
 Once SA node starts the heartbeat
 Impulse spreads to the AV node
 Impulse slows so atria can fill
 Then the atria contract
 At the AV node, the impulse passes through the
AV bundle, bundle branches, and Purkinje fibers
 Blood is ejected from the ventricles to the aorta
and pulmonary trunk as the ventricles contract
 Ventricles contract almost simultaneously
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Heart Contractions
Figure 11.6
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Electrocardiography
 Used to make a visible record of the heart’s
contractions
 Called an electorcardiogram
 EKG or ECG
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Electrocardiogram
 P Wave
 Depolarization of atria (contract)
 QRS Wave
 Repolarization of atria (rest)
 Depolarization of Ventricles
 T Wave
 Repolarization of Ventricles
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Figure 13.14
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Artificial Cardiac Pacemakers
 Continuously
charging
pacemakers
 Stimulate the heart
at a set rhythm
 Demand
Pacemakers
 Stimulate the heart
only when it is
below a set
minimum
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Artificial Cardiac Pacemakers
 Inferior to the heart
 Can’t speed up the heart when necessary
 Can’t slow down when needed
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The Heart: Regulation of Heart Rate
 Increased heart
rate
 Sympathetic
nervous system
 Crisis
 Low blood
pressure
 Hormones
 Exercise
 Decreased blood
volume
 Emotions
 Anxiety, fear,
anger
 Increased blood
temperature
 Epinephrine
 Thyroxine
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The Heart: Regulation of Heart Rate
 Decreased heart
rate
 Parasympathetic
nervous system
 Cold receptors
 Emotions- grief and
pain
 High blood pressure
or blood volume
 Decreased venous
return
 Release
Acetylcholine (Ach)
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Cardiac Pressorflexes
 Receptors sensitive to changes in pressure
(baroreceptors)
 Aortic baroreceptors
 Carotid baroreceptors
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Cardiac Pressorflexes
Detect increase
In blood pressure
Sends to
Brain
Decrease in
Blood Pressure
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SA Node
Releases
Ach
Heart Rate
decreases
Cardiac Arrythmia’s
 Arrythmia- abnormal beating of the heart
 Tachycardia—rapid heart rate over 100 beats
per minute
 Bradycardia—slow heart rate less than 60
beats per minutes
 Sinus Arrythmias- variation of heart during
breathing cycle
 Increases during inspiration
 Decreases during expiration
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The Heart: Cardiac Cycle
 Complete heartbeat or pumping cycle
 Atria contract simultaneously
 Atria relax, then ventricles contract
 Systole = contraction
 Diastole = relaxation
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Filling Heart Chambers: Cardiac Cycle
Left atrium
Right atrium
Left ventricle
Right ventricle
Ventricular
filling
Atrial
contraction
Mid-to-late diastole
(ventricular filling)
Isovolumetric
Ventricular
contraction phase ejection phase
Isovolumetric
relaxation
Ventricular systole
(atria in diastole)
Early diastole
Figure 11.7
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Filling Heart Chambers: Cardiac Cycle
Left atrium
Right atrium
Left ventricle
Right ventricle
Ventricular
filling
Mid-to-late diastole
(ventricular filling)
Figure 11.7, step 1a
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Filling Heart Chambers: Cardiac Cycle
Left atrium
Right atrium
Left ventricle
Right ventricle
Ventricular
filling
Atrial
contraction
Mid-to-late diastole
(ventricular filling)
Figure 11.7, step 1b
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Filling Heart Chambers: Cardiac Cycle
Left atrium
Right atrium
Left ventricle
Right ventricle
Ventricular
filling
Atrial
contraction
Mid-to-late diastole
(ventricular filling)
Isovolumetric
contraction phase
Ventricular systole
(atria in diastole)
Figure 11.7, step 2a
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Filling Heart Chambers: Cardiac Cycle
Left atrium
Right atrium
Left ventricle
Right ventricle
Ventricular
filling
Atrial
contraction
Mid-to-late diastole
(ventricular filling)
Isovolumetric
Ventricular
contraction phase ejection phase
Ventricular systole
(atria in diastole)
Figure 11.7, step 2b
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Filling Heart Chambers: Cardiac Cycle
Left atrium
Right atrium
Left ventricle
Right ventricle
Ventricular
filling
Atrial
contraction
Mid-to-late diastole
(ventricular filling)
Isovolumetric
Ventricular
contraction phase ejection phase
Isovolumetric
relaxation
Ventricular systole
(atria in diastole)
Early diastole
Figure 11.7, step 3
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Atrial Systole
 When atria contract
 Sends blood to ventricles
 AV valves are open
 SL valves closed
 Ventricles fill with blood
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Isovolumetric Ventricular Contraction (IVC)
 Before SL valves open
 Pressure in ventricle increases
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Ejection
 SL valves open
 Blood goes to ventricles
 Blood is ejected
 Residual Volume- the blood that remains in the
heart at the end of the ejection period
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Isovolumetric Ventricular Relaxation (IVR)
 Between the closing SL valves and opening of AV
valves
 AV valves won’t open until the pressure in the
atrial chambers is above that in the relaxing
ventricles
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Passive Ventricular Filling (PVR)
 When blood rushes into the ventricles and they fill
up again
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Copyright © 2009 Pearson Education, Inc., publishing as Benjamin Cummings
Please note that due to differing operating
systems, some animations will not appear
until the presentation is viewed in
Presentation Mode (Slide Show view). You
may see blank slides in the “Normal” or
“Slide Sorter” views. All animations will
appear after viewing in Presentation Mode
and playing each animation. Most
animations will require the latest version of
the Flash Player, which is available at
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Heart Sounds
 Heard through a stethoscope
 Lubb-dubb
 Systyolic sound
 First sound, longer and louder
 Caused by contraction of ventricle and closing
of AV valves
 Diastolic sound
 Second sound, shorter and sharper
 Caused by closing of SL valves
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Hemodynamics
 Term to describe the changing circulation of
blood
 Blood must be shifted from less active areas to
more active areas
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Primary Principle of Circulation
 Control of circulation comes from Newton’s law of
motion
 1st law- fluid doesn’t flow when pressure is the
same in all parts
 2nd law- fluid only flows when pressure is
higher in one area than in another
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Heart Sounds
 Heart murmur
 Incomplete closing of the valves
 Fairly common
 Most do not need treatment
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The Heart: Cardiac Output
 Cardiac output (CO)
 Amount of blood pumped by each side
(ventricle) of the heart in one minute
 Stroke volume (SV)
 Volume of blood pumped by each ventricle in
one contraction (each heartbeat)
 Usually remains relatively constant
 About 70 mL of blood is pumped out of the left
ventricle with each heartbeat
 Heart rate (HR)
 Typically 75 beats per minute
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Control of Arterial Blood Pressure
 Primary determinant of arterial blood pressure is
volume of blood in arteries
 Arterial blood volume is directly proportional
to arterial blood pressure
 Two most important factors influencing arterial
pressure through their influence on arterial
volume
 Cardiac output
 Peripheral resistance
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Cardiac Output
 Is the amount of blood pumped by each ventricle
in one minute
 Primary indicator of the functional capacity of
circulation to meet demands of physical activity
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Cardiac Output
 Stroke volume- volume of blood pumped by each
ventricle in one contraction
 Heart rate is typically 75 beats per minute
 Q = S.V. x H.R.
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The Heart: Cardiac Output
 CO = HR  SV
 CO = HR (75 beats/min)  SV (70 mL/beat)
 CO = 5250 mL/min
 The greater the stroke volume, the greater the
cardiac output, but only if heart rate remains the
same
 Anything that tends to change HR or SV tends to
change Q, arterial volume, and arterial blood
pressure in the same direction
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Target Heart Rate
 Maximum HR = 220-age
 Target HR = Max HR – resting HR x .7 + resting HR
 Any increase in cardiac output is directly
proportional to an increase in action for aerobic
metabolism
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Startling’s Law of the Heart
 The longer, or more stretched the heart fibers are
at the beginning of a contraction, the stronger the
contraction will be.
 Amount of blood in the heart determines how
stretched the fibers are
 The more blood returned to the heart per minute,
the more stretched the fibers are and the stronger
the contraction is.
 Startling’s Law ensures that increase amounts of
blood returned to the heart are pumped out of it
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Peripheral Resistance
 Peripheral resistance is the resistance to blood
flow imposed by the force of friction between
blood and the walls of its vessels
 Arterial blood pressure tends to vary directly with
peripheral resistance
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Peripheral Resistance
 Causes of friction
 Viscosity- the thickness of blood
 Length of the vessel
 Diameter of the vessel
 Arterioles contract and dilate and change the
resistance to blood flow.
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Peripheral Resistance
 Peripheral resistance determines pressure by
controlling the rate of arteriole runoff
 The amount of blood that runs out of the
arteries and into the arterioles
 The greater the resistance the less runoff and
the more blood left in the arteries and the
higher the blood pressure
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Peripheral Resistance
 Blood viscosity come from red blood cells
 The more red blood cells, the thicker the blood
 Anemia or hemorrhage can cause a decrease
in blood viscosity, which can lower peripheral
resistance and arterial blood pressure
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Vasomotor Control Mechanism
 Influence blood pressure by changing blood
distribution (hemodynamics) and diameter of
arterioles
 Smooth muscle of tunica media that allows
this change
 Sympathetic fibers is smooth muscle of vessels
cause them to constrict and increase pressure
 Dilate they decrease pressure
 Heat and alcohol causes vasodialation
 Nicotine, intense fear or anger, and cold causes
vasocontriction and rise in blood pressure
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Vasomotor Pressorreflexes
Cardiac baroreceptors
Detect increase
Pressure
Decrease
Heart Rate
Inhibits
Vasocontrictor
center
Pressure
Decreases
Vessel
Dialates
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Vasomotor Pressorrelexes
 Located in the aorta and carotid artery
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Vasomotor Chemoreflexes
 Chemoreceptors located in the aortic arch and
carotid body
 Sensitive to excess carbon dioxide- hypercapnia
 Less sensitive to deficiency of blood oxygenhypoxia
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Medullary Ischemic Reflex
 Activates when carbon dioxide builds up in the
brain
 hypercapnia
 controls blood vessels to send oxygen to brain
 If too little oxygen, this system can’t operate
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Pulse
 Pulse
 Pressure wave of blood
 Monitored at “pressure points” in arteries where
pulse is easily palpated
 Pulse averages 70–76 beats per minute at rest
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Venous Return to Heart
 Each time diaphram contracts, changes pressure
in vena cava and causes blood to flow back to
heart
 Skeletal muscle contractions act as booster
pumps
 valves in veins prevent blood from falling back
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Minute Volume of Blood
 Minute Volume of blood
 amount of blood circulating through the body
per minute
 Poiseuille’s Law Minute Volume = Pressure Gradient
Peripheral Resistance
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Blood Pressure
 Measured with a sphygmomanometer
 amount of air pressure equal to arterial
pressure
 Measured with the auscultatory method
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Measuring Arterial Blood Pressure
Figure 11.20a
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Measuring Arterial Blood Pressure
Figure 11.20b
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Measuring Arterial Blood Pressure
Figure 11.20c
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Measuring Arterial Blood Pressure
Figure 11.20d
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 Systolic—pressure at the peak of ventricular
contraction
 Diastolic—pressure when ventricles relax
 Write systolic pressure first and diastolic last
(120/80 mm Hg)
 Pressure in blood vessels decreases as distance
from the heart increases
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Comparison of Blood Pressures
in Different Vessels
Figure 11.19
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Blood Pressure: Effects of Factors
 BP is blood pressure
 BP is affected by age, weight, time of day,
exercise, body position, emotional state
 CO is the amount of blood pumped out of the left
ventricle per minute
 PR is peripheral resistance, or the amount of
friction blood encounters as it flows through
vessels
 Narrowing of blood vessels and increased
blood volume increases PR
 BP = CO  PR
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Blood Pressure: Effects of Factors
 Neural factors
 Autonomic nervous system adjustments
(sympathetic division)
 Renal factors
 Regulation by altering blood volume
 When blood pressure too high, kidneys
allow more water to leave body in urine,
which results in thinner blood and
decreased pressure
 Renin—hormonal control
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Blood Pressure: Effects of Factors
 Temperature
 Heat has a vasodilating effect
 Cold has a vasoconstricting effect
 Chemicals
 Various substances can cause increases or
decreases
 Diet
 Debated, but some believe a diet low in salt,
saturated fates and cholesterol will help
prevent hypertension
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Variations in Blood Pressure
 Normal human range is variable
 Normal
 140–110 mm Hg systolic
 80–75 mm Hg diastolic
 Hypotension
 Low systolic (below 110 mm HG)
 Often associated with illness
 Hypertension
 High systolic (above 140 mm HG)
 Can be dangerous if it is chronic
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Arterial Vs. Venous Bleeding
 Blood escapes from an artery in spurts and
gushes out
 Blood leaving a vein in a uniform fashion
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Velocity of Blood
 When a liquid flows from one cross-sectional size
to an area with a larger cross-sectional size, its
velocity slows
 Why would capillaries have a slow velocity?
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Pulse Mechanism
 The alternate expansion and recoil of an artery
 A pulse can be felt because arterial walls can
expand and contract
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Where can pulse be felt
 Can be felt wherever an artery lies over a bone
 Common pulse points
 Radial artery
 Carotid artery
 Brachial artery
 Femoral artery
 Facial Artery
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Pulse
Figure 11.18
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Pulse Wave
 Pulse wave dissipates as it travels away from the
heart
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Venous Pulse
 Only exists in large veins
 Not as important as arterial pulse
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Capillary Exchange
 Substances exchanged due to concentration
gradients
 Oxygen and nutrients leave the blood
 Carbon dioxide and other wastes leave the
cells
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Capillary Exchange: Mechanisms
 Direct diffusion across plasma membranes
 Endocytosis or exocytosis
 Some capillaries have gaps (intercellular clefts)
 Plasma membrane not joined by tight
junctions
 Fenestrations (pores) of some capillaries
 Found where absorption is a priority like
intestinal capillaries
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Capillary Exchange: Mechanisms
Figure 11.22
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Fluid Movements at Capillary Beds
 Blood pressure forces fluid and solutes out of
capillaries
 Osmotic pressure draws fluid into capillaries
 Blood pressure is higher than osmotic pressure at
the arterial end of the capillary bed
 Blood pressure is lower than osmotic pressure at
the venous end of the capillary bed
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Fluid Movements at Capillary Beds
Figure 11.23
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Developmental Aspects of
the Cardiovascular System
 A simple “tube heart” develops in the embryo and
pumps by the fourth week
 The heart becomes a four-chambered organ by
the end of seven weeks
 Few structural changes occur after the seventh
week
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Congenital Heart Defects
 Congenital means present at birth
 Maternal infection and ingestion of drugs during
first three months of pregnancy are major causes
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Aerobic Exercise and the heart
 Heart will hypertrophy and cardiac output
increases if exercise regularly aerobically
 Pulse rate and blood pressure decrease
 Clears fatty deposits from blood vessel walls
 Must be regular exercise
 Many weekend athletes are myocardial
infarction victims
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Developmental Aspects of
the Cardiovascular System
 Aging problems associated with the
cardiovascular system include
 Venous valves weaken
 Varicose veins
 Progressive atherosclerosis
 Loss of elasticity of vessels leads to
hypertension
 Coronary artery disease results from vessels
filled with fatty, calcified deposits
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Certified Surgical Technologist
 Use their knowledge of anatomy to assist
surgeons
 Keep operating area sterile
 Use knowledge of surgical tools to assist
physician
 Must anticipate Dr.’s next move and are their
extra eyes during a procedure
 Must complete an accredited training program
and pass national certifying exam
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Cycle of Life
 As a person ages, blood pressure increases
 As a person ages, pulse rate decreases
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Hypertension
 Cause of most office visits to physicians
 140/90 is hypertension
 Primary Hypertension- has no known cause
 Secondary Hypertension
 Caused by pregnancy, kidney disease, or
other cause
 Genetics play a huge role
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Hypertension
 Males have higher rates of hypertension
 Women more likely to die from a heart attack
 Tends to be higher in African Americans
 Direct relationship between age and hypertension
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Hypertension
 Other risk factors include
 Obesity
 Calcium deficiencies
 High alcohol and caffeine intake
 Smoking
 Lack of exercise
 Type “A” personalities
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Hypertension
 Complications of untreated hypertension
 Ischemic heart disease and heart failure
 Kidney failure
 stroke
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Hypertension
 Known as the “silent killer”
 No overt signs
 Headaches, dizziness, and fainting may occur
 Need regular screenings to detect
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Orthostatic Hypertension
 Temporary low blood pressure and dizziness
when rising suddenly from a reclining position
 Common among elderly
 Aging sympathetic system reacts slowly to
postural changes and blood pools in lower
limbs
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Circulatory Shock
 Failure of the circulatory system to adequately
deliver oxygen to the tissues
 Many types of circulatory shock
 Cardiogenic Shock
 Results from any type of heart failure
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Circulatory Shock
 Hypovolemic Shock
 Results from the loss of blood volume in the
blood vessel which leads to low blood
pressure
 Hemmorhage is a common cause
 Also caused by loss of interstitial fluid
common in chronic diarrhea, vomiting,
dehydration, or severe burns
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Circulatory Shock
 Neurogenic Shock
 Results from widespread dilation of blood
vessels
 Caused by injury to the spinal cord or medulla,
depressive drugs,
 Anaphylatic Shock
 Results from allergic reaction
 Causes blood vessels to dialate
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Circulatory Shock
 Septic Shock
 Complication where infectious agents release
toxins into the blood
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