Exam Final: Ch 14 Cardiac Output Flashcards
Cardiac Output (CO)
= volume of blood pumped/min by each ventricle
- (SV)(HR)
Stroke volume (SV)
- blood pumped/beat by each ventricle
- Ex: 70 – 80 ml/beat and average HR = 70 BPM
- CO = SV x HR thus at rest, CO ~ = 5500 ml/min = 5.5L….
- TL blood vol. in body is also ~5.5 L
therefore, during exercise CO
↑ so does rate of blood flow through circulation
Without neuronal influences, SA node will
will drive heart at rate of its spontaneous activity
chronotropic effect)
Normally Symp & Parasymp activity influence HR
Autonomic innervation of SA node is
- main controller of HR because nerve fibers modify rate of spontaneous depolarization
- Symp (↑ HR)
- Parasymp (↓HR)
NE & Epi stimulate
stimulate opening of pacemaker HCN channels
this depolarizes SA faster, increasing HR
ACH promotes opening of
- K+ channels
the resultant K+ outflow counters Na+ influx, slowing depolarization & decreasing HR
Cardiac control center of medulla
coordinates activity of autonomic innervation
Sympathetic endings in atria & ventricles can stimulate
increased strength of contraction
Stroke Volume
Is determined by 3 variables
- End diastolic volume (EDV)
- Total peripheral resistance (TPR)
- Contractility
End diastolic volume (EDV)
= volume of blood in ventricles at end of diastole
- ↑ EDV = ↑ SV; ↓ EDV = ↓ SV
Total peripheral resistance (TPR)
- impedance to blood flow in arteries
- ↑ TPR = ↓ SV; ↓ TPR = ↑ SV
Contractility
strength of ventricular contraction ↓ contractility = ↓ SV
EDV
is amount of blood in ventricles just before they contract = workload (preload) on heart prior to contraction
SV is directly proportional to
preload and contractility
strength of contraction varies directly with EDV
Total peripheral resistance
afterload which impedes ejection from ventricle
Frank-Starling Law of the Heart
States that strength of ventricular contraction varies directly with EDV
intrinsic property of myocardium
When EDV ↑, strength of ventricular contraction ↑, thus SV (blood pumped/beat by each ventricle) ↑
Extrinsic Control of Contractility
- At any given EDV
strength of contraction depends upon level of sympathoadrenal activity = (positive inotropic effect);
positive inotropic effect);
- NE (from symp. nerve endings) and Epi (from adrenal medulla) produce an increase in HR and contraction
2 ways CO is affected by sympathoadrenal activity
- positive inotropic effect on contractility
2. positive chronotropic effect on HR
Venous return
- return of blood to heart via veins
- controls EDV & thus SV & CO;
Venous return
dependent on
total blood volume & venous pressure
Veins hold most of blood in body (~70%) & are thus called
capacitance vessels;
capacitance vessels;
- Have thin walls & stretch easily to accommodate more blood w/o ↑ pressure (=higher compliance)
- have only 0-10 mm Hg pressure vs arteriole pressure of 90 – 100 mm Hg
Venous return is aided by
- Vasoconstriction caused by Symp (smooth muscle contraction)
- Skeletal muscle pumps (squeezes veins)
- Pressure drop during inhalation; promotes flow of venous blood to heart
Regulation of Blood Volume by Kidney
Blood volume ↓ as urinary excretion ↑
Urine formation begins with
- with filtration of plasma in renal capillaries = glomeruli;
- filtrate passes through and is modified by nephron
Volume of urine excreted
- can be varied by changes in reabsorption of filtrate
- adjusted according to needs of body by action of hormones
ADH (vasopressin)
released by
Posterior pituitary when osmoreceptors in hypothalamus detect high osmolality
ADH high osmolality from
excess salt intake or dehydration
high osmolality causes
- thirst and stimulates H20 reabsorption from urine;
- ADH release inhibited by low osmolality
Aldosterone
steroid hormone secreted by adrenal cortex
Aldosterone helps maintain
blood volume & pressure through reabsorption & retention of salt & water
Aldosterone Release stimulated by
salt deprivation, low blood volume, & low blood pressure
Renin-Angiotension-Aldosterone System
When there is a salt deficiency, low blood volume, or pressure, angiotensin II is produced
angiotensin II is produced
- starting w/ renin release from kidneys
- –> renin cleaves angiotensin into angiotensin I
- –> in lungs angiotensin converting enzyme (ACE) cleaves it to form angiotensin II
Angio II causes
- causes a number of effects all aimed at increasing blood pressure
- triggers vasoconstriction, aldosterone secretion, thirst
Atrial Natriuretic Peptide (ANP)
- ↑ blood volume is detected by stretch receptors in left atrium
- causes release of ANP (hormone)
ANP (hormone)
inhibits aldosterone, promoting Na+ (natriureses) excretion and water excretion to lower blood volume, also promotes vasodilation
Vascular Resistance to Blood Flow
- Determines how much blood flows through a tissue or organ
- Vasodilation = ↓ resistance = ↑ blood flow
- Vasoconstriction = ↑ resistance = ↓ blood flow
Blood Pressure (BP) is regulated by
- mainly by controlling HR, SV, & total peripheral resistance (TPR)
- Note: CO = HR X SV, thus BP = HR X SV X TPR
- An increase in any of these can result in increased BP
Sympathoadrenal activity raises
BP via arteriole vasoconstriction and by increased CO
kidney plays role in BP by
regulating blood volume & thus stroke volume
Baroreceptor Reflex Is activated by
changes in BP; which is detected by baroreceptors (stretch receptors) located in aortic arch and carotid sinuses
Increase in BP causes walls of aortic arch and carotid sinuses
to stretch, increasing frequency of APs
Baroreceptors are
tonically active and will send ↑ or ↓ frq APs to vasomotor & cardiac control centers in medulla
Baroreceptors is most sensitive to
to decrease & sudden changes in BP
Recall that when the parasymp (acts to ↓ BP) is on
the symp (acts to ↑ BP) is simultaneously turned off and vise versa
Baroreceptor reflex helps
maintain BP on beat-to-beat basis:
when going from laying to standing
BP ↓ b/c ~ 500 – 700 ml of blood moves from thoracic cavity to lower extremities –> ↓ venous return – > ↓ EDV –> ↓ SV and thus CO thus ↓ BP –> baroreceptors immediately ↓ frq of AP, which ↓ parasymp activity and ↑ symp activity
Measurement of Blood Pressure Is indirect via
auscultation (to examine by listening)
Measurement of Blood Pressure
- no sound is heard during
laminar flow (normal, quiet, smooth blood flow)
Korotkoff sounds can be heard when
sphygmomanometer cuff pressure is greater than diastolic (lowest BP) but lower than systolic (highest BP) pressure
cuff constricts
brachial artery creating turbulent flow & noise as blood passes
1st Korotkoff sound is heard at
at pressure that blood is 1st able to pass thru cuff; represents systolic pressure and last sound occurs when cuff pressure = diastolic pressure
Blood pressure cuff is inflated above
systolic pressure, occluding artery
as cuff pressure is lowered
blood flows only when systolic pressure is above cuff pressure, producing Korotkoff sounds
sounds are heard until
cuff pressure equals diastolic pressure, causing sounds to disappear
Pulse pressure
= (systolic pressure) – (diastolic pressure)
rise in pressure from diastolic to systolic levels =
= reflects stroke volume
Mean arterial pressure (MAP)
represents average arterial pressure during cardiac cycle
Mean arterial pressure (MAP)
has to be approximated because
period of diastole is longer than period of systole
MAP =
= diastolic pressure + 1/3 pulse pressure
Hypertension
- Is blood pressure in excess of normal range for age and gender
- (> 140/90 mmHg); afflicts about 20 % of U.S. adults
Primary or essential hypertension is caused by
complex & poorly understood mechanisms
Secondary hypertension is caused by
known disease processes
Primary (Essential) Hypertension
- Constitutes most of hypertensives
- ~ 95% of high BP cases; increase in peripheral resistance is universal; CO & HR are elevated in many
- Secretion of renin, Angio II, & aldosterone is variable
development of hypertension
- Sustained high stress (which increases Symp activity thus ↑ TPR and HR) and high salt intake act synergistically in
Prolonged high BP causes
thickening of arterial walls, resulting in atherosclerosis
Primary (Essential) Hypertension
- Kidneys appear to be
unable to properly excrete Na+ and H20
Dangers of Hypertension
- Patients are often asymptomatic until substantial vascular damage occurs
- Contributes to atherosclerosis, increases workload of the heart leading to ventricular hypertrophy and congestive heart failure, often damages cerebral blood vessels leading to stroke, these are why it is called the “silent killer”
Treatment of Hypertension
- includes lifestyle changes such as cessation of smoking, moderation in alcohol intake, weight reduction, exercise, reduced Na+ intake
Treatment of Hypertension
- Drug treatments
- include diuretics to reduce fluid volume, beta-blockers to decrease HR, calcium blockers, ACE inhibitors to inhibit formation of Angio II, & Angio II-receptor blockers
Circulatory Shock
Occurs when
- there is inadequate blood flow to, and/or O2 usage by tissues
- Cardiovascular system undergoes compensatory changes
- Sometimes shock becomes irreversible & death ensues
Severe allergic reaction can cause
a rapid fall in BP called anaphylactic shock
anaphylactic shock
Due to generalized release of histamine causing vasodilation
Rapid fall in BP called neurogenic shock can result from
decrease in Symp tone following spinal cord damage or anesthesia
Cardiogenic shock is
- common following cardiac failure resulting from infarction (myocardial necrosis caused by ischemia) that causes significant myocardial loss
- Severe arrythmias or valve damage
Septic Shock
- Refers to
dangerously low blood pressure resulting from sepsis (infection); Mortality rate is high (50-70%)
Septic Shock Often occurs as a result of
endotoxin release from bacteria
endotoxin
- Endotoxin induces NO production causing vasodilation and resultant low BP
- Effective treatment includes drugs that inhibit production of NO
Hypovolemic Shock
- Is circulatory shock caused by low blood volume
- E.g. from hemorrhage, dehydration, or burns
- characterized by decreased CO and BP
decreased CO & BP
Compensatory responses include
sympathoadrenal activation via baroreceptor reflex
Hypovolemic Shock
- low blood volume
- Results in low BP, rapid pulse, cold clammy skin (b/c of vasoconstriction), low urine output
- Blood is diverted to brain and heart at expense of other organs
Congestive Heart Failure
Occurs when CO is insufficient to maintain blood flow required by body
Congestive Heart Failure
- insufficient CO to maintain blood flow Caused by
myocardial infarction (most common), congenital defects, hypertension (↑afterload which impedes ejection from ventricle), aortic valve stenosis (thickened and hardened valve), disturbances in electrolyte levels
Congestive Heart Failure
- insufficient CO to maintain blood flow Compensatory responses are
similar to those of hypovolemic shock (sympathoadrenal activation)
- Causes ventricular hypertrophy and ↑ blood volume
Congestive Heart Failure
- Treatment
- Digitalis: (blockage of Na+/K+ pumps in myocardial cells –> ↓ Na+ driving force thus diffusion is ↓ and there is ↓ Na+ available for Na+/Ca2+ exchanger thus ↑ Ca2+ –> ↑ strength of contraction)
- Vasodilators like nitroglycerine, & diuretics
