Week 5 - Cardiac Output Flashcards
What is the Cardiac Cycle?
events that occur from the beginning of one heartbeat to the beginning of the next
-consists of two periods: diastole (relaxation/filling with blood) + systole (contraction/ejection)
Diastole
(Passive Ventricular Filling)
Cardiac Cycle
AV valves are open, blood flows from atria into relaxed ventricles
-accounts for most of ventricular filling
-semilunar valves closed
begins just after ventricular contraction
Diastole
(Active Ventricular Filling)
Cardiac Cycle
AV valves open, atria contract + complete ventricular filling
-semilunar valves closed
Systole
(Period of Isovolumic Contraction)
Cardiac Cycle
ventricular contraction causes the AV valves to close (beginning of vent. systole)
-semilunar valves remain closed
all 4 valves are closed
Systole
(Period of Ejection)
Cardiac Cycle
continued ventricular contraction pushes blood out of the ventricles, causing the semilunar valves to open
-AV valves are closed
Diastole
(Period of Isovolumic Relaxation)
Cardiac Cycle
blood flowing back towards the relaxed ventricles causes semilunar valves to close (beginning of vent. diastole)
-AV valves remain closed
all 4 valves are closed
Steps in the Cardiac Cycle
- Diastole: Passive Ventricular Filling
- Diastole: Active Ventricular Filling
- Systole: Period of Isovolumetric Contraction
- Systole: Period of Ejection
- Diastole: Period of Isovolumetric Relaxation
Why is Cardiac Output (C.O.) vital to homeostasis?
controls the amount of blood flow to tissues and prevents any undue stress on the heart
Cardiac Output
(C.O)
the volume of blood pumped each minute
C.O. = SV x HR
-generally proportional to body surface area
-depends on venous return/rate of flow to tissues
-proportional to energy requirements of the tissues (rate of flow to tissues depends on total peripheral resistance)
Heart Rate
Cardiac Output
varied by balance of sympathetic and parasympathetic influence on SA node
-sympathetic: stimulates HR (epinephrine/norepi)
-parasympathetic: inhibits heart by vagus nerve stimulation
-normally 60-100 bpm
directly proportional to C.O.
Filling of the ventricles results in:
Cardiac Output
end diastolic volume (EDV) =120-130 mL
Emptying of the ventricles results in:
Cardiac Output
stroke volume (SV) output = 70 mL
Remaining blood left over in the ventricles:
Cardiac Output
end systolic volume (ESV) = 50-60 mL
Ejection Fraction
(EF)
Cardiac Output
fraction / percentage of end-diastolic volume ejected + pumped out by the ventricle
-normal EF = about 55-60%
-less than 55% EF = heart failure
-EF increases during exercise
EF = SV / EDV
At rest, why is C.O. relatively unchanged in a long distance runner?
their SV is more effective because the heart muscle is strong + will pump more during systole, effectively decreasing HR
Stroke Volume
(SV)
Cardiac Output
the volume of blood pumped out by each ventricle per each contraction
-determined by preload, afterload + contractility
-SV = EDV - ESV
emptying of the ventricles
Cardiac Output is influenced by:
intrinsic + extrinsic control
-both factors increase SV by increasing strength of heart contraction
Intrinsic Control
Cardiac Output
-heart muscle operates short of optimal sarcomere length
-stretches it by bringing more blood back to the heart, increasing force of contraction (Frank Starling Law)
Extrinsic Control
Cardiac Output
Norepinephrine from sympathetic + epinephrine from adernal medulla increase the opening of Ca2+ channels
-more Ca2+ increases the force of contraction
End Diastolic Volume
Regulation of Stroke Volume
the amount of blood collected in a ventricle at the end of diastole
EDV = preload
End Systolic Volume
Regulation of Stroke Volume
the amount of blood remaining in a ventricle after contraction
Preload
Factors Determining SV
volume of blood in ventricles at the end of diastole (EDV)
gives the volume of blood that the ventricle has available to pump
Contractility
Factors Determining SV
the force that the muscle can create at the given length
-dependent on stretch and EDV
intrinsic strength of cardiac muscles
Afterload
Factors Determining SV
the back pressure exterted by blood in the large arteries leaving the heart
-the arterial pressure against which the muscle will contract
-end systolic wall stress/resistance
-increase in afterload = increased cardiac workload
(resistance left ventricle must overcome to circulate blood)
End Diastolic Volume is Affected by:
Factors Affecting SV
venous return or the volume of blood returning to the heart + preload (the amount that ventricles are stretched by the blood = EDV)
End Systolic Volume is Affected by:
Factors Affecting SV
-myocardial contractility force due to factors other than EDV
-afterload (back pressure exterted by blood in large arteries leaving the heart)
Increase in Parasympathetic Activity
Autonomic Control of C.O.
via M2 cholinergic receptors in the heart will decrease HR
-decrease HR to 20-40 bpm + decrease force of contraction by 20-30%
-releases ACh (increase permeability to K+)
-negative ionotropic effect (hyperpolarization + inhibtion)
-force of contractions reduced = decreased EF
by Vagus nerve stimulation
Increase in Sympathetic Activity
Autonmic Control of C.O.
via B1 + B2 adrenergic receptors throughout the heart will increase HR
-increase HR up to 200 bpm + double force of contraction
**-release norepinephrine from sympathetic postganglionic fiber / adrenal medulla **(increase permeability of Ca2+ and Na+)
-ventricles contract more forcefully -> increasing SV + EF, decreasing ESV
-positive ionotropic effect
In what conditions would you see an increase in preload?
-hypovolemia
-regurgitation of cardiac valves
-heart failure
In what conditions would you see an increase in afterload?
-hypertension
-vasoconstriction
(increase afterload = increase cardiac workload)
Afterload to LV:
aortic arterial pressure
afterload LV is greater than afterload RV
Afterload to RV:
pulmonary arterial pressure
Factors on C.O.
-preload
-afterload
-contractility
-heart rate
How does Preload affect C.O.
increased preload = increased C.O.
-more in -> more out
(Frank-Starling Mechanism)
How does Afterload affect C.O.
increased afterload = decreased C.O.
How does contractility affect C.O.
increased contractility = increased C.O.
How does HR affect C.O.
increased HR = increased C.O.
-pumping fast will eventually allow less blood to enter the heart -> decrease C.O.
dual effects; will increase to an extent, then decrease C.O.
Cardiac Reserve
the difference between resting and maximal C.O.
Normal C.O.
Limits of C.O.
about 5 L/min
Plateau C.O.
Limits of C.O.
13 L/min
Hypereffective Heart Plateau C.O.
Limits of C.O.
20 L/min
Hypoeffective Heart Plateau C.O.
Limits of C.O.
less than 5 L/min
Hypereffective Heart
Limits of C.O.
effected by:
-nervous excitation
-cardiac hypertrophy: exercise (marathon runners get 30-40 L/min) + Aortic Valve Stenosis
Hypoeffective Heart
Limits of C.O.
-valvular disease
-increased output pressure
-congenital heart disease
-myocarditis
-cardiac anoxia
-toxicity
Increased Venous Return =
increased EDV
(intrinsic control)
Frank Starling Law
the heart normally pumps out (during systole) the volume of blood returned to it during diastole
-heart muscle is normally (functioning at rest) short of it’s optimal sarcomere length
-increased preload -> increased stretch of muscle -> increased force of contraction -> increased SV
-cardiac muscle fibers contract more forcefully when stretched (preload), thus ejecting more blood (increased SV, decreased ESV)
-SV may increase due to greater contractility (ex. exercise) independent of EDV
only true for a normal, undiseased heart
Frank Starling Law: Venous Return (VR)
venous return (VR) increases when there is an increase in blood flow through the peripheral organs
-slow heartbeat and exercise increase venous return (VR), increasing SV
-increase VR -> increased EDV
-decreased VR -> decreased EDV
-any decrease in EDV = decrease in SV
-blood loss and extremely rapid heartbeat = decreased SV
peripheral blood flow is a major determinant of C.O.
Compensation for Heart Failure
Frank Starling Law
sympathetic stimulation: shifts Frank-Starling curve to the left, increasing contractility of the heart (trying to go towards normal heart function)
-compensatory increase in EDV due to increase in blood volume = increase in contraction
-ejects normal SV due to operating at a longer cardiac muscle fiber length
Venous Return (VR) + Filling Time Effects on EDV
-sympathetic: increased VR = increased EDV
-parasympathetic: decreased VR = decreased EDV
-sympathetic: increased filling time = increased EDV
-parasympathetic: decreased filling time = decreased EDV
EDV directly affects SV
Sympathetic + Parasympathetic Effects on Contractility of Muscle Cells
-sympathetic: increased contractility = increased ESV
-parasympathetic: decreased contractility = decreased ESV
contractility affects ESV -> affects SV
Vasoconstriction (increased cont.) v. Vasodilation (decreased cont.) Effects on Afterload
-vasoconstriction (increased contractility/sympathetic): increased afterload = increased ESV
-vasodilation (decreased contractility/parasympathetic): decreased afterload = decreased ESV
afterload effects ESV -> affects SV
EDV + ESV Effects on SV
-sympathetic: increased EDV = increased SV
-parasympathetic: decreased EDV = decreased SV
-sympathetic: increased ESV = decreased SV
-parasympathetic: decreased ESV = increased SV
Increased contractility is due to:
-increased sympathetic stimuli
-certain hormones (epi, norepi, thyroxine T4 - positive ionotropic effects)
-Ca2+ and some drugs (elevated by digitalis to interefere w/ Ca2+ removal from sarcoplasm)
Decreased contractility is due to:
-acidosis
-increased extracellular K+
-calcium channel blockers (beta blockers -olol prevent symp. stimulation - negative chronotropic effect)
Peripheral Resistance + C.O.
increasing peripheral resistance decreases C.O.
C.O. = arterial pressure / total peripheral resistance
Determinants of Venous Return (VR)
small increase in RA pressure -> dramatic decrease in VR
(mean systemic pressure)
pressure change is slight
VR + C.O.
-C.O. increases w/ atrial pressure (normal A. pressure = 10 mmHg)
-venous return decreases w/ atrial pressure
-working C.O. is where venous return curve meets cardiac output curve
Compensation for Increased Blood Volume
- increased C.O. increases capillary pressure, sending more fluid to tissues
- vein volume increases
- pooling of blood in the liver and spleen
- increased peripheral resistance reduces C.O.
Effects of Sympathetic Stimulation
- increases contractility of the heart
- decreases volume by contracting the veins
- increases filling pressure
- increases resistance
Disease States Lowering Total Peripheral Resistance
- Beriberi: insufficient thiamine; tissues starve because they cannot use nutrients
- AV fistula: ex. for dialysis
- Hyperthyroidism: reduced resistance cause by increased metabolism
- Anemia (lack of RBCs): effects viscosity and transport of O2 to the tissues
Disease States Lowering Cardiac Output
- Heart disease, valvular disease, myocarditis, cardiac tamponade, shock
- shock = nutrirional deficiency of tissues
- decreased venous return by: reduced blood volume, venous dilation (increased circulatory volume), venous obstruction
Hormonal Regulation of Blood Pressure
- renin
- ADH
- aldosterone
intra + extracellular ion conc. maintained for normal heart function
Hypocalcemia
Homeostatic Imbalances
reduced ionic calcium depresses the heart
Hypercalcemia
Homeostatic Imbalances
dramatically increases heart irritability and leads to spastic contractions
-high plasma Ca2+ (ECF)
-positive ionotropic
Hypernatremia
Homeostatic Imbalances
blocks heart contraction by inhibiting ionic calcium transport
-high plasma Na+ (ECF)
-negative chronotropic
Hyperkalemia
Homeostatic Imbalances
leads to heart block and cardiac arrest
-high plasma K+ (ECF)
-negative chronotropic
-used in lethal injection
Renin
Hormonal Regulation of BP
sympathetic stim.. hypotension, decreased sodium delivery -> kidney -> renin -> adrenal glands -> aldosterone -> kidney tubules retain water and increase BP / blood volume, systemic vasoconstriction, cardiac + vascular hypertrophy
Angiotensin
Hormonal Regulation of BP
angiotensin -> vasoconstrictors -> increased resistance + BP
Baroreceptor Reflex
Neural Control
stimulated by increase in aterial pressure (stretch)
-regulate the heart when BP increases or decreases
-involved in short term regulation of BP
-effect: negative chronotropic + ionotropic
Chemoreceptor Reflex
Neural Control
stimulated by decreased O2/pH or increased CO2
-effect: positive chronotropic + ionotropic
-less important in regulating cardiac function
Proprioceptor Reflex
Neural Control
stimulated by muscle and joint movement
-effect: increase HR during exercise
Role of Epinephrine
increases HR and contractility
-released from adrenal gland
(sympathetic stimulation)
Role of Thyroxin (T4)
increases HR
-released from thyroid gland
Autoregulation of the Heart
SV is autoregulated by ventricular filling (Frank-Starling Law)
Preload Increase Effect on EF
increased preload = increased EF
preload increase seen in AR, MR + anemia
Afterload Increase Effect on EF
afterload increase = EF decrease
afterload increase seen in AS
Angiographic Assessment
Tests for LV Function
determining actual motion of ventricle
Echocardiography
Tests for LV Function
allows measurement of EF in relation to cardiac filling and visualizing structures that are interfering with C.O. (ex. fluid in pericardial sac)
CT Scan
Tests for LV Function
excellent visualization of cardiac structures including reproducible measuremenat of wall thickness + ESV + EDV
MRI
Tests for LV Function
allows visualization even in patients with abnormal anatomy/geometry
Heart Failure
physiological state in which C.O. is insufficient for body’s needs
-problem with structure or function of heart impairs blood flow / supply
-EF less than 40%
reduction in myocardial efficiency -> produces changes w/in heart
Heart Failure Effects on C.O.
-reduced contractility (due to overload of ventricle)
-reduced SV (result of failure of diastole, systole, or both)
-reduced spare capacity
-increased HR (stimulated by increased sympathetic activity to maintain C.O.)
-hypertrophy of myocardium (due to terminally differentiated muscle fibers increasing in size in an attempt to improve contractility)
-enlargement of the ventricles (contributing to enlargement + spherical shape of failing heart)
Causes of CHF
(Congestive Heart Failure)
- Coronary Artery Disease (CAD)
- heart attack
- HTN
- Valve disorders
- inflammation
- kidney disease
- abnormal heart rhythms
- pulmonary HTN
- severe anemia
- hyperthyroidism
- hypothyroidism
Higher than normal EF (greater than 60%)
indicates presence of hypertrophic cardiomyopathy
Lower than normal EF (less than 55%)
heart is weakened (heart failure)
Systolic Heart Failure
decreased contractility
-enalrged heart fills w/ blood -> ventricles pump less than 50% of the blood
-failure of pump function of the heart
-decreased EF (less than 40-50%) -> inadequate C.O.
-caused by dysfunction of cardiac myocytes
-common mechanism of damage: ischemia -> infarction/scar formation
-EDV + pressure increase
-leads to pulmonary edema (left side of the heart)
-leads to peripheral edema (right side of the heart)
more readily recognized than diastolic HF
Diastolic Heart Failure
decreased filling of the ventricles
-stiff ventricles fill w/ less blood than normal -> ventricles pump out 60% of blood
-failure of ventricle to relax = stiffer wall
-decreased filling = decreased SV = decreased C.O. (despite normal EF)
-pulmonary edema (LHF)
-peripheral edema (RHF)
-sensitive to increases in HR
-diastolic function worsens with age
-limited exercise tolerance -> elevated pulmonary venous pressure -> increases work of breathing
may be asymptomatic
Etiologies of Systolic Heart Failure
- Coronary Artery Disease (65%)
- Idiopathic dilated cardiomyopathy
- Alcohol/toxing induced cardiomyopathy
- Infectious/inflammatory process
- Familial dilated cardiomyopathy
- Postpartum cardiomyopathy
- Stress induced cardiomyopathy
- Endorcine/nutritional causes
- Iron overload cardiomyopathy
- Tachycardia mediated cardiomyopathy
Epidemiology of Diastolic Heart Failure
-1/3 pts with CHF have DHF
-prevalence in pts greater than 75 y/old
-mortality = 5-8 % annually
-mortality directly related to absence of CAD
Epidemiology of Systolic Heart failure
-2/3 pts with CHF have SHF
-mortality rate = 10-15% annually
-mortality rate directly related to presence of CAD
Factors that Exacerbate Diastolic HF
- Uncontrolled HTN
- A Fib
- noncompliance with medications for HF
- myocardial ischemai
- anemia
- renal insufficiency
- NSAID use
- deitary indisrection w/ over indulgence of salty foods
Diagnosis of Diastolic HF
typical signs + symptoms of HF, plus:
-normal LV EF
-no valvular abnormalities on echocardiogram
