❌ is the quantity of blood pumped each minute into the aorta by the heart.
❌ is the quantity of blood flowing from the veins into the right atrium (RA) each minute.
VR and CO must ❌ each other except for a few heartbeats at a time when blood is temporarily stored in or removed from the heart and lungs.
Which of the following factors does NOT affect cardiac output?
Basal metabolic rate
Gender
Age
Body habitus
Increased energy requirements (exercise)
Cardiac Index = ❌ / ❌
m2 = ❌
The average CO for a resting adult is liters/minute
The average CI for a resting adult is liters/minute/m2
At what age is a person's cardiac function the highest?
10
20
30
40
Peripheral circulatory factors that affect the flow of blood from the veins into the heart provide the primary control of CO.
Blood flow does not increase in proportion to each tissue's metabolism.
If arterial BP is constant, long-term CO will typically have an ❌ relationship to total peripheral resistance.
This is a form of ❌ law.
The Frank-Starling law states that the ❌ of the heart increases in response to an an increase in the volume of blood filling the heart (end diastolic volume), when all other factors remain constant.
Another way to state this: a large volume of blood flows into the ventricle, the blood will stretch the walls of the heart, causing a greater expansion during diastole, which in turn increases the force of the contraction and thus the quantity of blood that is pumped into the aorta during diastole. The increased volume of blood stretches the ventricular wall, causing cardiac muscle to contract more forcefully.
According to the Frank-Starling curve, the normal heart can pump an amount of venous return up to what times the normal venous return before the heart becomes a limiting factor in the control of cardiac output?
2
2.5
3
3.5
Sympathetic stimulation and parasympathetic inhibition can significantly increase heart rate and contractility. The result of this combination is known as what kind of heart?
Effective
Hypoeffective
Hypereffective
Optimized
A number of factors can lead to a hypoeffective heart. Examples include increased arterial pressure (afterload), due to hypertension, valvular heart disease, and congenital heart disease. Select other causes of the hypoeffective heart.
Sympathetic nervous system inhibition
Sympathetic nervous system excitation
Pathological dysrhythmias
Acute coronary syndrome
The nervous system is instrumental in maintaining arterial blood pressure when peripheral blood vessels are ❌ and venous return and CO ❌.
Fill in the blanks for the following: Intense exercise increases decreases( increases, decreases ) SNS outflow, causing large vein constriction dilation( constriction, dilation ), and increase decrease( increase, decrease ) in heart rate and an increase decrease( increase, decrease ) in contractility.
Beriberi disease leads to a manifestation of insufficient dietary vitamin B1 (thiamine). The results of auto-regulatory compensation increases decreases maintains( increases, decreases, maintains ) cardiac output.
Select the other pathologic states that increase cardiac output:
Arteriovenous (AV) fistula
Hypothyroidism
Hyperthyroidism
Anemia
Conditions that produce low CO generally fall into one of two categories:
1. Abnormalities that ❌ the pumping effectiveness of the heart.
2. Abnormalities that cause venous return to ❌.
is the most common non-cardiac peripheral factor that decreases venous return.
Non-cardiac factors that decrease cardiac output due to decreased venous return include:
Obstruction of the large veins
Decreased tissue mass
Arteriovenous Fistula
The two primary factors that must be evaluated in the quantitative analysis of CO regulation are:
The pumping ability of the heart (cardiac output)
The heart's end-diastolic volume (preload)
Venous return curves
The pressure on the wall of the left ventricle during ejection (afterload)
The normal external pressure on the heart is equal to the normal pressure (which is -4 mmHg).
A shift to the right left( right, left ) reflects the increase RA pressure that will be required to fill the cardiac chambers to offset the increase decrease( increase, decrease ) in external pressure.
Select the following factors that can shift the CO curve:
Cyclical changes in intrapleural pressure during respiration
Breathing against a negative pressure
Positive pressure breathing
Opening the thoracic cage
Cardiac tamponade
Principle factors that affect VR to the heart from the systemic circulation: ◦ 1. Exerts a backward force on the veins to impede flow of blood from the veins into the RA ◦ 2. The degree of filling of the Measured by the mean systemic filling pressure (Psf) which forces the systemic blood toward the heart.
is the abbreviation for mean systemic filling pressure.
The principle factor that affects Venous Return to the heart from the systemic circulation is resistance to blood flow between the peripheral vessels and the RA.
The normal venous return curve demonstrates that if the pumping ability of the heart decreases, the RA pressure will rise fall stay the same( rise, fall, stay the same ), and the backward force of this rising pressure on the systemic vasculature will decrease increase( decrease, increase ) VR.
Without compensatory ANS reflexes, VR decreases to zero when the RA pressure rises to what number in mmHg?
4
5
6
7
When both arterial and venous pressure flow in the systemic circulation ceases increases decreases( ceases, increases, decreases ).
Most of the resistance to venous return occurs where?
Arterioles
Veins
Smaller arteries
Select what can compensate in resistance to venous return:
`small artery
aorta
arterioles
venuoles
What is another word for preload?
End-diastolic pressure
Venous return
Afterload
Regardless of the chamber, the is related to the chamber volume just prior to contraction.
Factors that increase preload include all except the following:
Increased venous return
Decreased venous compliance
Decreased thoracic blood volume
Increased thoracic blood volume
What is the pressure within the thoracic space between the organs (lungs, heart, vena cava) and the chest wall?
intrapleural pressure (Ppl)
Preload
Pulmonary filling pressure
intrarterial pressure
❌ has to do with venous return because the one-way valves in the veins of the legs and arms are instrumental in directing blood flow away from the limbs and towards the heart.
Veins within large skeletal muscle groups also undergo compression as muscles contract and decompress as the muscles relax.
The Oxygen Fick Method, indicator dilution method, echocardiography, and ventriculogram are all methods of measuring .
The Oxygen Fick Principle states that: (L/min) = 02 absorbed per minute by the lungs (mL/min) / arteriovenous 02 difference (mL/L of blood)
Place in order the electrical pathways of the heart.
1 2 3 4( 1, 2, 3, 4 ) AV node
1 2 3 4( 1, 2, 3, 4 ) SA node
1 2 3 4( 1, 2, 3, 4 ) Internodal pathway
1 2 3 4( 1, 2, 3, 4 ) Left and right bundles of Purkinje fibers
Identify the pace of each area of the heart.
SA Node: ❌
AV Node: ❌
Purkinje Fibers: ❌
Heart muscle _________________.
is single-nucleated
lacks gap junctions
is syncytial
lacks striations
❌ (where normal rhythmical impulse is generated) -> ❌ (conduct impulse from SA node to AV node) -> ❌ (delays impulse from atria to ventricles) -> ❌ (conducts impulse from atria to ventricles) -> Right & Left Bundle branches of Purkinje fibers (conduct impulse to ALL parts of the ❌)
There are almost no contractile fibers in the SA node.
The SA node is located in the of the right atrium, slightly below and lateral to the opening of the .
Which of the following is NOT a type of cardiac muscle ion channel?
Fast sodium channels
L-type calcium channels
Ligand-gated calcium channels
Potassium channels
The SA node has depolarization.
Select the membrane potential for the SA node.
-40 to -50
-30 to -40
-60 to -70
-55 to -60
At what membrane threshold potential do slow Na-Ca channels to open up?
-30 mV
-40 mV
-50 mV
-60 mV
Place what is happening in the SA node with its appropriate location.
Match the channels with the appropriate description:
❌ Rapid depolarizing phase of AP • Atrial and ventricular muscle & in Purkinje fibers • (inactive at -55)
❌ inherent leakiness of the SA node is responsible for self-excitation
❌ Responsible for repolarizing phase of AP in ALL cardiomyocytes
❌ •Depolarizing phase of AP • SA node and AV node • Also triggers contractions in all cardiomyocytes
•❌ to cause AP (leaky Na+ & Ca channels) -> Recovery from AP (K+ channels open) -> ❌ after AP is over (K+ channels remain open) -> Drift of the "Resting" Potential to ❌ (leaky Na+ & Ca channels) -> ❌ to elicit another cycle
The of the sinus nodal fibers to sodium and calcium ions causes their self-excitation.
The SA node has no true resting potential.
Label the contractile cell or autorhythmic cell.
Assign the appropriate label to what is happening in the ventricular myocyte.
Anterior interartrial band carries impulses to left atrium.
The delay in the AV node is:
0.04 seconds
0.09 seconds
0.10 seconds
.20 seconds
The delay in the AV bundle is:
.04
0.09
0.10
0.14
The total delay in AV node/AV bundle system is seconds.
The is located in the posterior wall of the right atrium immediately behind the tricuspid valve
The Bundle branches and then divide into extensive system of
Transmission time between A-V bundles and fibers is:
0.90 seconds
0.06 seconds
The Purkinje fibers transmit impulses faster slower( faster, slower ) than other fibers.
The Purkinje fibers are larger smaller( larger, smaller ) than ventricular muscle fibers.
The Purkinje fibers have high low( high, low ) levels of permeability of the gap junctions between successive cells in the conducting pathways.
The is the pacemaker
SA node discharges both the AV node & Purkinje fibers after during before( after, during, before ) either of these can undergo self-excitation.
Select the resting membrane potential of the ventricular muscle cell.
-85 to -90
-100 to -110
40 to 60
What doesn't happen when the AV node is blocked?
Impulse can’t get past atria to ventricles
Atria continue beating at normal SA node rate and rhythm
New pacemaker in Purkinje system takes over driving ventricular contraction 15 to 40 bpm
New pacemaker is Bachman Bundle, which takes over driving the ventricular contraction.
Sudden AV block: Delay in pickup of the heart beat is the “” syndrome
❌ (vagal) activation decreases conduction velocity (negative ❌) at the AV node • Decreases slope of Phase ❌ • leads to ❌ depolarization of adjacent cells, and reduced velocity of conduction
Parasympathetic fibers in the heart are nicotinic muscarinic( nicotinic, muscarinic ).
Acetylcholine released by nerve • Binds to cardiac c receptors • intracellular cAMP
Vagal Adrenergic Sympathetic( Vagal, Adrenergic, Sympathetic ) stimulation releases acetylcholine. This goes to muscarinic receptors that decrease cAMP. This causes increased K permeability, which decreases transmission of impulses. Ventricular escape occurs.
increases the vagal activity to the heart.
Sympathetic nerves release norepinephrine aCH cAMP( norepinephrine, aCH, cAMP ).
Sympathetic Parasympathetic( Sympathetic, Parasympathetic ) activation increases conduction velocity in the AV node • Rate of depolarization increased • i.e. slope of Phase 0 3 4( 0, 3, 4 ) increase • Leads to more rapiddepolarization of adjacent cellsàmore rapid conduction of action potentials • Positive Negative( Positive, Negative ) dromotropy
Normal delay of conduction thru AV node reducedàtime between atrial and ventricular contraction reduced • Increase in AV conduction velocity manifests as decrease increase( decrease, increase ) in P-R interval on EKG
is a beta blocker that's metabolized in the blood.
Parasympathetic Nerves • Releases acetylcholine norepinephrine( acetylcholine, norepinephrine ) • Binds to muscarinic nicotinic( muscarinic, nicotinic ) • Decreases Increases( Decreases, Increases ) conductivity of K and decreases increases( decreases, increases ) conductivity of Ca2+ • Decreases Increases( Decreases, Increases ) heart rate of rhythm and excitability of AV junctional fibers and AV node • Excitatory signals are no longer transmitted into the ventricles.
SympatheticNerves • Releases acetylcholine norepinephrine( acetylcholine, norepinephrine ) at sympathetic endings. • Binds to β1 β2( β1, β2 ) receptors • Decreases Increases( Decreases, Increases ) the rate of sinus nodal discharge. • Decreases Increases( Decreases, Increases ) the overall heart activity. • Decreases Increases( Decreases, Increases ) the permeability of Na+ and Ca2+ ions.
Phase 0 is .
Conduction velocity is altered by: Sympathetic stimulation (decreases increases( decreases, increases )) Vagal stimulation (decreases increases( decreases, increases )) Ischemia/Hypoxia: decreases increases( decreases, increases ) Drugs (adrenergic and cholinergic): increase or decrease
Label the effects of the parasympathetic and sympathetic nerve activations appropriately.
Key Difference in Pacemaker Cell AP
•The higher the slope of Phase 0 3 4( 0, 3, 4 ), the higher the rate •Vagal stimulation slows speeds( slows, speeds ) phase 4 depolarization •Rate slows •Catecholamines speed it up
Essentially/primary hypertension is ❌ percent of cases.
Secondary/demonstrable causes are ❌ percent of cases.
and H2O retention is the final common pathway shared by all of these etiologies; Interplay of these 2 determined by kidneys
Extracellular fluid volume increases, then arterial pressure decreases increases( decreases, increases ) • increase in arterial pressure, then the kidneys to lose retain( lose, retain ) Na+ and water then returns arterial BP to return to normal
The depicts the effect of increasing arterial BP on urinary output (UOP).
Fill in the blanks for the renal function curve.
• ❌ mm Hg = UOP = 0 • ❌ mm Hg = normal UOP • ❌ mm Hg = 6-8 times normal
Over time, output must = intake • The point at which this occurs is where the two lines intersect is known as the . • The equilibrium point tends to be at an arterial BP of mm Hg
If arterial BP decreases increases( decreases, increases ) then the loss of H2O and Na+ will be greater than the intake → a decrease increase( decrease, increase ) in fluid volume and BP will decrease increase( decrease, increase ) until the arterial pressure falls exactly back to the equilibrium point
If arterial BP falls below the equilibrium point, intake of Na+ and H2O will be greater less( greater, less ) than the output → an decrease increase( decrease, increase ) in fluid volume and BP until the arterial pressure returns exactly back to the equilibrium point
This equilibrium point for the kidneys will occur as long as (1) of salt and water and (2) of salt and water remain in balance
2 primary ways to change long-term arterial pressure levels • Shifting of the renal output curve to a different pressure • Changing level of and Na+ intake
can cause the renal output curve and equilibrium point to shift to the right.
As the intake of water/salt decreases increases( decreases, increases ), the equilibrium point shifts to the right (160 mm Hg) • If there were a decrease increase( decrease, increase ) in water/salt intake, the equilibrium point and the arterial BP would also decrease
Effect of Total Peripheral Resistance TPR
Acutely, if TPR decreases increases( decreases, increases ), arterial BP decreases increases( decreases, increases ) • Arterial pressure = CO x TPR
If renal vascular resistance (RVR) is NOT affected (i.e., increased when TPR is increased), then the equilibrium point for BP will will not( will, will not ) change
Changes in TPR do not typically affect the long-term short-term( long-term, short-term ) arterial pressure level
Which of the following conditions does NOT have a long-term effect on TPR and therefore equilibrium point.
Beriberi
AV shunts
Pulmonary disease
Paget's disease
Diabetes mellitus
An increase in TPR without any change in renal resistance would:
Transiently increase arterial pressure
Transiently increase sodium and water excretion
Decrease extracellular fluid (ECF)
All of the above
autoregulation— blood volume has decreased increased( decreased, increased ) then tissue blood flow decreases increases( decreases, increases ) throughout body; constricts vasodilates( constricts, vasodilates ) blood vessels everywhere
As Na+ intake increases, two things happen: • ECF osmolality decreases increases( decreases, increases ) → stimulation of the thirst center to drink more water to return the ECF salt concentration to normal • This excess water intake → ↑ ECFV • The increased osmolality also stimulates the release of ADH Angiotensin Aldosterone( ADH, Angiotensin, Aldosterone ) → kidney reabsorption of H2O → ↑ ECFV
The first stage in a volume-loading hypertension is an increase in . The reduction in total peripheral resistance is more related to a effect.
The initial increase in BP is the result of the rise in CO.
2nd stage – • HTN exists • CO returns to near • At same time TPR occurs
Which of the following doesn't happen several weeks following initial-onset volume loading?
Hypertension
Significant increase in TPR
Nearly complete return of ECFV, BV, and CO back to normal.
Significant decrease in TPR.
Angiotensinogen-converting enzyme (ACE) lives mostly in where?
Liver
Lungs
Kidneys
Heart
Where is renin mostly made and stored?
Which enzyme in the blood and tissues inactivates angiotensin II?
Angiotensin I
Renin
Angiotensinases
Aldosterone
Angiotensin Effect on Retention of Salt/Water By Kidneys 1. Direct renal effects • Renal arteriole • Less blood flow thru kidneysàless fluid filtered thru glomeruli into the tubules • Slowedbloodflowresultsinlessperitubularcapillariespressureàrapidreabsorption of fluid from tubules • Act directly on tubular cells to#tubular of sodium & water
causes aldosterone secretion by adrenal glands • Results in significant in sodium reabsorption by renal tubules then H2Oretention, which leads to in fluid volume and an increase in BP
Which of the following does not increase renal excretion of Na and water-increasing BP?
Angiotensin II
Atrial natriuretic peptide
Sympathetic nervous system
Endothelin
Factors that decrease renal excretion of Na & Water to increase BP: 1. ❌ 2. ❌ 3. ❌ 4. ❌
Factors that Increase Renal Excretion of Na and Water, Reducing Blood Pressure 1. ❌ 2. ❌ 3. ❌
Atrial natriuretic peptide is secreted from the .
❌ • Constricts renal arteriolesàless blood flow to kidneys • Stimulates aldosterone secretionàincreases Na+ reabsorption • Directly stimulates Na+ reabsorption in proximal tubules, loops of Henle, distal tubules and collecting tubules ❌ • secreted by adrenal glands • Sodium reabsorption which is followed by water reabsorption • ❌ • Constricts renal arterioles, reducing GFR; low levels of SNS activation acts on alpha receptors on renal tubular cells increasing Na reabsorption; also stimulates release of renin and AGII formation • ❌ • Amino peptide in endothelial cells released in response to vessel trauma • Intense vasoconstriction
❌ ¤ Causes decreased Na and H2O reabsorptionà#UOPàreturn blood volume to normalà$BP ̈❌ ¤Vasodilator ¤ Basal level of NO in kidneys, helps maintain renal vasodilation allowing normal renal excretion of salt/water ̈❌ ¤ At low doses, stimulates dopamine- 1 receptors nCause renal vessel vasodilation nStimulates natriuresis
Use the dropdown to choose the appropriate stage in the cardiac cycle: Diastole Systole( Diastole, Systole ): Muscle re-establishing Na/K/Ca gradient
Diastole Systole( Diastole, Systole ): Contraction of muscle & ejection of blood from chambers
Diastole Systole( Diastole, Systole ): Muscle stimulated by action potential
Diastole Systole( Diastole, Systole ): Relaxation of muscle & filling chambers with blood
Drag and drop to the appropriate location on the cardiac cycle:
❌: Also known as the atrial wave, represents the spread of depolarization
❌: Ventricle depolarization
❌: Ventricular repolarization
Choose if the following descriptions match the atria or the ventricles:
Atria Ventricles( Atria, Ventricles ): Contraction enhances ventricular filling.
Atria Ventricles( Atria, Ventricles ): Blood flows from the RV and LV into the pulmonary artery and aorta
Atria Ventricles( Atria, Ventricles ): Blood flows from the IVC and SVC
True or false: The amount of blood pumped out of the RV will always equal the amount of blood pumped out of the LV.
The fullest the ventricle will be is the end diastolic volume (EDV). This number is what?
40 to 50 mL
50 to 100 mL
110 to 120 mL
150 to 200 mL
The emptiest the ventricle will be is the end systolic volume (ESV). What number is this?
100 to 150 mL
The comparison of the end diastolic volume to the end systolic volume is what?
Total peripheral resistance
Ejection fraction or stroke volume
Arterial pressure
The average ejection fraction in a healthy adult is what?
30 percent
40 percent
50 percent
60 percent
Select the two factors that can change the EDV and the ESV.
Strength of contraction
Increases in diastolic filling
Drag and drop the appropriate part of the heart to the area it works.
❌: Deoxygenated blood from RA
❌: Deoxygenated blood from IVC and SVC
❌: Oxygenated blood from LA
❌: Oxygenated blood from pulmonary circulation
The atrium is the stronger weaker( stronger, weaker ) pump of the heart.
The left right( left, right ) ventricle sends blood to the pulmonary circulation.
The left right( left, right ) ventricle sends blood to the peripheral circulation.
Name the three types of cardiac muscle in alphabetical order:
muscle
/ conductive muscle
Which of the following is a difference between cardiac muscle and skeletal muscle?
Striations
Actin and myosin filaments
Low-Resistance intercalated disks
Heart muscle is a of many heart muscle cells. When one cell becomes excited the action potential spreads to all of them
Identify the three characteristics of cardiac muscle and how an impulse travels.
❌
Contraction of cardiac muscle is initiated by the SA node AV node Bundle of His Purkinje fibers( SA node, AV node, Bundle of His, Purkinje fibers ).
Action Potentials:
The resting membrane potential of cardiac muscle is ❌.
The action potential of cardiac muscle is ❌ millivolts.
The plateau lasts ❌ seconds in ventricular muscle -- much longer than skeletal muscle.
Which of the following is responsible for the influx of intracellular calcium in cardiac muscle?
Intracellular sarcoplasmic reticulum
Activation of the dihydropridene (DHP) channels
Activation of the ligand-gated channels
Passive sodium flow
In cardiac muscle, after the outflow of K+ ions during an action potential (AP), the permeability to K+ ions decreases increases( decreases, increases ) tremendously.
This prevents the early return of the AP voltage to its resting level.
Action potentials of the cardiac cell is much longer shorter( longer, shorter ) than the AP of the nerve cell.
Label the portions of the ventricular muscle action potential:
Put the steps of rapid depolarization of a cardiac cell in order:
❌ and ❌
Put the steps of initial re-polarization in order for cardiac muscle:
1. ❌
2. ❌
3. ❌
4. ❌
5. ❌.
6. ❌ channels.
SA node action potential has fewer more the same amount( fewer, more, the same amount ) phases than other cardiac muscle types.
Place in order the phases of the SA node.
Phase 0: ❌
Phase 3: ❌
Phase 4: ❌ & intrinsic ❌ depolarization.
❌ During this time, the cardiac muscle cannot be re-excited.
❌ Cell can be excited, but the signal must be very strong. Example is an early or "premature" contraction.
Cardiac T-tubules are five times larger smaller( larger, smaller ) than skeletal muscle T-tubules.
Excess Ca causes ❌.
Low Ca causes ❌.
Atrioventricular (AV) valves allow blood flow in one direction FROM atria to ventricle.
❌: Between RA & RV
❌ Between LA & LV
The semilunar valves are the outlet valves of the ventricles. They provide blood from each ventricle into large outflow tract vessel.
❌: Between RV & Pulmonary artery
❌: Between LV & aorta
Label the parts of the Atrial Pressure Wave:
Diastole
-Isovolumic relaxation -A-V valves close open( close, open ) -Rapid inflow of blood -Diastasis -Slow flow into ventricle -Atrial systole -Extra blood in following P wave. -Accounts for 20-25 % of filling
Systole 1. Isovolumic contraction 2. A-V valves close open( close, open ) ventricular press>atrial press 3. Aortic valve opens 4. Ejection phase 5. Aortic valve closes
Aortic Pressure Curve
1. Aortic pressure starts to decrease increase( decrease, increase ) during systole after the aortic valve opens
2. Aortic pressure decreases increases( decreases, increases ) toward the end of the ejection phase. 3. Aftertheaorticvalvecloses,an incisura occurs because of sudden cessation of back-flow toward left ventricle. 4. Aortic pressure decreases increases( decreases, increases ) slowly during diastole because of the elasticity of the aorta.
= (SV/EDV) x 100
Compute the following to calculate ejection fraction:
EDV = 150 End-Systolic Volume = 50
55%
60%
67%
70%
If heart rate is 70 and stroke volume is 70, what is the cardiac output?
3.5 L/min
4 L/min
4.9 L/min
6 L/min
The normal value for ejection fraction is ❌ percent.
An EF less than ❌ percent is associated with significant left ventricular impairment.
Select the normal valve area for the Aortic valve.
1.5 to 3.0
2.5 to 4.5
3 to 5
4 to 6
What is the normal valve area for the mitral valve?
1 to 3
Mean Pressure Gradient (mmHg) 1. Aortic <5 3 2( 5, 3, 2 ) 2. Mitral <5 3 2( 5, 3, 2 )
Because of smaller opening, velocity through aortic & pulmonary valves exceed are less than( exceed, are less than ) that through the A-V valves.
Label the ventricular pressure/volume loops.
Know these key points from Ray's powerpoint.
Increased contractility decreases increases( decreases, increases ) stroke volume.
Increased preload decreases increases( decreases, increases ) stroke volume.
Increased afterload decreases increases( decreases, increases ) stroke volume.
Increasing the arterial pressure in the aorta does not decrease the CO until the MAP rises above what?
80
100
120
160
Frank-Starling Law
Intrinsic ability of the heart to adapt to increasing volumes of inflowing blood
Greater the heart muscle is stretched during filling, the greater lesser( greater, lesser ) force of contraction, the greater amt of blood pumped to aorta
The Frank-Starling Relationship says that
Decreased Increased( Decreased, Increased ) ventricular filling
Decreased Increased( Decreased, Increased ) Preload
Decreased Increased( Decreased, Increased ) LVEDP
Decreased Increased( Decreased, Increased ) Stroke Volume
What are the ways to increase cardiac output?
Decrease Increase( Decrease, Increase ) contractility
Decrease Increase( Decrease, Increase ) preload
Decrease Increase( Decrease, Increase ) after load
Change the rate
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