Regulation of Cardiac Output and Venous Return by Dr. Roomi

7/28/2019 Regulation of Cardiac Output and Venous Return by Dr. Roomi

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CARDIAC OUTPUT AND

VENOUS RETURN

BY

DR. MUDASSAR ALI ROOMI(MBBS, M. PHIL)


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STROKE VOLUME (SV)

S.V is the amount of blood pumped out byeach ventricle during each beat. Whenheart rate is normal (72/min), it is 70ml(60-80ml).

It is the difference between EDV & ESV =120 50 = 70ml.


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CARDIAC OUTPUT

CARDIAC OUTPUT (CO): Quantity ofblood pumped into the aorta each minuteby the heart. In a resting supine man, it is5L/min C.O = ARTERIAL PRESSURE (Ohms

Law) TPR

C.O = STROKE VOLUME (SV) X HEART RATE (HR)

C.O = 70ml x 72 beats/min = 5000ml = 5 L(approx)


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EJECTION FRACTION: is the fraction of

EDV that is ejected out by each ventricle

per beat. Normally it is 60-65%.


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CARDIAC INDEX: It is the correlation

between resting C.O & body surface area.

C.I = C.O / min / m2 of body surface

70kg man has body surface area = 1.7 m2

So, C.I = 5L/min = 3L / min / m2 (approx)

1.7m2


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CARDIAC RESERVE: is the maximumamount of blood that can be pumped outby the heart above normal value.

SIGNIFICANCE: In normal persons, C.Oincreases during stress like exercise.

C.R = 300-400% (in young adult)

C.R = 200-250% (in old age)C.R = 500-600% (in athletes)

C.R = 0% approx (in cardiac diseases)


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VENOUS RETURN is the quantity of bloodflowing from the veins into the right atrium eachminute.

Normally V.R = C.O (Frank starling law)


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FACTORS AFFECTING C.O:

PHYSIOLOGICAL FACTORS

PATHOLOGICAL FACTORS


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PHYSIOLOGICAL FACTORS

1. AGE:

CHILDREN = less C.O (due to low B.Vol) & C.I of children >C.I

of adults (due to less body surface area).

OLD AGE = less C.O (due to low metabolic activity).

2. SEX: In FEMALES: C.O = less,

C.I = more (due to less surface area)

In MALES: C.O = more,

C.I = less (due to more body surface area)

3. BODY BUILD:

C.O is more if body build is greater


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PHYSIOLOGICAL FACTORS (cont)

4. DIURNAL VARIATION:

C.O = low in morning (due to low BMR)

C.O = more in day time (due to high BMR)

5. TEMPERATURE:

C.O = increases if temp increases above 30C.

6. EMOTIONAL CONDITIONS:

C.O = increases by 50-100% in Anxiety & excitement.

Mechanism: Release of CATS increased H.Rate & Force of

contraction.


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7. AFTER MEALS:

C.O = increased during 1st hour after meal.

8. EXERCISE:

C.O = increased (depending on severity of exercise).

MECHANISM: Increase in H.Rate & Force of contraction.

9. HIGH ALTITUDE:

C.O = increased

MECHANISM: Due to hypoxia secretion of adrenaline.


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10. POSTURE:

C.O = decreases when recumbent upright position.

MECHANISM: Pooling of blood in lower limbs, when we

stand up from lying position.

11. PREGNANCY: C.O = increased by 45-60% in later months of pregnancy.

12. SLEEP:

C.O = reduced / unchanged during sleep.


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PATHOLOGICAL FACTORS:

1. PYREXIA / FEVER:

C.O = increased (rapid metabolism)

2. ANEMIA:

C.O = increased (due to hypoxia secretion of adrenaline).

3. ABNORMAL THYROID FUNCTION:

HYPERTHYROIDISM: C.O increases (due to increased BMR).

HYPOTHYROIDISM: C.O decreases (due to decreased BMR).


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4. ABNORMAL HEART CONDITIONS:

ATRIAL FIBRILLATION: C.O is decreased (due to incomplete

filling).

INCOMPLETEHEART BLOCK with coronary sclerosis or myocardial

degeneration: C.O is decreased (due to defective pumping).

CCF: C.O is less (due to weak contraction of heart).

5. ABNORMAL CIRCULATORY CONDITIONS:

SHOCK: C.O = less (due to poor pumping & circulation).

HEMORRHAGE: C.O = less (due to low blood volume).


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DISTRIBUTION OF Cardiac Output TO

VARIOUS ORGANS:

BLOOD LEFT VENT. SYSTEMICCIRCULATION:

LIVER = 1500ml = 30%

KIDNEYS = 1300ml = 26%SKELETAL MUSCLES = 900ml = 18%

BRAIN = 800ml = 16%

SKIN+BONE+GIT = 300ml = 6%

HEART = 200ml = 4%

TOTAL = 5000ml = 100%


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REGULATION OF C.O:

C.O = STROKE VOL. X HEART RATE

C.O REGULATING FACTORS INCLUDE: 1. FACTORS REGULATING S.V (EDV-ESV)

2. FACTORS REGULATING HEART RATE


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FACTORS AFFECTING EDV :

1. V.R (most important factor)

2. M.S.F.P

3. SYMPATHETIC STIMULATION

4. SKELETAL MUSCLE PUMP5. GRAVITY

6. RESPIRATORY PUMP

7. DURATION OF DIASTOLE

8. DISTENSIBILITY OF VENTRICLE

9. ATRIAL CONTRACTION


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FACTORS AFFECTING ESV :

1. FORCE OF HEART CONTRACTION

(FRANK STARLING LAW)

2. AFTER LOAD

3. SYMPATHETIC /VAGUS NERVES

4. CONDITION OF MYOCARDIUM

5. HORMONES/DRUGS WHICHINCREASE CONTRACTILITY OF HEART


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FACTORS AFFECTING EDV:

1. VENOUS RETURN:

Most important factor.

Amount of blood which returns to heart/min.

Basic factors affecting V.R:

V.R = ARTERIAL B.P

TPR

V.R = MEAN SYSTEMIC FILLING Pr Rt. At. PrRESISTANCE TO V.R

V.R = MSFP-RAP

RVR


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2. MSFP: Mean Systemic Filling Pressure is average pressure

in systemic blood vessels which tends to push the

blood towards the heart, when there is no activecirculation. It indicates the degree of filling of bloodvessels.

MSFP depends on:A) how much vessel is filled with blood

B) compression from outside Normal MSFP = 7mmHg (MCQ)

MSFP is affected by blood volume, sympatheticStimulation & contraction of skeletal muscles.(Directly proportional)

More Blood Volume more MSFP more V.R (in bloodloss low B.V low V.R)

Symp. StimULATION VenoConstriction more V.R

Skeletal muscle contraction more MSFP more V.R


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RIGHT ATRIAL PRESSURE = C.V.P = 0in most of Cardiac Cycle.

RVR (RESISTANCE TO V.R) is resistance

offered by veins against the return of blood= 1.4mmHg/L

So V.R = MSFP-RAP

RVRV.R = 7-0 = 5L

1.4


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Effect of hormones & drugs etc which increaseC.O: (byincreaseing contraction of heart)1. Cats

2. Thyroxine

3. Glucagon4. Increased temperature

5. Caffeine

6. Theophylline

7.

Digitalis8. Calcium ions


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Factors which decrease C.O By

depressing the heart:

1. Heart failure

2. Hypoxia

3. Acidosis

4. Barbiturates

5. Beta adrenergic blockers


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FLOW CHART OF C.O:

C.O

H.RATE STROKE

VOLUME

EDV ESV

CARDIAC CONTRACTILITY

NERVOUS STIM.

DRUGS & MET

CARDIAC NUTR

PRELOAD

STARLING LAW

AFTER LOAD

ART. Pr

TEMP

SYMP ST

P.SYM INHIB

IMPULSES FROM

CVS RECEPTORS& BRAIN CENTERS

FILLING TIME

ATRIAL CONTR

DIST OF VENT

VR

ART BP & TPR MSFP

THOR.

MOVE&I.Th.Press. B.VOL SYMP ST SK MUS CONTR


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RELATION BETWEEN H.R & C.O:

Generally when H.R increases C.O

increases. (but the limit is 150/min)

Between 150-180 beats/min, there is noincrease in C.O.

Beyond 180-190 beats/min, C.O decreases,

with increasing heart rate. It is because of tooshort diastole


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NERVOUS CONTROL OF HEART

RATE:

Heart beat is autonomous but is modified

by nervous mechanisms:

1) Autonomic nerves supplying the heart:

Sympathetic

Parasympathetic

2) Vasomotor centre (effected by impulses

from different parts of the body).


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EFFECTS OF SYMPATHETIC STIMULATION

1) +ve CHRONOTROPIC EFFECT: Increase in heart rate.

2) +ve INOTROPIC EFFECT: Increased force of contraction.

3) +ve DROMOTROPIC EFFECT: INCREASED CONDUCTIVITY IN HEART.

4) +ve BATHMOTROPIC EFFECT:

INCREASED EXCITABILITY OF HEART.


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EFFECTS OF VAGAL STIMULATION

1)ve CHRONOTROPIC EFFECT:

SLOWING OF H.R.

2) SLIGHTve IONOTROPIC EFFECT:

Decrease force of contraction Only slight effect because vagal fibers do not supply

ventricular muscle.

3)ve DROMOTROPIC EFFECT:

Slowing of conduction in heart & AV nodal delay is

prolonged.

4)ve BATHMOTROPIC EFFECT:

Decreased excitability of heart.


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Factors affecting venous

return1. Vis a tergo (force from behind).2. The pressure gradient

3. Vis a Fronte (force from front) : Right

Ventricular Contraction. Sucking force isproduced

4. Muscle venous pump (peripheral heart)

5. Thoracoabdominal pump or Respiratory

Pump6. Venous reservoirs

7. Effect of posture and gravity


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Cardiac Output Curves

F t Th t C C


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Factors That Can Cause

Hypereffective Heart:

1. Sympathetic stimulation

2. hypertrophy of the heart muscle.

Factors That Cause a HypoeffectiveHeart:

1. Coronary artery blockage, causing

a heart attack

2. Inhibition of sympathetic excitation

of the heart3. Pathological factors that cause

abnormal heart rhythm or rate of

heartbeat

4. Valvular heart disease

5. Increased arterial pressure against

which the heart must pump, such

as in hypertension

6. Congenital heart disease

7. Myocarditis

8. Cardiac hypoxia


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Cardiac output curves at different levels of

intrapleural pressure and at different

degrees of cardiac tamponade


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Venous Return

Definition: it is the quantity of blood flowing fromthe veins into the right atrium each minute.

Normally V.R = C.O (Frank starling law)VENOUS RETURN = (MEAN SYSTEMIC FILLING PRESSURE

RIGHT ATRIAL PRESSURE)/ RESISTANCE TO VENOUSRETURN


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VENOUS RETURN CURVE

Pressure Gradient for

Venous ReturnWhen

This Is Zero, There Is

No Venous Return.


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Increase in Blood

Volume increases

MSFP

SympatheticStimulation increases

MSFP.


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Increase in MSFP shifts the VR curve to

the right and vice versa.


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EFFECT OF TPR ON VENOUS RETURN

Decrease in TPR

causes a clockwise

rotation of the VR

curve and vice versa.


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Combinations of the major patterns of venous return curves,

showing the effects of simultaneous changes in mean systemic

filling pressure (Psf) and in resistance to venous return.


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Cardiac Output and

Venous Return Curves combined

The point at which the

CO and VR curves

intersect each other is

the equilibrium orsteady state point.

At this point CO and

VR are equal.


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Cardiac Output and

Venous Return Curves combined

Cardiac output can be

changed by altering

the CO curve or VR

curve or both thecurves

simultaneously.


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Regulation of Cardiac Output and Venous Return by Dr. Roomi

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