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CARDIAC OUTPUT AND VENOUS RETURN

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

STROKE VOLUME (SV)


S.V is the amount of blood pumped out by each ventricle during each beat. When heart rate is normal (72/min), it is 70ml (60-80ml). It is the difference between EDV & ESV = 120 50 = 70ml.

CARDIAC OUTPUT
CARDIAC OUTPUT (CO): Quantity of blood pumped into the aorta each minute by the heart. In a resting supine man, it is 5L/min

C.O = Law)

ARTERIAL PRESSURE TPR

(Ohms

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

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

EJECTION FRACTION: is the fraction of EDV that is ejected out by each ventricle per beat. Normally it is 60-65%.

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

CARDIAC RESERVE: is the maximum amount of blood that can be pumped out by the heart above normal value. SIGNIFICANCE: In normal persons, C.O increases 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)

VENOUS RETURN is the quantity of blood flowing from the veins into the right atrium each minute. Normally V.R = C.O (Frank starling law)

FACTORS AFFECTING C.O:


PHYSIOLOGICAL FACTORS PATHOLOGICAL FACTORS

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). 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)
C.O is more if body build is greater

2. SEX:

3. BODY BUILD:

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. C.O = increases by 50-100% in Anxiety & excitement. Mechanism: Release of CATS increased H.Rate & Force of contraction.

6. EMOTIONAL CONDITIONS:

PHYSIOLOGICAL FACTORS (cont)


7. AFTER MEALS:

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


C.O = increased (depending on severity of exercise). MECHANISM: Increase in H.Rate & Force of contraction. C.O = increased MECHANISM: Due to hypoxia secretion of adrenaline.

8. EXERCISE:

9. HIGH ALTITUDE:

PHYSIOLOGICAL FACTORS (cont)


10. POSTURE:

C.O = decreases when recumbent upright position. MECHANISM: Pooling of blood in lower limbs, when we stand up from lying position. C.O = increased by 45-60% in later months of pregnancy.
C.O = reduced / unchanged during sleep.

11. PREGNANCY:

12. SLEEP:

PATHOLOGICAL FACTORS:
1. PYREXIA / FEVER:

C.O = increased (rapid metabolism)


C.O = increased (due to hypoxia secretion of adrenaline). HYPERTHYROIDISM: C.O increases (due to increased BMR). HYPOTHYROIDISM: C.O decreases (due to decreased BMR).

2. ANEMIA:

3. ABNORMAL THYROID FUNCTION:


4. ABNORMAL HEART CONDITIONS:

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


INCOMPLETE HEART 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). SHOCK: C.O = less (due to poor pumping & circulation). HEMORRHAGE: C.O = less (due to low blood volume).

5. ABNORMAL CIRCULATORY CONDITIONS:


DISTRIBUTION OF Cardiac Output TO VARIOUS ORGANS:


BLOOD LEFT VENT. SYSTEMIC CIRCULATION: LIVER = 1500ml = 30% KIDNEYS = 1300ml = 26% SKELETAL MUSCLES = 900ml = 18% BRAIN = 800ml = 16% SKIN+BONE+GIT = 300ml = 6% HEART = 200ml = 4% TOTAL = 5000ml = 100%

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

FACTORS AFFECTING EDV :


1. V.R (most important factor) 2. M.S.F.P 3. SYMPATHETIC STIMULATION 4. SKELETAL MUSCLE PUMP 5. GRAVITY 6. RESPIRATORY PUMP 7. DURATION OF DIASTOLE 8. DISTENSIBILITY OF VENTRICLE 9. ATRIAL CONTRACTION

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 WHICH INCREASE CONTRACTILITY OF HEART

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. Pr RESISTANCE TO V.R V.R = MSFP-RAP RVR

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 active circulation. It indicates the degree of filling of blood vessels. 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, sympathetic Stimulation & contraction of skeletal muscles. (Directly proportional)
More Blood Volume more MSFP more V.R (in blood loss low B.V low V.R) Symp. StimULATION VenoConstriction more V.R Skeletal muscle contraction more MSFP more V.R

RIGHT ATRIAL PRESSURE = C.V.P = 0 in 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 RVR V.R = 7-0 = 5L 1.4

Effect of hormones & drugs etc which increase C.O: (by increaseing contraction of heart)
1. 2. 3. 4. 5. 6. 7. 8.

Cats Thyroxine Glucagon Increased temperature Caffeine Theophylline Digitalis Calcium ions

Factors which decrease C.O By depressing the heart:


1. 2. 3. 4. 5.

Heart failure Hypoxia Acidosis Barbiturates Beta adrenergic blockers

FLOW CHART OF C.O:


C.O
H.RATE TEMP P.SYM INHIB SYMP ST IMPULSES FROM CVS RECEPTORS & BRAIN CENTERS ART BP & TPR THOR. MOVE& I.Th.Press. B.VOL FILLING TIME STROKE VOLUME

ATRIAL CONTR DIST OF VENT VR

EDV

ESV
AFTER LOAD ART. Pr

PRELOAD STARLING LAW

CARDIAC CONTRACTILITY
MSFP

CARDIAC NUTR NERVOUS STIM. DRUGS & MET SYMP ST SK MUS CONTR

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 no increase in C.O. Beyond 180-190 beats/min, C.O decreases, with increasing heart rate. It is because of too short diastole

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).

EFFECTS OF SYMPATHETIC STIMULATION


1) +ve CHRONOTROPIC EFFECT:

Increase in heart rate.


Increased force of contraction.

2) +ve INOTROPIC EFFECT:

3) +ve DROMOTROPIC EFFECT:

INCREASED CONDUCTIVITY IN HEART.


INCREASED EXCITABILITY OF HEART.

4) +ve BATHMOTROPIC EFFECT:

EFFECTS OF VAGAL STIMULATION


1) ve CHRONOTROPIC EFFECT:

SLOWING OF H.R.
Decrease force of contraction Only slight effect because vagal fibers do not supply ventricular muscle.

2) SLIGHT ve IONOTROPIC EFFECT:


3) ve DROMOTROPIC EFFECT:

Slowing of conduction in heart & AV nodal delay is prolonged.


Decreased excitability of heart.

4) ve BATHMOTROPIC EFFECT:

Factors affecting venous return


1. Vis a tergo (force from behind). 2. The pressure gradient 3. Vis a Fronte (force from front) : Right Ventricular Contraction. Sucking force is produced 4. Muscle venous pump (peripheral heart) 5. Thoracoabdominal pump or Respiratory Pump 6. Venous reservoirs 7. Effect of posture and gravity

Cardiac Output Curves

Factors That Can Cause Hypereffective Heart:


1. 2.

Sympathetic stimulation hypertrophy of the heart muscle.

Factors That Cause a Hypoeffective Heart:


1.

2.

3.

4. 5.

6. 7. 8.

Coronary artery blockage, causing a heart attack Inhibition of sympathetic excitation of the heart Pathological factors that cause abnormal heart rhythm or rate of heartbeat Valvular heart disease Increased arterial pressure against which the heart must pump, such as in hypertension Congenital heart disease Myocarditis Cardiac hypoxia

Cardiac output curves at different levels of intrapleural pressure and at different degrees of cardiac tamponade

Venous Return
Definition: it is the quantity of blood flowing from the 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 VENOUS RETURN

VENOUS RETURN CURVE


Pressure Gradient for Venous ReturnWhen This Is Zero, There Is No Venous Return.

Increase in Blood Volume increases MSFP Sympathetic Stimulation increases MSFP.

Increase in MSFP shifts the VR curve to the right and vice versa.

EFFECT OF TPR ON VENOUS RETURN


Decrease in TPR causes a clockwise rotation of the VR curve and vice versa.

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.

Cardiac Output and Venous Return Curves combined


The point at which the CO and VR curves intersect each other is the equilibrium or steady state point. At this point CO and VR are equal.

Cardiac Output and Venous Return Curves combined


Cardiac output can be changed by altering the CO curve or VR curve or both the curves simultaneously.