Q:1 a) Briefly discuss the two types of blood flow.

(4 marks)

th
b). give formula of Poiseuille’s law (4 power law). (1 mark)

TYPES:

1. STREAM-LINE / LAMINAR FLOW &

2. TURBULENT FLOW

LAMINAR BLOOD FLOW: (0.5*3= 1.5 marks) any three points

• Blood flows in layers or laminae. (0.5 mark)
• A thin layer of blood in contact with vessel wall does not move. (0.5 mark)
• Next layer moves with a slow velocity & further next with higher velocity.
• At centre of vessel, maximum velocity. (0.5 mark)
• Unidirectional & without noise or sound. (0.5 mark)

TURBULENT FLOW: (0.5*3= 1.5 marks) any three points

• Blood flows in different directions. (0.5 mark)
• Blood mixes within itself. There are eddy currents in blood flow. (0.5 mark)
• This type of flow is accompanied by noise or sound. (0.5 mark)
• Tur ula e a e deter i ed & e pressed i ter s of REYNOLD’“ NUMBER. (0.5 mark)
• Normally in all vessels blood flow is streamlined, except ascending aorta & pulmonary trunk, where normally there is some
turbulance.
Diagram: 1 mark

Poiseuille’s law: (1 mark)

• F = π Δ P r4
• 8nl
• F = Rate of blood flow, Δ P = pressure difference, r = radius of vessel wall, n = viscosity of blood & l = length of vessel.

Q.2: a) Briefl des ri e the CN“ is he i respo se. Wh it is alled last dit h respo se of the od
(2+1 marks)

b). what is vasovagal syncope? (2 marks)

a) CNS ISCHAEMIC RESPONSE: 2marks

• It is activated when mean B.P falls below 60 mmHg (0.5 mark)
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 • Blood flow to the brain dec  ischemia of brain ( including vasomotor centre). (0.5 mark)
• From vasomotor centre discharge excessively occurs along sympathetic nerves (1 mark)
this leads to :
1. Tachycardia
2. Vasoconstriction
3. Increased Blood Pressure back towards normal –
“last ditch response?

(1 mark)
It is one the most powerful stimulant of the sympathetic vasoconstrictor nerves.
• This response is the last attempt of body to safe life, called last ditch response.

b). what is vasovagal syncope? (2 marks)


Emotional Fainting—Vasovagal Syncope.


vasodilatory reaction occurs in people who experience intense emotional disturbances that cause fainting.
In this case, the muscle vasodilator system becomes activated, and at the same time, the vagal cardioinhibitory center transmits strong signals to the


heart to slow the heart rate markedly.
The arterial pressure falls rapidly, which reduces blood flow to the brain and causes the person to lose consciousness.

Q.3: a). Give an account of circulatory changes that occur as a result of muscular exercise. (4 marks)

b). Define cardiac index. (1 mark)

Key3

1) INCREASE IN SKELETAL MUSCLE BLOOD FLOW:

 At rest 3-4 ml/100g/min.
 During severe Ex. 20x  (i-e, 50-100ml/100g/min).
 This is due to:
a) B.P

b) opening of dormant capillaries

c) stimulation Of symp. Vasodilator fibers at onset of Exercise.

d) Local metabolic factors is very imp in sk.muscle.Blood flow. In tissue hypoxiathere is release of Vasodilatirs:

Adenosine,H+, K+, PGs, Bradykinin, ADP, ATP, Lactic acid, Pyruvic acid, temp, Ca++.

All these factors are present in physical activity thus blood flow is increased.

(0.5 mark)

2) EFFECT ON THE HEART:

Due to SYMP.stimul. & PARASYMP inhibition there is TACHYCARDIA (H.Rate:180-200/min).

Stroke vol.  & thus C.O (4-6X)

 V.R (due to thoracoabd. & sk.mus. pump), there is venoconstriction as a result E.D.V& E.S.V (due to forceful vent. Contraction)
M.S.F.Pr 

(0.5 mark)

 3) EFFECT ON CIRCULATION:
due to contraction of Liver & Splenic capsule, additional amount of blood enter into general circulation.

All the blood vessel show Vasoconstricton Except Cerebral, Coronary & in the active Skeletal Muscles.

(0.5 mark)

 4) CUTANEOUS BLOOD SUPPLY:

In the beginning of Exercise there is Cutaneous V.C.

As Ex. Progresses, more heat production leading to Sweatingas a resu Cutaneous V.D.(to facilitate heat loss from the body).
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 (0.5 mark)

 5) CEREBRAL BLOOD VESSELS:

They remain dilated.

Cerebral blood flow is UNCHANGED

(0.25 mark)

 6) CORONARY BLOOD FLOW:

There is Coronary V.D.

Coronary blood flow 4-6x

(0.5 mark)

 7) SPLANCHNIC BLOOD FLOW & 8) RENAL BLOOD FLOW:

There is Splanchnic & Renal V.C .

Because of this about 2.5L Blood is directed towards active muscle as a result

Active Skeletal Muscle V.D.

(0.5 mark)

 EFFECT OF Exercise ON B.P:

A) Severity of Exercise:

( Mild, Moderate, Severe.)

Mild Ex: BOTH SYSTOLIC & DIASTOLIC B.P

Mod Ex: systolic 

Severe : SYSTOLIC B.P 

BUT DIASTOLIC 

Due to accumulation of metabolites in sk.mus. V.D (0.5 mark)

b) .Cardiac Index: (1) mark

 The cardiac output per square meter of body surface area.


2
In an average human being of 70 kg average cardiac index is about 3L/min/m .

Q:4. A person rises from sitting to standing position suddenly. He feels dizzy due to postural hypotension. But after sometime the condition
becomes normal.

a) Give the sequence of events that helped in normalizing the blood pressure in this case.
b) Which nerves take part in this reflex?

(3+2 marks)

key:4

A) standing from sitting  blood pooling in legs  postural hypotension  decreased pressure sensed by baro-receptors

•  impulses to VMC  Sympathetic stimulation & parasympathetic inhibition

• peripheral vaso-constriction, increase in contractility of heart & heart rate  increase in cardiac output  increase in blood pressure
back to normal

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B)

• Impulses from CAROTID BARO-RECEPTORSHering NGlossopharyngeal Nerve.

(1 mark)

Those from AORTIC BARORECEPTORS carried by VAGI

(1 mark)

Q.5: Define cardiac output. List the factors which regulate cardiac output. Name at least two methods for determining the cardiac output.
(1+3+1 marks)

th
Key: 15 Ref: p 111, Guyton 11 Ed & p 234 Ganong

Cardiac output: it is the blood pumped out of heart in one minute. 5-5.5 L/min. 1 mark

Factors which regulate cardiac output:

As cardiac output is the product of stroke volume and heart rate so all factors affecting these ultimately affect cardiac output.

Mechanism of relation of Heart rate to cardiac output.

The basic mechanisms by which cardiac output is regulated by heart are:

 Intrinsic cardiac regulation of pumping in response to changes in volume of blood flowing into the heart. This follows
Frank Starling mechanism according to which the greater the heart muscle is stretched during filling the greater is the
force of contraction and the greater the quantity of blood pumped in the aorta (0.5)

 The autonomic nervous system: Sympathetic stimulation increases rate and force of contraction that lead to an increase
in cardiac output. Parasympathetic stimulation on the contrary causes decreased heart rate with slight effect on force of
contraction as well.

(0.5)

HEART RATE AFFECTING FACTORS: (0.5)

Heart beat is autonomous but is modified by nervous mechanisms:

1) Autonomic nerves supplying the heart:

a) Sympathetic

b) Parasympathetic

2) Vasomotor centre (affected by impulses from different parts of the body).

EDV AFFECTING FACTORS: (Any 4 = 1 mark)

• 1. Venous return (most important factor) or Pre-load

• 2. M.S.F.P (Mean Systemic Filling Pressure)

• 3. B.P or After-load
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 • 4. SYMPATHETIC STIMULATION or peripheral resistance

• 5. SKELETAL MUSCLE PUMP

• 6. GRAVITY

• 7. RESPIRATORY PUMP

• 8. NEGATIVE PRESSURE IN SYSTOLE

• 9. FILLING TIME

• 10. DURATION OF DIASTOLE

• 11. DISTENSIBILITY OF VENTRICLE

• 11. ATRIAL CONTRACTION

ESV AFFECTING FACTORS: (Any 2 = 0.5 mark)

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:

Examples: Thyroxine & Glucagon

6. FACTORS WHICH DECREASE C.O.:

Examples: Heart failure, Hypoxia, Acidosis, Barbiturates, Beta adrenergic blockers

Q.6. A 50 years old barber gradually develops elongated, tortuous & dilated veins in the legs.

a. What is this condition called as?

b. Enlist factors that affect venous return.

c. How are veins controlled by nervous system?

d. How do inspiration & expiration affect venous return? (1+2+1+1)

UHS MBBS (I) ANNUAL 2009, Q:3, Goal Ed. 2011

Key: 6 Reference: pp 176-178, 204, 240 Guyton 11th Ed.

a. Condition: Varicose veins (1)

b. Factors affecting venous return (V.R):

(Any 4 = 2 marks)

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 Basic factors affecting Venous return are:

i) Arterial blood pressure: Directly proportional

• (V.R = ARTERIAL B.P

• TPR)
ii) Total peripheral resistance (TPR) or resistance to venous return

• (RVR): Inversely proportional.

• (V.R = ARTERIAL B.P
• TPR)
iii) Mean systemic filling pressure (MSFP)

• V.R = MSFP – Rt. At. Pr

• RESISTANCE TO V.R
• (MSFP is affected by blood volume, sympathetic stimulation & contraction of skeletal muscles. It is directly proportional to all these).
iv) Blood volume (More Blood volume will lead to more arterial pressure & more

enous return)

v) Sympathetic stimulation (Sympathetic Stimulation will cause vasoconstriction & more venous return)

vi) Contraction of skeletal muscles (Skeletal muscle contraction causes more pressure & more venous return). Venous pump & venous
valves (unidirectional flow)

• vii) Right atrial pressure (V.R = MSFP – Rt. At. Pr

• RESISTANCE TO V.R)
viii)Intra-abdominal pressure effect on venous pressure of leg (rise in intra-abdominal pressure due to pregnancy, large tumors or
ascites).Increase in intra-abdominal pressure resists venous return.

ix) Gravitational pressure effect on venous pressure (in standing posture, gravity negatively effects venous return)

c) Control of veins by nervous system:

• Sympathetic nervous system stimulation causes venoconstriction & thus decreases the volume of the veins. This can push blood into
heart & thus play a major role in regulation of heart pumping
(1)

d) Effect of Inspiration & expiration on heart rate:

• There is negative intra-thoracic pressure in inspiration, due to descent of diaphragm (when volume increases, pressure decreases
a ordi g to Bo le’s la ) so e ous retur i reases due to su tio effe t thora i pu p & i e ersa.
(1)

Q.7: A middle aged man riding on a bicycle was hit by a speedy car. He fell on the ground and got multiple injuries. He was taken to the
emergency department of a nearby hospital after one hour. He was bleeding profusely from his wounds. He was drowsy. On examination,
his radial pulse was rapid and thready. His skin was pale, cold and clammy. Arterial blood pressure was 70/50 mmHg. 1+1+3 (2008, UHS)

a).what is your diagnosis?

b).what was the cause of rapid pulse, and his cold clammy skin?

c). how will you manage such a case?

Ans:

a). hypovolumic shock due to excessive blood loss. 1 mark

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b). sympathetic stimulation causes tachycardia and vasoconstriction of the blood vessels in skin (leading to clod and clammy skin). 1 mark

c). EMERGENCY MANAGEMENT OF THE CASE: 3 marks

• Evaluate vital signs of the patient:

– Blood Pressure, Respiration Rate, Pulse, Temperature.

• Simple measures e.g. raising the legs to increase venous return towards heart.

• Control bleeding from the bleeding points.

• Blood transfusion should be given ideally because this is a case of shock caused by hemorrhage.

• Plasma expander e.g. dextran may be given if blood is not available.

• Rehydrate the patient by giving normal saline or ringer lactate.

• Monitor urine output in order to prevent acute renal failure.

• Sympathomimetics drugs e.g. dopamine and epinephrine may be given to increase the blood pressure.

Q.8: a).Enlist various mechanism of arterial blood pressure regulation. 3

b). What is renin angiotensin mechanism? Briefly describe its significance. 1+1

Ans:

a). VARIOUS MECHANISM OF ARTERIAL BLOOD PRESSURE REGULATION.

1. RAPIDLY-ACTING ARTERIAL B.P. CONTROL MECHANISMS: 1 mark

• Baroreceptor feedback mechanism.

• Chemoreceptor mechanism.

• Atrial and pulmonary artery reflex.

• Atrial reflex to kidneys or volume reflex.

• Bainbridge reflex.

• CNS ischemic response.

2. INTERMEDIATE TIME-PERIOD ARTERIAL B.P. CONTROL MECHANISMS: 1 mark

• Renin-angiotensin vasoconstrictor mechanism.

• Stress-relaxation mechanism.

• Capillary fluid shift mechanism.

3. LONG-TERM ARTERIAL B.P. CONTROL MECHANISMS: 1 mark

• Renal-body fluid mechanism.

• Renin-angiotensin-aldosteron mechanism.

b). RENIN-ANGIOTENSIN SYSTEM: 1 mark

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 • Renin is synthesized and stored in modified smooth muscle cells in afferent arterioles of the kidney.

• Renin is released in response to a fall in pressure.

• Renin acts on a substance called angiotensinogen to form a peptide called angiotensin I.

• AI is converted to AII by a converting enzyme located in the endothelial cells in the pulmonary circulation.

PHYSIOLOGICAL ACTIONS OF THE RENIN ANGIOTENSIN SYSTEM (RAS): 1 mark

• Causes vasoconstriction.

• Causes sodium (Na+) retention by direct and indirect actions on the kidney. in this way it allows a normal person to maintain a
normal blood pressure despite large variations in salt intake.

RELATION OF RENIN ANGIOTENSIN SYSTEM WITH DISEASE:

 In heart failure, liver failure and renal artery stenosis this system is activated and causes fluid retention (edema) in the body.
 In uncompensated heart failure it causes fluid retention leading to irreversible shock.
 Tumor of renin secreting cell may lead to hypertension.
 Angiotensin converting enzyme inhibitors (captopril, enalapril) are antihypertensive drugs.

Q.9: Define edema. How is interstitial fluid formed? Explain with starling forces acting on the systemic capillaries.

Ans:

Edema: 1 mark


The swelling of soft tissues as a result of excess water accumulation in interstitial space is called as edema.
Edema is often more prominent in the lower legs and feet toward the end of the day as result of pooling of fluid from the
upright position maintained during the day. This sort of edema is usually seen in heart failure.

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  Upon awakening from sleeping, patients can have swelling around the eyes referred to as "periorbital edema." This
type of edema is seen in cases of nephritic syndrome.

Formation of interstitial fluid: 4 marks (1 for each force)

Four primary hydrostatic and colloid osmotic forces (Starling forces) determine fluid movement through the capillary membrane
into the interstitial space:

1. The capillary hydrostatic pressure (Pc): which tends to force fluid outward through the capillary membrane.
2. The interstitial fluid pressure (Pif), which tends to force fluid inward through the capillary
membrane when Pif is positive but outward when Pif is negative.
3. The capillary plasma colloid osmotic pressure (Pc), which tends to cause osmosis of fluid inward through the capillary
membrane.
4. The interstitial fluid colloid osmotic pressure (Pif), which tends to cause osmosis of fluid outward through the capillary
membrane.

ANALYSES OF STARLING FORCES ACTING ON CAPILLARY:

 Total outward forces are 28.3 mmHg.

 Total inward force is 28 mmHg.
 Net outward force is 0.3 mmHg and this is responsible for net interstitial fluid.

Q.10: How is coronary blood flow regulated? Briefly describe the mechanisms. 5 marks

Ans:

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Norma Coronary Flow at rest is equal to 225 ml/min.

FACTORS REGULATING CORONARY BLOOD FLOW: 1 mark

+
1) Local metabolism of myocardium by virtue of vasodilator substances e.g. adenosine, K ions, CO2 bradykinin, Prostaglandins and
EDRF.

2) Myocardial O2 consumption which is directly proportional to pump work.

3) Autonomic nerves (sympathetic and parasympathetic).

4) Hormones (epinephrine and nor-epinephrine, thyroxine).

5) Heart Rate.

6) Aortic diastolic B.P ( coronary blood flow increases during diastole.).

7) Anemia & polycythemia.

8) Body temperature (directly proportional).

EFFECT OF LOCAL METABOLISM OF MYOCARDIUM ON CORONARY BLOOD REGULATION: 1 mark

 Coronary blood flow is auto regulated according to O2 consumption & demand (directly proportional).

 When PO2 in myocardium fallshypoxia (due to increased consumption).

 This hypoxia causes release of vasodilators in the myocardium. The most important one is adenosine.

 ATP  ADP + Adenosinecoronary vasodilation.

EFFECT OF SYMPATHETIC STIMULATION ON CORONARY BLOOD FLOW: 2 marks

• Direct effect: in most of the cases this causes Coronary vasoconstriction. It is less important in overall regulation of coronary blood
flow.

• Indirect effect: (more important!) More heart rate & contraction  more myocardial metabolism & O2 consumption  more
vasodilators causing Vasodilatation of coronaries.

EFFECT OF PARASYMPATHETIC STIMULATION ON CORONARY BLOOD FLOW: 1 mark

• Direct effect: coronary vasodilatation

• Indirect effect: decreased heart rate & contraction  decreased myocardial metabolism & O2 consumption  less vasodilators and
less Vasodilatation of coronaries leading to less blood flow.

Team edu Blog 2013 MBBS Section 03338801993

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