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Flashcards in Circulation Deck (14):

What local factors affect vasodilation and vasoconstriction/Discuss the local factors affecting arteriolar tone. Discuss the hormones that influence arteriolar tone.

1. Local factors
- Vasodilation: Increase CO2, reduce pH, reduce O2, high temp, increase lactate, high K, adenosine, histamine, prostacyclin
- Vasoconstriction: Low temp, auto regulation, endothelin, thromboxane A2

2. Hormonal factors
- Vasodilation: Bradykinin, histamine
- Vasoconstriction: Adrenaline and noradrenaline acting on a1-receptors, vasopressin from posterior pituitary, Angiotensin 2


What is auto-regulation of tissue blood flow? What are the proposed mechanisms involved in auto-regulation?

1. Auto-regulation is maintenance of normal blood flow despite changes in blood pressure by changing vascular resistance

2. Mechanisms involved
- Myogenic theory: Distension of vessel wall -> Increased stretch -> Smooth muscle contraction
- Metabolite theory: Low blood flow to area -> Accumulation of vasodilatory metabolites -> Vasodilation -> Increase blood flow
- Endothelin products: Endothelium produces endothelin, Thromboxane A2 which causes vasoconstriction and nitric oxide, prostacyclin causing vasodilation
- Neurohumoral substances: Vasoconstriction caused by adrenaline, noradrenaline, vasopressin, angiotensin 2 and vasodilation caused by bradykinin, ANP, histamine
- Neural: Vasoconstriction by sympathetic nervous system via a1-receptors and vasodilation by parasympathetic nervous system via muscarinic receptors


Describe the central neural control affecting arteriolar tone. Describe the volume/atrial stretch reflex?

1. Centre neural control of arteriolar tone
- Vasomotor centre in medulla of CNS which has vasoconstrictor and vasodilator areas
- Triggered by peripheral baroreceptors, peripheral chemoreceptors, higher neural centres
- Peripheral baroreceptors in carotid sinus and aortic arch are triggered by changes in blood pressure -> Mainly inhibits vasoconstrictor area
- Peripheral chemoreceptors in carotid body and aortic body are triggered by hypoxia -> Mainly excites vasoconstrictor area
- Noradrenergic fibres running from vasoconstrictor area down spinal cord to arteriolar smooth muscles -> Vasoconstriction

2. Stretch of atrium causes reflex renal afferent arteriolar vasodilation


What other general effects do endothelin have on the cardiovascular system?

- CVS: Positive inotropic and chronotropic
- Neurohumoral: Increase ANP, renin, aldosterone production
- Renal: Reduce GFR and renal blood flow


What are baroreceptors and where are they located? What is their mechanism of action? What is their action in the setting of acute blood loss/hypovolaemia?

1. Baroreceptors are stretch receptors found in the adventitia layer of vessels. Located in
- Carotid sinus
- Aortic arch
- Pulmonary circulation
- L + R atrium

2. Mechanism of action
- Baroreceptors when distended or stretched are stimulated
- Causes inhibitory effects on SYMPATHETIC nervous system and excitatory effects on parasympathetic nervous system
- Leading to vasodilation, decrease BP, HR, and CO

3. In hypovolaemia,
- There is less stretch or distension on baroreceptors
- Reduced baroreceptors firing
- Causes excitatory effect on sympathetic nervous system and inhibitory effect on parasympathetic nervous system
- Leading to vasoconstriction, increase BP, reflex tachycardia


What are the effects of rapid transfusion of 1L normal saline into a normovolemic patient? Is the effect sustained? What is the mechanism of excretion of this fluid?

1. Rapid IV infusion into a normotensive patient causes
- Increase in intravascular volume
- Increase in mean systemic BP
- Increase preload
- Increase cardiac output as per Frank-Starling law

2. This effect is not sustained due to pressure autoregulation
- Increase intravascular volume sensed by baroreceptors
- Baroreceptors are distended and stimulated
- Inhibits sympathetic nervous system
- Stimulates parasympathetic nervous system
- Causing vasodilation
- Net effect is reduction in BP to normal range

3. Excretion of excess fluid is by the kidneys due to glomerulotubular imbalance
- Increase in intravascular volume causes increase in hydrostatic pressure and decrease in oncotic pressure
- Less Na + H20 reabsorbed in PCT
- More Na + H20 excreted


What is the effect of chronic HTN on baroreceptors? What changes in arterial blood pressure does baroreceptors respond to? What is the set point?

1. Chronic HTN
- In chronic HTN, baroreceptors resets to a higher “set point”
- Maintains normal basal activity at higher blood pressure
- Reversible

2. Baroreceptors in
- Carotid sinus -> More sensitive than aortic arch baroreceptors -> Responds to increase and decrease BP
- Aortic arch -> Responds to increase BP

3. Set point is
- Neutral MAP for vasomotor centre
- Usually around 100mmHg


Describe the factors that affect blood flow to the myocardium

1. Blood flow is determined by Poiseuille’s Law = [Pressure difference x pi x radius^4]/[viscosity x length]
- Pressure differences between arteries and veins
- Changes in radius of vessel
+ Local factors causing
> Vasodilation - Low O2, high CO2, high pH, high temp, adenosine, K, NO
> Vasoconstriction - Thromboxane A2, endothelin
+ Neural factors causing
> Vasodilation - Parasympathetic nervous system
> Vasoconstriction - Sympathetic nervous system
- Viscosity of blood


How is blood pressure maintained in the setting of acute blood loss? What other factors influence vasomotor centre?

1. 3 phases of compensation in acute blood loss
A. Seconds/minutes
- Baroreceptors -> reduced stretch and stimulation -> stimulates sympathetic and inhibits parasympathetic nervous system
- Chemoreceptors -> stimulated due to low O2, high CO2, low pH
- Overall effect is vasoconstriction, increase BP, HR and CO
B. Minutes/hours
- Renin-angiotensin system stimulated due to reduced perfusion
- Causes vasoconstriction
C. Long term compensation
- Renal compensation via aldosterone
- Increases Na + H20 reabsorption -> increase blood volume

2. Vasomotor centre can be influenced by
- Direct stimulation: Changes in pO2, pCO2
- Excitatory inputs: Cortex via hypothalamus, pain pathways, chemoreceptors
- Inhibitory inputs: Cortex via hypothalamus, baroreceptors


Please draw a diagram of the changes in systolic and diastolic pressure as blood flows through the systemic circulation. How does the total cross sectional area of vessels change through the systemic circulation?

1. Changes in pressure in systemic circulation
- Small pressure change in large and medium sized arteries
- Rapid fall in pressure in small arterioles
- Mean pressure at the end of arterioles between 30 - 40 mmHg
- Pulse pressure at the end of arterioles is 5 mmHg

2. Total cross sectional area (TA) is largest in the capillaries and venules
- 10x more than arterioles


Describe the cardiovascular effects that occur during a Valsalva manoeuvre. Which phase of Valsalva is responsible for reverting SVT?

1. Onset of straining
- Phase 1: Straining causes increase intrapleural pressure -> squeezes pulmonary vessels -> increase blood flow into L atrium -> increase SV + CO -> increase arterial BP
- Phase 2: Persistent increased intrapleural pressure -> reduced venous return -> reduce CO -> reduce BP -> sensed by baroreceptors -> triggers peripheral vasoconstriction -> prevents further fall of BP

2. Offset of straining
- Phase 3: Offset of straining reduces intrapleural pressure -> increase flow into pulmonary vessel -> transient reduction of flow into atrium -> decrease CO -> transient decrease in BP
- Phase 4: CO normalises -> increases BP -> pumps against peripheral constricted vessels -> overshoot of BP -> sensed by baroreceptors -> triggers vagus response -> reflex bradycardia

3. SVT can be reverted in
- Phase 4 of Valsalva which increases vagal response


Describe the ABO system. Describe the Rhesus system.

1. ABO system is used to classify blood types
- Inherited via Mendelian dominance A and B antigens
- 4 blood types
+ A: A antigen, anti-B antibodies
+ B: B antigen, anti-A antibodies
+ AB: A + B antigen, no antibodies, universal recipient
+ O: No antigens, anti-A + anti-B antibodies, universal donor

2. Rhesus system is found on RBC only
- C, D, E antigen but only D antigen is clinically important
- Rh +ve: +ve D antigen
- Rh -ve: -ve D antigen
- Clinically important in pregnancy in a Rh -ve mother -> Fetus may be Rh +ve -> Fetus circulation may leak into maternal’s circulation during pregnancy or delivery -> Maternal develops anti-Rh D antibodies -> Next pregnancy antibodies may cross placental -> Causes hemolytic disease of newborn, potential miscarriage


What is the normal central venous pressure (CVP) at rest? Describe the factors that determine CVP.

1. Central venous pressure is
- Pressure in the RA at rest
- Normally ranges between -5 to +5

2. Factors determining CVP is the balance between the venous return and the ability of the heart to pump out from the R atrium
- Factors that affect venous return: Volume status, intrapleural pressure, intra-abdominal pressure, sympathetic/parasympathetic stimulation
- Factors that affect contractility: Presence of heart disease, cardiac failure, myocardial infarct, arrhythmia, atrial fibrillation, valvular disease, cor pulmonale or pulmonary HTN


What factors affect cerebral blood flow? What is the mechanism of Cushing’s response? What is the Monro-Kellie doctrine? What is meant by the term autoregulation of cerebral blood flow? What substances are important for brain metabolism? Describe how blood flow can vary in different parts of the brain.

1. Factors affecting cerebral blood flow (CBF = MAP - ICP)
- Mean arterial pressure
- Intracranial pressure
- Mean venous pressure
- Blood viscosity
- Local constricting/dilating factors affecting cerebral arterioles -> pH, CO2

2. Cushing’s response is the physiological response to increased intracranial pressure
- Results in Cushing’s triad -> Increase systemic BP, reduce HR + RR
- Increase in ICP -> Decrease in cerebral blood flow (CBF) -> Cerebral ischaemia -> Activates sympathetic nervous system -> Increase systemic BP to increase cerebral perfusion -> Triggers baroreceptors -> Activates parasympathetic nervous system -> Reflex reduce in HR + RR via vagus nerve

3. Monro-Kellie doctrine explains that the cranium is a fixed box and therefore
- Volume of CSF (75mls), blood (75mls) and brain parenchyma is relatively constant
- Change in any one will cause the other 2 factors to compensate
- Eg: Increase in ICP compresses on cerebral vessels reducing CBF

4. Cerebral blood flow autoregulation
- The blood flow to the brain is maintained relatively constant despite variations in arterial pressure within the range of 65 - 140 mmHg
- Outside the range, the blood flow changes with arterial pressure

5. Brain metabolism dependent on
- Glucose: Main energy source
- Oxygen: 20% body O2 consumption
- Glutamate
- Amino acids in prolonged starvation

6. Blood flow varies in brain due to
- Active neurons attracting blood flow and oxygen
- Marked variation in blood flow with activity of neurons