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ACEM Viva > Physiology - Circulation > Flashcards

Physiology - Circulation Flashcards

1
Q

What are the basic factors that determine the rate of flow of blood through a vessel

A

Hagen-Poiseuille formula:
Pressure difference
Diameter
Length
Viscosity

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2
Q

What factors cause turbulent flow in a blood vessel

A

-probability of turbulent flow is determined by Reynold’s number:

Re = fluid density x diameter x velocity / viscosity

  • the higher the value of Reynold’s number, the higher the chance of turbulence
  • turbulence is usually present at branching points of arteries and constriction points, reduced viscosity
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3
Q

Why is blood flow slower in capillaries

A
  • velocity relates to total cross-sectional area:
velocity = flow / cross sectional area
  • capillary total cross-sectional area is 1000x that of the aorta, thus low velocity but same flow
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4
Q

What is the relationship between pressure and wall tension in blood vessels of different size

A 
Law of Laplace: 
Tension = Pressure x Radius / 2x wall thickness

The smaller the radius the lower the tension and thus less likely to rupture

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5
Q

What is the relationship between pressure and wall tension in the heart

A
  • increased ventricular volume means increased radius and thus increased tension and increased work required to overcome
  • ventricular dilation means more tension required to generate the same pressure = more work
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6
Q

Draw a diagram of the changes in systolic and diastolic pressure as blood flows through the systemic circulation

A
  • pressure falls very slightly in large and medium sized arteries because resistance to flow is small
  • pressure falls rapidly in small arteries and arterioles, which are the main sites of vascular resistance
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7
Q

How does the total cross-sectional area of a vessel change through the systemic circulation

A

capillaries have the largest cross sectional area

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8
Q

Describe the central neural control affecting arteriolar tone.

A
  • cardiovascular system is under central neural control coming from parts of the brainstem, forebrain and insular cortex
  • the vasomotor center is located in the rostral ventrolateral medulla, major source of excitatory input to the sympathetic nerves
  • influenced by:
    direct stimulation = CO2, hypoxia
    excitatory inputs = chemoreceptors (peripheral and central, cause vasoconstriction and influence respiration)
    inhibitor inputs = baroreceptors (stimulation inhibits sympathetic discharge), pain, lung inflation
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9
Q

Describe the bainbridge (atrial stretch) reflex

A 
A protective mechanism that adjusts heart rate in response to changes in blood volume, helping to maintain cardiovascular stability and optimize cardiac performance.
  • increase in heart rate due to an increase in central venous pressure
  • increase in volume is detected by stretch receptors in both sides of atria
  • impulse travels to the CNS, modulating sympathetic and parasympathetic pathways to the SA node, causing increased HR
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10
Q

What is the set point

A

neutral MAP for the vasomotor center at around 100mmHg

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11
Q

Describe the receptors that respond to a fall in blood pressure

A

baroreceptors: in carotid sinus, aortic arch, wall of atria, SVC, IVC, pulmonary veins
- respond to stretch in adventitia, with distension causing inhibition of sympathetic discharge

chemoreceptors:
- peripheral = in carotid body and aortic body, responds to low O2, high CO2 by increasing respiration and vasoconstriction
- central = in medulla, responds to high CO2 by stimulating vasomotor areas in medulla, leading to vasoconstriction

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12
Q

What are baroreceptors, where are they located and what is their mechanism of action

A

Stretch receptors present in the adventitia of heart and blood vessels that respond to pressure changes

location: carotid sinus, aortic arch, walls of right and left atria, entrance of SVC and IVC, pulmonary veins

mechanism: stimulation by distension travels down CN IX afferents (carotid sinus) to medulla (NTS -> CVLM -> RVLM), ultimately leads to inhibition of tonic sympathetic discharge, causing vasodilation, reduced HR/CO/BP

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13
Q

What is the baroreceptor mechanism in acute blood loss (hypotension)

A

less stretching of baroreceptors leads to reduced discharge to the medulla and an overall increase in sympathetic discharge

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14
Q

What is the effect of chronic hypertension on the activity of arterial baroreceptors

A

they reset to maintain normal basal activity at elevated blood pressures (reversible)

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15
Q

Discuss local factors that affect arteriolar tone (what is autoregulation, what local factors cause vasodilation/vasoconstriction)

A

1) autoregulation: capacity of tissues to regulate their own blood flow
-maintain constant blood flow by compensating pressure changes with peripheral resistance
-myogenic theory: intrinsic contractile response to SM stretch
-metobolic theory: production of vasoactive substances by active tissue
vasodilation in response to low O2, high CO2, high osmolality, high temperature, low pH, high lactate, high K+, histamine
vasoconstriction in response to trauma, low temperature, serotonin

2) substances secreted by endothelium
- prostacyclin = promotes vasodilation
- nitric oxide = causes vasodilation
- endothelin = causes vasoconstriction

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16
Q

Discuss the hormones that influence arteriolar tone

A
  • kinins = bradykinin and kallidin, cause relaxation of vascular SMC
  • natriuretics = ANP, BNP, CNP, work by antogonising vasoconstrictors
  • adrenaline = vasodilation of skeletal muscle via beta-2
  • noradrenaline = vasoconstriction via alpha-1
  • vasopressin = potent arteriolar vasoconstrictor
  • angiotensin II = general arteriolar vasoconstrictor
  • serotonin = local vasoconstriction post injury
  • adenosine = vasodilatory on cardiac muscle (not skeletal muscle)
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17
Q

What effects do endothelins have on the cardiovascular system

A

vasoconstriction
positive inotrope
positive chronotrope
causes renin release
decreases GFR and renal blood flow

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18
Q

Describe the factors that control blood flow to the myocardium

A

1) Local factors
- vasodilation = low O2, high CO2, high temperature, low pH, high K+, adenosine
2) Innervation of coronary arterioles
- alpha adrenergic receptors = vasoconstriction
- beta adrenergic receptors = vasodilation
3) Pressure differences: flow of blood from high pressure to low pressure
- flow better during diastole (because heart compresses coronary vessels when it contracts)
4) Viscosity of blood

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19
Q

What happens to cardiac output during exercise

A

increased cardiac output:
increased HR, increased venous return, increased myocardial contractility

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20
Q

Describe the factors controlling blood flow through skeletal muscle during exercise

A
  • local factors: increased blood flow by vasodilation due to low O2, high CO2, high lactate, high K+, low pH, high temperature
  • other factors: sympathetic vasoconstriction, circulating adrenaline
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21
Q

What other circulatory changes occur in the body during exercise

A
  • increased cardiac output due to sympathetic discharge
  • constriction of peripheral arterioles not in skeletal muscle secondary to sympathetic discharge (coronary and cerebral spared)
  • contraction of capacitance vessels (veins) secondary to sympathetic discharge leading to increased venous return
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22
Q

What factors affect cerebral blood flow?

A

factors that affect cerebral blood flow:
MAP, MVP, ICP, viscosity and local factors (CO2 level)

  • intracranial pressure is determined by brain mass (1400g), csf volume (75ml) and blood volume (75ml)
  • autoregulation maintains cerebral blood flow at arterial pressures of 65-140mmHg
  • cerebral perfusion pressure is the pressure gradient causing blood flow to the brain (CCP = MAP - ICP)
23
Q

What is the Monro-Kellie doctrine?

A

cranial compartment is incompressible and volume inside the cranium is fixed
brain tissue, csf and blood create a state of volume equilibrium

24
Q

What is the mechanism of the Cushing response?

A
  1. increased ICP leads to decreased CBF
  2. rostral ventrolateral medulla RVLM ischaemia
  3. increased sympathetic outflow
  4. increased BP
  5. activates the baroreceptor reflex
  6. vagal stimulation with decreased HR and RR
25
Q

What is meant by the term autoregulation of cerebral blood flow and draw a diagram

A

the process by which CBF is maintained at a constant rate (750ml/min) despite variation of MAP of 65-140mmHg

26
Q

Describe how blood flow can vary in different parts of the brain

A

active neurons attract blood flow and oxygen in excess of needs

27
Q

What substances are important for brain metabolism (what proportion of total body oxygen does the brain consume)

A

oxygen (20% of body oxygen consumption)
glucose (main energy source)
glutamate (converted to glutamine)

28
Q

What energy substrates can be used by the brain

A

glucose
glutamate

in prolonged starvation:
amino acids, lipids and proteins

29
Q

How is brain perfusion maintained in brain injury?

A
  • aim is to maintain cerebral perfusion pressure
  • CPP = MAP - ICP
  • when ICP is high, need to increased MAP to maintain CPP
  • achieved by Cushing’s reflex:
    1) hypertension via increased sympathetic activity to the cardiovascular system (alpha 1 adrenergic receptor) with initial tachycardia and arterial constriction
    2) vagal stimulation and reflex bradycardia
30
Q

What is the coronary blood flow at rest

A

250ml/min or 5% of cardiac output

31
Q

Describe the coronary artery blood flow during the cardiac cycle

A
  • greater flow during diastole because of vessel compression during systole
  • blood flow to left ventricle subendocardium only occurs during diastole and thus is most vulnerable
  • blood flow occurs in right ventricle continuously
32
Q

What are the factors that affect coronary blood flow

A

1) autoregulation = local factors causing vasodilation (low O2, high CO2, low pH, high K+)
2) neural = inotropic and chronotropic effects
3) phase of cardiac cycle = flow is higher in diastole
4) disease states = coronary artery disease, valve disease, heart failure

33
Q

What chemical factors cause coronary vasodilation

A

low O2
high CO2
high H+
high K+
high lactate
adenosine

34
Q

What receptors govern coronary blood flow (describe the neural regulation of coronary blood flow)

A
  • alpha receptors = vasoconstriction
  • beta receptors = vasodilation
  • vagal nerve stimulation = dilates coronaries
35
Q

What factors can decrease coronary artery blood flow?

A
  • physiological = tachycardia (causes shorter diastole)
  • pathological = CAD, heart failure, aortic stenosis (causes increased LV pressure), vasospasm
36
Q

Describe the mechanisms of venous return to the heart

A
  • thoracic pump = inspiration results in negative pressure in thorax and positive pressure in abdomen
  • muscle pump = contraction of muscles around the veins in the limbs during activity (venous valves with one way flow)
  • differential resistance = resistance in large veins near the heart is less than peripheral veins
  • heartbeat sucks blood from great veins into atria during systole
37
Q

What is the normal CVP at rest and what factors determine the CVP

A
  • pressure in the SVC or right atrium, normally 0-6mmHg
  • determined by a balance between venous return and ability of the heart to pump out of right atrium

factors affecting venous return = gravity, intra-abdominal pressure, volume status, vascular tone, tamponade, tumour
factors affecting ability of heart to pump = myocardial contractility, hypertrophy, cardiac failure, mi, arrhythmia

  • decreased CVP = fluid loss, blood loss, loss of arterial tone, myocardial depression, poor ventricular filling (tachycardia)
  • increased CVP = excessive fluid replacement, CCF, positive pressure ventilation, increased thoracic pressures
38
Q

What is the normal value for venous return in a healthy human heart and what factors influence it

A

5-5.5L/min

circulating blood volume
sympathetic/parasympathetic tone
right atrial pressure

39
Q

What is the relationship between right atrial pressure and venous return

A

as right atrial pressure increases, venous return decreases

40
Q

What percentage of cardiac output goes to the kidney

A

renal blood flow is 1.2-1.3L/min or 25% of cardiac output

41
Q

How is renal blood flow regulated

A

1) autoregulation
- contractile response of afferent arteriole SMC to stretch

2) chemicals
- NA = constricts renal vessels, reduces renal blood flow
- dopamine = renal vasodilation, increases GFR
- angiotensin II = constricts efferent > afferent arterioles, GFR remains stable
- prostaglandin = increases blood flow to cortex, decreases blood flow to medulla
- acytylcholine = renal vasodilation, increases renal blood flow

3) neural
- stimulation of renal nerves causes increase in renin secretion and Na+ resorption and renal vasoconstriction
- low MAP causes reduced baroreceptor firing with sympathetic stimulation causing vasoconstriction and reduced RBF

42
Q

How can renal blood flow be measured

A

Fick’s principle:
blood flow = amount of substance taken up per unit time / arteriovenous difference

uses PAH to measure renal plasma flow and estimated renal blood flow from plasma flow

43
Q

Describe the differences in regional blood flow within the kidney

A

cortex: high blood flow, low O2 extraction
medulla: low blood flow, high O2 extraction

44
Q

Describe the physiological characteristics of renal blood flow

A
  • renal blood flow is 25% of the cardiac output
  • glomerular capillary pressure is 40% of systemic arterial pressure
  • after passing through glomerulus, the efferent arteriole becomes the peritublar capillary network and renal veins
  • renal cortex gets higher blood flow but has lower O2 extraction than the medulla
45
Q

What is hypovolaemic shock

A

systemic hypoperfusion due to reduced effective circulating blood volume resulting in impaired tissue perfusion and hypoxia

46
Q

How is blood pressure maintained in the setting of acute blood loss

A

1) Seconds to minutes
- baroreceptors have reduced firing activity, thus increased sympathetic discharge
- chemoreceptors are stimulated, leading to peripheral vasoconstriction and rise in BP

2) Minutes to hours
- decreased renal blood flow causes activation of renin-angiotensin-aldosterone system
- blood volume changes
- fluid shift through capillaries

3) Longer term
- renal compensation via aldosterone and EPO (increases RBC production in 10 days+)
- salt intake

47
Q

Describe the non-cardiovascular compensatory responses to shock

A

1) efferent arterioles constrict more than afferent, GFR falls less than RPF, causing increased filtration fraction

2) increased renin activates the RAAS with increased AGII = Na+ reabsorption, increased aldosterone/ADH, vasoconstriction
aldosterone - promotes Na+ and H2O retention and lowers K+ in plasma
vasopressin (adh) - translocates water channels, causes vasoconstriction and increases secretion of ACTH

3) osmoreceptors detect high osmotic pressure and activate thirst mechanism

48
Q

What are the types of immunoglobulins and what is the clinical significance of each

A

IgG: most common, involved in complement activation, only one that can cross the placenta

IgA: dimer found in mucosal areas for localised protection of external secretions

IgM: pentamer expressed on surface of B cells, pentamer, early immunity before sufficient IgG is formed

IgD: mainly acts as antigen receptor on B cells, activates basophils and mast cells

IgE: binds to allergens, involved in type 1 hypersensitivity, releases histamine from basophils and mast cells

49
Q

Draw a typical immunoglobulin molecule and label the parts

A

Fab: antigen binding site, has variable regions

Fc: mediates reactions

50
Q

What are the features of innate immunity

A
  • non-specific, generalised defence mechanism
  • immediate response, first line
  • stages: recognition of microbes, activation of various mechanisms, elimination
  • components: epithelial cells, phagocytes, dendritic cells, natural killed cells, mast cells, complement, cytokines
  • recognition of microbes: pathogen recognition receptors (PRRs) are cell components that recognise pathogen-associated molecular patterns (PAMPs) on microorganisms; examples: toll-like receptors, mannose receptors, nod-like receptors
  • adaptive immunity activation
51
Q

What are the features of acquired immunity

A
  • consists of mechanisms stimulated by microbes, develops later and is stronger than innate
  • components: lymphocytes, dendritic cells, macrophages
    1) T lymphocytes = T cell receptor on T cell recognises antigens presented by MHC on surface of APC

helper T cell binds to class II MHC and stimulates B cells and macrophages

cytotoxic T cell binds to class I MHC and directly kills infected cells

2) B lymphocytes = recognise antigen via B cell antigen receptor complex

develop into antibody factories and make immunoglobulins IgG, IgA, IgM, IgD, IgE

3) Dendritic cells = most important APC and initiate T cell response
4) Macrophages = able to phagocytose microbes, secrete mediators of inflammation and initiate tissue repair

52
Q

Describe the ABO blood types and their inheritance

A
  • RBC contain different antigens on their membrane surfaces called agglutinogens
  • blood contains antibodies (agglutinins) against some antigens (agglutinogens)
  • the main agglutinogen systems are the A and B system and the Rh system
    1) A and B system
  • A and B antigens are inherited as Mendelian dominants
  • types:

A = A antigen, anti-B antibody

B = B antigen, anti-A antibody

AB = A and B antigen, no antibody (AB+ universal recipient)

O = no antigen, anti-A and anti-B antibody (O- universal donor)

2) Rh system
- composed of C, D, E antigens (D is most antigenic)
- types:

Rh+ = D antigen present

Rh- = no D antigen present, anti-D antibody present when injected with Rh+ cells

-if Rh- mother gives birth to a Rh+ baby, small amount of fetal blood leaks into maternal circulation at delivery

→ mother generates Rh antibodies (IgG that can cross the placenta)

→ during next pregnancy, maternal agglutinins cross placenta and attack Rh+ fetus

→ give IgG antibody to Rh- mother within 24 hours of exposure to Rh+ infant

→ maternal development of Rh antibodies is suppressed

53
Q

Why is group O- blood used as universal donor

A
  • group O- blood has no surface antigens and both anti-A and anti-B antibodies
  • blood will not be attacked by recipient antibodies as no surface antigens are present

ACEM Viva (39 decks)

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