Anatomy - Hypertension Flashcards
(83 cards)
1
Q
What are the different things to remember in Darcy’s law of flow?
A
- Flow = ‘delta’ pressure / resistance
- ‘delta’ p = pressure gradient between arteries and veins, created by heart pumping
- Resistance = measure of degree which blood vessel resists blood flow
- Flow = directly related to pressure difference
- Flow = inversely related to resistance
2
Q
What is the equation for Poiseuille’s law of flow?
A
3
Q
What effects does longer vessel, + viscosity and + radius have on flow?
A
Lower flow
Lower flow
Greater flow
4
Q
What does the graph for relative flow against relative radius look like?
A
5
Q
What is the resistance equation?
A
6
Q
What are the properties of small arteries and arterioles?
A
- ability to change radius
- pressure change
- Must decrease pressure before capillay entry
7
Q
How do you calculate total peripheral resistance?
A
Arterial - venous pressure / cardiac output
8
Q
What is laminar blood flow?
A
Largest velocity in the centre of blood vessel
9
Q
What is the function of arterial compliance?
A
Provides filtering / smoothing
10
Q
What is the function of venous compliance?
A
Provides capacity for storage (reservoir blood), which is reduced by constricting veins
11
Q
What 4 things is venous return affected by?
A
- Affected by venomotor tone (constriction)
- Affected by venous valve competence
- Affected by skeletal muscle pump –> leg muscle contraction squeezes blood from superficial vein to deep vein to heart
- Affected by respiration –> inspiration decreases intra-thoracic pressure & increases intra-abdominal pressure hence provides a pressure gradient to assist blood flow to the heart
12
Q
What are the 3 determinants of blood vessel radius?
A
- Active tension exerted by smooth muscle
- Passive elastic wall properties
- Blood pressure inside of vessel
13
Q
What does an increase in vessel radius lead to?
A
- wall tensions
- Aneurysm
14
Q
What things does active control of vessel calibre allow?
A
- Allows redistribution of blood flow
- Allows control of pre/post capillary sphincters
- Allows regulation of vascular tone and control of blood pressure
15
Q
What is vascular tone?
A
Degree of constriction / dilatation
16
Q
What does vasomotor tone refer to?
A
Arteries and arterioles
17
Q
What does venomotor tone refer to?
A
Veins and venules
18
Q
What factor causes vasoconstriction?
A
Noradrenaline:
- Released from sympathetic
- Binds to alpha receptors
19
Q
What factor causes vasodilatation?
A
Noradrenaline:
- Released by sympathetic
- Binds to beta receptors in skeletal muscle
20
Q
What effect do certain hormoenes have on smooth muscle vessel contraction?
A
Catecholamines:
- Noradrenaline / adrenaline
- Constrict / dilate
Peptides:
- Vasopressin, angiotensin = constrict
- Bradykinin = dilate
21
Q
What intrinsic mechanisms affect vessel contraction/dilatation?
A
- Endothelium-derived vasorelaxants (PGI2, NO, EDHF)
- Endothelium-derived vasoconstrictors (endothelin)
- Metabolites
- Myogenic (autoregulation of blood-flow)
22
Q
What effects do certain metabolites have on vessels?
A
23
Q
What factors contribute to extrinsic control?
A
- Nerves
- Hormones
- Regulate arterial bp
24
Q
How is cerebral blood flow regulated?
A
- 14% cardiac output at rest
- Neural control = alpha vasoconstriction
- Autoregulation resets during hypertension and abloshed by hypercapnia
- H+, K+, adenosine, hypercapnia, hypoxia = vasodilatation
- Mechanical = constrained in rigid cranium, influenced by VSF pressure
- Medullary ischaemic reflex = special feature
25
How is coronary blood flow regulated?
* 4% of cardiac output
* Neural = secondary effect on flow due to cardiac function and metabolism changes
* Sympathetic stimulation = B-mediated increase in HR and stroke volume, increasing oxygen consumption
* Local = Hypoxia, hypercapnia, adenosine = vasodilation
* Hormones = adrenaline
* Mechanical = major influence on flow during cardiac cycle – peak flow = early diastole, 0/- at onset of systole
* Special features = parallelism between metabolism and flow
26
How is skin blood flow regulated?
* 4% cardiac output at rest in thermoneutral environment
* Neural = arterioles = weak innervation, A-V anastomoses = dense innervation
* Local = arterioles = myogenic autoregulation, AV anastomoses = no autoregulation and no reactive hyperaemia, endothelin = may be involved in pathological states, i.e. Raynauds
* Hormones = angiotensin, vasopressin, noradrenaline, adrenaline = vasoconstriction
* Special features = thermoregulation is primary function, sweat glands = sympathetic cholinergic innervation, causes vasodilation vie bradykinin release, i.e.
27
How is skeletal blood flow regulated?
* 15% cardiac output at rest
* Neural = rest – important alpha vasoconstriction, some beta vasodilatation, some sympathetic cholinergic vasodilatation – exercise – little neural influence, some beta vasodilation
* Local = rest – neural control override autoregulatory mechanisms – exercise – local metabolites = major influence
* Hormones = adrenaline at low concentrations = beta vasodilatation
* Mechanical = muscle pumping
* Special features = capacity to increase flow in exercise 20-fold, active hyperaemia, large increase in flow post-occlusion- reactive hyperaemia (increased blood flow)
28
How is splanchnic blood flow regulated?
* Superior mesenteric = 10% cardiac output, hepatic = 25% cardiac output
* Neural = intestinal: moderate a vasoconstriction, hepatic: important a venoconstriction
* Local = intestinal: importantly influenced by local peptides, hepatic: portal vein - no autoregulation, hepatic artery - good autoregulation
* Hormones = G-I hormones (gastrin, cholecystokinin) vasodilate; vasopressin, angiotensin constrict potently
* Special features = intestinal circulation exhibits functional hyperaemia following feeding. Intense vasoconstriction can lead to damage and release of toxins à Vasoconstriction (neurohumoral) beneficial in baroreflex but can be detrimental in haemorrhage/septic shock
29
How is renal blood flow regulated?
* 25% cardiac output
* Neural = important a vasoconstriction; some b vasodilatation. Renin secreting cells have a sympathetic innervation (b adrenoceptors)
* Local = good autoregulation of flow over a wide pressure range
* Hormones = noradrenaline, adrenaline, angiotensin = constriction. Vasopressin = vasodilatation via prostaglandin/NO release. Dopamine = vasodilatation
* Mechanical = renal capsule may restrict flow in pathological states
* Special features = excretory function of kidney depends on (autoregulation). Vascular connections provide for capacity to regulate afferent/efferent resistances
30
How is pulmonary blood flow regulated?
* 100% cardiac output
* Neural = a vasoconstriction
* Local = hypoxia causes vasoconstriction = augmented by hypercapnia - possibly mediated by endothelin. NO = dilatation - may be used therapeutically - Pulmonary hypertension: - possible therapeutic strategies include endothelin receptor antagonism and NO inhalation
* Mechanical = flow is affected by changes in alveolar pressure and lung volume. Increase in flow = recruitment and distension of micro vessels = decrease in vascular resistance - If alveolar pressure \> intravascular pressure, flow reduced. Lung inflation reduces resistance in extra-alveolar vessels (traction) and increases resistance in intra-alveolar vessels (compression)
* Special features = thin walled vessels with low resistance, low vasoconstrictor capacity. Hydrostatic pressure (10mmHg) \< colloid osmotic pressure (25mmHg) which favours reabsorption
31
How do you calculate mean blood pressure?
What is the reason for this?
diastolic bp + 1/3 pulse pressure
Spoends more time in diastole than systole
32
What are the 2 systolic bp determinants?
* Stroke volume
* Aortic elasticity (elastic absorbs energy from systole, so less elkastic = + bp)
33
What are the 3 diastolic bp determinants?
* Peripheral resistance (+ = + bp)
* Aortic elasticity (- = - bp as less energy to give back during diastole)
* Heart rate (- = - bp because greater run-off time)
34
How do you calculate mean arterial bp?
Cardiac output X total peripheral resistance
35
How is arterial blood pressure controlled?
* Pressure sensors in circulation (baroreceptors in carotid sinus and aortic arch) --\> **afferent input**
* Integration systems in CNS --\> **efferent output**
* Effector mechanisms via ANS --\> PNS and SNS activation supplying heart (NA on alpha 1/2 = vasoconstriction = + TPR)
36
What are the order of events for the medulla integration systems in controlling arterial bp?
37
What are the properties of the pressor area in arterial bp control?
Tonically active
Tonically inhibited by baroreceptors
38
What are the properties of the depressor area in arterial bp control?
Not tonically active
Activated by increase in baroreceptor afferent nerve discharge
39
What are the order of events when arterial bp decreases?
40
What are the order of events when arterial bp increases?
41
What happens to dbp and sbp upon standing from lying down?
DBP = increases
SBP = decreases
42
What 3 things determine solvent movement across capillaries?
Diffusion
Filtration
Pinocytosis
43
What are the 2 components of bulk flow?
Filtration
Reabsorption
44
What is filtration favoured by?
Capillary hydrostatic pressure (Pc)
Interstitial fluid colloid osmotic pressure (πi)
45
What is reabsorption favoured by?
Capillary colloid osmotic pressure (πc)
Interstitial fluid hydrostatic pressure (Pi)
46
What are the properties of capillary hydrostatic pressure (Pc)?
* Major determinant of fluid movement
* Depends on:
* pre/post capillary resistances
* venous pressure
* (arterial pressure)
* If an arteriole constricts
* increase pressure upstream
* decrease pressure downstream
* Precapillary constriction reduces Pc
47
What are the properties of interstitial fluid colloid osmotic pressure (Pi)?
* Normally minor determinant of fluid movement
* Depends on the presence of protein in interstitium hence capillary permeability to protein - normally very low
48
What are the properties of capillary colloid osmotic pressure (Pc)?
* Major determinant of fluid movement
* Depends upon:
* synthesis/breakdown of protein (liver)
* capillary permeability to protein
* abnormal protein loss (kidney damage)
49
What are the properties of interstitial fluid hydrostatic pressure (Pi)?
* Normally minor determinant of fluid movement
* Depends upon:
* interstitial fluid volume
* compliance of organ
* effective drainage
* Lymphatic system provides drainage
* Lymphatic vessels are valved & highly permeable to protein
* Lymph flow rate ~ 2-4 litres/day - returns excess filtered fluid and 95% of protein lost from vascular system back to the circulation (subclavian vein)
50
What does right sided heart failure lead to?
Peripheral oedema
51
What does left sided heart failure lead to?
Pulmonary oedema
52
What factors affect capillary fluid transfer?
Capillary hydrostatic pressure (+Pc = + filtration)
Plasma colloid osmotic pressure (+πc = + reabsorption)
53
What are some causes of secondary hypertension?
* Renal disease
* Renovascular disease
* Conn’s syndrome
* Cushing’s syndrome
* Hyperthyroidism
* Phaeochromocytoma
* Pregnancy
* Drugs (e.g. NSAIDs, corticosteroids, sympathomimetics)
54
What are the goals of hypertension treatment?
* Reduction in cardiovascular damage.
* Preservation of renal function.
* Limitation or reversal of left ventricular hypertrophy.
* Prevention of Ischaemic Heart Disease.
* Reduction in mortality due to stroke and myocardial infarction
* Get systolic \< 140 mmHg
* Get diastolic \< 90 mmHg
55
How do you calculate blood pressure?
Cardiac output X total peripheral resistance
56
How do ACEIs work and their contraindications?
Aldosterone = water retaining and sodium retaining (cough from + bradykinin)
ACEIs = prevent aldosterone production by inhibiting angiotensin ii
Contraindication = renal artery stenosis as + decrease in BP, can be fatal
57
How do AT1 receptor antagonists work?
Block angiotensin 2 at angiotensin 1 receptor
Less likely to give rise to a cough
58
How do calcium channel inhibitors work and their contraindications?
Reduce bp and cause vasodilatation
Rate-limiting = + cardiac tissue effect
Contraindication with heart failure as they worsen it - DHPs = + favourable, + action on vascular smooth muscle
59
How do diuretics work and their side effects?
Inhibit na+/cl- transporter, prevent reabsorption so ions excreted, followed by water
Circulating volume reduced
Side effects = hypokalaemia, postural hypotension, impaired glucose control
60
What are the properties of alpha blockers?
Block alpha adrenoceptors
Reduce bp
Used as last resort as side effects poorly tolerated
61
How do beta-blockers work and their contraindications?
Reduce renin release
Reduce sympathetic drive to heart and reduce cardiac output
Contraindicated = asthma, used with caution in COPD
62
What is apoptosis?
Intracellular mechanism
63
What are the treatment guidelines for hypertension + type 2 diabetes, \<55 + non-black and \>55 or black?
64
What is necrosis and the different types?
Extracellular mechanism
Coagulative, liquefactive, caseous, fat and fibrinoid necrosis - infarction (ischaemic necrosis), gangrene (ischaemic necrosis with some putrefaction)
65
What is infarction?
An area of ischemic necrosis due to abrupt cessation of the arterial supply (‘arterial infarction’) or venous drainage (‘venous infarction’)
66
What factors affect infarction development?
* Vascular occlusion
* Nature of vascular supply
* Rate of occlusion development
* Type of tissue (have different vulnerabilities to hypoxia à neurons = 2-3mins, myocardium = 20-40 mins, fibroblast = many hours)
67
How do you characterise infarctions based on their colour?
* Based on amount of haemorrhage
* Pale or white infarct (A): solid organs such as heart & spleen
* Red or haemorrhagic infarct (V): in loose spongy tissue rich in blood supply or has dual blood supply such as lung
68
What are the 2 origins of causes of infarction?
Arterial
Venous
69
What are the two types of infarction infection?
* Septic: causes by septic emboli such as vegetation of SBE
* Bland: caused by aseptic emboli or thrombi. Most common
70
What is the morphology of infarction?
* Infarct is usually wedge shaped with occluded artery at apex and base at periphery (if serosa- fibrinous exudate)
* Margins: early poorly defined slightly haemorrhagic but later well defined
* Inflammatory response followed by reparative response - finally scar tissue
71
What are the causes of arterial infaction?
* Occlusion by EMBOLUS
* Occlusion by ATHEROMA + THROMBOSIS
* Occlusion by ATHEROMA WITH PLAQUE FISSURE
* Occlusion by ATHEROMA ALONE
* Other cases: arterial spasm or arterial trauma
72
What are the stages of infarction (timeline)?
* 0-12 hours - early stages of cell death
* 12 - 24 hours - necrotic muscle fibres apparent microscopically
* 24 - 72 hours - acute inflammatory reaction to dead muscle
* 3 - 14 days - macrophagic removal of debris and vascular granulation tissue formation
* 14 - 21 days - fibrous granulation tissue formation
* 21 - 56 days - scar formation and cicatrisation
73
What are the early complications of arterial infarction?
* Sudden death due to cardiac dysrhythmia
* Sudden death due to acute left ventricular failure
* Rupture of myocardium -\> haemopericardium
* Rupture of papillary muscle -\> acute valve failure-\>LVF
* Mural thrombus on infarct -\> embolism -\> stroke & others
* Fibrinous Pericarditis & extension of MI
74
What are the late complications of arterial infarction?
* Chronic LVF
* Ventricular aneurysm
75
What are the properties of a renal infarct?
* Usually due to emboli from L side of heart
* Wedge-shaped
* Pale area with hyperaemia around
* Heals by scar formation
76
What are the properties of cerebral infarct?
_Causes are:_
* Atherothrombotic in extra-cerebral arteries
* Embolic
* Watershed (Border zone) infarct: hypoperfusion & microembolisms
77
What is this and how does it heal?
Liquefaction necrosis
Heals by astrocytic gliosis
78
What are the properties of gangrene?
* Type of necrosis caused by vascular insufficiency following injury or infection
* Infarction of extremities or bowel
* Foot and leg most common. Often in diabetics
* Only solution is amputation
* Types = dry, wet or gas
79
What are the 2 causes of gangrene?
* Thrombus occluding atheromatous ilio-femoral artery
* Thromboembolism from left side of heart
80
What are the properties of venous infarction?
* Can occur when the entire venous drainage from an organ or tissue is, and remains, completely obstructed.
* Three common examples:
* Bowel infarction e.g. volvulus, hernial strangulation.
* Testis infarction, due to torsion.
* Ovarian infarction, due to torsion.
81
What are the events of venous infarction?
* Veins become obstructed, usually by extrinsic pressure
* Tissues become congested with blood, venules and capillaries being engorged with blood which cannot escape
* Pressure in capillaries and venules rises so high that:
* Many of them rupture, with leakage of blood
* Arterial blood cannot enter, so hypoxia ensues
* Tissues become congested, hypoxic and necrotic
82
What is this?
Volvulus
* Colon has twisted on its vascular pedicel
* Venous outflow obstructed
* Venous infarction ensued
83
What is this?
Venous infarction - torsion of testes
* Twisted spermatic cord
* Plexus of veins are compressed
* Blood cannot drain out of tested or epididymis
* Venous infarction occurs
