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103 theme 3 > How the CVS fails > Flashcards

How the CVS fails Flashcards

1
Q

what is a stroke

A

Rapid loss of brain function due to loss of perfusion to parts of the brain (cerebrovascular accident)

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2
Q

what are the types of stroke

A

Haemorrhagic (cerebral blood vessel rupture) or ischaemic (cerebral blood vessel blockage)

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3
Q

what are causes of blood vessels bursting

A

Stresses – high pressure (high BP or downstream blockage), turbulent flow, large diameter (high wall tension), low compliance (high stiffness)
Damage
Trauma (eg transluminal procedures), atherosclerosis, diabetes

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4
Q

how much tension is placed on vessel walls

A

Tension in a cylinder is the force (tangential to the circumference of the cross section) that is trying to rip the wall apart
In a cylinder it is proportional to P x radius
The larger the vessel, the greater the wall tension

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5
Q

what is compliance

A

The change in volume caused by a change in pressure

eg Low compliance = a change in pressure results in a very little change in volume

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6
Q

what causes turbulent flow and what does it cause

A

causes of high speed, branching, low viscocity

caused by junctions, mixing and obstacles Iatherosclerosis, endothelial damage)

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7
Q

what does the endothelial layer in vessels do

A

Blood vessel tone (local control of perfusion, vasodilation – NO)
Fluid filtration (blood brain barrier, CSF, kidney, GI secretions)
Haemostasis esp fibrinolysis
White cell recruitment (atherosclerosis)
Angiogenesis
Hormone trafficking – transcytosis eg insulin

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8
Q

what is acute myocardial infarction

A

A region of heart tissue dying or dead

Usually caused by blocked coronary artery

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9
Q

what are symptoms of MI

A

Onset takes mins – extremely painful
Reduces capacity of heart to pump
Large or multiple infarcts > heart failure
AMIs can be fatal due to arrythmia or heart failure

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10
Q

What causes atherosclerosis

A

hyperlipidaemia, immune action or unknown aetiology (asymptomatic but can lead to other disorders, narrowing of arteries)

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11
Q

what is coronary artery disease

A

results from coronary obstruction
Angina or asymptomatic
Primary cause is atherosclerosis

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12
Q

what is a plaque rupture

A

When a fibrous cap of a plaque bursts open
Atheromas are relatively safe (even at 50% occlusion, if ruptures in coronary artery then can lead to thrombus or embolism and an MI)

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13
Q

what happens in response to a MI

A

Sympathetic nervous system releases adrenaline and noradrenaline in response to pain and haemodynamic abnormalities
Helps compensate as leads to increase in HR and contractility

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14
Q

What are the risks related to MI compensatory action

A

increased peripheral resistance and risk of arrythmia)

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15
Q

what is pulmonary oedema

A

Fluid accumulation outside of blood vessel (in lungs esp alveoli)
Impaired gas exchange or O2 diffusion path is lengthened

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16
Q

what causes pulmonary oedema

A

Caused by left heart failure (damming of blood > hydrostatic pressure > increase in pulmonary circulation)

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17
Q

what are symptoms of pulmonary oedema

A

dyspnoea/orthopnoea (trouble breathing)

>hypoxia

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18
Q

what is ascites and peripheral oedema

A

Ascites is the accumulation of fluid in peritoneal cavity, many causes inc HF
Peripheral oedema is swelling of tissues esp ankles, many causes esp chronic low output HF)

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19
Q

what is compensation

A

Maintaining homeostasis of physiological function despite stressors or malfunction
Eg HF to maintain CO, inc plasma volume (net inc in pressure) and sympathetic activity (inc net amount of pumping) (starling’s law)

20
Q

what is decompensated HF

A

A medical emergency (failure of heart to maintain adequate blood circulation after long standing vascular disease = respiratory distress

21
Q

what is cardiac remodelling

A

Growth of cardiac muscle (changes in size, shape, function)
Caused by injury (MI, hypertension, valve disease, response to increased afterload or preload)
Result in hypertrophy or dilation
Compensatory initially to pathological later

22
Q

how can cardiac remodelling be treated

A

Treat inhibit ACE inhibitors or spironolactone

23
Q

what is ventricular hypertrophy

A

Response to work
Eg Athlete’s heart
Eccentric (dilate due to volume overload)
Concentric (thicken due to pressure overload)

24
Q

what is ADH

A

(aka vasopressin)

Causes kidneys to reabsorb more water (decrease diuresis), secreted from posterior pituitary, a peptide

25
Q

what is aldosterone

A

Causes kidneys to reabsorb more NaCl (more H20), directly decreases natriuresis to decrease diuresis, secreted from adrenal cortex, steroid

26
Q

what does decreased diuresis do to BP

A

increase it as it antagonises ADH and aldosterone leading to fluid loss

27
Q

what does angiotensin do

A

increases pressure
Vasoconstriction, increases fluid retention (inc aldosterone secretion by adrenal cortex, inc Na+ retention). Increase ADH secretion by posterior pituitary
Contributes to ventricular hypertrophy and remodelling

28
Q

what is RAAS

A

The rein-angiotensin-aldosterone system

Angiotensinogen turns to angiotensin I by RENIN (enz), ACE (enz) turns it to angiotensin II

29
Q

What do thiazide (and thiazide like) diuretics do

A

Eg indapamide

Blocks reabsorption at DCT (distal convoluted tubule)

30
Q

What do loop diuretics do

A

eg furosemide

Block reabsorption in thick loop

31
Q

what do K+ sparing diuretics do

A

eg spironolactone

Inhibits aldosterone receptors in cortical collecting duct

32
Q

what is chronic low output heart failure

A

CO low due to accumulated damage, chronic condition with a 5 year survival rate, abbreviated as heart failure, can also have high output HF

33
Q

what is decompensated HF

A

ME > rapid death if untreated

34
Q

What are CLO symptoms if they effect the LHS of the heart

A

resp symptoms (R heart pumps to lungs but left atrium is too full so hydrostatic pressure increases in pulmonary circulation) > Congestive heart failure (pulmonary vasculature is congested, extreme if fluid leaks into lungs from BVs)

35
Q

What are CLO symptoms if they effect the RHS of the heart

A

systemic symptoms (increase in central venous pressure leading to peripheral oedema)

36
Q

What are CLO symptoms regardless of heart side effected

A

Reduced CO, sympathetic activation to compensate (inc HR and PR)

37
Q

what are symptoms and signs of HF

A

Fatigue (esp exertion`0
Peripheral oedema
Dyspnoea (orthopnoea, cant breath lying down), paroxysmal nocturnal dyspnoea)
HF is physiological, MI is anatomical

38
Q

what unites all forms of HF

A

fluid retention as its compensation (initially homeostatic) but eventually does more harm than good (dyspnoea, ascites, ankle oedema)

39
Q

what is cariogenic shock

A

Critically low perfusion due to low CO (ME, usually fatal)
Insufficient perfusion of tissues esp the heart
Progresses by positive feedback

40
Q

what is the definition of shock

A

Def og shock SBP< 90 mmHg (systolic BP)

Treatments aggressive intravenous fluid and O2 + airway maintained

41
Q

what are treatments for chronic HF

A

ace inhibitors, diuretics, beta blockers which all interfere with body’s homeostatic response to low CO (stop going too far)

42
Q

What is the body’s homeostatic response to low CO

A

Inc sympathetic activity (fast response) -Inc HR, contractility and vasoconstriction
Kidney accumulates fluid (slower) -Dec GFR, inc venous pressure, return and preload

43
Q

What is the kidney evolved to deal with

A

Kidney evolved to cope with haemorrhage not HF

44
Q

how does low output compare to ow volume

A

Heart failure (normal pressure (inc vascular resistance), ends with shock, rare before 50)
vs
Haemorrhage (loss of fluid leads to loss of pressure, ends with shock, any age (due to trauma)).

45
Q

how does the kidney respond to decompensated heart failure

A

responds as if haemorrhage
increase plasma volume (compensate for poor renal tissue perfusion, fluid overload)
Heart unable to pump extra fluid (fluid damming leads to increased venous hydrostatic pressure, increase back pressure, further damage, positive feedback loop)
Capillaries leak fluId into tissues (eg lungs and ankles)
Lungs can’t exchange O2 and CO2

46
Q

what are the goals for treating low output HF

A

Prevent acute decompensated heart failure
Counteract cardiac remodelling
Minimise symptoms

103 theme 3 (20 decks)

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