How the CVS fails Flashcards
what is a stroke
Rapid loss of brain function due to loss of perfusion to parts of the brain (cerebrovascular accident)
what are the types of stroke
Haemorrhagic (cerebral blood vessel rupture) or ischaemic (cerebral blood vessel blockage)
what are causes of blood vessels bursting
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
how much tension is placed on vessel walls
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
what is compliance
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
what causes turbulent flow and what does it cause
causes of high speed, branching, low viscocity
caused by junctions, mixing and obstacles Iatherosclerosis, endothelial damage)
what does the endothelial layer in vessels do
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
what is acute myocardial infarction
A region of heart tissue dying or dead
Usually caused by blocked coronary artery
what are symptoms of MI
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
What causes atherosclerosis
hyperlipidaemia, immune action or unknown aetiology (asymptomatic but can lead to other disorders, narrowing of arteries)
what is coronary artery disease
results from coronary obstruction
Angina or asymptomatic
Primary cause is atherosclerosis
what is a plaque rupture
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)
what happens in response to a MI
Sympathetic nervous system releases adrenaline and noradrenaline in response to pain and haemodynamic abnormalities
Helps compensate as leads to increase in HR and contractility
What are the risks related to MI compensatory action
increased peripheral resistance and risk of arrythmia)
what is pulmonary oedema
Fluid accumulation outside of blood vessel (in lungs esp alveoli)
Impaired gas exchange or O2 diffusion path is lengthened
what causes pulmonary oedema
Caused by left heart failure (damming of blood > hydrostatic pressure > increase in pulmonary circulation)
what are symptoms of pulmonary oedema
dyspnoea/orthopnoea (trouble breathing)
>hypoxia
what is ascites and peripheral oedema
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)
what is compensation
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)
what is decompensated HF
A medical emergency (failure of heart to maintain adequate blood circulation after long standing vascular disease = respiratory distress
what is cardiac remodelling
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
how can cardiac remodelling be treated
Treat inhibit ACE inhibitors or spironolactone
what is ventricular hypertrophy
Response to work
Eg Athlete’s heart
Eccentric (dilate due to volume overload)
Concentric (thicken due to pressure overload)
what is ADH
(aka vasopressin)
Causes kidneys to reabsorb more water (decrease diuresis), secreted from posterior pituitary, a peptide
what is aldosterone
Causes kidneys to reabsorb more NaCl (more H20), directly decreases natriuresis to decrease diuresis, secreted from adrenal cortex, steroid
what does decreased diuresis do to BP
increase it as it antagonises ADH and aldosterone leading to fluid loss
what does angiotensin do
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
what is RAAS
The rein-angiotensin-aldosterone system
Angiotensinogen turns to angiotensin I by RENIN (enz), ACE (enz) turns it to angiotensin II
What do thiazide (and thiazide like) diuretics do
Eg indapamide
Blocks reabsorption at DCT (distal convoluted tubule)
What do loop diuretics do
eg furosemide
Block reabsorption in thick loop
what do K+ sparing diuretics do
eg spironolactone
Inhibits aldosterone receptors in cortical collecting duct
what is chronic low output heart failure
CO low due to accumulated damage, chronic condition with a 5 year survival rate, abbreviated as heart failure, can also have high output HF
what is decompensated HF
ME > rapid death if untreated
What are CLO symptoms if they effect the LHS of the heart
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)
What are CLO symptoms if they effect the RHS of the heart
systemic symptoms (increase in central venous pressure leading to peripheral oedema)
What are CLO symptoms regardless of heart side effected
Reduced CO, sympathetic activation to compensate (inc HR and PR)
what are symptoms and signs of HF
Fatigue (esp exertion`0
Peripheral oedema
Dyspnoea (orthopnoea, cant breath lying down), paroxysmal nocturnal dyspnoea)
HF is physiological, MI is anatomical
what unites all forms of HF
fluid retention as its compensation (initially homeostatic) but eventually does more harm than good (dyspnoea, ascites, ankle oedema)
what is cariogenic shock
Critically low perfusion due to low CO (ME, usually fatal)
Insufficient perfusion of tissues esp the heart
Progresses by positive feedback
what is the definition of shock
Def og shock SBP< 90 mmHg (systolic BP)
Treatments aggressive intravenous fluid and O2 + airway maintained
what are treatments for chronic HF
ace inhibitors, diuretics, beta blockers which all interfere with body’s homeostatic response to low CO (stop going too far)
What is the body’s homeostatic response to low CO
Inc sympathetic activity (fast response) -Inc HR, contractility and vasoconstriction
Kidney accumulates fluid (slower) -Dec GFR, inc venous pressure, return and preload
What is the kidney evolved to deal with
Kidney evolved to cope with haemorrhage not HF
how does low output compare to ow volume
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)).
how does the kidney respond to decompensated heart failure
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
what are the goals for treating low output HF
Prevent acute decompensated heart failure
Counteract cardiac remodelling
Minimise symptoms
