heart failure and oedema Flashcards
how is the blood volume distributed through veins, arteries etc.
- veins = 64%
- Arteries/arterioles = 15%
- capillaries = 5%
- heart = 7%
- lungs = 9%
how is blood resistance distributed trhough veins, arteries etc.
- arteries/arterioles = 66%
- capillaries = 27%
- veins = 7%
what happens in the capillary beds
- transfer of nutrient and waste products
- under smooth muscle control for constriction/relaxation
- precapillary sphincter controls regional flow
- gaps between endothelial cells allow diffusion
describe the distribution of water within the body
- intracellular fluid compartment = 2/3 of total body water within cells
- extracellular fluid compartment = 1/3 total body water. 80% intersitial fluid, 20% blood plasma
describe how extracellular fluid is balanced
plasma and interstitial fluid are in dynamic equilibrium. 2 things determine direction of equilibrium:
- hydrostatic pressure (force exerted against inner capillary wall promoting formation of tissue fluid (net filtration pressure OUT)
- colloid osmotic pressure (exerted by plasma proteins promoting fluid reabsorption INTO circulatory system
how does hydrostatic pressure aid in the exchange of fluid in tissues
hydrostatic pressure is higher in the arterial end than the venous end.
- pressure must push fluid OUT at arteriole end to force nutrients into tissues
- pressure must allow fluid to re enter the circulatory system at the venous end to allow waste products to be removed from tissues
describe this graph
at the start of the capillary beds (arteriole end) hhydrostatic pressure is greater than osmotic pressure (which stays the same throughout) to push fluid out into the tissues. this is beneficial because it forces fluid carrying nutrients and oxygen into the tissues.
at the end, (the venous end) hydrostatic pressure falls below osmotic pressure, allowing waste products to reenter the capillary beds.
remember: hydrostatic is pressure OUT of vessels and osmotic is pressure IN
describe how starlings forces determine whether fluids are going in or out of vessels
starling force = (hydrostatic pressure in the capillary + colloid osmotic pressure of the intersitial fluid) - (hydrostatic pressure in the interstitial fluid + colloid pressure of the blood plasma)
what are the functions of the lymphatic system
- Assists in circulation of body fluid between cells and bloodstream (returns tissue fluid to circulation)
- protects body against foreign materials (carries to lymph nodes)
- transports dietary fats
what is oedema
- an excessive accumulation of intersitial fluid (may be free fluid in cavities)
- can be localised or general
- starlings forces are out of balance (increased outward filtration pressure, decreased inward absorption pressure = leaky vessels)
what causes increased outward filtration pressure?
decreased inward pressure?
increase outward:
- increased arterial pressure (dont see this clinically b/c of pressure decrease in venous and capillary end)
- increased venouc pressure (by either obstruction of the vessels locally or generalised increase in venous pressure
decreased inward:
- Fall in plasma COP
- protein loss
- reduced protein synthesis
what causes oedema
- vasogenic (leaky vessels) caused by local inflammation or generalised vasculitis
- lymphatic disease
- hyperaemic/hydrostatic caused by localised obstruction, high venous pressures (heart failure)
- osmotic caused by low plasma COP
what are the clinical findings of oedema
- can be localised or generalised
- fluid in skin (pitting oedema)
- fluid within tissue in a body system (lungs if L sided heart failure, brain if vascular disease)
- free fluid in body cavities (pleural fluid in cats = heart failure, free fluid in abdomin in dogs (ascites) = right sided heart failure)
what are the 2 words used to describe heart failure
- congenital
- acquired
desccribe the development of acquired heart disease
- develops later in life
- > 95% of all heart diseases (very common)
- require medical therapy
what are the primary causes of acquired heart failure
- degenerative valvular disease (aortic or mitral)
- heart muscle disease (cardiomyopathy)
- valve/endocardial infection
- pericardial disease
- rate/rhythm abnormalities
describe degenerative valvular disease
- develops later in life
- cause unknown
- may/may not develop into heart failure
- regurgitation into atrium during systole (compare atrial and aortic/pulmonic pulses
- picked up as murmur
- causes jet lesions caused by abnrormal flow of pressure
describe heart muscle diseases
- cardiomyopathy (especially in large breed dogs like dobermans)
- develops later in life
- cause unknown
- usually develops into heart failure
- in the cat rarely dilated
- usually restrictive (stiff heart)
- or hypertrophic (heart is thick walled)
describe dilated cardiomyopathy
- in the dog usually dilated if have cardiomyopathy
- disease of the heart muscle
- muscle function becomes poor
- heart does not pump effectively
compare eccentric hypertrophy and concentric hypertrophy
- eccentric occurs with volume loading (valve incompetence/ dilated CMO)
- concentric occurs with pressure load (hypertension or aortic/pulmonic stenosis)
compare acute vs chronic heart failure
acute:
- rare
- vascular disease and acute myocardial infarction (heart attack)
chronic:
- most common
- usually degenerative conditions
explain pathophysiology of heart failure
whatever the cause, cardiac output falls and is detected as a drop in blood pressure
-degenerative valve disease (regurgitation means less forward flow into the aorta)
dilated cardiomyopathy (forward flow falls due to poor contractility
restrictive/hypertrophic cardiomyopathy (forward flow falls because heart cannot fill)
what mechanisms are activates to restore blood pressure in heart failure
- SNS activation
- RAAS (renin angiotensin aldosterone system)
- cardiac enlargement (later)
what are the effects of the compensatory mechanisms of heart failure and how can they cause adverse effects long term
- HR increases
- contractility increased
- vasoconstriction
- salt and water retention
- cardiac enlargement
all of these are ideal in the short term, but long terms can worsen heart function or cause lean on effects to other organs
- HR and contractility increase = sick heart works harder = increased O2 demand but O2 availibility is decreased
- vasoconstriction = increased afterload = CO falls more = valves leak more
- salt and water retention = volume of blood returned to heart increases, volume of fluid in vessels increases, pressure in capillaries increases = oedema develops
- cardiac enlargement = AV valves leak more sue to stretch, O2 demand increases, O2 supply decreases = cells die and if not replaced scar tissue forms = contractility falls more
