how the cardiovascular system fails Flashcards
1
Q
what is stroke and what are the different types? 3
A
- rapid loss of brain functions due to loss of perfusion to parts of the brain
- hemorrhagic- cerebral blood vessel rupture
- ischaemic- cerebral blood vessel blockage
2
Q
what can cause a blood vessel to burst? 8
A
- high pressure
- high blood pressure or downstream blockage
- turbulent flow
- large diameter/ high wall tension
- low compliance/ high stiffness
- trauma
- atherosclerosis
- diabetes
3
Q
explain vessel wall tension? 3
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 (there is more trying to tear the vessel apart)
4
Q
what is laminar flow?
A
- slow at the edges
5
Q
what is turbulent flow? 2
A
- can be caused by high speed, branching and low viscosity
- turbulence can be caused by junctions, mixing and obstacles (atherosclerosis, endothelial damage)
6
Q
what are the activities of the endothelium? 6
A
- blood vessel tone= local control of perfusion and vasodilation due to NO secretion
- fluid filtration for tissues surrounding the blood vessel (blood brain barrier, CSF, kidney, GI secretions)
- haemostasis: especially fibrinolysis
- white cell recruitment: atherosclerosis
- angiogenesis
- hormone trafficking= transcytosis (transportation across the inside of a cell)(insulin)
7
Q
what is an acute myocardial infarction? 6
A
- a region of heart tissue that is dying or dead
- usually caused by a blocked coronary artery
- onset takes minutes
- reduces hearts capacity to pump
- large or multiple can lead to heart failure
- can be fatal
8
Q
what is atherosclerosis? 4
A
- a disease process
- results in the furring of arteries
- asymptomatic but can lead to other disorder
- results from hyperlipidaemia, immune action of unknown aetiology
9
Q
what is coronary heart disease? 5
A
- a disease process resulting in obstruction of arteries supplying the heart tissue
- angina/ asymptomatic
- primary cause is atherosclerosis
- treat with drugs for hyperlipidaemia, angina or hypotension
- treat with stenting or surgically replacing clogged vessels
10
Q
explain plaque rupture? 2
A
- when the fibrous cap of a plaque bursts open
- atheroma are relatively safe even if they occlude 50% of a vessel, but if the plaque ruptures in a coronary artery it can cause a thrombus or MI
11
Q
what are the sympathetic activity during a MI? 4
A
- sympathetic nervous system releases adrenaline and noradrenaline during acute MI
- this is in response to pain and haemodynamic abnormalities
- sympathetic activities also help to compensate during heart failure
- it leads to increased heart rate and contractility, increased peripheral resistance and increased risk of arrhythmia
12
Q
what are the forces on water molecules in a capillary?
2
A
- net pressure= hydrostatic pressure (out) and osmotic pressure (in)
- pushes water out at arterial end and pulls in at venous end
13
Q
what is pulmonary oedema? 4
A
- fluid accumulates in lungs (especially alveoli)
- causes impaired gas exchange and the process of O2 diffusion is lengthened
- this is caused by left heart failure- damming of blood vessels leads to hydrostatic pressure increase in the pulmonary circulation
- symptoms= dyspnoea/orthopnoea (trouble breathing lying down) which leads to hypoxia
14
Q
what are ascites? 2
A
- accumulation of fluid in the peritoneal cavity
- many causes including heart failure
15
Q
what is peripheral oedema? 2
A
- swelling of tissues
- many causes including chronic low output heart failure
16
Q
what is compensation?
in heart faliure?
A
- maintaining homeostasis of a physiological function despite stressors of malfunctions- happens via endogenous physiological feedback
- in heart failure, to maintain adequate cardiac output despite damage, there needs to be an increase in plasma volume and increase in sympathetic activity
17
Q
what is decompensated heart failure? 3
A
- a medical emergency
- the failure of the heart to maintain adequate blood circulation after long-standing vascular disease (previously compensated)
- respiratory distress
18
Q
what is cardiac remodelling? 5
A
- growth of cardiac muscle, changes in shape, size and function
- caused by injury (MI, heart failure, valve response)
- the result is hypertrophy or dilation
- compensatory initially-pathological later
- treated by ACE inhibitors or spironolactone
19
Q
explain ventricular hypertrophy? 4
A
- response to work
- athlete’s heart
- eccentric= dilate due to volume overload
- concentric= thicken due to pressure overload
20
Q
what is ADH? 4
A
- antidiuretic hormone
- causes kidneys to reabsorb more water and decreases diuresis (losing water via kidneys into the urine)
- secreted from posterior pituitary gland
- peptide
21
Q
what is aldosterone? 5
A
- causes kidney to reabsorb more NaCl (and thus more H2O)
- directly decreases natriuresis (excretion of sodium in urine)
- which decreases diuresis
- secreted from the adrenal cortex
- steroid
22
Q
what does angiotensin II do? 7
A
- increases pressure
- vasoconstriction
- increased fluid retention
- increased aldosterone secretion by adrenal cortex
- increases Na+ retention
- increases ADH secretion by posterior pituitary
- contributes to ventricular hypertrophy and remodelling
23
Q
describe the renin-angiotensin-aldosterone system (RAAS)? 5
A
- angiotensinogen
- enzyme renin
- angiotensin I
- enzyme ace
- angiotensin II (active vasoconstrictor)
24
Q
what do diuretics do?
name 3 different types
A
lead to loss of fluid at nephron
- thiazide like
- indapamide
- blocks reabsorption at DCT
- loop
- furosemide
- blocks reabsorption in the thick
- K+ sparing
- spironolactone
- inhibits aldosterone receptors in cortical collecting duct
25
Q
what is heart faliure?
A
- when cardiac output is insufficient for meeting needs of the body and lungs
26
Q
what is chronic low output heart failure? 2
A
- cardiac output is low, usually due to accumulated damage to the heart
- chronic condition with poor 5-year survival rate
27
Q
what is left heart failure? 5
A
- respiratory systems
- right heart pumps into lungs but left atrium is too full
- increased hydrostatic pressure in pulmonary circulation
- ‘congestive’- pulmonary vasculature is congested
- in extreme conditions- fluid leaks out of blood vessels and into the lungs
28
Q
what is right heart failure? 2
A
- increased central venous pressure
- leads to peripheral oedema
29
Q
what is heart failure symptoms and signs? 4
A
- fatigue (especially during exertion)
- peripheral oedema
- dyspnea
- orthopnea
30
Q
what is fluid retention? 3
A
- the thing that unites all forms of heart failure
- compensation= initially homeostatic
- eventually does more harm than good= dyspnea, ascites, ankle oedema
31
Q
what is cardiogenic shock? 6
A
- critically low perfusion due to low cardiac output
- medical emergency, usually fatal
- insufficient perfusion of tissues, especially the heart
- progresses by positive feedback
- includes SBP < 90 mmHg
- aggressive intravenous fluid and oxygen +airway maintained
32
Q
what are the normal treatments for chronic heart failure? 4
A
- ACE inhibitors
- diuretics
- beta blockers
these all interfere with the body’s response to low cardiac output
33
Q
what is the homeostasis for cardiac output? 9
A
- increased sympathetic activity (fast response)
- increased heart rate and heart contractility
- vasoconstriction
- kidney accumulates fluid (slow response)
- decreased glomerular filtration rate
- increased central venous pressure
- increased venous return
- increased preload
the goal of pharmacotherapy for heart failure is to stop both of these processes
34
Q
explain what the kidney is evolved to cope with? 3
A
- haemorrhage no heart failure, these look the same to the kidney
- heart failure- normal pressure, ends with shock
- haemorrhage- loss of fluid leads to loss of pressure, ends with shock
35
Q
explain the process of decompensated heart failure? 8
A
- kidney increases plasma volume to compensate for poor perfusion of renal tissue
- the kidney responds as if there is haemorrhage which leads to fluid overload
- the heart is unable to pump the extra fluid
- fluid damming leads to increased venous pressures
- increased back pressure further damages the heart
- positive feedback loop
- the capillaries leak fluid into the tissues
- the lungs cannot perform gas exchange
36
Q
what are the treatment goals of low output HF? 3
A
- prevent acute decompensated heart failure
- counteract cardiac remodelling
- minimize symptoms
