PBL 4 - clinical heart failure Flashcards
1
Q
what is the definition of clinical heart failure?
A
a state in which the CO fails to meet the body’s demands
2
Q
what does clinical heart failure clinically manifest as a triad of?
A
- typical signs
- typical symptoms
- a cardiac deficit resulting in reduced cardiac output (CO)
or increased filling pressures
3
Q
fluid makes up what % of the body?
A
60%
4
Q
what is the fluid of the body divided into?
A
intra-cellular and extra-cellular compartments
5
Q
what do all the cells in the body bask in?
A
ECF
6
Q
the ECF is moved around the body in what 2 phases?
A
- movement through the vasculature — blood and associated plasma pumped around the body
- movement from the capillaries to the interstitial fluid or interstitial space
7
Q
compared to ICF, what is ECF rich in?
A
rich in — Na+, Cl-, HCO3-, glucose
8
Q
compared to ECF, what is ICF rich in?
A
K+, Mg++, phosphates, amino acids (proteins)
9
Q
in terms of the levels of Na+ and K+, what is important for the cells’ function and survival?
A
vital that the level of sodium in cells is very low and the levels of potassium inside cells is elevated
10
Q
what does ECF also carry?
A
oxygen and nutrients such as glucose, amino acids and fats, and it carries away waste products such as CO2
11
Q
approx what % of ECF is plasma?
A
20%
12
Q
how long does it take at rest for plasma to be circulated around the body?
A
about a minute
13
Q
how are capillaries well adapted for ECF to reach the cells?
A
- densely packed — every cell in the body is very close to a capillary
- thin-walled
- clefts in the capillary wall — pores which allow some fluid and substances to go through them — allow very fast movement of water and water-soluble substances to the interstitial space
14
Q
how do fat soluble substances move from the plasma to interstitial space? (+ give examples of fat-soluble substances)
A
- eg. O2, CO2, nitrates, alcohol
- can cross lipid belayer of the cell membranes
- can therefore cross the surface of capillaries anywhere very quickly
15
Q
how do water soluble substances move from the plasma to interstitial space? (+ give examples of water soluble substances)
A
- eg. water, sodium, chloride
- go through the pores
- pores vary in size (eg. large in liver)
16
Q
by what process to substances move across?
A
diffusion
17
Q
by what process does water move across?
A
osmosis
18
Q
what is capillary pressure?
A
blood pressure inside the capillaries — drives fluid out of the capillary
19
Q
what is capillary pressure opposed by?
A
interstitial fluid pressure = usually lower than capillary pressure (sub atm in a lot of places)
20
Q
what is plasma colloid osmotic pressure? what is it opposed by?
A
essentially plasma proteins (largely albumin) pulling water towards them — opposed by interstitial fluid colloid osmotic pressure but there is less protein inside the interstitial fluid
21
Q
what do the pressures affecting the movement of water from the plasma to the interstitial space look like on a diagram?
A
22
Q
what is the effect of an increase in capillary pressure or a decrease in plasma colloid pressure and what can this lead to?
A
- causes more fluid to leave the capillary into the interstitial space
- can cause oedema
23
Q
label this interstitium
A
24
Q
approx what fraction of the body’s volume is interstitium?
A
1/6
25
approx 1% of the interstitium is made up of what and how can this change in oedema?
free-flowing fluid — up to 50% in oedema
26
why are ions such as Na+ and K+ drawn into cells by proteins?
because the proteins are negatively charged
27
what follows the ions entering the cells?
water
28
what is between the interstitial fluid and intracellular space?
cell membrane = lipid bilayer
29
what moves across cell membranes into ICF by diffusion?
- fat soluble molecules (eg. O2, CO2, N, alcohol) — cross freely by simple diffusion
- not-fat solubles such as H2O require channel proteins called aquaporins — allow H2O molecules to quickly diffuse across the cell membrane through pores in single file
30
where are aquaporins also located?
RBCs — 100x the volume of the RBC crosses through aquaporins every second - very fast
31
what factors affect diffusion?
- conc
- charge
- pressure — pushes molecules out
32
explain facilitated diffusion?
- uses carrier proteins — very specific in order for conformational change to occur
- bind to the substance and allow it to diffuse from one side to another after forming a conformational change
- eg. sodium channels
33
what features of carrier proteins must be specific?
- diameter
- shape
- charge
- chemical bonds
34
what kind of relationship is present between conc and rate of diffusion in simple diffusion?
linear
35
what kind of relationship is there between conc and rate of diffusion in facilitated diffusion and why?
non-linear — limiting factor as the carrier protein needs to change shape twice before being able to transport a further molecule across the membrane
36
what would a graph look like showing simple and facilitated diffusion, and Vmax?
37
what uses active transport to cross cell?
- different ions — Na+, Ca++, H+, K+, Fe+++, Cl-, urate, amino acids
- allows for different concentrations of substances
38
describe the NaK-ATPase Pump
- binds 2 K+ on outside of cell and 3 Na+ on inside of the cell
- this activates the ATPase
- ATPase breaks down ATP to ADP + P — releases energy
- this energy is used by the channel to undergo a conformational change which takes the Na+ out of the cell and K+ into the cell
- every time this happens, 3 Na+ leave and 2K+ enter — net loss of 1 +ve ion every time — inside of cell membrane becomes -ve as you are losing one Na+
- some water can follow it via osmosis from inside to outside — partly responsible for the cells not swelling up with too much water and bursting
39
what are the 3 parts of the neurohormonal response to a decreased CO?
- sympathetic nervous system
- Renin Angiotensin Aldosterone System (RAAS)
- Anti Diuretic Hormone (ADH)
40
how does a reduced stroke volume result in difficulty in blood returning to the heart?
- reduced SV
- reduction in systemic BP
- reduced forward flow of blood
- blood stays in LV — hard for blood to enter the LV as the forward flow is poor
- increase pressure in LA
- blood returning from lungs to LA struggles to return
- increased pressure in pulmonary vasculature
- RV pressure increases
- RA pressure increases
- difficult for blood to return to the heart
BACKFLOW OF PRESSURE AND REDUCED BP
41
what do baroreceptors detect with a lowered BP?
reduced stretch
42
where are baroreceptors located?
carotid bifurcation and arch of the aorta
43
what kind of signals does the vasomotor centre (in brain stem) receive?
sensory signals
44
what does the vasomotor centre do?
sends signals via the sympathetic chain to the heart telling it that it needs to increase the HR and strength of heart contraction to increase the CO
45
what does the sympathetic system also cause in response to a drop in BP?
vasoconstriction of arteries and veins — very quickly — increases BP
46
what activates the RAAS?
renin
47
renin is released in response to what and from where?
released by the kidneys in response to decreased BP
48
what does the RAAS result in and how does this increase SV?
vasoconstriction (angiotensin II) and salt + water retention (aldosterone)— increases circulated volume — increases stretch of heart muscle — increases SV
49
where is ADH released from?
posterior pituitary gland
50
what does ADH release result in?
thirst (increased water intake) and fluid retention — results in dilation of blood and dilution all hyponatraemia (= low sodium levels in the serum = poor prognostic marker)
51
what does ECF expansion help increase?
helps increase the myocardial stretch — causes increased myocardial contractility
52
what does an increased myocardial stretch result in the release of?
natriuretic peptides such as brain NP(BNP)
53
how does the release of natriuretic peptides such as BNP counteract the ECF expansion and prevent heart failure from worsening?
- causes natruiresis (passing sodium into the urine) — causes loss of salt and water, hence counteracting the ECF expansion
- causes vasodilation — counteracts vasocontriction — prevents heart failure from worsening
54
in the long term, what causes damage to the heart and heart failure to become worse?
- prolonged ECF expansion
- vasoconstriction
- increased myocardial contractility
- increased HR
55
what happens to BNP levels in heart failure?
levels are elevated
56
what is BNP primarily released by and in response to what?
release primarily by the ventricular myocardium in response to wall stress such as volume expansion and pressure overload
57
what does BNP cause?
natriuresis and dilation of blood vessels — reduces BP
58
how does cardiac stretch affect the cardiac output?
the more there is cardiac stretch, the more the cardiac output improves
59
natriuretic peptides are released secondary to what?
released secondary to cardiac stretch
60
draw a diagram of the nuerohormal response
61
how can chronic fluid retention impact heart failure and CO?
- no further improvement in CO (if there is a lot of damage to the heart muscle, the increased ECF volume and increased stretch of the myocardium does not make much improvement in the SV)
- increased workload on already damaged heart
- pulmonary and peripheral oedema
62
what do the Frank-Starling curves look like for normal, mild and severe dysfunction?
63
describe the mechanism of oedema caused by heart failure
- the backflow of pressure in HF causes the venous pressures to eventually increase
- this causes the capillary pressure to increase which causes more fluid to filtrate out of the capillaries
- there is more circulating volume and more salt + water retention which will again cause more fluid to cross the capillary membrane
64
what causes elevated venous pressure in the legs?
gravity
65
why is pressure in the capillaries also elevated?
leakage of fluid into the tissue spaces (oedema)
66
how can chronic sympathetic activation due to HF lead to apoptosis/necrosis of heart cells?
- increased energy demand on the heart — tells it to be stronger and faster
- vasoconstriction — increases BP so harder for heart to pump blood from the LV into the aorta where there is a high BP
- worsening ischaemia
- apoptosis/necrosis of heart cells
67
how does increased sympathetic activation affect survival?
the survival is worse in the lung run the more the sympathetic system needs to be activated
68
can a size of a heart attack affect the activated of the SNS?
yes - the larger the heart attack, the more the SNS needs to be activated
69
how can chronic RAAS activation lead to apoptosis?
- hypertrophy of the heart muscle — heart becomes stiff and filling becomes difficult
- fibrosis — heart becomes stiff
- apoptosis
70
what are some typical symptoms of heart failure?
- dyspnoea
- orthopnoea
- paroxysmal nocturnal dyspnoea (PND)
- fatigue/reduced exercise tolerance
71
what is orthopnoea and what is it due to?
= worsening breathlessness when lying flat
| - due to the effect of gravity on fluid in the body
72
what is paroxysmal nocturnal dyspnoea?
episodes of fluid buildup on the lungs when people are sleeping, causing them to wake up from their sleep gasping for breath
73
what are severe symptoms of HF?
- pleural effusions
- swelling of the abdomen
- pulmonary oedema
74
what are typical signs of HF?
- elevated JVP
- basal crackles
- dullness to percussion in lung bases if there is pleural effusion
- pitting oedema
- tachycardia due to sympathetic activation
- third heart sound (S3 Gallop) — manifestation of the stiffening of the heart muscle (chronic RAAS activation)
75
describe clinical heart failure management
