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PBL SEM 2 > PBL 4 - clinical heart failure > Flashcards

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

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2
Q

what does clinical heart failure clinically manifest as a triad of?

A
  1. typical signs
  2. typical symptoms
  3. a cardiac deficit resulting in reduced cardiac output (CO)
    or increased filling pressures
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3
Q

fluid makes up what % of the body?

A

60%

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4
Q

what is the fluid of the body divided into?

A

intra-cellular and extra-cellular compartments

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5
Q

what do all the cells in the body bask in?

A

ECF

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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
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7
Q

compared to ICF, what is ECF rich in?

A

rich in — Na+, Cl-, HCO3-, glucose

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8
Q

compared to ECF, what is ICF rich in?

A

K+, Mg++, phosphates, amino acids (proteins)

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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

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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

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11
Q

approx what % of ECF is plasma?

A

20%

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12
Q

how long does it take at rest for plasma to be circulated around the body?

A

about a minute

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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
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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
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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)
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16
Q

by what process to substances move across?

A

diffusion

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17
Q

by what process does water move across?

A

osmosis

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18
Q

what is capillary pressure?

A

blood pressure inside the capillaries — drives fluid out of the capillary

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19
Q

what is capillary pressure opposed by?

A

interstitial fluid pressure = usually lower than capillary pressure (sub atm in a lot of places)

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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

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21
Q

what do the pressures affecting the movement of water from the plasma to the interstitial space look like on a diagram?

A
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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
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23
Q

label this interstitium

A
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24
Q

approx what fraction of the body’s volume is interstitium?

A

1/6

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25
Q

approx 1% of the interstitium is made up of what and how can this change in oedema?

A

free-flowing fluid — up to 50% in oedema

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26
Q

why are ions such as Na+ and K+ drawn into cells by proteins?

A

because the proteins are negatively charged

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27
Q

what follows the ions entering the cells?

A

water

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28
Q

what is between the interstitial fluid and intracellular space?

A

cell membrane = lipid bilayer

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29
Q

what moves across cell membranes into ICF by diffusion?

A
  • 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
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30
Q

where are aquaporins also located?

A

RBCs — 100x the volume of the RBC crosses through aquaporins every second - very fast

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31
Q

what factors affect diffusion?

A
  • conc
  • charge
  • pressure — pushes molecules out
32
Q

explain facilitated diffusion?

A
  • 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
Q

what features of carrier proteins must be specific?

A
  • diameter
  • shape
  • charge
  • chemical bonds
34
Q

what kind of relationship is present between conc and rate of diffusion in simple diffusion?

A

linear

35
Q

what kind of relationship is there between conc and rate of diffusion in facilitated diffusion and why?

A

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
Q

what would a graph look like showing simple and facilitated diffusion, and Vmax?

A
37
Q

what uses active transport to cross cell?

A
  • different ions — Na+, Ca++, H+, K+, Fe+++, Cl-, urate, amino acids
  • allows for different concentrations of substances
38
Q

describe the NaK-ATPase Pump

A
  • 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
Q

what are the 3 parts of the neurohormonal response to a decreased CO?

A
  • sympathetic nervous system
  • Renin Angiotensin Aldosterone System (RAAS)
  • Anti Diuretic Hormone (ADH)
40
Q

how does a reduced stroke volume result in difficulty in blood returning to the heart?

A
  • 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
Q

what do baroreceptors detect with a lowered BP?

A

reduced stretch

42
Q

where are baroreceptors located?

A

carotid bifurcation and arch of the aorta

43
Q

what kind of signals does the vasomotor centre (in brain stem) receive?

A

sensory signals

44
Q

what does the vasomotor centre do?

A

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
Q

what does the sympathetic system also cause in response to a drop in BP?

A

vasoconstriction of arteries and veins — very quickly — increases BP

46
Q

what activates the RAAS?

A

renin

47
Q

renin is released in response to what and from where?

A

released by the kidneys in response to decreased BP

48
Q

what does the RAAS result in and how does this increase SV?

A

vasoconstriction (angiotensin II) and salt + water retention (aldosterone)— increases circulated volume — increases stretch of heart muscle — increases SV

49
Q

where is ADH released from?

A

posterior pituitary gland

50
Q

what does ADH release result in?

A

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
Q

what does ECF expansion help increase?

A

helps increase the myocardial stretch — causes increased myocardial contractility

52
Q

what does an increased myocardial stretch result in the release of?

A

natriuretic peptides such as brain NP(BNP)

53
Q

how does the release of natriuretic peptides such as BNP counteract the ECF expansion and prevent heart failure from worsening?

A
  • 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
Q

in the long term, what causes damage to the heart and heart failure to become worse?

A
  • prolonged ECF expansion
  • vasoconstriction
  • increased myocardial contractility
  • increased HR
55
Q

what happens to BNP levels in heart failure?

A

levels are elevated

56
Q

what is BNP primarily released by and in response to what?

A

release primarily by the ventricular myocardium in response to wall stress such as volume expansion and pressure overload

57
Q

what does BNP cause?

A

natriuresis and dilation of blood vessels — reduces BP

58
Q

how does cardiac stretch affect the cardiac output?

A

the more there is cardiac stretch, the more the cardiac output improves

59
Q

natriuretic peptides are released secondary to what?

A

released secondary to cardiac stretch

60
Q

draw a diagram of the nuerohormal response

A
61
Q

how can chronic fluid retention impact heart failure and CO?

A
  • 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
Q

what do the Frank-Starling curves look like for normal, mild and severe dysfunction?

A
63
Q

describe the mechanism of oedema caused by heart failure

A
  • 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
Q

what causes elevated venous pressure in the legs?

A

gravity

65
Q

why is pressure in the capillaries also elevated?

A

leakage of fluid into the tissue spaces (oedema)

66
Q

how can chronic sympathetic activation due to HF lead to apoptosis/necrosis of heart cells?

A
  • 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
Q

how does increased sympathetic activation affect survival?

A

the survival is worse in the lung run the more the sympathetic system needs to be activated

68
Q

can a size of a heart attack affect the activated of the SNS?

A

yes - the larger the heart attack, the more the SNS needs to be activated

69
Q

how can chronic RAAS activation lead to apoptosis?

A
  • hypertrophy of the heart muscle — heart becomes stiff and filling becomes difficult
  • fibrosis — heart becomes stiff
  • apoptosis
70
Q

what are some typical symptoms of heart failure?

A
  • dyspnoea
  • orthopnoea
  • paroxysmal nocturnal dyspnoea (PND)
  • fatigue/reduced exercise tolerance
71
Q

what is orthopnoea and what is it due to?

A

= worsening breathlessness when lying flat

- due to the effect of gravity on fluid in the body

72
Q

what is paroxysmal nocturnal dyspnoea?

A

episodes of fluid buildup on the lungs when people are sleeping, causing them to wake up from their sleep gasping for breath

73
Q

what are severe symptoms of HF?

A
  • pleural effusions
  • swelling of the abdomen
  • pulmonary oedema
74
Q

what are typical signs of HF?

A
  • 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
Q

describe clinical heart failure management

A

PBL SEM 2 (44 decks)

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