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Cardiovascular system > Lecture 18- The Pathophysiology of heart failure > Flashcards

Lecture 18- The Pathophysiology of heart failure Flashcards

1
Q

what is heart failure

A

‘An inability of the heart to meet the demands of the body’ ‘ A clinical syndrome (collection of signs and symptoms) of reduced CO, tissue hypoperfusion, increased pulmonary pressures and time congestion (e.g. tissue oedema”

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2
Q

what enables the heart to work as an effective pump?

A

input = blood enters the heart via the atria output= leaves the heart via the pulmonary aortic arteries

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3
Q

conditions that affect inout and output lead to impairment of cardiac function

A

impairment of: one way valve, chamber size, functioning muscle

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4
Q

one way valves make sure

A

blood just goes in one direction

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5
Q

conditions which affect valves

A

mitral stenosis and aortic regurgitation

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6
Q

chamber size

A

If too small reduced preload (reduced SV, reduced CO)

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7
Q

functioning muscle

A

has to have adequate blood supply to contract in a coordinated fashion- MI would deteriorate muscle very quickly

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8
Q

most common causes of HF

A

Ischaemic heart disease (coronary heart disease)

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9
Q

IHD/ CHD cxause

A

myocardial dysfunction e.g. through fibrosis (scarring- doesn’t conduct impulse as well)–> remodels the heart

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10
Q

other causes of heart failure

A
  • hypertension
  • aortic stensosis
  • cardiomyopathies
  • arrhythmias
  • other valvular or myocardial structural diseases
  • pericardial diseases
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11
Q

hypertension can cause heart failure due to

A

increased after-load on ventricles and accelerates atherosclerosis

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12
Q

aortic stenosis can cause HF

A

increased after load on ventricles

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13
Q

cardiomyopathies can cause HF

A

hypertrophy/ dilated

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14
Q

rarely HF can occur

A

can occur if a grossly elevated demand on cardiac output e.g. sepsis, severe anaemia, thyrotoxicosis (high output heart failure)

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15
Q

Measuring the ability of the heart to meet demands of the body

A

CO= SV x HR

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16
Q

SV

A

volume ejected by a ventricle in a single heart beat

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17
Q

what influences stroke volume

A

preload myocardial contractility afterload

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18
Q

pre-load

A

volume in ventricles at the end of diastole = EDV (the stretch on the ventricle just before contraction) o Increasing this will increase SV

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19
Q

increased contractility increases

A

SV

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20
Q

after load

A

total peripheral resistance (what the heart has to pump against) o The higher the after-load the small the SV

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21
Q

frank-starling rule

A
  • The more ventricular distention during diastole = greater volume ejected (SV) during systole (up to a certain point)
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22
Q

why is CO reduced in heart failure

A

due to reduced stroke volume

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23
Q

reduced preload (reduced EDV) due to

A

o Impaired filling of the ventricle during diastole  Ventricular chamber too stiff/ not relaxing enough  Ventricular walls thickened (hypertrophied)

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24
Q

reduced myocardial contraction causes

A

ejection problem- space available is not reduced but poor ventricular contraction so unable to empty it as well)

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25
Q

why can’t muscle produce same force of contraction with a given volume within the ventricle (EDV)

A

 Muscle walls thinned/fibrosed e.g. due to ischaemia

 Chambers enlarged (overstretched sarcomeres) e.g. cardiac remodelling due to hypertension

 Abnormal or uncoordinated myocardial infarction e.g. ischaemia

26
Q

increased after load due to

A

increased pressure against which the ventricle contracts - aortic stenosis - chronic severe hypertension

27
Q

heart failure is classified according to ejection fractions

A
  • Systolic heart failure (HFrEF)- ejection problem
  • Diastolic heart failure (HFpEF)- filling problem
28
Q
  • Systolic heart failure (HFrEF)- ejection problem
A
  • Heart failure with reduced ejection fraction - Contractility problem - Most common type
29
Q

-Diastolic heart failure (HFpEF)- filling problem

A
  • Heart failure with reduced ejection fraction - Filling problem
30
Q

normal ejection fraction is

A

>50% (typically 60%)

31
Q

ejection fraction=

A

amount of blood pumped out of the ventricle/ total amount of blood in ventricle

32
Q

how can the heart be failing if EF is maintained

A
  • “Filling problem”: o Ventricle ejects less volume in a heartbeat (SV reduced) as less volume to begin with (less space) o Fraction of what is availabClassifying heart failure … according to ventricle involvedle to eject is still >50% o Hence ejection fraction preserved
33
Q

Classifying heart failure … according to ventricle involved

A

left or right or biventricular ventricular heart failure

34
Q

left ventricle heart failure

A

most common

 Will displace apex to the left

 Often results in right ventricular hypertrophy

35
Q

why does left sided heart failure result in right ventricular hypertrophy

A
  • During left sided heart failure due to increased resistance in the LA and LV, less blood from the pulmonary vein will enter the LA.
  • This causes more blood to be held in pulmonary circulation
  • Increased afterload (what the heart has to work against) for in the right ventricle
  • Hypertrophy of the right ventricle
36
Q

biventricular heart failure also known as

A

congestive heart faulure

37
Q

right ventricle heart failure can occur in isolation, secondary to

A

chronic lung disease (cor pulmonale)  Much less common than left ventricular heart failure  Most common cause of RV heart failure is LV heart failure

38
Q
  • Increased LV filling in the healthy heart leads
A

to a big increase in CO (gradient of curve)

39
Q
  • Increase LV filling in failing heart leads
A

to a very little increase in CO o Eventually leads to worsening CO (curve flips) o Markedly increased LVEDP (in an attempt to increase SV) result in falling CO and development of pulmonary congestion

40
Q

how does the body respond to a falling CO

A

neuro-hormonal activation (Baroreceptors and RAAS)

41
Q

neuronhormonal activation is helpful in

A

healthy hearts

42
Q

neuronhormonal activation is unhelpful in

A

unhealthy heart

43
Q

neurohormonal activation in a healthy heart will ultimately lead to an

A

increased cardiac demand and a further reduction in stroke volume (further deterioration in cardiac output and the condition) *cardiotoxic effects*

44
Q

Clinical signs and symptoms of heart failure

A

Symptoms: o Fatigue/ lethargy o Breathlessness o +/- leg swelling

45
Q
  • Signs (and symptoms) due to increased interstitial fluid (oedema)
A

o Pulmonary tissue (left sided)

o Peripheral tissues (i.e. lower limbs) (right sided)

46
Q

starling forces

A
  • Hydrostatic forces greater than oncotic pressure at arterial end due to increased blood pressure
  • Hydrostatic pressure lower than oncotic pressure at venous end
  • Oncotic pressure stays stable
47
Q

tissue fluid accumulation occurs when

A

gradient between hydrostatic and onctoic pressure less favoruable for fluid returning to capillary

48
Q

oncotic pressure

A

stays constant throughout circulation

49
Q

hydrostatic pressure

A

decreases fromt he arterial end to the venous end

50
Q

Pulmonary oedema

A
  • accumulation of fluid in interstitial lung tissue
51
Q

Pitting oedema

A
  • accumulation of fluid in interstitial peripheral tissues
52
Q

when does pitting (peripheral) oedema occur?

A

right ventricular heart failure

53
Q

when does pulmonary oedema occur?

A

left ventricular heart failure

54
Q

signs and symptoms of left ventiruclar heart failure

A
  • fatigue/lethargy
  • breathlessness (exertional)
  • pulmonary oedema- basal pulmonary crackles
  • orthopnoea
  • paroxysmal nocturnal dyspnoea
  • cardiomegaly (displaced apex beat- indicates enlarged LV)
55
Q

displaced apex beat- indicates

A

enlarged LV

56
Q

orthnopnoea

A

shortness of breath

57
Q

Paroxysmal nocturnal dyspnoea

A

shortness of breath that occurs in the middle of the night

58
Q

signs and symptoms of right ventiruclar heart failure

A
  • fatigue/ lethargy
  • breathlessness
  • peripheral oedema (pitting- in legs due to gravity)
  • raised jugular venous pressure
  • tender, smooth enlarged liver (liver congestion)
59
Q
A
60
Q

Raised jugular venous pressure

A

Measurement of the pressure in the right internal jugular vein can be used as a direct reflection of pressures in the right side of the heart

61
Q
A

Cardiovascular system (30 decks)

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