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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
why can't muscle produce same force of contraction with a given volume within the ventricle (EDV)
 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
increased after load due to
increased pressure against which the ventricle contracts - aortic stenosis - chronic severe hypertension
27
heart failure is classified according to ejection fractions
- **Systolic heart failure (HFrEF)**- ejection problem - **Diastolic heart failure (HFpEF)**- filling problem
28
- Systolic heart failure (HFrEF)- ejection problem
- Heart failure with reduced ejection fraction - Contractility problem - Most common type
29
-Diastolic heart failure (HFpEF)- filling problem
- Heart failure with reduced ejection fraction - Filling problem
30
normal ejection fraction is
\>50% (typically 60%)
31
ejection fraction=
amount of blood pumped out of the ventricle/ total amount of blood in ventricle
32
how can the heart be failing if EF is maintained
- “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
Classifying heart failure … according to ventricle involved
left or right or biventricular ventricular heart failure
34
left ventricle heart failure
most common  Will displace apex to the left  Often results in right ventricular hypertrophy
35
why does left sided heart failure result in right ventricular hypertrophy
* 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
biventricular heart failure also known as
congestive heart faulure
37
right ventricle heart failure can occur in isolation, secondary to
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
- Increased LV filling in the healthy heart leads
to a big increase in CO (gradient of curve)
39
- Increase LV filling in failing heart leads
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
how does the body respond to a falling CO
neuro-hormonal activation (Baroreceptors and RAAS)
41
neuronhormonal activation is helpful in
healthy hearts
42
neuronhormonal activation is unhelpful in
unhealthy heart
43
neurohormonal activation in a healthy heart will ultimately lead to an
increased cardiac demand and a further reduction in stroke volume (further deterioration in cardiac output and the condition) \*cardiotoxic effects\*
44
Clinical signs and symptoms of heart failure
Symptoms: o Fatigue/ lethargy o Breathlessness o +/- leg swelling
45
- Signs (and symptoms) due to increased interstitial fluid (oedema)
o Pulmonary tissue (left sided) o Peripheral tissues (i.e. lower limbs) (right sided)
46
starling forces
* 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
tissue fluid accumulation occurs when
gradient between hydrostatic and onctoic pressure less favoruable for fluid returning to capillary
48
oncotic pressure
stays constant throughout circulation
49
hydrostatic pressure
decreases fromt he arterial end to the venous end
50
Pulmonary oedema
- accumulation of fluid in interstitial lung tissue
51
Pitting oedema
- accumulation of fluid in interstitial peripheral tissues
52
when does pitting (peripheral) oedema occur?
right ventricular heart failure
53
when does pulmonary oedema occur?
left ventricular heart failure
54
signs and symptoms of **left** ventiruclar heart failure
* fatigue/lethargy * breathlessness (exertional) * pulmonary oedema- basal pulmonary crackles * orthopnoea * paroxysmal nocturnal dyspnoea * cardiomegaly (displaced apex beat- indicates enlarged LV)
55
displaced apex beat- indicates
enlarged LV
56
orthnopnoea
shortness of breath
57
Paroxysmal nocturnal dyspnoea
shortness of breath that occurs in the middle of the night
58
signs and symptoms of **right** ventiruclar heart failure
* fatigue/ lethargy * breathlessness * peripheral oedema (pitting- in legs due to gravity) * raised jugular venous pressure * tender, smooth enlarged liver (liver congestion)
59
60
Raised jugular venous pressure
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

Cardiovascular system (30 decks)

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