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Cardiovascular MBCHB2 > Lecture 26: Heart Failure Mechanisms 2021 > Flashcards

Lecture 26: Heart Failure Mechanisms 2021 Flashcards

1
Q

Describe Ca movement in the myocyte:

A
  • Ca fluxes through the T tubule during Plateau due to the L-type Ca channels.
  • Ca passes through the DHPR channels in the t tubules and binds to the aligned RyR2 receptors on the SR
  • This is the Ca spark and there is Ca induced Ca release.
  • Ca binds to troponin C and this allows contraction to occur
  • Ca is removed from the cell my SERCA2A, Na/Ca (NCX) pump and CaATPase
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2
Q

What regulates SERCA2a and its speed of action?

A

Phospholambam

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3
Q

What defines cardiac hypertrophy?

A

Cardiac ventricular dilation

Increased ventricular wall thickness

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4
Q

In general terms what can cause a change in cardiac structure?

A

A change in haemodynamic load can lead to a change in cardiac structure.

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5
Q

What are the types of haemodynamic loads?

A

Volume Overload

Pressure Overload

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6
Q

What is volume overload?

A

The EDV is increased and the blood pushes on the ventricular walls causing increased pressure during diastole.

This leads to a change in cell signalling and thus a change in cell structure.

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7
Q

What is pressure overload?

A

The aortic pressure increase (i.e hypertension) and the ventricle needs to develop higher pressures to open the aortic valve in systole.

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8
Q

Can pressure and volume overload occur at the same time?

A

Yes i.e an obese person with hypertension

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9
Q

Is the hypertrophic phenotype rigid?

A

No it is dynamic.

A increased ventricle thickness (pressure overload) can end up in a decompensated heart failure and ventricle dilation.

Its a continuum

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10
Q

What is the problem with increased ventricular wall thickness?

A

Increase in cardiomyocyte size is not necessarily accompanied by increased capillary density, therefore oxygen and nutrient supply may be limited.

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11
Q

What is the problem with volume overload?

A

Volume overload is past the point of optimal ‘frank starling’ increase in force with myocyte stretch. i.e less overlap b/c too much stretch.

LaPlaces law describes the decrease in pressure with an increase in radius. Tension = p.r but tension limited.

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12
Q

What are the causes of cardiac hypertrophy?

A
  • Hypertension (pressure overload)
  • Valve disease (pressure and volume overload)
  • MI, regional dysfunction with volume overload.
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13
Q

What do insults on the heart cause?

A

Increased cardiac work leading to increased wall stress and cell stretch.

= Increased wall thickness or dilation

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14
Q

What does cardiac hypertrophy result in? (symptoms)

A

Cardiac dysfunction characterised by:

  • Heart Failure (systolic/diastolic)
  • Arrhythmias
  • Neurohumoral stimulation
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15
Q

Why does heart failure occur?

A

Early adaptations (to cardiac insult) to preserve function (i.e hypertrophy) can become maladaptive and the heart function fails to meet the demands of the body.

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16
Q

What are the types of heart failure?

A

Systolic failure (impaired contraction) or diastolic function (impaired relaxation) or both.

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17
Q

What does echocardiography obtain from systolic measurements?

A
  • Fractional shortening

- Ejection fraction (<40% in HF)

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18
Q

What are the types of heart failure?

A

Systolic heart failure (HFrEF)

Diastolic heart failure (HFpEF)

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19
Q

What is systolic heart failure?

A

Systolic heart failure: Impaired heart contraction

Heart Failure with Reduced Ejection Fraction

20
Q

What is diastolic heart failure?

A

Diastolic heart failure: Impaired heart relaxation

Heart Failure with Preserved Ejection Fraction

21
Q

What is the structural changes preemptive of HFrEF?

A

Enlarged ventricles = more blood

22
Q

What is the structural change prior to HFpEF?

A

Stiff ventricles fill less blood than normal

23
Q

What happens to the PV loop in diastolic dysfunction?

A

Ventricular compliance is reduced (increased ventricular stiffness) and LV volume is smaller.

PV-loop is smaller, and EDV is less.

24
Q

How does fibrosis contribute to diastolic dysfunction?

A

Increased cell death in heart failure;

  • Collagen forms b/w myocytes = interstitial fibrosis
  • Fibroblasts activated
  • affects compliance and electrical conduction
  • increased risk of cardiac dysfunction and arrhythmias.
25
Q

What causes prolonged Ca levels in diastolic dysfunction and what does it cause?

A

The NCX and SERCA are slowed.

This results in prolonged Ca and this results in; delayed myofilament lengthening and cellular relaxation is impaired.

26
Q

Discuss gender and heart failure:

A

Occurs equally

  • Females less researched due to hormonal influence
  • Still dont have perfect regime for female treatment which will differ due to hormonal influence
27
Q

What are the cardinal symptoms of heart failure?

A

HF is complex clinical syndrome

Characterised by

  • Shortness of breath
  • Exercise limitation and fatigue
  • Clinical signs of peripheral and/or pulmonary congestion

AND SECONDARY to abnormalities of cardiac structure and function

Diagnosis of exclusion as the signs are same for COPD etc.

28
Q

What are the big symptoms of HF?

A
  • Dyspnoea (usually with exertion (cant breath)
  • Orthopnea (lying down)
  • Paroxysmal nocturnal dyspnoea (sleeping)
  • Fatigue (low O2, sleep)

Fluid in the lungs contribute to these factors and when lying down it goes from being at the base to throughout

29
Q

Why is there pulmonary congestion in heart failure?

A

Following HF in the LV then theres an increase in LV EDP which in turn raises pulmonary pressure, increased filtration through cap. wall. and thus fluid in lungs.

30
Q

What are some physical findings in HF?

A
  • Elevated JVP
  • Hepatojugular reflex (push on it and pops back)
  • 3rd heart sound (turbulent filling during diastole)
  • Laterally displaced apex (Cardiomeagly)
31
Q

What investigations can you do for a HF patient?

A

ECG
BNP (found to be elevated in HF)
Chest x-ray
Echo

32
Q

Why does the heart balloon out in HF?

A

Increased pressure = increased wall tension and the wall stretches

33
Q

Whats normal ejection fraction?

A

55-75%

34
Q

What is HFpEF?

A
  • Symptoms
  • 50%< EF
  • Diastolic dysfunction and/or structural changes

Diastolic dysfunction discussed earlier

Typical in hypertension / afterload increase

35
Q

What does clinical data show for the sex differences?

A

Females:

  • HFpEF
  • 10+ years older than men
  • Hypertensive
  • Better long term survival
  • Experience greater oedema, exercise intolerance, depression, reduced quality of life
36
Q

Describe the types of cardiac remodelling in HF?

A

Diastolic remodelling: Increased heamodynamic related wall distension = Increased sarcomere addition in series = inc. myocyte length. (inc volume and difficulty shortening)

Concentric remodelling: Inc. wall stress during systole results in sarcomeres added in parallel = inc. thickness, reduced volume (stiffer heart with inc. collagen content)

37
Q

What does laPlace’s law predict in HF?

A

T = P*r / wall thickness

Thus, HFrEF = Inc. tension (more stretch)
HFpEF = Reduced tension but less filling

38
Q

Describe the cycle of HFrEF;

A

Increased wall stress during during diastole. i.e aortic insufficiency or myocardial infarction

  • > Increased diastolic wall stress
  • > Sarcomere addition in SERIES
  • > Cardiac myocyte elongation
  • > Increased cavity volume

= Heamodynamic effect, increased filling, impaired ejection (Further drives diastolic wall stress)

39
Q

Describe the cycle of HFpEF;

A

Increased wall stress during systole i.e aortic stenosis or hypertension

  • > Increased systolic wall stress
  • > Sarcomere addition in PARALLEL
  • > Cardiac myocyte thickening
  • > Increased wall thickness

= Heamodynamic effect, Imparied ejection, impaired filling (increased systolic wall stress)

40
Q

What are some of the neurohormonal compensations for heart failure?

A

Reduced CO =

  • Dec. BP, baroreceptor unloading = Symp. Activation
  • Red. renal BF = RAAS activation
  • Increased Na and H2O reabsorption (inc preload)
  • Increased vasoconstriction (inc afterload)
41
Q

What happens to the pressure volume loop in HFrEF?

A
  • Decreased systolic pressure
  • Decreased Stroke volume

i.e the pressure slope decreases and the EDV increases (curve right shifts and down)

42
Q

What happens to the PV loop in compensatory HFrEF?

A
  • Increased venous return = increased EDV and thus increased ESP thus driving SV towards normal.

(think about how it would look on graph)

43
Q

Describe the PV loop for HFpEF;

A
  • Diastolic dysfunction
    = Impaired filling and reduced diastolic volume
    = Increased EDP and reduced SV (i.e loop smaller, left and up) (ESP not changed)
44
Q

Describe the PV loop for HFpEF with compensation;

A
  • EDP is increased b/c inc. Venous return thus ensuring SV is maintained but risking flash pulmonary oedema
45
Q

Describe what HF can lead on to?

A
  • Impaired exercise tolerance (deconditioning)
  • GI and Renal failure
  • Pulmonary oedema and respiratory complications
  • Increased SNA = increased chance of arrhythmia and sudden death
46
Q

What are some treatment options for HF?

A
  • Weight loss
  • Exercise
  • Diuretic
  • ACE inhibitors / ARB / Aldosterone inhibitors
  • Beta blockers
  • Digoxin
  • Anti-arrhythmitics
  • Nitrates (reduced afterload)

Cardiovascular MBCHB2 (31 decks)

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