Session 7 Heart Failure Flashcards Preview

Personal Integrative > Session 7 Heart Failure > Flashcards

Flashcards in Session 7 Heart Failure Deck (26)
Loading flashcards...

What is heart failure?

Heart failure is state in which heart fails to maintain an adequate circulation for the needs of the body despite an adequate filling pressure.

    A pathophysiological state in which an abnormality of cardiac function is responsible for the failure of the heart to pump blood at a rate commensurate with requirements of the metabolising tissues.

    A clinical syndrome caused by an abnormality of the heart and recognised by a characteristic pattern of haemodynamic, renal, neural and hormonal responses. 


Describe the aetiology of heart failure

    Ischaemic Heart Disease is the primary cause of Systolic HF (~70%) e.g. previous MI

    Other causes of HF:


Dilated cardiomyopathy (non-ischaemic)

  • Bugs (viral/bacterial/mycobacteria)
  • Alcohol/drugs/poisoning
  • Pregnancy (peri-partum)
  • Idiopathic

Valvular Heart Disease / Congenital

Restrictive Cardiomyopathy e.g. amyloidosis (deposition in LV wall)

Hypertrophic Cardiomyopathy

Pericardial disease

High-output heart failure

Arrhythmias (e.g. if patient doesn’t receive treatment for AF => dilation of ventricles)


Describe the progression of heart failure

NYHA Functional Classification

    Class I: no symptomatic limitation of physical activity

    Class II:

  • Slight limitation of physical activity
  • Ordinary physical activity results in symptoms
  • No symptoms at rest

    Class III:

  • Marked limitation of physical activity
  • Less than ordinary physical activity results in symptoms
  • No symptoms at rest

    Class IV:

  • Inability to carry out any physical activity without symptoms
  • May have symptoms at rest
  • Discomfort increases with any degree of physical activity.

Heart failure prognosis is worse than most cancers – very severe!


Describe the clinical syndromes in heart failure

in clinical practice, heart failure is often divided into:

    Right sided heart failure

    Left sided heart failure

    Biventricular (congestive) cardiac failure

    Systolic heart failure (‘pump failure’)

    Diastolic heart failure (failure of relaxation)



Draw the Starling Curve in Mild and Gross Heart Failure

Starling’s Law of the Heart: the force developed in a muscle fibre depends on the degree to which the fibre is stretched


What happens in Systolic Dysfunction

: failure of the left ventricle to pump properly

    Increased LV capacity (LV dilatation)

    Reduced LV cardiac output

    Thinning of the myocardial wall

  • Fibrosis and necrosis of myocardium
  • Activity of matrix proteinases

    Mitral valve incompetence (doesn’t close properly => functional mitral regurgitation (structurally normal))

    Neuro-hormonal activation

    Cardiac arrhythmias 


What structural changes would you see in diastolic and systolic heart failure?

    Ventricular remodelling after acute infarction

  • Expansion of infarct (hours to days)
  • Global remodelling (days to months)

    Ventricular remodelling in diastolic and systolic heart failure

  • Diastolic heart failure: hypertrophied heart
  • Systolic heart failure: dilated heart


What does cardiac output depend on?

Heart rate

Myocardial contractility




What is Diastolic Dysfunction

Diastolic Dysfunction (Heart Failure with Normal Ejection Fraction)

    20-50% of heart failure patients

    Key factors:

  • Frequently elderly and female
  • Often history of hypertension/diabetes/obesity

    Normally LV function but concentric left ventricular hypertrophy

    Hospitalisation and mortality similar to systolic HF

    Diagnosis is less clear cut

    Little clinical outcome study data to guide therapy


Describe Diastolic Dysfunction procedures

    Reduced LV compliance

    Impaired myocardial relaxation

    Impaired diastolic LV filling (but with increased LA and PA pressures)

    Unable to compensate by increasing LV EDP (Frank Starling)

    Low cardiac output results

    Triggers neuro-hormonal activation as per systolic heart failure.


What is preload and afterload?


Preload: end diastolic volume – initial stretching of the cardiac myocytes prior to contraction.

Afterload: pressure that the chambers of the heart have to generate to eject blood – the end load against which the heart contracts to eject blood.


What is meant by Neuro-Hormonal Activation?

    Sympathetic Nervous System

    Renin-Angiotensin-Aldosterone System

    Natriuretic Hormones

    Anti-Diuretic Hormone


    Prostaglandins/Nitric Oxide

    Kallikrien System

    Tissue Necrosis Factor - alpha


Describe the up-regulation of the Sympathetic Nervous System in HF

    Baroreceptor-mediated response (baroreceptors innervated by glossopharyngeal and vagal afferents) to increase heart rate

    Early compensatory mechanism to improve CO:

  • Cardiac contractility
  • Arterial and venous vasoconstriction
  • Tachycardia

    However long-term deleterious effects

B-adrenergic receptors are down-regulated/uncoupled


  • Induces cardiac hypertrophy/myocyte apoptosis and necrosis via alpha-receptors (direct cardiotoxicity)
  • Induce up-regulation of the RAAS

Reduction in heart rate variability (reduced parasympathetic nervous system and increased sympathetic nervous system) (vicious cycle)


Describe RAAS

The Renin-Angiotensin-Aldosterone System (RAAS)

    RAAS is commonly activated in HF:

  • Reduced renal blood flow
  • SNS induction of renin from macula densa

    Renin converts Angiotensinogen into Angiotensin I.

    Angiotensin I is converted into Angiotensin II by Angiotensin Converting Enzyme (lungs and vasculature)


What are the effects of elevated AT2?

Potent vasoconstrictor

Promotes LVH (left ventricle hypertrophy) and myocyte dysfunction

Promotes aldosterone release

Promotes Na+/H2O release

Stimulates thirst by central action?


What are renal effects in HF?

    GFR is maintained in early HF by haemodynamic changes at the glomerulus.

    Increased Na+/H2O retention due to neuro-hormonal activation.

    However in severe HF, renal blood flow falls (reduced renal perfusion) leading to reduced GFR (via vasoconstriction) and a subsequent rise in serum urea and creatinine.

    This can be exacerbated by treatment inhibiting the actions of Angiotensin II


What are the symptoms of left heart failure


    Exertional dyspnoea (at rest = severe) (struggle to eat)

    Orthopnoea (number of pillows)

    Paroxysmal nocturnal dyspnoea (opening windows)

    Ankle swelling (often minimised) (due to RAAS activation => Na+ + H2O retention)

    Chest pain




What are the signs of heart failure?

    Overt breathlessness



    Blood pressure: depends on aetiology

    Cardiomegaly (displaced apex beat, may be sustained)

   3rd or 4th heart sound (gallop murmur)

    Functional murmur of mitral regurgitation (systolic blowing murmur)

    Basal pulmonary crackles

    Peripheral oedema (compared to RHF)

    Peripheral oedema and basal pulmonary crackles due to fluid overloading but in LHF, JVP is unlikely to be raised. 


Describe the aetiology of right heart failure?

    Chronic Lung Disease

    Pulmonary embolism/pulmonary hypertension

    Pulmonary/tricuspid valvular disease

    Left-to-right shunts (ASD/VSD)

    Isolated right ventricular cardiomyopathy

    The most frequent cause is secondary to left heart failure


What are the symptoms/signs of 'pure' right heart failrue?

    (Relate to distension and fluid accumulation in areas drained by the systemic veins) (congestion)

    Fatigue, dyspnoea, anorexia, nausea

    Increased JVP

    Tender, smooth hepatic enlargement

    Dependent pitting oedema


    Pleural effusion


How would you investigate heart failure?


  • Full blood count (look at Hb to see if anaemia is exacerbating HF)
  • Renal function and electrolytes (is there renal function impairment or concurrent renal disease? Any drug contraindications?)
  • Glucose/Lipids
  • BNP (brain natural peptide)

    ECG (left bundle branch block is often associated with dilated cardiomyopathy

    CXR – to detect cardiomegaly

  • Kerley lines are a sign seen on chest radiographs with interstitial pulmonary oedema. They are thin linear pulmonary opacities caused by fluid or cellular infiltration into the interstitium of the lungs.

    Echocardiography – gold-standard



Describe the management of heart failure principles. What are the aims of pharmacological therapy?

    Correct underlying cause (is there underlying ischaemia? Consider stenting, angiography)

    Non-pharmacological measures

    Pharmacological therapy

  • Symptomatic improvement
  • Delay progression of heart failure
  • Reduce mortality

    Treat complications/associated conditions/cardiovascular risk factors e.g. arrhythmia


Describe what lifestyle modification would involve

Reduce salt

Reduce alcohol

Increase aerobic exercise

Decrease blood pressure


What would pharmalogical therapy involve?

Diuretics (loop) (initial therapy furosemide)



Beta-blocker (add-on therapy to ACEi/ARB)

Spironolactone (add-on therapy to ACEi/ARB) – can especially be beneficial in isolated RHF so consider early on

(Digoxin) (Maybe suitable for AF? Uncertain how advantageous)

(Inotropes – acute setting)

Phosphodiesterase inhibitors – acute setting

Aniarrhythmics (if rhythm disturbance)


What would cardiac surgery involve?

Heart transplantation

Mechanical assist devices

Underlying cause

  • E.g. valve surgery
  • Revascularisation (PCI, CABG)
  •     Implantable pacemakers

    Biventricular pacing (to allow synchronous pumping of the heart e.g. in LBBB – can significantly improve cardiac output)

        Implantable defibrillators (if risk of ventricular fibrillation)


What do you need to remember about ACEi/ARBs and hyperglycaemia in acute HF?

ACE inhibitors inhibit Angiotensin Converting Enzyme breaking down bradykinin. Bradykinin leads to vasodilation as it increases the production of Nitric Oxide. An accumulation of bradykinin in the lungs leads to a cough.

Angiotensin Receptor blockers block AT1 receptors leading to ATII binding to AT2 receptors. This has a beneficial effect as it increases the production of nitric oxide leading to vasodilation.

Patients with acute HF: hyperglycaemia has a significant impact on mortality => require aggressive treatment