FRCA Notes

Heart Failure

The curriculum asks for knowledge on both 'heart failure – systolic vs diastolic, high vs low cardiac output' and 'fluid challenge and heart failure'.

Resources

  • Heart failure is a complex clinical syndrome characterised by impaired cardiac filling or ejection
  • There are multiple causes, either a primary myocardial disorder or secondary to other (typically cardiovascular) pathology
    • Ischaemic heart disease is the commonest primary cause
    • Hypertensive disease is the commonest secondary cause
Myocyte death Myocyte dysfunction Circulatory dysfunction
Ischaemic heart disease Cardiomyopathy Valvular heart disease
Myocarditis Endocrine disease e.g. thyroid, cortisol Severe hypertension
Alcohol Nutritional deficiencies Pericardial constriction
Cytotoxic drugs Protracted, severe anaemia
Diabetes mellitus

HF-pEF

  • This describes a state of heart failure with a preserved ejection fraction, historically called 'diastolic heart failure'
  • HF-pEF typically occurs in older patients due to age-related changes in the cardiovascular system, which cause impaired myocardial relaxation
  • Chronic disease states, including obesity, HTN, CKD, COPD and OSA may play a role

  • Impaired myocardial relaxation leads to abnormal ventricular filling, pulmonary congestion and symptomatic dyspnoea/oedema
  • The pressure-volume relationship of the ventricle is altered such that for a given LVEDV, there is a higher LVEDP

Adaptive responses

  • Acute failure of LV contractility (of any aetiology) leads to LV distension with accumulated blood
  • There is raised LV end-diastolic volume and thus LVEDP
  • This initially causes myocyte stretch, and therefore increased contractility via the Frank-Starling mechanism
  • However, over time the declining stroke volume leads to volume overload and ventricular dilatation

  • The medullary cardiovascular centres are triggered in response to reduced arterial pressure, leading to sympathetic activation and vasopressin release
  • Pulmonary congestion leads to hypoxia and hypercarbia, which further stimulates central sympathetic activation
    • Sympathetic activation
      • Tachycardia
      • Increased contractility
      • Peripheral vasoconstriction
    • Vasopressin release
      • Water The medullary cardiovascular centres are triggered in response to reduced arterial pressure
      • Peripheral vasoconstriction

  • The combination of sympathetic activation & renal hypoperfusion triggers renin release and RAAS activation
    • Salt and water retention ensues

  • Remodelling is the term used to describe these mechanical and neurohumoral factors which:
    • Induce myocardial hypertrophy
    • Increase ventricular size: atrial and ventricular dilatation
    • Increase ventricular wall stress
    • Reduce ventricular compliance due to fibrosis

Maladaptive responses

  • The adaptive responses seen in HF evolved as temporary measures to support blood pressure during exertion, haemorrhage or dehydration in those with normal hearts
  • In the modern clinical setting, they become maladaptive, eventually exacerbating the issues

  • The adapative measures initially raise:
    • LVEDV and LVEDP
    • Cardiac output through higher contractility and heart rate
    • MAP through higher CO and SVR

  • In the long-run they become detrimental by:
    • Increasing myocardial oxygen demand through higher contractility and afterload
    • Reducing myocardial oxygen supply through tachycardia, impaired relaxation and arrhythmia generation
    • Promoting pulmonary oedema due to venoconstriction and RAAS-mediated sodium and water retention

  • The increased LV wall stress & oxygen demand renders the hypertrophied LV susceptible to subendocardial ischaemia

Pressure-volume loop

  • In LV failure, the LV pressure-volume loop demonstrates:
    • Rightwards shift of ESV, due to impaired contractility
    • Raised EDV, due to impaired myocardial relaxation
    • Reduced width i.e. reduced stroke volume, due to higher ESV

  • Diagnosis typically requires the presence of both signs and symptoms

Investigations

  • Bloods to exclude causes e.g. haemochromatosis, thyroid disease, acromegaly, thiamine deficiency

  • Serum BNP (or NT-pro-BNP)
    • Secreted by ventricular myocytes in response to stress
    • It inhibits the RAAS; reduces sodium reabsorption and increases GFR
    • BNP level correlates to the severity of the heart failure
    • Can be a useful screening, diagnostic and prognostic tool

  • ECG is typically abnormal:
    • LVH
    • Conduction defects
    • Evidence of current ischaemia or previous infarction
    • P-mitrale
    • AF

  • TTE
    • May be diagnostic e.g. valvular disease, RWMA, dilatation, LVOT evaluation
    • May show raised LA pressure, LA dilatation and impaired LV diastolic dysfunction i.e. HF-pEF
    • Can help judge severity according to ejection fraction

  • MRI | radionuclide scanning | coronary angiography
    • May yield further information about aetiology and severity

Class A-D

Class Description
A
At risk of HF		 At risk for heart failure but no symptoms, structural or functional heart disease
B
Pre-HF		 No current or previous symptoms of HF but structural heart disease, increased filling pressures or other risk factors
C
Symptomatic HF		 Current or previous symptoms of HF
D
Advanced HF		 HF symptoms interfering with ADLs or lead to repeated hospitalizations

NYHA Classification

  • Patients with Class C or D heart failure can be further classified based on their symptomatology to aid management
Stage Description
I No limitation of physical activity
Ordinary physical activity does not cause undue fatigue, palpitation or shortness of breath
II Slight limitation of physical activity but comfortable at rest
Ordinary physical activity results in fatigue, palpitation, shortness of breath or chest pain
III Marked limitation of physical activity but comfortable at rest
Less than ordinary activity causes fatigue, palpitation, shortness of breath or chest pain
IV Symptoms of heart failure at rest
Any physical activity causes further discomfort


Class A

  • Multi-professional disease management
  • Exercise rehabilitation
  • Aggressive treatment of risk factors such as HTN, smoking, DM and dyslipidaemia

Class B

  • Medicate with the 'four pillars of heart failure management
  • These have been shown to reduce mortality and/or reduce episodes of decompensation requiring hospitalisation

    1. ACE-Inhibitor
      • Or Sacubitril/Valsartan (a combination neprilysin inhibitor/ARA) if ACE-I not tolerated or symptomatic despite maximal dose

    2. β-blockers e.g. bisoprolol

    3. Mineralocorticoid receptor antagonist e.g. spironolactone or eplerenone

    4. SGLT2 inhibitors e.g. dapagliflozin or empagliflozin

Class C & D

  • Approximately 25% with moderate-to-severe HF have LBBB; LV contraction becomes asynchronous and they may benefit from a CRT if:
    • EF <35%
    • QRS >120ms
    • Poor functional status despite maximal medical therapy

Treat other contributory factors

  • Reduce hospitalisations & mortality by treating contributory causes

    • Factor Treatment
    Volume overload Diuretics
    AF Digoxin
    Catheter ablation
    Coronary artery disease CABG
    Aortic stenosis Surgical repair or TAVI
    Mitral regurgitation Surgical repair, MICS or transcatheter repair
    Sinus rhythm but high HR Ivabradine
    Iron deficiency IV iron

  • Select patients may be appropriate for mechanical circulatory support ± cardiac transplant

HF-pEF

  • No strong evidence that any medical therapies alter outcome in HF-PEF, however:
    • Patients should be screened for, and have treated, any potential comorbidities associated with HF
    • Diuretics can be used for the treatment of symptomatic fluid overload, typically loop diuretics first line
    • Many of these patients are already on some blend of ACE-I/ARA, β-blocker or mineralocorticoid receptor antagonist for treatment of other pathologies

  • Neprilysin is an endogenous endopeptidase which metabolises BNP, reducing its natriuretic effects
    • Sacubitril is a neprilysin inhibitor, which reduces breakdown of BNP
    • This therefore increases natriuresis from BNP
    • It is indicated for HF-pEF in combination with angiotensin receptor antagonists

  • Acute decompensations in those with existing heart failure can be triggered by a number of different aetiologies
  • As ever, one should find and treat the underlying cause where possible

Clinical features & diagnosis

  • Symptoms: dyspnoea, fatigue, worsening oedema (or escalating diuretic requirement), chest pain, palpitations
  • Signs:
    • Tissue hypoperfusion e.g. oliguria, reduced mentation, cool peripheries
    • Tachycardia
    • Tachypnoea
    • Hypoxia
    • Hypotension

  • Investigations
    • Raised BNP or NT-pro-BNP
    • Raised lactate
    • Raised troponin e.g. new ACS
    • ECG - new ischaemia, dysrhythmia
    • CXR - pulmonary oedema
    • TTE - reduce LVEF, valve pathology etc

Respiratory support

  • Aim target saturations 94-98% (or even lower)
  • Administering oxygen to non-hypoxic patients can cause:
    • Coronary vasoconstriction and reduced CBF by up to 30%
    • Negative pulmonary effects from oxygen toxicity

  • CPAP e.g. 10cmH2O
  • NIV is associated with reduced rates of intubation and improved respiratory parameters but no evidence it improves survival
Benefits of CPAP in acute heart failure
↓ LV afterload
Improving myocardial oxygen supply
Recruiting alveoli
Promote redistribution of extravascular lung water
↓ work of breathing
↓ intra-pulmonary shunting

Preload management

  • Reduce LA pressure to alleviate pulmonary congestion and reducing the excessive LVEDV
  • Consider continuing chronic therapy (e.g. mineralocorticoid antagonists) unless contra-indicated
  • Achieved through:
Target Actions
Venomotor relaxation Loop diuretic
Nitrates
Hydralazine
Morphine
Reduce circulating volume Loop diuretic
Ultrafiltration
Manage tachycardia/AF β-blockers
Digoxin

Afterload reduction

  • High, or sometimes even 'normal', afterload reduces cardiac output by:
    • Reducing stroke volume achieved by the failing ventricle
    • Increased myocardial oxygen demand, rising further impediment to contractility

  • Contributors to afterload include high systemic arterial pressure (LV), raised pulmonary pressures (RV) and increased ventricular radius
  • Should target SBP <110mmHg initially although MAP should be guided by evidence of tissue perfusion

  • Treatment options include:
    • IV nitrates
    • Inodilators
    • Reduce pulmonary pressures e.g. reverse hypoxia, acidosis, hypercarbia, consider pulmonary vasodilators e.g. NO, milrinone
    • IABP
    • Continuing ACE-I where possible

Augment contractility

  • Optimise oxygenation
  • Ensure normal plasma pH
  • Ensure normal plasma potassium, magnesium, calcium and phosphate levels

  • Don't start de novo beta blockers, and consider pausing existing beta blockade
  • Treat thyroid hormone or cortisol deficiency if present

  • Use of inotropes if there is hypotension and shock, although not shown to improve outcomes in acutely decompensated heart failure
  • No evidence to suggest superiority of any one of:
    • Dobutamine (often first line)
    • Dopamine
    • Milrinone
    • Levosimendan
    • Adrenaline

Other

  • Rate titration of those with pacemakers or CRTs
  • Mechanical support using IABP
  • VAD or V-A ECMO as a bridge to transplantation

Perioperative management of the patient with heart failure


  • Acute heart failure is associated with high perioperative risk and patients should have elective surgery delayed
  • Cardiology input to ensure optimisation of medications

Investigations

  • Bloods
    • FBC
    • U&E
      • Electrolyte derangement may occur due to diuretic therapy
      • Renal dysfunction/cardiorenal syndrome may imply poorly optimised
    • LFTs
    • Clotting profile if on anticoagulants
    • G&S depending on surgery

  • ECG
  • Consider up-to-date TTE if no recent echo
  • May need perioperative management of implanted devices such as PPMs, CRTs or ICDs

  • Functional assessments e.g. CPET depending on the nature of the surgery

Drug management

  • ACE-I and ARA
    • Continuation is associated with perioperative hypotension
    • Are often stopped 48hrs pre-operatively, although the evidence base for doing so isn't robust

  • SGLT2 inhibitors
    • Generally discontinued owing to the risk of euglycaemic DKA, volume depletion and electrolyte disturbance if continued
    • Discontinuation risks exacerbation of HF symptoms

  • MRA
    • Generally continued
    • Can contribute to PONV, electrolyte disturbance and hypovolaemia

  • β-blockers
    • Generally continued

  • Patients may be on drugs such as digoxin, loop diuretics, ivabradine - all are generally continued in the perioperative period
  • May need to manage anticoagulants if patient has concomitant AF

Monitoring and access

  • AAGBI
  • Low threshold for arterial line
  • Consider CVC if anticipated need for vasoactive drugs
  • Consider CO monitoring
  • Depth of anaesthesia monitoring may help titrate anaesthetic and reduce its cardio-depressant effects

Anaesthetic technique

  • No evidence to suggest that GA or regional/neuraxial techniques are superior

  • Neuraxial techniques benefit from:
    • Decreasing afterload thus improving CO without increasing oxygen demand
    • Reducing pain-associated tachycardia and hypertension, which may induce ischaemia
    • Avoiding cardio-depressant GA drugs
  • However they may also cause:
    • Sympatholysis, precipitating large, sudden drops in BP
    • Reductions in preload due to peripheral venodilation

Haemodynamic goals

Cardiovascular feature Goal of management Rationale
Heart rate Avoid tachycardia Preserves diastolic time
Heart rhythm Maintain sinus rhythm
Aggressively treat arrhythmia		 Ensures atrial kick aids filling against high LVEDP
Preload Maintain adequate preload/high CVP Facilitates filling of poorly compliant LV
Contractility Avoid myocardial depression E.g. use cardiostable agents such as BZD or opioids
Afterload Prevent increases in afterload May precipitate LV failure


  • Consider HDU or CCU level care for those at high risk
  • Restart paused HF medications as soon as possible post-operatively
  • Multimodal analgesia and anti-emesis as standard