Heart failure

Introduction

• Poor prognosis with 50% mortality at 5 years
• Hospitalisation marks higher mortality than matched non-hospitalised patients
• Pathophysiology
  • Definition: A complex clinical syndrome that results from any structural or functional impairment of ventricular filling or ejection of blood
  • Upregulation of neurohormonal systems to maintain perfusion ultimately increase myocardial workload, wall tension and myocardial oxygen demand
  • Natriuretic peptides (ANP, BNP and CNP) are the counter-regulatory response to the neurohormonal system activation
  • Vicious circle in APO results from rising blood pressure, reduced cardiac output and further increased systemic vascular resistance, repeatedly

Classification

• Phenotypes
  • Hypertensive AHF: Relatively preserved LV fx, SBP >140, APO and <48hrs duration
    • Control BP first as may be more fluid shift than overload
  • Pulmonary oedema: Respiratory distress, desaturation and CXR
    • Early BiPAP/CPAP to avoid intubation
  • Cardiogenic shock: SBP <90 with tissue hypoperfusion
    • Consider structural or ischaemic cause. Often benefit from vasopressors and invasive haemodynamic monitoring
  • Acute on chronic HF: Typical onset over days with peripheral oedema and not meeting above criteria
  • High-output failure: High CO, tachycardic, warm extremities and pulmonary congestion
    • E.g. anaemia or thyrotoxicosis
  • Right heart failure: Raised JVP, hepatomegaly, peripheral oedema and may have hypotension
    • Pulmonary disease, valvular disease (TR) or OSA
    • Treatment rests with treatment of underlying disorder, often without volume removal as low-output state may co-exist

Causes

• Myocardial ischaemia: Acute or chronic
• Systemic hypertension
• Cardiac dysrhythmias (esp. AF with RVR)
• Valvular dysfunction
  • AS, AR (consider IE or dissection)
  • MS, MR (consider papillary muscle rupture, ruptured chordae tendinae, IE)
  • Prosthetic valve dysfunction
• Cardiomyopathy
  • HOCM
  • Dilated
  • Restrictive
  • Alcohol, cocaine, thyrotoxicosis, myxoedema
• Myocarditis: Radiation or infection
• Constrictive pericarditis
• Cardiac tamponade
• Anaemia

Systolic vs. diastolic failure (old paradigm)

• Systolic = LVEF <50%
  • Results in afterload sensitivity
  • With circulatory stress e.g. walking, failure to improve contractility with rising venous return results in increased cardiac pressures, pulmonary congestion and oedema
• Diastolic dysfunction (aka HF with preserved EF)
  • Impaired ventricular relaxation
  • Reduced LV compliance necessitates higher atrial pressures to ensure adequate filling, creating
    preload sensitivity
  • Common in chronic hypertension with LV hypertrophy
  • Coronary artery disease also contributes as diastolic dysfunction is seen early in cardiac ischaemia

Latest classification

• Heart failure with normal ejection fraction (HFnEF)
  • EF > 55% for women and >60% for men
  • Still have heart failure but minimal proven therapies
  • Still benefit from volume status management and reversible cause treatment
• Heart failure with mildly reduced ejection fraction (HFmrEF)
  • EF 40-55% in women or 40-60% in men
  • New group that likely benefit from neurohormonal treatments
• Heart failure with reduced ejection fracture (HFrEF)
  • EF <40%
  • Definitively benefit from all therapies and have highest mortality/morbidity

Diagnosis

• There is no singular historical or physical exam finding that achieves sensitivity and specificity >70%
• Initial global clinical assessment has sensitivity of 61% and specificity of 86%
• Hx of heart failure has sensitivity of 60% and specificity of 90% (+LR 5.8)
• Symptom with highest sensitivity is dyspnoea on exertion (84%)

• Most specific symptoms are PND, orthopnoea and oedema (76-84%)
  • Orthopnoea is a late symptom due to redistribution of splanchnic/limb fluid into central circulation. Nocturnal cough is a frequent manifestation and often overlooked (Harrison’s)
  • PND often occurs 1-3 hours after retiring to bed and is not rapidly relieved by sitting up (unlike orthopnoea)
  • Cheyne-Stokes respiration occurs with periodic apnoea/dyspnoea due to impaired sensitivity to reduced PaO2 and subsequent dyspnoea as PaCO2 rises

• Historical precipitating factors
  • Non-adherence to salt/fluid restriction or medication
  • Renal failure (esp. missed dialysis)
  • Substance abuse e.g. meth, cocaine, ethanol
  • Poorly controlled HTN
  • Iatrogenic e.g. recent negative inotrope change, NSAID/steroid initiation, inappropriate therapy reduction, new antiarrhythmics

• Examination
  • S3 has higher LR+ for acute heart failure (LR+ 11)
    • Absence does not rule out acute heart failure however
  • Abdominojugular reflex +LR 6.4
  • Raised JVP + LR 5.1
  • Clinical judgement and a single BNP have similar accuracy
  • Pulmonary crackles may be absent in chronic HF due to increased lymphatic drainage from alveoli
  • Pleural effusions tend to be bilateral and are more common in biventricular failure (if unilateral, more often right sided)

• CXR
  • Up to 20% of patients have CXR without classic signs on first presentation to ED (particularly in late-stage heart failure)
  • Alveolar oedema – Loss of visible vessels in peri-hilar region, fluffy patches of consolidation +- air bronchograms
  • Interstitial oedema – Kerley B lines
  • Pulmonary congestion – Upper lob diversion
  • Pleural effusions – Blunted costophrenic angles, fluid in fissure
  • Cardiomegaly – C:T ratio >0.5

• ECG
  • May reveal underlying cause or precipitant
  • New AF has higher +LR for heart failure

• Biomarkers
  • BNP may add value in the undifferentiated dyspnoeic patient in the ED
  • May elevate later in flash APO
  • Marked rise is associated with worse short-term outcomes
  • BNP <100 makes HF unlikely (sensitivity 90%)
  • BNP >500 akes HF likely (specificity 90%)

• POCUS
  • 1) Is pulmonary congestion evident?
    • Sonographic B lines: >2 in any one sonographic window along anterior and anterolateral chest is highly specific
  • 2) Is elevated CVP evident?
    • IVC >2cm and <50% collapsible
    • Look for RV strain also to ensure no evidence for PE or clinically significant TR as alternative diagnosis
  • 3) What is the LVEF?
    • Visual estimation into normal, moderately reduced and severely reduced

Treatment

• Airway and breathing take precedence
  • NIV reduces intubation rates and improves respiratory distress and metabolic disturbance compared to standard therapy alone
  • Unclear if reduces hospital mortality
  • I&V if necessary
• Hypotensive HF
  • Seen in 3% of cases
  • Consider ischaemia and reperfusion therapy
  • Early inotropes and invasive monitoring indicated

• Hypertensive AHF
  • Prompt recognition (SBP >150) and afterload reduction with vasodilators
  • Nitroglycerin
    • Reduces MAP by reducing preload, and afterload at high doses
    • May have coronary vasodilatory effects, reducing myocardial ischaemia and improving cardiac function
    • 400mcg S/L at one per minute until relief or IV infusion started
    • IV 5-10mcg/min titrated up to 200mcg/min based on BP and symptoms
    • Start high and titrate down rapidly as very short half-life (2 min)
    • If hypotension <90 ensues and persists with cessation, consider volume depletion or RV infarct and treat with N/S boluses
    • Risk of methaemaglobinaemia if prolonged use
  • Nitroprusside
    • Second-line if persistent symptoms and HTN despite GTN 200mcg/min
    • More potent arterial vasodilator
    • 0.3mcg/kg/min titrated up every 5-10 minutes to 10mcg/kg/min
    • Risk of thiocyanate toxicity if prolonged, high-dose or renal/liver failure
    • End-point is control of LV filling pressures to prevent intubation
  • Loop diuretics
    • If continued symptoms despite BP control
    • Likely has pulmonary venodilation effect producing benefit without diuresis
    • Frusemide alone without vasodilators INCREASES mortality and worsen renal function
  • Contraindications to vasodilators
    • If signs of hypoperfusion/SBP< 90
    • Flow-limiting, preload-dependent states such as RV infarct, aortic stenosis, HOCM or volume depletion increase the risk
    • Therapy in these situations is aimed at decreasing the outflow gradient by slowing the heart rate and cardiac contractility with IV beta-blockers in ICU setting
    • If co-existent shock in HOCM, phenylephrine or noradrenaline are preferred to raise systemic BP without increasing cardiac contractility

Treatment

• Normotensive heart failure
  • Diuresis first with further treatment based on response to therapy
    • Loop diuretics provide rapid symptom relief of congestive symptoms and improved effects of ACEi by reducing intravascular volume
    • IV dosing preferred (most pt’s will have bowel wall oedema limiting absorption of oral preparations)
    • Effective within 10-15 minutes
    • Frusemide 20-40mg IV push
      • If prior use, give 1-2.5x previous total daily dose, divided in half and given q12h
      • Bumetanide 1-3mg IV (1mg = 40mg frusemide)
      • Torsemide 10-20mg IV (20mg = 40mg frusemide)
    • DOSE trial
      • Higher doses produce more rapid response with slight decrease in renal function
    • Adverse effects include hypocalcaemia, hypokalaemia, hypomagnesaemia, ototoxicity (if used with aminoglycoside)
    • If symptoms worsen or fail to improve, double dose and repeat in 30-60 minutes

Treatment

• Normotensive HF
  • Ultrafiltration
    • No benefit seen over bolus diuretic therapy
    • Consider if all medical strategies not effective in obvious volume overload
  • Morphine
    • Relieves congestion and anxiety BUT is associated with need for mechanical ventilation, prolonged hospitalisation, ICU admission and mortality
    • If desired for venodilation or pain control, 2-4mg IV boluses with close monitoring is an option
    • This trial only used morphine in severe cases so probably biased but definitely has a secondary role to loop diuretics and nitrates
  • Nesiritide
    • Vasodilator (recombinant BNP) with no significant effect on hospitalisation or mortality (ASCEND-HF trial)
    • Increased risk of hypotension
    • Optional if nitrates ineffective or contraindicated

Treatment

• Normotensive HF
  • ACEi and ARB’s
    • Not utilised in the ED for acute management but indicated for chronic heart failure with reduced EF
  • Beta-blockers
    • Reduce mortality in chronic heart failure but generally witheld in acute heart failure due to risk of deterioration
    • May have a place in management of rate-related failure but very dangerous
• Drugs to avoid
  • CCB
    • Myocardial depressant activity (like beta-blockers)
    • Trials show no benefit and worse outcomes
  • NSAID’s
    • Risk of sodium and water retention, blunt the effect of diuretics +- renal impairment and may increase morbidity and mortality

Treatment

• Hypotensive heart failure
  • HFrEF/HFmrEF
    • Optimise preload ( judicious use of fluids given likely APO)
    • Add inotrope
      • Dobutamine 2.5mcg/kg/min titrated up to 20mcg/kg/min is first-line
      • Adrenaline is an alternative although small RCT’s have shown increase in refractory cardiogenic shock (in revascularised MI), arrhythmias, in-hospital mortality and worsened vital organ perfusion as compared to dobutamine + noradrenaline
    • Add vasopressor
      • Noradrenaline agent of choice
    • If SBP <90 probably better of starting with vasopressor and adding inotrope given the old adage of dobutamine reduces BP in 1/3, doesn’t change in 1/3 and increases BP in 1/3
    • Consider mechanical device as bridge to decision
  • HFnEF
    • Optimise preload
    • Consider dynamic LV outflow obstruction
      • May require beta-blocker, vasopressor and gentle diuresis
    • Inotropes are NOT indicated and positive chronotropic agents will cause deterioration

Treatment

• Anticoagulation
  • 1.3-2.4% annual risk of stroke in HF
  • Warfarin indicated if HF and AF or HF with history of systemic or pulmonary emboli
  • If documented LV thrombus, need 3 months of therapy
• Aspirin is recommended for HF patients with IHD to prevent MI and death
• ICD
  • Prophylactic use in NYHA II-III reduces sudden cardiac death
  • Should be considered for these patients with EF <30-35% who are already on optimal background therapy
  • May be combined with biventricular pacemaker (CRT)

Treatment

• Cardiac resynchronisation therapy
  • 1/3 of patients with depressed EF and symptomatic HF have QRS >120ms
  • Mechanical consequences of inter- or intraventricular conduction disturbance include suboptimal ventricular filling, reduced LV contractility, prolonged duration of MR and paradoxical septal wall motion
  • CRT reduces severity of MR, mortality, hospitalisation, reversal of LV remodelling and improved QoL and exercise capacity
  • Indicated for patients in sinus rhythm with EF <35% and QRS >120ms and those who remain symptomatic (NYHA III-IV) despite optimal medical therapy

Disposition

• Need to consider clinical gestalt, physiological risk profile and barriers to self-care/support
  • Caregiver support, hospitalisation history, symptom monitoring, education, access to medical care, disease knowledge, medication adherence all come into consideration
• Is ED SSU an option?
  • Studies have shown this can be safely done if no high-risk markers
  • Can monitor for complete symptom resolution within 12-24 hours (typical), can have BP/UO/weight/HR monitoring, any further diagnostic testing organised (labs, echo) and can perform heart failure education, confirm outpatient appointments and arrange follow-up

Disposition

• Exclusion criteria for SSW/Discharge
  • Positive troponin
  • BUN >40mg/dL
  • Creatinine >3mg/dL
  • Sodium <135
  • New ischaemic changes
  • New onset acute HF
  • IV vasoactive infusions being titrated
  • Significant cormorbidities requiring acute interventions
  • RR >32 or NIV
  • Signs of poor perfusion
  • Poor social support and/or follow-up

Disposition

• High-risk markers (seen in 50%)
  • Renal dysfunction
  • Low BP
  • Low serum sodium
  • Elevated BNP
  • Elevated troponin
• Studies have shown 75% of patients will respond to therapy, will have no identifiable high-risk features and can be discharged home
  • Rates of re-admission are similar to or better than those that are admitted
  • Outpatient follow-up within 5 days reduces re-admission rates
• If inadequate response to initial therapy, high-risk features need admission

The Summary

Rapid Review – Acute Heart Failure

•   6 phenotypes and each will require different management priorities
  • Hypertensive
  • APO
  • Cardiogenic Shock 
  • Acute on chronic HF
  • High-output HF (anaemia, anorexia, thryotoxicosis) 
  • RV failure 
• S3 heart sound had greatest Sp on clinical exam 
• CXR findings  
  • Bilateral interstitial oedema
  • Alveolar infiltrates 
  • Fluid in the fissues
  • Kerley B lines 
  • Increased apical vascularity 
  • Pleural effusion 

Introduction

• Defined as a complex clinical syndrome that results from any structural or functional impairment of ventricular filling or ejection of blood.
• Neurohormonal compensation results in increased after load, increased wall tension and increased myocardial oxygen demand. This results in a vicious cycle of increasing workload, remodelling and worsening pump function. 

Clinical Features/Discriminating Features 

• Signs of LV failure:
  • Bilateral creps in lung fields
  • Varying degrees of hypotension 

• Signs of RV failure:
  • Elevated JVP
  • Peripheral oedema 
  • +ve hepato-juglar reflex 

• Careful cardiac examination should be undertaken:
  • Any new murmurs?
    • Specifically AS, Systolic murmur of HOCM, any new murmur of mitral valve could be due to prolapse. Tricuspid murmur could be from IE. 
  • Apex beat will be mid-clavicular line if acute event or laterally displaced if old cardiac remodelling has already occurred. 

• ECG —> DO THIS EARLY AS MI IS ONE OF THE FEW REVERSIBLE CAUSES 

• Chest XR
  • Demonstrates pulmonary congestion/oedema with:
    • Bilateral interstitial oedema
    • Alveolar infiltrates 
    • Fluid in the fissues
    • Kerley B lines 
    • Increased apical vascularity 
    • Pleural effusion 

• Bedside Ultrasound (Lungs + Heart + IVC):
  • B-lines throughout the lung fields
    • > 2 b-lines in 1 USS window 
  • Possible pleural effusions bilaterally
  • Enlarged and non-collapsing IVC
    • >2cm and < 50% collapse with respiration when measured at the hepatic vein. 
  • May demonstrate dilated LV with poor systolic function OR collapsed LV with dilated RV in RV infarct (could also be PE) 
  • In EF preserved HF can demonstrated signficant wall thickening (LVH or HOCM) 
  • Assess for RWMA if ischaemia 
  • May see evidence of valve insufficiency
  • Also check for pericardial effusion 

• Haemodynamic Criteria for Cardiogenic Shock;
  • Sustained hypotension (SBP < 90mmHg)
  • Reduced Cardiac Index (< 2.2L/min/m2) 
  • Elevated pulmonary artery occlusion pressure (> 18mmHg) 

• Lab Tests
  • BNP
    • < 100 —> very unlikely to be heart failure
    • > 500 —> likely to be component of heart failure 
    • Overall clinical decision making just as good, not useful test in ED 
  • Evidence of High Risk Heart Failure
    • New renal dysfunction
    • Low serum sodium
    • Elevated TnI
    • Elevated Lactate 

Management – Hypertensive Heart Failure

• Resus Management
  • Airway + Breathing
    • Only required if APO or altered mental state 
    • Generally trial of GTN and NIV before committing to invasive ventilation
    • SEE BELOW (CARDIOGENIC SHOCK) FOR DETAILS
  • Circulation
    • Required for cardiogenic shock —> SEE BELOW 

• Definitive Management
  • Management of hypertension
    • GTN
      • sublingual 400mcg every 10 mins, target systolic BP 120 – 140 
      • Infusion
        • Start at 50mcg/min and titrate to systolic BP 120 – 140
          • max 200mcg/min 
        • Conservative Mx could start infusion at 10mcg/min and titrate up, however likely to need larger doses 
      • Be wary of GTN in pre-load dependent disease states
        • RV infarct
        • HOCM
        • Critical AS 
        • Pericardial Effusion 
    • Sodium Nitroprusside
      • 2nd line therapy, to start when GTN running at 200mcg/min and still not achieving BP targets 
      • Start at 0.3mcg/kg/min, increase to max 10mcg/kg/min 
      • Be wary of thiocyanate toxicity in large doses or prolonged infusions 
  • IF APO a component of presentation
    • CPAP or BiPAP 
    • CPAP
      • Start 6cmH2O and titrate to oxygenation and respiratory effort 
    • BiPAP
      • Further utility if patient has type 2 respiratory failure associate with APO 
      • Also useful if significant work of breathing 
      • Can start for most patients at IPAP 12 and EPAP 6
      • Titrate to sats >94% (increase EPAP for hypoxia) 
      • Titrate to PCO2 35 – 45 (increase IPAP for hypercarbia) 
  • Medications to avoid in APO/acute cardiac failure
    • Calcium channel blockers
    • Beta blockers 
  • NOTE – Frusemide has no morbidity improvement for acute hypertensive cardiac failure and may worsen renal function. Should only be used once HTN has been controlled. 

• Supportive Management
  • Supplemental oxygen to maintain sats >94% 
  • Anti-emetics if nausea 
  • If chest pain, provide analgesia 

• Colleagues Expectation
  • K >4.0
  • Mg >1.0 

• Disposition
  • Depends on severity and underlying cause 
  • Most require admission
  • If GTN infusion will require coronary care ward environment 

Management – APO Heart Failure

• Resus Management
  • Airway + Breathing
    • Only required if APO or altered mental state 
    • Generally trial of GTN and NIV before committing to invasive ventilation
    • SEE BELOW (CARDIOGENIC SHOCK) FOR DETAILS
  • Circulation
    • Required for cardiogenic shock —> SEE BELOW 

• Definitive Management
  • CPAP or BiPAP
    • CPAP
      • Start 6cmH2O and titrate to oxygenation and respiratory effort 
    • BiPAP
      • Further utility if patient has type 2 respiratory failure associate with APO 
      • Also useful if significant work of breathing 
      • Can start for most patients at IPAP 12 and EPAP 6
      • Titrate to sats >94% (increase EPAP for hypoxia) 
      • Titrate to PCO2 35 – 45 (increase IPAP for hypercarbia) 
  • Diuretic
    • Frusemide 40mg IV (or double normal dose for patient) 
  • Medications to avoid in APO/acute cardiac failure
    • Calcium channel blockers
    • Beta blockers 

• Supportive Management
  • Supplemental oxygen to maintain sats >94% 
  • Anti-emetics if nausea 
  • If chest pain, provide analgesia 

• Colleagues Expectation
  • K >4.0
  • Mg >1.0 

• Disposition 
  • Depends on severity and underlying cause 
  • Most require admission
  • If GTN infusion will require coronary care ward environment 

Management – Cardiogenic Shock

Emergency management of cardiogenic shock is only a temporising measure. The patient will only benefit from either revascularisation (if AMI) OR surgical intervention. 

• Resus Management
  • Airway + Breathing
    • All shocked patients should receive supplemental oxygen, esp in cardiogenic shock
    • If PPV is required in cardiogenic shock, patients will generally require intubation. Non-invasive ventilation with BiPAP or CPAP might buy some time, but often patients are uncooperative and their haemodynamics don’t allow for NIV. However NIV should be used as a bridge to intubation and delayed sequence induction. 
    • IF RV failure is suspected hold off on intubation as long as possible, as switching to positive-pressure ventilation will decrease the pre-load and could lead to further deterioration and arrest
    • IF LV failure is more likely early intubation with PPV will likely benefit the patient as respiratory failure and worsening hypoxia will be mitigated 

• AN APPROACH TO INTUBATING THE CARDIOGENIC SHOCK PATIENT
  • Optimise the haemodynamics and oxygenation prior to RSI or DSI
    • Small fluid bolus
    • Start inotropes (Adrenaline 5mcg/min titrate) 
    • Pre-oxygenate with BiPAP 12/6 with FiO2 100%, use ketamine 0.5mg/kg as dissociative agent prior if patient not compliant 
    • Alternative to BiPAP is using c-circuit with PEEP with patient spontaneously breathing 
    • Apply sub nasal oxygen 
  • For the RSI
    • Direct laryngoscopy with bougie (or VL if difficult airway predicted) 
    • High dose fentanyl alone preferred (500 – 1000mcg) + Rocuronium 1.2mg/kg
      • Fentanyl is not a true general anaesthetic and will take longer to have effect in this setting given longer arm-brain circulation time
    • If ketamine used for DSI, use ketamine + rocuronium
      • Risk of vasoplegia with ketamine remains given patient sympathetically maxed out
      • Tachycardia not beneficial when LV is struggling to meet demand already
    • Push dose pressor available (Adrenaline 10 – 50mcg bolus) 
    • Bag the patient once apnoea to avoid any apnoeic period 
  • Ventilation Settings
    • SIMV mode
    • 6mL/kg tidal volume + 16 breaths/minute 
    • Insp Support – 10cmH2O 
    • Peep 10mmHg 
    • FiO2 100%, titrate ASAP 
  • Sedation Strategy
    • Fentanyl 0.5 – 2mcg/kg/hour +
    • Midazolam 0.05 – 0.15mg/kg/hr 
    • Can consider low-dose propofol (0.5-2mg/kg) instead of midazolam. Dosing is key.
• Circulation – Improve the cardiac pump function
  • Trial of fluid bolus is not unreasonable, however if pulmonary congestion, don’t give fluids
    • NOTE fluid bolus is KEY MANAGEMENT for RV infarct or critical AS 
    • 10mL/kg normal saline bolus 
  • Correct any electrolyte abnormalities:
    • K+ target 4.0 – 5.0
    • Mg target 1.0 – 1.2
    • Ca target > 1.0 (ionised Ca) 
  • Manage the hypotension:
    • Adrenaline 0.05 – 0.5mcg/kg/min (3mg in 50mL start at 10mcg/min) OR;
    • Noradrenaline 0.05 – 0.5 mcg/kg/min PLUS Dobutamine 2.5mcg/kg/min 
    • Avoid pure alpha agonists along (Metaraminol/Phenylephrine) as they increase after load without improving pump function (but may be very useful in critical AS)
    • If hypotension persists despite inotrope support —> requires intra-aortic balloon pump
    • In acute mitral valve failure, consider dobutamine alone or combination of dobutamine + nitroprusside to increase cardiac output and also decrease after load. 
• Diagnosis
  • Look for STEMI
  • Look for pericardial effusion
  • Look for valve failure 
  • Look for alternate diagnosis 

• Definitive Management
  • Acute MI with cardiogenic shock
    • Requires URGENT revascularisation
      • PCI is preferred method
      • Thrombolytic therapy demonstrated in SHOCK trial to be ineffective due to low drug delivery to coronary arteries due to low cardiac output. Therefore thrombolysis unlike to be effective in cardiogenic shock caused by MI
      • However if there’s significant delay to PCI thrombolytics should still be give as thrombolysis was still better for mortality outcomes then supportive therapy alone 
  • Mechanical Issue (valve failure etc)
    • Requires urgent surgical intervention
    • Patients will also benefit from early angiography to assess for any potential stentable lesions to improve cardiac perfusion

• Supportive Management
  • Antiemetics may be required
  • Analgesia as required 
  • IDC should be placed

• Patient Expectation
  • Explain severity
  • Explain potential poor prognosis
  • If > 75 years old or multiple co-morbidities, establish ceiling of care 

• Family
  • Involve them early
  • Invite them into the resuscitation 
  • Explain situation, management required and likely disposition
  • Social worker involvement is recommended 

• Disposition
  • Patients with cardiogenic shock are best managed in a hospital with:
    • Cardiac catheterisation facilities
    • Cardio-thoracic surgical services 
    • Cardiac ICU 

Key Decision Points/Consultant Level Thinking

• Heart failure should be considered a symptom, not a diagnosis. Ascertain the underlying cause of the heart failure as this will dictate management.
  • Ischaemia
  • Systemic Hypertension 
  • Dysrhythmia
  • Valvular dysfunction
  • Cardiomyopathy
    • HOCM
    • Dilated vs Restrictive 
    • Alcohol, cocaine, thyrotoxicosis, sepsis, anorexia 
  • Myocarditis 
  • Tamponade 
  • Anaemia 
• Treat the phenotype in front of you, don’t blindly apply a ‘package of care’ treat the pathology with clear targets. 
  • Hypertensive —> Vasodilators 
  • APO —> BiPAP/CPAP
  • Cardiogenic Shock —> Inotropes
  • Acute on chronic HF —> frusemide titration
  • High-output HF (anaemia, anorexia, thryotoxicosis) —> treat underlying cause 
  • RV failure —> often pre-load responsive, caution with GTN 

Critical Interventions for this Topic (what will actually make a difference to outcomes)

• Look for reversible causes early as nothing can be ‘reversed’ in ED
  • STEMI —> needs PCI
  • Valve Failure —> needs surgical intervention
  • Tamponade —> needs drain
  • Cardiomyopathy —> if restrictive or HOCM is pre-load dependent 

Last Updated on July 15, 2024 by Andrew Crofton