Acute Heart Failure

Key Differential Diagnoses

COPD
ARF
Nephrotic syndrome, and other causes non-cardiac oedema

Key Investigations

CXR, ECG (MI?)
O2 saturation ± ABG
Urinalysis (nephrotic?)
FBC, ESR, CRP
U+E, LFT, Bone, Glucose, Troponin T (MI?)

Key Treatment

Sit up
OYXGEN (high flow)
IV MORPHINE 2.5-5.0 mg
SL GTN 1-2 tabs ± IV GTN infusion 10-200 mcg/min (start high)
PO/IV FUROSEMIDE 40 mg od (80 mg if creat 120-200; 120 mg if 200-400; 250 mg, if 400+)
SC ENOXAPARIN 1 mg/kg (esp, if in AF)
    ± ?ACS protocol, if ?MI
    - ie Rx STEMI appropriately (PCI? Thrombolysis?)
        ± Rx of ?arrythmia
        ± Rx endocarditis

Key Management Decisions

ECHO (not necessary acutely, will need later to exclude valvular heart diease or cardiomyopathy)
CCU/ITU
DC Cardioversion (if new AF/flutter, and <24h)

Introduction

• Acute heart failure (or CCF, LVF, RVF, fluid overload, pulmonary oedema etc) are not diagnoses. They are syndromes with a pathological cause, which may or may not be the heart. Why call it 'heart' failure then? This is because whatever the cause, the clinical syndrome is, in part, secondary to heart failure
• For example, there is no distinction between the clinical presentation of AHF secondary to ARF, nephrotic syndrome or ALF
• If it is the heart, then which bit? The 5 main possibilities are IHD (new event), valvular heart disease (new), worsening of previous cause of CCF (especially not taking current medications), iatrogenic (eg too much IV fluid; especially on surgical wards) and arrthymia (rarely the sole cause). Myocarditis/cardiomyopathy, congenital heart disease or accelerated hypertension are rare
• Diagnosis is initially clinical, supported by chest x-ray, ECG, urinalysis, blood tests and echocardiography. If AHF is very quick, symptoms and signs of LVF/pulmonary oedema are initially present, without signs of RVF
• AHF can be very satisfying to treat. In a hour, a patient can transform from gasping in resus, to sitting up and chatting - after GTN, furosemide, high-flow oxygen and being asked to sit-up
• 1/3rd have no previous history (then 40% due to ACS). 80% have MR (usually functional) on ECHO. 1/3rd have normal EF. In-hospital mortality is 5-10% (40% if cardiogenic shock)

Definition 

Difficult! An acute abnormality of cardiac structure or function that reduces the heart's ability to eject blood (systolic dysfunction) or fill with blood (diastolic dysfunction)

Epidemiology

Prevalence = 3-20 cases/1000 pop; 1/3rd no previous history of AHF
>65y = >100/1000 pop

Types

LVF/pulmonary oedema
BiVF/CCF
'Pure' RVF; rare, suggests pulmonary hypertension. Exclude PE    

Causes

1. IHD (new event, ie exclude MI); 40% new (de novo) cases of AHF due to ACS
2. (new) Valvular heart disease (especially AS, MR). Does the patient need an operation? Is this endocarditis?
3. Worsening of known CCF (atrial arrthymias, endocarditis 'on top of' previous lesion, ischaemia, sepsis, non taking current medications)
4. Iatrogenic (too much IV fluid, especially post-op)
5. Arrthymia
Note: arrthymias are common in AHF (usually AF); but rarely the sole cause; AHF can be multifactorial eg known CCF secondary to MR, now worsened by 'fast AF' or new MI; 1/3rd have no previous history
Accelerated hypertension
Myocarditis/Cardiomyopathy (including alcohol)
Congenital (ASD, VSD etc)

Symptoms

Of LVF
Cough, wheezing (hence phrase 'cardiac asthma'), frothy (sometimes blood-stained) sputum; occasionally frank haemoptysis
SOB, feeling of suffocation
Of RVF
RUQ pain (a medical cause of abdominal pain)
Ankle swelling
Note: can be non-specific eg collapse; or, of cause eg chest pain in an MI  

Key questions

"How long have you been SOB?"
"How far can you walk?"
"Do you get SOB when you lie down at night, or ever wake up SOB?"  
"Have you ever had a heart attack or angina before?"
"Has anyone changed your tablets in the last 4-6 weeks?"

Signs

Of cause
Eg, splinters in endocarditis (start with the nails)
Of LVF
SOB
Tachycardia
Pulsus alternans
Increased or decreased pulse volume (BP can be high or low in AHF)
Triple or gallop rhythym
Murmur (Endocarditis? Valvular or congenital cause?)
>Basal crackles, wheeze
Of RVF
L parasternal heave
Raised JVP (giant CV waves)
Ascites
Ankle swelling
RUQ tenderness (liver distension) or pulsatile hepatomegaly   
Of cardiogenic shock
Cold, pale, sweaty, anxious
Hypotension, oliguric/anuric
Note: BP is variable, low (in shock), normal or high (accelerated BP or AR). Generally speaking higher BP is 'better' as it shows the heart is contracting reasonably

• The heart and kidneys are intrinsically related. As cardiac ouput (and perhaps BP) decrease, renal blood flow and GFR decrease, and blood flow within the kidneys is redistributed
• In order to maintain BP, the homeostatic response is to increase tubular resorption, leading to Na and water retention (oedema)
• Eventually, when CO/BP decrease critically, there is insufficient blood flow to the kidneys, and ARF will ensue (remember 1/5th of CO goes to kidneys)
• At this point, the patient has a lethal combination of cardiogenic shock and ARF/oliguria. BP is usally too low to dialyse, and death is likely. Blood flow is further redistributed away from the kidneys during exercise, but renal blood flow improves during rest, possibly contributing to nocturia

Blood

FBC, CRP/ESR (?endocarditis)
U+E, LFT (bilirubin raised in liver failure; albumin low in liver failure and nephrotic syndrome), Bone, Glucose, Mg
Troponin T (acute MI?)
BCx3 (before AB), if ?endocarditis
TFTs
O2 Saturation ± ABG

Other

Key investigations

ECG
CXR

Specialist investigations

• ECHO is NOT the key test: AHF is a clinical diagnosis
• On ECHO, 80% have MR, usually functional; and 1/3rd have normal EF
• Also ECHO is also notoriously unreliable in terms of prognosis - ie, EF can be poor during an acute episode but much better when the patient is treated
• Almost all patients seem to have functional MR (± TR) but this is rarely the stuctural cause of the problem
• Also 'No vegetations' on ECHO also ≠ 'no endocarditis'. Again, it is a clinical diagnosis, at least initially
• Cardiac catheter is sometimes necessary
• Where available, BNP should be measured (high in AHF, normal in COPD)

Differential diagnosis

COPD (pulm oedema can cause 'cardiac asthma')
Note: may have both AHF and COPD (smoking is a risk factor for IHD and COPD; and COPD can cause cor pulmonale)   
ARF
Nephrotic syndrome, and other causes non-cardiac oedema
Other causes fluid overload: ALF, Iatrogenic
Pulmonary fibrosis (fine inspiratory crackles sound the same; clues are: slower onset, clubbing and crackles in all zones, and CXR)

Treatment
(first line)

Drugs   
SL GTN 1-2 tabs
GTN infusion 10-200 mcg/min (start high, if systolic BP >100 mmHg)
Note: some clinicians would wait to see the effect of these drugs before giving a diuretic
PO/IV FUROSEMIDE 40 od; 80 mg if creatinine 120-200 mcmol/L; 120 mg if 200-400; 250 mg, if 400+)
SC ENOXAPARIN 1 mg/kg od (esp, if in AF); consider ACS protocol, if ?MI, or unexplained pulmonary oedema
± IV MORPHINE 2.5-5.0 mg (care, if severely hypoxic; eg give in dilute form slowly, or not at all)
± Rx of arrthymia (eg digoxin for AF); ± iv AB for ?endocarditis
Note: even though arrthymias are not often the cause of AHF, often when the patient is unwell, it is not clear if a tachycarrthymia is cause or effect (eg patient could be in chronic AF, then tachycardia of LVF 'causes' fast AF; in these situations, Rx as if it is the cause). There is debate regarding the relative importance of nitrates vs diuretic/opiate in AHF: [Ref] . Some also think, there is no role for opiates in acute pulmonary oedema: [Ref] . There is no role for ACE inhibitors in acute heart failure, unlike CCF: [Ref]

           
IV line
SIT UP (patients in resus often in poor position)
OXYGEN, high flow; hypoxia kills BUT remember in the acute situation that hypoventilation and hypercapnia are a risk. Also remember that COPD is a common co-morbidity in (especially elderly) patients
ECG monitoring

Key management decisions

Stop

If bradycardic, stop digoxin/amiodarone/beta-blocker. If ARF (or hyperkalaemic, or both) stop ACEi. Beta-blocker and ACEi may need to be restarted later

Treatment
(second line)

Drugs               
ITU: inotrope, if cardiogenic shock does not respond to first line therapy

Procedures           
Urinary catheter, CVP line, arterial line
Non-invasive ventilation (eg CPAP), if hypoxic despite Rx; hypercapnia is an ominous sign, and should make you consider:
ITU: Ventilation, intra-aortic balloon pumping
Note: rarely ultrafiltration can be life saving (if patient moribund); if you cannot access this quickly, venesection is the equivalent 'older' alternative; one of the authors has used this technique on several occasions, to good effect

Admit?

Always

Bed plan

Medical admission ward (for <48h admission)   
± Cardiology (if >48h)
± CCU/ITU

Referrals

Medical          
Cardiology
± ITU

Other
Cardiac nurse (may help with ECG interpretation)

Complications

Cardiogenic shock
Cardiac arrest
Respiratory arrest

Prognosis, risk factor stratification

Mortality 5-10% (40% if cardiogenic shock). Poor prognosis, if: older, high urea, hyponatraemia, respiratory rate, low BP; first published in 1967 but still useful:  [Ref]
Survival of patients with a new diagnosis of heart failure: a population based study. Cowie MR et al. Heart; 83:505–510, 2000; [Ref]

2° Prevention +
Health promotion

• Heart failure clinic/heart failure nurse specialist
• Drugs: keep taking 'mainstay of Rx' = ACEi, betablocker + spironolactone (or eplerenone) ± aspirin and HMG CoA reductase inhibitor
• Education: Na/fluid restriction, stop smoking, appropriate weight and fitness levels
• Correction of underlying conditions (eg attend CT surgical referral)

Don't forget

• Exclude MI
• ECHO is not needed immediately
• But, nonetheless, ask yourself this question: 'does the patient need an operation?'
• Is this endocarditis?
• Arrythmias common (esp AF); rarely cause, but may need treating
• Follow up in heart failure clinic

Red flags

• Poor response, to first line treatment (above)
• Cardiogenic shock