Heart failure

A clinical syndrome with current or prior:

• Symptoms, signs or both caused by a structural or functional cardiac abnormality

Corroborated by at least one of:

• Increased natriuretic peptide concentrations
• Objective evidence of cardiogenic pulmonary or systemic congestion through imaging or haemodynamic measurement at rest or during exercise

We prefer 'not enough squeezy'.

• The heart fails to pump the fluid it is given forward
• If there aren't any valves, then fluid backs up (pulmonary oedema)
• If there are valves, then the chamber starts to distend (ventricle)
• Pressure in the aorta and carotids drops
• Oxygen supply to the brain drops
• The brain smashes the panic button
• Sympathetic tone increases, fluid and salt are retained
• The heart is then overloaded with more fluid that it can't handle
• The oxygen demand of the myocytes also increases
• The arterioles constrict to increase the blood pressure and divert blood to the head
• The heart is now pumping harder and faster against more resistance, with less time in diastole to supply itself with oxygen

Hello spiral of doom.

Working on the simple premise that if the heart isn't working properly, fluid is going to back up behind it, you can use clinical symptoms to figure out which side of the heart is the main problem.

• Normalish systolic blood pressure, lungs clear, swollen ankles - right heart
• Slim ankles, crackly chest and short of breath - left heart
• Crackly chest, can't lie flat, swollen ankles, big JVP - both

Both often happens after a protracted period of left heart failure, as the right starts to fail as well.

As always this is an oversimplification and there of course are textbook-loads of nuance involved.

This is a very simple classification:

• Have they crashed through the door in shock and pulmonary oedema after taking a bunch of funny drugs at a festival?
• Or have they had fifteen years of cardiology clinic letters with a gradual progressive drop in their exercise tolerance?

This classification of course tells you nothing of the pathophysiology of which side of the heart is the main issue or during what phase of the cycle, but it gives you an idea of the urgency with which it requires managing.

The heart muscle isn't pushing hard enough, and the fluid isn't flowing forward properly.

• The ventricle is floppy and often dilated
• There is a reduced ejection fraction
• Fluid backs up behind the ventricle causing the tell tale symptoms signs and symptoms

Causes:

• Ischaemia
• Cardiomyopathy
• Myocarditis

The ventricle is reasonably capable of squeezing pretty hard, enough to empty the fluid contained within it, but like most type A workaholic anaesthetists it's not very good at relaxing.

• The ventricle doesn't relax properly, or quickly enough
• It doesn't fill as well
• Less volume available to eject during systole
• Lower cardiac output

The ejection fraction may still be high, but a high fraction of a lower volume is still a lower cardiac output.

This is where the ridiculous HEFF PEFF thing comes from - heart failure with preserved ejection fraction - it just means the squeezy phase isn't the main issue, it's the filly phase.

Causes:

• Age
• Hypertension
• Diabetes
• Atrial fibrillation

Atrial fibrillation is key here because a stiff ventricle relies heavily on the atrial kick to squeeze as much fluid into it before it squirts it into the aorta.

Seemingly robust patients can decompensate rapidly if they flip into AF on the table.

• Low means the metabolic demand of the patient's body is fairly normal, the heart just isn't pumping effectively enough to meet it
• High means the heart is pumping fine, maybe even better than normal, but the demand is so high it's still not enough

Think thyrotoxicosis, severe sepsis, anaemia, AV fistuale

This might not be the first thing you do, or an immediate fix, but it often gets forgotten, hence we've written it first.

• If the heart is failing because they were previously dependent on their atrial kick,
• and their low potassium from vomiting due to bowel obstruction has just flipped them into atrial fibrillation
• Then giving some potassium might solve a lot of your (and their) problems

Don't forget magnesium, for no reason other than you like magnesium because you're an anaesthetist and magnesium is amazing.

Other causes to think about:

• Sepsis
• Hypoxia from respiratory pathology
• Electrolyte disturbance
• Thyroid and other endocrine issues

Oxygen is frequently helpful for improving myocardial oxygen delivery, however avoid overoxygenating a patient that doesn't need it, as you'll just induce coronary vasoconstriction.

• 92 - 94% saturations is fine

What's more interesting is whether pressure helps.

CPAP

• Pulmonary oedema will be improved by increased intrathoracic pressure
• Increased intrathoracic pressure will reduce the pressure gradient between the inside of the ventricle and the outside of the heart
• This reduces the myocardial workload for the left ventricle
• The right ventricle however won't be so pleased, as the intrathoracic pressure will squeeze the pulmonary vasculature and increase the after load on the right heart
• CPAP will also help with alveolar recruitment and oxygenation

BiPAP

• All the benefits of CPAP plus help with work of breathing

IPPV

• All the benefits of BIPAP pluse more control over the pattern of ventilation
• All the added risks and cardiovascular silliness of having to give an anaesthetic to a bad heart

The main downside is that intrathoracic pressure will compress the IVC and SVC and reduce venous return, so pressure needs to be used with caution.

• Rapid capacitance vessel venodilation reduces preload and unloads the heart
• Diuresis reduces the unhelpful fluid and salt retention from the medulla smashing its big red button

Emergency beetroot.

• Stuff with nitrates in it will cause rapid and profound arterial and venous dilatation
• This dramatically reduces afterload and preload
• It also dramatically reduces systolic pressure and thus cerebral perfusion pressure
• It also generates a reflex tachycardia which might cause as many problems as it solves

A headache for everyone involved.

• Encourage the myocyte to work harder
• More squeezy means more oxygen delivery
• More oxygen delivery to heart means happier myocyte
• Hopefully the myocyte is more happy about the extra oxygen than it is unhappy about the extra speedy squeezy

Inopressors (adrenaline)

• Stronger contraction and more resistance
• Better immediate blood supply to brain
• Much harder work for heart

Inodilators (dobutamine)

• Stronger contraction but less resistance
• Lower blood pressure but better forward flow
• Better for heart but might not be enough for brain

Often a combination of both is needed (noradrenaline and dobutamine) to please both organs as much as possible.

Milrinone and levosimendan

• Same idea as vasodilators but for the right heart
• Reduce the pulmonary vascular resistance
• Increase contractility of the right heart

Can absolutely tank your systolic pressures, so use with caution.

• A variety of effects including a mild potassium sparing diuresis
• Prevents pathological remodelling of the heart
• More of a chronic therapy
• Should be offered once renal function and hyperkalaemia improve

• Reduce afterload
• Reduce preload
• Reduce remodelling
• Reduce sympathetic activity
• Again more of a chronic therapy that should only be started once renal function and blood pressure stable

Ah the age-old 'if drugs don't work let's try some lightning' approach.

• Cardiac resynchronisation therapy is a special form of pacing
• By triggering the right and left heart to contract at the same time, the efficiency of the heart as a whole improves

This is getting silly now.

• Wouldn't it be cool if the systemic vascular resistance could be really low when the heart is trying to squeeze
• But then higher when the heart is relaxing so the coronaries get some decent flow?
• Well let's shove an enormous helium filled balloon in the most important blood vessel and rapidly inflate and deflate it with every heartbeat
• Inflate at the beginning of diastole to shove blood back into the coronaries
• Deflate at the beginning of systole to reduce resistance and effectively suck blood out of the ventricle

A nice idea.

Very much a temporary solution as a bridging therapy to either help the heart recover or to buy time until a definitive treatment becomes available.

Here's our post on balloon pumps.

Ah we're running out of ideas now aren't we.

• If not responding to pharmacological diuresis, then mechanical diuresis may be considered
• Use if fluid overload is the main issue and you're convinced they can tolerate the haemodynamic challenge of going onto the filter

More commonly used in patients who have end stage renal failure and a then bit of heart failure on top, where fixing the fluid overload for the kidneys will then make the heart calm down.

The control freak's dream - just let me do it for you.

• Entirely replaces the function of the lungs and heart
• Buys time either for heart to recover or a definitive procedure to be done
• Brings its own host of thrombotic and infective complications with it

Ventricular assist devices may offer a slightly more permanent mechanical solution, but are beyond the scope of this post.

• Hypertrophic cardiomyopathy
• Amyloid cardiomyopathy
• Pulmonary hypertension
• Constrictive pericarditis
• Coronary artery disease

Pre-op

• Optimise where possible
• Establish severity - NYHA/BNP/Echo/recent decompensations
• Assess functional status and exercise tolerance
• Continue beta-blockers, ACEi, spironolactone but hold ACEi on the morning of surgery
• Optimise volume status, avoid hypo/hypervolaemia

Intra-op

• Lots of monitoring - AoA standard plus invasive blood pressure
• Low threshold for central line and inotropes/vasopressors
• Loco-regional anaesthetic techniques where possible, but caution with big drops in SVR with spinal anaesthesia - epidural might better
• General anaesthesia - cardiostable induction, high opioid, lower hypnotic
• Avoid hypoxia
• Avoid hypotension - goal directed fluid therapy
• Avoid anaemia
• Avoid acidosis
• Avoid big swings in preload and afterload
• Maintain sinus rhythm
• Avoid tachycardia

Post-op

• HDU/ICU
• Multimodal analgesia to avoid hypoventilation
• Early mobilisation
• Careful fluid monitoring
• Continue heart failure medications