Past paper SAQs concerned with heart failure have been unsurprisingly common in the past papers, considering the prevalence of this in our daily workload. What is surprising is that they have focued extensively on right heart failure. In fact, the second paper of 2018 contained two questions on this topic. As no massive breakthroughs or upheavals have occurred in the literature, one might surmise that recently one of the examiners has completed a PhD on the subject, or otherwise the topic of right ventricular dysfunction forms a special interest area for them. Whatever the reason, by using past papers as a shadow curriculum the CICM candidate might come to the concusion that for the purposes of revision the left ventricle is a useless vestigial organ which has zero importance in critical care.
The past paper questions on heart failure have consisted of the following SAQs:
In spite of the dextrocentricity (Right-wingedness? Left hemineglect?) of the past papers, this chapter is an effort to address all heart failure in a way which lends a structure to one's approach to a generic CCF question. It is of course difficult to do so in a manner which is comprehensive, given that heart failure management is a massive daunting topic. In order to approach this in a systematic manner, I have separated the problems of heart failure into the variables which govern cardiac output, and the means of manipulating those variables. The approach resembles that of the similar chapter from the section on cardiothoracic intensive care.
The definitive resource for this is probably this 2013 guideline statement by the AHA/ACC. Unless otherwise reported, it is my source for most of the information below. For the sane exam candidate who may be disinclined to read the entire fifty-page document, of particular interest may be Section 7.3.2, Pharmacological Treatment for Stage C HFrEF. For Question 17 from the second paper of 2009, the single most useful article on right heart failure was the JACC review by Lahm et al (2010). From Oh's Manual, one needs to be familiar with Chapter 24 (Acute heart failure) by Nicholas Ioannou, Pratik Sinha and David Treacher.
Idiopathic and infiltrative
Endocrine and environmental
|Management of preload||Management of afterload||Management of contractility||Cheating|
Increase cardiac output by unnatural means:
Decrease the organism's demand for cardiac output
There are several methods of managing preload in heart failure. Typically, with LV failure the LV preload needs to be on the lower side, because high LV preload tends to lead to pulmonary oedema. In contrast, with RV failure the preload needs to be high (but not too high) because the useless RV is essentially a passive conduit into the pulmonary circulation.
Preload has all sorts of precise and imprecise definitions created by intelligent people - but it is essentially the volume of blood which manages to make its way back to the heart during diastole. Generally speaking, in manipulating preload we have only two major choices: we can either change the volume, or the venous compliance. Volume can be changed by adding or removing fluids of some sort. Venous compliance can range from 30 to 300ml/mmHg, and can be manipulated by vasoactive substances.
Diuretics: If there is evidence of fluid overload, one normally reaches for the diuretics. The general tendency of heart failure patients to become boggy with fluid has resulted in a Class I recommendation in favour of diuretic use. Loop diuretics are recommended as a start. In order to increase the fluid loss, one may add a thiazide (the increase in the delivery of sodium to the distal tubule will improve the activity of frusemide).
Fluid restriction begins to play more of a role once the patient is extubated and begins to complain of thirst to teir attending relatives. Bottles and jugs are brought. Oedema ensues. At the early intubated stage, it is much easier to have fine control over fluid balance.
Aldosterone receptor antagonists (such as spironolactone) are recommended not only for their diuretic effect (which is minor), but also because they seem to improve mortality by another effect, perhaps related tot he role of the renin-angiotensin-aldosterone system in the development of CCF. The RALES trial demonstrated a 30% improvement in mortality for patients receiving spironolactone.
Venodilators such as hydralazine and nitrates are useful in decreasing preload in patients whose renal function does not permit the use of diuretics (eg. if they produce no urine).
Question 17 from the second paper of 2009 has asked specifically about the management of right heart failure. General principles of heart failure management are preserved in this context, but the approach required to optimise RV preload is dramatically different. The RV requires a higher filling pressure, and you can never guess precisely how high it has to be without experimenting. Traditional means of assessing fluid responsiveness are ineffective in RV failure.
Beta blockers: Question 12 from the second paper of 2000 discusses the role of cardioselective beta blockers in the management of heart failure. This role seems to be largely related to the improvement in cardiac contractility associated with the increase in diastolic time. During a nice long diastole your useless floppy ventricle can fill with blood to a satisfactory point (i.e. where its Frank-Starling relationship allows it to contract with a satisfactory force). Another beneficial aspect of beta blockade is the limits it puts on cardiac conduction and automaticity. The beta-blocked patient is less likely to develop a lethal MI-inducing tachycardia while mowing their lawn, or to develop VT. Cardiac oxygen consumption is decreased, and because of decreased contractility the subendocardial blood flow is better. This mortality benefit has been demonstrated both in cardioselective and non-selective beta blockers. Bisoprolol, carvedilol and metoprolol all decrease mortality, but carvedilol is not cardioselective.
The main disadvantage of beta-blockade in the context of critical illness is the fixed cardiac output. With beta blockade, the ICU patient is unable to reflexively increase their contractility or heart rate in response to stress. Sepsis and trauma rapidly demonstrate the advantages of a working sympathetic nervous system among non-beta-blocked people. Less important disadvantages include lethargy, nightmares and depression.
Pacing may improve A-V synchrony, and result in an improvement of ventricular preload. Unfortunately, frequently the atrial conducting system is fairly shot by the time you get your dual-chamber pacemaker. The atria may be very dilated by this stage, and their contractility may be impaired by fibrosis. A specific situation where atrial pacing is very beneficial is functional mitral regurgitation, where the dilated noncontractile atrium stretches open the mitral valve annulus and increases the severity of MR: in this context, maintaining a sinus rhythm could produce some benefit by decreasing or reversing the MR, thereby maintaining haemodynamic stability (Al Qahtani et al, 2019).
Realistically, you can do little about this variable. Ventricular compliance in the standard heart failure patient is not amenable to any specific therapy. A stupid-level answer to this question would be "keep them from infarcting"; an ischaemic LV is much less compliant than a healthy one (Bardet et al, 1977). Obviously, sometimes there are easily reversible compliance problems (for instance, a pericardial effusion which could be drained) but this is not something you can routinely rely upon. In the context of recent cardiothoracic surgery you could even open the chest and allow the pericardial sack to remain open, which is the ultimate compliance-improving trick.
In the presence of severe diastolic heart failure, one may be able to improve diastolic function (or at least prevent a deterioration in diastolic function) by manipulating the lusitropy, i.e. the relaxation of the myocardium. This is an active process which is mediated by the removal of calcium from the cell, and depends on SERCA proteins. Generally, positive lusitropy is viewed as a property of catecholamine inotropes, which phosphorylate phosphholamban (thus stimulating the removal of calcium from the cytosol and into the sarcoplasmic reticulum by SERCA), and troponin-I, (thus inhibiting calcium interaction with troponin-C). It is hard to track down precisely which papers this comes from, but it is reproduced in Kam (Principles of Physiology for the Anaesthetist) and in Achilles Pappano and Withrow Weir's Cardiovascular Physiology. It is a property observed with β-agonists such as dobutamine; for example Parker et al (1991) were able to demonstrate "significant acceleration of isovolumetric relaxation" in patients both with normal LV function and with CCF. Conversely, β-blockers tend to inhibit lusitropy.
Afterload can be reduced by arterial vasodilators such as ACE-inhibitors, nitroprusside, hydralazine, and numerous others. the whole point is to achieve an increase in cardiac output without any additional myocardial workload. Unfortunately, there is only so far you can push this: it is important to maintain some blood pressure, so as to maintain a gradient for flow into capillary beds. It is also important to maintain a certain diastolic pressure to ensure coronary arterial perfusion
ACE-inhibitors and angiotensin II receptor blockers (ARBS) earn a Class I recommendation from the AHA. This recommendation rides on the back of many trials. For instance, The CONSENSUS study (1988) demonstrated an improvement in both mortality and NYHA grade with the use of enalapril, which is one of the drugs asked about in Question 14 from the first paper of 2000. These drugs have been placed in the "afterload reduction" basket, but in actual fact their mortality benefit may be due to their influence on cardiac remodelling. Other drugs with purely afterload-reducing effects would include prazocin and hydralazine. An ancient article (Mason, 1978) reports that the effect of these drugs is to increase cardiac output and reduce the symptoms of fatigue.
This strategy has benefits in the context of mitral regurgitation, where forward flow is improved by decreasing systemic vascular resistance (Stevenson et al, 1990). It is effective even in aortic stenosis (mild and moderate AS will still benefit, according to a 1980s paper by Greenberg et al). In severe AS, no amount of fiddling with peripheral resistance will be of any benefit: the limiting resistance is at the level of the valve.
In order to improve forward flow in right heart failure, a pulmonary vasodilator is sometimes used. The modern arsenal consists of nitric oxide, prostacycline, bosentan and sildenafil. On a slightly different shelf one may place milrinone and levosimendan, which will dilate the pulmonary circulation along with the systemic.
Oxygen: The pursuit of normoxia is of some importance. Hypoxic pulmonary vasoconstriction is to be avoided; oxygen is a cheap and easy way to optimise pulmonary vascular resistance. Lahn et al (2010) recommend aiming for an SpO2 in excess of 92%.
Avoidance of excessive PEEP: all positive respiratory pressure is transmitted to the pulmonary circulation and is counterproductive in right heart failure. It adds to afterload and is to be avoided. Typically, these people do not have any indications for high pressure mechanical ventilation (unless ARDS is their primary pathology). Ask yousrelf: am I doing this person any favours by continuing to ventilate them? Would they be better off try it themselves on some high-flow nasal prongs?
Avoidance of hypercapnea: In the weird backwards-world of the pulmonary circulation, everything that normally causes vessel dilation has the opposite effect. CO2 increases pulmonary arterial pressure and RV afterload. After 4 hours of hypercapnea (created experimentally with an FiCO2 of 10mmHg) healthy volunteers had an increase in PA pressure from 22mmHg to 32mmHg (Balanos et al, 2003).
Pulmonary vasodilators: Of these, the ones in common use are inhaled prostacycline, inhaled nitric oxide and systemic sildenafil. Of nitric oxide, a 2015 review by Benedetto et al writes "this remarkable story has experienced a roller-coaster ride with high hopes and nearly universal demonstration of physiological benefits but disappointing translation of these benefits to harder clinical outcomes". Inhaled nitric oxide can sure dilate some porcine pulmonary arteries, but it doesn't seem to save lives. Presently, the only guidelines supporting its use are feeble expert recommendations from Europe.
Digoxin may improve contractility, and may control the rate of AF with atrial systolic benefits. In the ICU, digoxin is frequently inappropriate as a rate control agent for AF because of its ineffectiveness in the presence of increased sympathetic tone. However, it may have a role to play as a positive inotrope irrespective of the underlying rhythm. In the community, digoxin does appear to improve the symptoms of heart failure, even in people who are in sinus rhythm, though it does not seem to decrease mortality. Specifically, hospitalisation rates were improved. Digoxin is probably the only orally bioavailable inotrope in the current repertoire. All others (eg. the ill-fated attempt to feed milrinone to outpatients) have failed hideously. Inotropes for cardiogenic shock are discussed elsewhere.
The AHA recommend cardiac resynchronisation therapy (CRT) for patients who have an LVEF less than 35% and a LBBB with a QRS duration of greater than 150 msec. CRT in this group may improve ventricular contractile function, diminish secondary mitral regurgitation, and reverse ventricular remodeling.
This broad topic includes such weirdness as the hormonal contribution to cardiac function (eg. from insulin, glucagon, thyroxine) as well as the all-important maintenance of the various electrolyte gradients. The AHA makes statements to scoff at diet modification or supplements, but the situation is very different at the ICU level. Critically ill patients have enough reasons to have impaired cardiac metabolism and their endocrinology is deranged. They may be septic and their cardiac mitochondria may have been disabled by cytokines and endotoxin. They may have a relative adrenal insufficiency. Thiamine deficiency or hypothyroidism may be occult in this population. In short, anything is worth a try.
The following list of correctable negatively inotropic metabolic variables is offered in Oh's Manual. To the canonic list, the author has added a few italicised variables.
Let us say you have a "fixed" cardiac output. That cardiac output will increase by 30% if we increase your heart rate from 70 to 90. The temporary pacemaker is an ideal device for this, because it does not have the side-effects of chronotropic drugs. Similarly, controlling an unnaturally high rate (eg. the 150 bpms of 2:1 conducted atrial flutter) is beneficial as it will improve diastolic filling.
Heart failure is by definition the failure fo the heart to produce a cardiac output which satisfies the body's needs. If one can do nothing about the cardiac output, it is therefore logical to make changes to the demand side of the equation. One may begin with beta-educing the demand for cardic output comes in several flavours, and included sedation, paralysis, hypothermia, and the use of mechanical ventilation.