2   Why has Mr D gone into LVEF following his AMI?

3   What is an LVEF?

4   What is the significance of determining LVEF following an echocardiogram and potential future events?

5   Describe the mode of action of IV nitrates

6   Explain the contraindications of giving IV nitrates to a person with acute left ventricular failure

7   What is the mode of action of frusemide?

8   What are the benefits of giving IV frusemide in left ventricular failure?

9   What are opioids?

10   What is the significance of using IV diamorphine in acute left ventricular failure?

11   What likely side-effects should the nurse anticipate?

ANSWERS

1 Prior to Mr D’s acute AMI, how would his heart have worked as a pump?

A Normal cardiac output (CO) is the product of heart rate (HR) and stroke volume (SV). HR is determined by the rate of spontaneous firing at the sinoatrial node but can be modified by the autonomic nervous system. The vagus nerve acts on muscarinic receptors to slow the heart, whereas the cardiac sympathetic fibres stimulate beta adrenergic receptors and increase HR. Stroke volume is determined by three main factors:

•   preload;

•   afterload;

•   contractility.

Preload is the stretching of the muscle fibres in the ventricles (both right and left). This stretching results from blood volume in the ventricles at end diastole (the relaxation filling period of the cardiac cycle). According to Starling’s Law, the more the heart muscle stretches during diastole, the more forcefully it contracts during systole (the contraction phase of the cardiac cycle). Think of preload as being like a balloon stretching as air is blown into it – the more air blown into the balloon the greater the stretch.

AFTERLOAD

This is the resistance to ventricular ejection and is caused by resistance to flow in the systemic circulation, referred to as systemic vascular resistance. This is determined by the diameter of the arterioles and pre-capillary sphincters – the narrower or more constricted, the higher the resistance. The level of systemic vascular resistance is controlled by the sympathetic system which, in turn, controls the tone of the muscle in the wall of the arterioles, and hence the diameter.

CONTRACTILITY

Contractility refers to the inherent ability of the myocardium to contract normally. Contractility is the amount of stretch present in the myocardium muscle fibres at the end of diastole. This is also influenced by preload. So in effect if returned blood flow to the right side of the heart is compromised in any way then ultimately this will have an effect on the amount of blood returning to the left side of the heart. This can affect afterload (Barrett et al. 2009).

As the heart is a closed system it needs to function effectively and requires that both sides pump the same amount of blood over time. If the output of the left heart ventricle were to fall below that of the right, blood would accumulate in the pulmonary circulation. Likewise if the right side were to pump less efficiently than the left then blood would accumulate in the systemic system (Porth 2011).

2 Why has Mr D gone into LVEF following his AMI?

A Mr D has been diagnosed and treated for an AMI. Any occlusion of the anterior descending branch of the left coronary artery can lead to an anterior wall infarction (death of muscle tissue). This occurs if the heart muscle is starved of rich oxygenated blood and as a result the portion of the muscle that has been occluded dies (necrosis). This is affecting Mr D’s heart’s pumping ability.

Because the left ventricle has the largest coronary blood supply, it is the most likely to be involved in MI. Any damage to the left ventricular myocardium through infarction leads to reduced contractility and abnormal movements of the walls of the ventricle (akinetic and hypokinetic contraction); this has had a greater significance as Mr D also has a history of hypertension.

The result is reduced cardiac output or a need for the ventricle to increase its workload to maintain the same cardiac output. This in turn can lead to an increase in muscle bulk (hypertrophy) or an enlargement of the chamber itself (dilation). These physical changes are known as ‘remodelling’ and although they are a compensatory mechanism the result can be a negative effect as the ventricle becomes overstretched and the fibres lose their elasticity. Further, a dilated heart can also change the shape of the atrioventricular valves, which can in turn lead to regurgitation (Nicholson 2007).

Left-sided heart failure associated with elevated pulmonary venous pressure and decreased cardiac output explain Mr D’s situation – he is presenting with breathlessness, weakness, pulmonary congestion and associated confusion (Woods et al. 2010).

3 What is an LVEF?

A As Mr D has a diagnosis of left ventricular systolic dysfunction (LVSD) the pumping action of his heart is reduced, weakened and/or compromised. This can be quite common following an AMI. A common clinical measurement of the left ventricle, via an echocardiogram, is LVEF.

•   The LVEF is a calculation of how much blood is ejected out of the left ventricle (stroke volume), divided by the maximum volume remaining in the left ventricle at the end of diastole (when the heart relaxes).

•   A normal LVEF in a healthy person is around 55–75%. Left ventricular systolic heart failure shows as a decreased fraction of <50%.

•   Mr D has been diagnosed as having an LVEF of 40%. At anything less than 50% his heart can start to have serious problems with its pumping ability, as a direct consequence of his MI (NICE 2010).

The final action of these drugs is that they dilate the coronary arteries, thereby increasing blood and oxygen supply to the myocardium (Nicholson 2007). For IV administration the starting dose should be low and increased gradually until relief of symptoms is achieved or blood pressure is adversely affected. As IV nitrates are vasodilators it is an important part of nursing care that blood pressure is monitored closely and that IV nitrates are adjusted accordingly. The systolic blood pressure should not drop by >20mmHg and if it does then the dose should be reduced if the systolic blood pressure is <100mmHg. A diastolic blood pressure of >60mmHg is necessary for adequate coronary artery perfusion.

Gardner et al. (2008) clarify that there is evidence that the combination of IV nitrates and frusemide is superior to high-dose diuretic treatment alone in the management of pulmonary oedema.

6 Explain the contraindications of giving IV nitrates to a person with acute left ventricular failure

A The contraindications of giving IV nitrates to a person with acute left ventricular failure are that they can cause hypotension (low blood pressure) as a consequence of vasodilation. The supply of blood to the heart is dependent on blood pressure remaining above a critical level; this means that a sufficient pressure to force blood into the coronary arteries is maintained. If it falls below the critical level the heart becomes short of oxygen and this can lead to chest pain. As a person ages a low blood pressure can reduce cerebral blood flow which can ultimately lead to impaired functioning of the brain and confusion (Jordan 2009).

7 What is the mode of action of frusemide?

A Frusemide belongs to a group of drugs called diuretics. Their mechanism of action is to work on the kidneys to increase urine volume by reducing salt and water reabsorption from the tubules (BNF 2012). There are several different sodium channels that exist in the renal tubules and, because of this, different diuretic drugs act at different sites along the tubule, providing different molecular actions and clinical side-effects (Dawson et al. 2005). Frusemide is a loop diuretic which acts at the thick ascending segment of the Loop of Henle, which eventually leads into the distal tubule.

Frusemide can cause the excretion of 15–25% of filtered sodium as opposed to the normal 1% or less. This action alone can result in profound diuresis (remember that where sodium goes, water will follow it). The mechanism of action of loop diuretics is that they inhibit the sodium/potassium/chloride co-transporter in the luminal membrane which inevitably increases the amount of sodium reaching the collecting duct. Because of this there is an increase in potassium and proton secretion. Loop diuretics have a venodilatory action which is renowned for bringing relief of clinical symptoms such as acute pulmonary oedema and heart failure in as little as 30 minutes by the IV route (NICE 2010).

A The benefit of giving IV frusemide to a patient like Mr D with acute left ventricular failure is that if the patient is showing signs of fluid retention (pulmonary oedema) and is acutely unwell the dose of diuretic can be titrated up quickly to achieve the desired effect (DH 2000). Another benefit is that by removing excess water and by causing vasodilation, the pressure on the heart (preload) is inevitably reduced and consequently the heart is not put under as much strain. This can lead to a marked reduction in breathlessness (Nicholson 2007).

As with any drug there are always some side-effects and the main ones for frusemide are:

•   hypotension;

•   hypokalaemia;

•   hyponatraemia;

•   hypovolaemia;

•   hyperuricaemia.

9 What are opioids?

A

•   Opioids are drugs that are either naturally occurring (e.g. morphine) or chemically synthesized. They work by interacting with specific opioid receptors to produce the pharmacological effect of analgesia.

•   They are also considered to be anxiolytic (reduce anxiety) and are likened to endorphins and encephalins, which are the body’s mood changers and analgesics in time of great stress.

•   Sometimes, sedation, mental detachment or euphoria are the predominant effects of a dose of diamorphine (BNF 2012).

10 What is the significance of using IV diamorphine in acute left ventricular failure?

A As Mr D has gone into acute heart failure, the left ventricle fails and afterload increases. Pressure then rises in the left atrium and left ventricle, while hydrostatic pressure rises and fluid is forced out into the lung tissues, leading to pulmonary oedema. Opioids have a venodilatory effect, and because of this they can be used to reduce afterload. They also have the effect of making the patient feel calmer and dissociated from their body.

When a patient goes into acute MI like Mr D they appear very distressed due to their breathlessness, which can make them feel totally out of control. At this time their ‘fight and flight’ response becomes activated, which makes them feel worse. Administering IV diamorphine calms the patient, allowing time for the nitrates and diuretics to take effect (Nicholson 2007).

11 What likely side-effects should the nurse anticipate?

A Some of the adverse side effects of diamorphine include:

•   reduction in sensitivity of the respiratory centre to CO₂, which can lead to shallow and slow respirations and should be monitored carefully;

•   hypotension and reduced cardiac output;

•   activation of the vomiting centre due to stimulation of the chemoreceptor trigger zone (CTZ) – an antiemetic such as cyclizine should also be administered (Dawson et al. 2005).