VOL: 97, ISSUE: 17, PAGE NO: 36
Mandy Sheppard, RGN, is an independent training and development consultant
The key function of the heart is to pump oxygenated blood from the lungs to all the body cells via the left side of the heart and arterial circulation.
The cells use the oxygen to perform cell function. The main waste product of that cell function is carbon dioxide and that returns via the venous circulation to the right side of the heart and ultimately the lungs.
There are two main prerequisites to enable the heart to circulate blood around the body. One is that there is an adequate circulating volume, for example, the patient is not hypovolaemic. The second is the ability of the heart to pump that fluid, in other words, how well the heart muscle can contract (contractility). The two act in partnership: a good pump is of little value where there is insufficient fluid. Equally, a good circulating volume will be of little value without a pump to move it around. A deficiency in either can produce the clinical signs of poor perfusion: hypotension, compensatory tachycardia and peripheral vasoconstriction and oliguria.
Inotropic drugs (‘inotropes’) have the ability to alter the contractility of cardiac muscle, which will subsequently influence how effectively the heart can pump.
There are inotropic drugs that can improve cardiac contractility and therefore perfusion, for example dobutamine, dopexamine or adrenaline. These are known as positive inotropes. There are also drugs, given for other purposes, which as a side-effect can have a detrimental effect on contractility. These are known as negative inotropes and examples include beta-blockers and calcium antagonists. Only positive inotropes will be discussed here.
How inotropes work
Inotropes stimulate receptors that are part of the sympathetic nervous system. There are three main types of receptor which, when stimulated, have specific actions (Table 1).
Inotropes are primarily given for the beta-1 effect of increased contractility, but different inotropes have varying effects on the other receptors. For example, adrenaline does achieve increased contractility (beta-1) but, particularly at higher doses, also stimulates the alpha-receptors and may cause peripheral vasoconstriction. But in addition to achieving increased contractility (beta-1), dobutamine can stimulate the beta-2 receptors and cause vasodilation. This is an important phenomenon for nurses to appreciate for two main reasons. First, to recognise that a change in the patient’s condition - for example, the development of cool peripheries - may be purely a side-effect of the inotrope causing vasoconstriction or may signal a deterioration in perfusion for other reasons. Second, some patients may poorly tolerate some side-effects. For example, patients with existing poor cardiac function may find it difficult to maintain haemodynamic stability in the presence of an increased heart rate. The varying effects of inotropes on the different receptors may influence the choice of inotrope used in certain patients.
Key points of inotrope therapy
1. Inotropes have an extremely short half-life. Consequently, they can be given only as continuous infusions and should never be stopped abruptly, but should be decreased gradually;
2. The clinical features of hypotension, tachycardia, oliguria and decreased perfusion can be the result of hypovolaemia, inadequate cardiac function or a combination of both. Before starting inotrope therapy, hypovolaemia must be excluded and if necessary the patient should be fluid resuscitated;
3. When starting inotrope therapy, the dose should be increased until the desired effect is achieved, as opposed to starting with a high dose and decreasing it until the effect is maintained;
4. As the drugs are titrated to the effect on blood pressure and perfusion, the method of administration has to be accurate and requires an infusion device and a dedicated infusion line;
5. Most inotropes have to be given via a central line because of their vasoconstrictive nature which, if peripheral extravasation occurs, can cause local tissue necrosis. However, some can be further diluted and given peripherally. One disadvantage of this method of administration is that the dilution required may result in the patient receiving an unwanted volume of fluid merely to deliver the drug;
6. All cells require oxygen to function and myocardial muscle cells are no exception. When the heart is required to work harder, by increasing contractility and/or heart rate with inotropes, the cells will require more oxygen to do so. This is known as increased myocardial oxygen demand. When caring for patients receiving inotrope therapy, it is important where possible to meet that increased demand for oxygen by maintaining arterial oxygen saturations, with respiratory interventions if necessary, and ensuring adequate haemoglobin levels to transport the oxygen;
7. As inotropes exert an effect on receptors, which in turn can affect cardiac contractility and heart rate, patients must be closely observed and monitored to (a) titrate therapy and (b) identify any side-effects. The following are minimum monitoring requirements:
- Electrocardiograph (ECG) monitoring for heart rate and rhythm;
- Blood-pressure monitoring - minimum of non-invasive blood pressure (NIBP) but some patients may require continuous arterial blood-pressure monitoring;
- Accurate fluid intake and output records;
- Patient observation for peripheral perfusion and temperature, and level of consciousness;
- Pulse oximetry (to be used with caution if the patient has reduced peripheral perfusion);
- General cardiorespiratory observations including blood-glucose estimations.
Inotropes are normally prescribed as micrograms per kilogram of body weight per minute - mcg/kg/min. There are many types of calculation that can be used. One example is shown in Box 1.
Lew Hick, 66, was transferred to a medical ward from the coronary care unit (CCU) where he had been for three days after a myocardial infarction. On transfer Mr Hick was warm and well perfused. His pulse was 85bpm and regular, his blood pressure 130/90. He was also attached to a pulse oximeter with a saturation reading of 97%. He had a peripheral venflon in situ. He had no relevant medical history and his progress in the CCU had been uneventful.
Four hours after transfer Mr Hick deteriorated. His heart rate increased to 120bpm and he looked pale, with beads of sweat on his forehead. His hands and feet were cold to the touch. He did not complain of chest pain. Since being in hospital he had been passing urine into a bottle. A urinary catheter had been inserted while he was in the CCU, but he found it uncomfortable and became agitated so it was removed.
Mr Hick had not passed urine since arriving on the ward and felt no desire to do so. A blood-pressure reading revealed hypotension at 90/65mmHg. His saturations had dropped to 91%, but the signal was poor because of reduced peripheral perfusion. A 12-lead electrocardiogram was performed but was inconclusive. Mr Hick was attached to an ECG monitor and given oxygen.
The CCU had no empty beds and none of the patients could be transferred so it was decided that Mr Hick would be treated on the ward with inotropes to support his blood pressure while investigations and tests were performed to determine the cause of his sudden deterioration. A central line was inserted under aseptic conditions into his right internal jugular vein. A chest X-ray confirmed correct positioning and there was no evidence of a pneumothorax after the insertion.
Dobutamine was prescribed to start at 2.5mcg/kg/min, administered via a syringe driver with a 50ml syringe. The dobutamine was supplied in 20ml vials which contain 250mg of the drug, which was then further diluted with 30ml of 5% dextrose. This provides 250mg of dobutamine in 50ml of fluid, that is 5mg/ml or 5,000 mcg/ml. Mr Hick’s weight was 80kg. The calculation was as follows: 80kg (Mr Hick’s weight) x 2.5 (dose of drug in mcg/kg/min) x 60 divided by 5,000 (concentration of drug in mcg/ml) equals 2.4ml/hr.
The syringe was labelled and an infusion line was attached which was primed with the solution. The syringe was then inserted into the syringe driver, which was set at 2.4ml/hr. The infusion line was labelled ‘dobutamine’ to avoid other drugs or infusions being given into the central line which would deliver a bolus of the inotrope. Mr Hick’s heart rate and rhythm were continuously monitored and his blood pressure taken every five minutes.
After 10 minutes, his blood pressure had not changed and it was decided to increase the dose to 5mcg/min which, using the above calculation, meant the infusion rate had to be increased to 4.8ml/hr. This resulted in a decrease in Mr Hick’s blood pressure to 85/55mmHg. It was felt that this was due to the vasodilating effects of dobutamine and although Mr Hick had been assessed before starting the infusion and it had been agreed that he had an adequate circulating volume, 200ml of Gelofusine, a plasma expander, was rapidly infused via the peripheral venflon. This resulted in an improvement and his blood pressure increased to 125/85mmHg. After a further 10 minutes, his blood pressure remained between 120-125/75-85mmHg and it was agreed to maintain the dobutamine dose at 5mcg/kg/min.
Mr Hick’s heart rate settled between 80-95bpm and as his peripheral perfusion improved it was decided to attach a pulse oximeter probe. His blood glucose was measured every four to six hours (inotropes can sometimes cause high blood-glucose levels) and a strict fluid balance chart was maintained.
To minimise myocardial oxygen demand, measures such as bedrest, placing items within reach and avoiding any anxiety or distress triggers, such as pain or worry, were incorporated into the care plan. A pressure area risk assessment was done as Mr Hick was on bedrest and had had a period of reduced peripheral circulation.
- The patient’s name has been changed