5: A systems approach

Section 5 A systems approach

In this section some common medical and surgical conditions that you will meet on the wards are considered and care and management of the patient is discussed. In some areas a problem-solving approach has been used and the care planned in a little more detail following the activities of living. Using these examples as a guide, you will be able to plan the care for other patients using this section.

5.1 The cardiovascular system

More than 40% of patients admitted to medical wards in the United Kingdom have some form of cardiovascular disease and more than 1 in 3 people in the UK die from cardiovascular disease (CVD). Death rates from CVD in those under 75 years of age have fallen by 38% since 1995. Cardiovascular disease includes:

Myocardial infarction.

Cardiac arrhythmias.

Ischaemic heart disease (IHD) or coronary heart disease (CHD) is caused by an inadequate blood flow via the coronary arteries to the heart muscle. This leads to angina and possibly a myocardial infarction. Deaths from CHD in the UK have halved since 1988 but in 2008, 88 000 people still died in the UK from CHD (British Heart Foundation 2011). CHD accounts for approximately 40% of all deaths in the developed world.

CHD is usually due to a narrowing caused by deposits of atheroma (fatty plaques) in the coronary arteries. These plaques may rupture and cause complete occlusion to a coronary artery resulting in death of the myocardial muscle and a myocardial infarction.

Hypertension

Hypertension is a raised blood pressure and is present in about 1 in 3 of the UK population over 55 years of age. Many of the patients you nurse are likely to be on medication to reduce their blood pressure. A blood pressure of 135/85 or below is regarded as normal by the World Health Organization (WHO).

Hypertension is a most important risk factor for diseases of the cardiovascular system, including stroke, coronary heart disease and peripheral vascular disease. Diseases of the cardiovascular system kill more people in Britain than all other causes of death combined and hypertension is sometimes called the ‘silent killer’.

Patients have raised blood pressures and feel well. They may have no symptoms but the raised blood pressure may be slowly damaging their bodies. The risk to the person rises progressively as the blood pressure rises. The patients that you nurse with cardiovascular disease (CVD) may have had raised blood pressure for many years.

The control of hypertension can lead to the prevention of its cardiovascular complications. A raised systolic blood pressure is now regarded as being more significant than a raised diastolic pressure as a risk factor for CVD and isolated systolic hypertension is associated with a two to three times greater death rate from heart disease (Table 5.1).

Table 5.1 British Hypertension Society (BHS) classification of blood pressure levels

Category	Systolic BP (mmHg)	Diastolic BP (mmHg)
Optimal BP	< 120	< 80
Normal BP	< 130	< 85
High normal BP	130–139	85–89
Grade 1 hypertension (mild)	140–159	90–99
Grade 2 hypertension (moderate)	160–179	100–109
Grade 3 hypertension (severe)	> 180	> 110
Isolated systolic hypertension (grade 1)	140–159	< 90
Isolated systolic hypertension (grade 2)	> 160	< 90

These levels will be at least 5 mmHg lower if ambulatory monitoring of blood pressure is used or home monitoring of blood pressure. The reader is referred to the full NICE guidelines on Hypertension.

In the vast majority of cases there is no definite cause of hypertension and the term essential or primary hypertension is used.

There are risk factors associated with essential hypertension and these include:

Genetic factors (high blood pressure tends to run in families).

Low birthweight.

High salt intake.

High alcohol intake.

Only in less than 10% of patients can a definite cause be found for the raised blood pressure. This is called secondary hypertension.

The commonest cause is kidney disease, especially diabetic nephropathy. Other causes are mostly endocrine and include:

Phaeochromocytoma (tumour of the adrenal medulla).

Conn’s syndrome (hyperaldosteronism).

Cushing’s disease (overactivity of the adrenal cortex or due to administration of long-term steroids).

Hyperthyroidism.

Acromegaly (excessive growth hormone in adulthood).

Hyperparathyroidism.

Malignant hypertension is a dangerous form of accelerated hypertension where the blood pressure rises rapidly and diastolic blood pressure is > 120 mmHg. This may lead to progressive kidney failure, retinal haemorrhages, heart failure, cerebral oedema and stroke. If no treatment is given less than 20% of these patients survive for 1 year.

Diagnosis

All adults should have their blood pressure checked at least every 5 years. In mild hypertension lifestyle changes alone may be recommended at first and these may include weight loss, reduction in salt intake, safe exercise, stopping smoking and stress reduction. In 2011, the NICE guidelines recommended the use of ambulatory blood pressure monitoring when diagnosing hypertension:

A blood pressure in the doctor’s surgery of 140/90 mmHg or more is followed by ambulatory blood pressure monitoring (ABPM) at home. If this is higher than 135/85 mmHg this is classed as Stage 1 hypertension.

Stage 2 hypertension is a clinic reading of 160/100 mmHg or higher followed by ABPM average of 150/95 mmHg.

In severe hypertension the clinic systolic BP is 180 mmHg or higher or the clinic diastolic BP is 110 mmHg or higher.

Medication

The British Hypertension Society (BHS) and the National Institute for Health and Clinical Excellence (NICE) have together issued guidelines on the pharmacological management of hypertension (www.nice.org.uk).

Step 1

For those younger than 55 years of age, angiotensin-converting enzyme (ACE) inhibitors, e.g. ramipril or an angiotensin receptor blocker (ARB) such as losartan (used if intolerance such as a cough with ACE-inhibitors) are the first-line treatment.

For those over 55 years of age or black patients of any age, calcium channel blockers, e.g. diltiazem, are the first-line therapy. If these are not suitable because of the presence of oedema, or intolerance or heart failure then a thiazide diuretic, e.g. chlortalidone or indapamide should be given rather than the conventional bendroflumethiazide.

Step 2

A CCB in combination with either an ACE inhibitor or an ARB.

Step 3

If the hypertension is not controlled further drugs are added to the regimen and a patient may be taking an ACE inhibitor or an ARB, a diuretic and a calcium channel blocker for hypertension.

Step 4

If still not controlled then an alpha-blocker such as doxazosin or a beta-blocker such as atenolol are added to the drugs already being taken.

Angiotensin-converting enzyme (ACE) inhibitors – these drugs block the formation of angiotensin II from angiotensin I that is manufactured from renin, produced by the kidney. As these drugs may cause a sudden drop in blood pressure, the first dose is given before going to bed at night. If the patient cannot tolerate an ACE inhibitor (usually due to the side-effect of a dry cough) then an angiotensin-II receptor blocker (antagonist) (ARB) such as losartan should be prescribed.

Diuretics – bendroflumethiazide was the commonest and a small dose of 2.5 mg daily is usually prescribed. This drug has some vasodilatory action. The current guidelines replace bendroflumethiazide with chlortalidone or indapamide.

Beta-blockers should not be given to patients with airway obstruction. The commonest drug used is atenolol which is a cardioselective beta-blocker commonly used in the treatment of angina.

Calcium antagonists – amlodipine is an example. These drugs cause vasodilatation and are also useful in clients with angina. Side-effects include headache and flushing.

Patients admitted with a very raised blood pressure will usually have this controlled slowly rather than giving drugs to act quickly by the intravenous route. The aim is to reduce the diastolic blood pressure to < 110 mmHg over approximately 24 hours.

Low blood pressure

Often a fall in blood pressure is more significant than the absolute value and monitoring of blood pressure is an activity that as a nurse you will be performing daily.

A sytolic blood pressure of less than 90 mmHg is considered low. A systolic BP less than 70 mmHg will:

Lead to reduced tissue perfusion throughout the body and a state of shock.

Reduce the blood supply to the heart.

Reduce renal blood flow and thus reduce urine output – leading to renal tubular necrosis.

Reduce blood flow to the brain and eventually lead to unconsciousness. It may result in permanent brain damage.

Causes of hypotension

Depletion in blood volume:

– Blood loss as a result of trauma, a leaking aneurysm, bleeding from the gastrointestinal tract or postoperatively

– Dehydration from any cause such as diabetic ketoacidosis and diarrhoea or vomiting

– Loss of serous fluid from severe burns.

– Myocardial infarction

– Pulmonary embolism (if very large)

– Depression of the myocardium due to acidosis or septicaemia

– Drugs that depress the contractility of the heart, e.g. beta-blockers.

Large fall in peripheral resistance:

– Septicaemia

– Peritonitis

– Pancreatitis

– Anaphylactic shock

– Neurogenic shock.

Management

This will depend on the cause of the hypotension.

Record observations of blood pressure, pulse and respirations as prescribed.

When the blood pressure is low, the pulse rate will usually be increased (tachycardia).

The respiratory rate may also be increased, as in acidosis or haemorrhage, but in severe instances the rate may be reduced and respirations may be shallow.

Fluid replacement may be commenced by intravenous infusion and a plasma expander such as Gelofusine may be given.

If blood has been lost the doctor will group and crossmatch the patient and order a transfusion.

The urine output has to be closely monitored as hypotension can lead to impaired renal function. It may be necessary to catheterize the patient if the urine output falls and it should remain above 30 ml per hour.

Oxygen may be prescribed.

The patient may be anxious and will need reassurance.

Investigations such as an electrocardiogram, chest X-ray and blood cultures to identify infection may be ordered.

Postural (orthostatic) hypotension

This is a drop in systolic blood pressure of at least 20 mmHg on standing from sitting or lying down positions.

Normally reflex actions compensate for changes in gravity on standing which could cause venous pooling. If the autonomic nervous system is not functioning so well, especially in the elderly, the sympathetic response may not occur. Postural hypotension may also occur for other reasons such as venous pooling in pregnancy, vasodilator drug action, prolonged immobility or a low blood volume such as may occur with diuretic use.

Postural hypotension is often accompanied by dizziness, blurring or loss of vision and fainting.

Coronary artery disease

This is due to coronary atherosclerosis and presents as stable angina or acute coronary syndrome (ACS). ACS includes unstable angina, ST elevation myocardial infarction (STEMI) and non ST elevation myocardial infarction (NSTEMI). The latter two are differentiated by the electrocardiogram (ECG) tracing.

Fatty atheromatous plaques are laid down on the endothelium of the arteries. They start as ‘fatty streaks’ and progress to cause narrowing of the vessel. The plaque may eventually leak and rupture, attracting platelets and forming a thrombus, resulting in a myocardial infarction.

The focus now is on primary prevention as we know that certain risk factors are associated with the development of atheroma. Some of these we are not able to change such as:

Family history.

Others we may be able to change with treatment. These include:

Raised blood cholesterol and lipids (hyperlipidaemia).

Diabetes mellitus.

Lack of exercise.

Diet high in saturated (animal) fats.

Moderate alcohol consumption (one or two drinks per day) is associated with a reduced risk of CAD but if intake is high the risk of CAD increases.

CVD risk level is now assessed using prediction charts that take into account the above risk factors. These charts are printed in the back of the British National Formulary (BNF) and are used to determine whether medication such as drugs to reduce cholesterol should be prescribed to those free of symptoms.

Those with symptoms of angina or previous heart attacks are at high risk and should be treated intensively to reduce further risk.

The National Service Framework (NSF) has set standards of care with the aim of reducing CAD-related deaths in the under-75-year age group by 40% by the year 2010. These guidelines are available on the Department of Health website at www.dh.gov.uk.

Angina pectoris

This is pain, usually in the chest, felt as a result of lack of blood supply (ischaemia) to the heart. There is a narrowing of the coronary vessels, usually due to deposits of atheroma but sometimes due to spasm. Coronary blood vessels usually need to be narrowed by at least 70% for the pain of angina to be felt.

Types of angina

Stable angina – ‘angina of effort’ – the commonest form.

Variant (Prinzmetal’s) angina – may occur at rest – usually due to spasm of a coronary artery.

Nocturnal angina – wakes the patient up – may occur with vivid dreams.

Unstable angina (see acute coronary syndrome) – rapidly worsening angina of recent onset or occurring at rest.

Clinical features of stable angina

The pain is usually in the chest but may extend down the left arm or both arms or into the neck and jaw.

Some patients may experience pain just in the arm, the neck, the jaw or the back.

It is usually described as a tightness or squeezing pain, gripping or a heavy discomfort.

The pain is brought on by exertion (angina of effort), excitement or extreme cold, all of which increase the oxygen demand of the myocardium.

The pain fades fairly rapidly on rest.

A glyceryl trinitrate (GTN) tablet sublingually or GTN spray buccally usually gets rid of the pain.

The pain will always occur after a similar amount of physical exertion.

The distribution of the pain will be the same each time but in more severe attacks it may extend further.

Sometimes the pain of angina is mild and the patient confuses it with heartburn or ignores it.

Management of stable angina

This patient is likely to be treated in the community and their condition will be explained to them. Stable angina has an annual mortality of less than 2% so the patient will be informed of the good prognosis.

General advice will aim to restore normal exercise capacity and will include:

Cessation of smoking.

Weight loss if necessary.

Treatment of hypertension if present.

Treatment of raised cholesterol levels if necessary.

Dietary advice on how to achieve a low saturated fat intake and a low salt intake.

Pharmacological management

Nitrates

These may be given in several forms and relieve the pain of angina by causing vasodilatation. They are coronary vasodilators but also reduce the work of the left ventricle by reducing venous return due to venodilatation. All nitrates may produce a troublesome headache.

GTN may be given as a tablet sublingually or as an aerosol spray. Its onset of action is very rapid, 1–2 minutes, and its duration of action is under 30 minutes. The spray has a longer storage life.

GTN may also be given in the form of a sustained-release transdermal patch where the GTN is absorbed through the skin.

Isosorbide mononitrate and isosorbide dinitrate are both longer-acting nitrates that are given once or twice daily.

Tolerance and reduced therapeutic effects may occur with prolonged use of long-acting nitrates, including transdermal patches. The patches should be removed for several consecutive hours in each 24-hour period to prevent this from happening.

Beta-blockers

Contraindicated in asthma, beta-blockers reduce the heart’s demand for oxygen and also reduce pulse rate and blood pressure.

An example of a general beta-blocker is propranolol, but cardioselective beta-blockers such as atenolol are usually used. These block the beta-1 receptors in the heart in preference to the beta-2 receptors found in other parts of the body, e.g. the bronchi, but are still not regarded as safe in those with asthma.

Calcium antagonists

These vasodilate and may be used in angina or hypertension. An example is amlodipine.

Aspirin

Used as an antiplatelet drug, aspirin prevents platelets sticking together and so reduces the chance of a thrombus (blood clot) and a coronary event.

All patients with angina should take aspirin 75 mg daily unless contraindicated.

Lipid-lowering drugs

As a raised low-density lipoprotein (LDL) cholesterol is a risk factor for CHD, statins such as atorvastatin are prescribed if the total cholesterol is above 4.8 mmol/l.

These drugs reduce the total cholesterol by inhibiting an enzyme in the liver that allows the manufacture of cholesterol from saturated fats.

Coronary angioplasty and stenting

Percutaneous transluminal coronary angioplasty (PTCA) is a procedure in which a segment of atheromatous artery is dilated by a balloon that has been introduced on the tip of a very thin catheter using X-ray fluoroscopy. Intra-coronary stents are usually inserted into the artery to prevent restenosis. These are thin wire-mesh structures that act as permanent linings to keep the coronary artery patent. Sometimes drug-eluting stents are used in a further attempt to prevent restenosis at the site of the stent. NICE has issued guidance on the use of stents in CAD and this is available on their website.

Surgical treatment of angina

Coronary artery bypass grafting

The narrowed coronary artery that is causing the angina is replaced by a graft usually taken from the internal mammary artery (less likely to narrow over time) or saphenous leg vein. Patients with severe three-vessel CAD can also be grafted. The number of CABG procedures annually in the UK has increased from 15 700 in 1991 to approximately 25 000 in 2010. The NSF for CHD set targets for revascularization rates by percutaneous coronary intervention (PCI) and coronary artery bypass grafting (CABG).

Acute coronary syndromes

This term is used to describe ST-elevation myocardial infarction (STEMI), non-ST-elevation myocardial infarction (NSTEMI) and unstable angina. The plaque is now rupturing or has eroded and platelet adhesion has occurred. Sometimes it is difficult to differentiate between unstable angina and a myocardial infarction – the term ACS is therefore used to describe both.

Cocaine is a powerful coronary vasoconstrictor and raises blood pressure and pulse rate. Cocaine users may present with chest pain and a minority may go on to ischaemia and infarction.

Unstable angina

More ominous symptoms than stable angina.

The episodes of pain are more frequent.

They may occur without obvious cause and at rest.

Some patients present atypically with pleuritic pain, indigestion or dyspnoea.

12-lead ECG may be normal in ACS but there may be ST depression and T-wave inversion.

The patient is admitted to hospital.

Urgent angiography is required for diagnosis and treatment in those in danger of progressing to myocardial infarction or death.

Anti-platelet drugs are vitally important. Aspirin is given but other anti-platelet drugs such as clopidogrel are additionally used.

Low-molecular-weight heparins such as enoxaparin are used as anticoagulants.

Beta-blockers may be given to reduce the demand of the heart for oxygen and nutrients.

Statins and ACE inhibitors are also routinely given in ACS and appear to stabilize the plaque.

Coronary revascularization is recommended.

Myocardial infarction (MI) occurs when the muscle cells in the myocardium die due to ischaemia. MI is diagnosed by the clinical history, a 12-lead ECG and biochemical markers such as troponin I and T and creatinine-kinase-MB that are raised.

ST elevation myocardial infarction

This is a heart attack or coronary thrombosis that presents with an ECG showing ST elevation. A blood clot (thrombus) occurs in one of the coronary arteries supplying the heart muscle with oxygen and nutrients. The lack of blood supply leads to death of the area supplied by that artery. The word ‘infarct’ means death.

In the UK someone has a heart attack approximately every 2 minutes and about 105 000 people die each year from heart attacks. Approximately half of these people die in the first hour following infarction. Death is usually due to cardiac arrhythmias and in hospital the patient will usually be nursed in a coronary care unit where members of staff are experienced and equipment is available. If an arrhythmia occurs, it can be treated immediately and DC countershock administered in ventricular fibrillation if needed.

Clinical features

Chest pain which is tight or crushing in nature; 80% of patients have this.

The pain may be similar to that of angina, but more severe.

The pain lasts longer than angina – usually more than 20 minutes.

Pain may radiate to the arms, throat and jaw.

The pain may not respond to sublingual GTN and morphine is usually needed.

Nausea and vomiting may occur.

Always ask patients about the type of pain they have – their vocabulary may help to confirm the diagnosis.

The elderly or diabetic patient may sometimes have a ‘silent’ MI where no chest pain is experienced and the symptoms are atypical – dyspnoea, fatigue and syncope may be present.

Early medical management

The patient is likely to be very frightened so the nurse will need to offer reassurance, using a calm and confident manner.

The main aim is revascularization:

A 12-lead ECG should be done as soon as the patient is admitted. If this baseline ECG is normal (rare) it should be repeated every 15 minutes for as long as the patient is still in pain.

The patient will be connected to a cardiac monitor for immediate detection of cardiac arrhythmias. These are common following a STEMI.

An intravenous cannula will be inserted to allow drugs to be given easily and immediately.

Blood samples will be taken for cardiac markers (see below), full blood count (FBC), biochemistry, lipids and glucose.

Analgesia will be given as needed to try to keep the patient pain free. This is likely to be IV diamorphine 2.5–5 mg and an anti-emetic if needed, e.g. metoclopramide 10 mg.

The patient will be made comfortable using the headrest and pillows.

Oxygen may be prescribed if the oxygen saturation measured by pulse oximetry is below 94% (British Thoracic Society Guidelines).

Observations of blood pressure and pulse will be monitored half hourly at first.

It is important that the blocked coronary artery be made patent again as soon as possible and blood flow re-established to the cardiac muscle. The first choice is primary PCI (percutaneous coronary intervention) by angioplasty if available, but if angioplasy is not available a fibrinolytic drug (‘clotbuster’) will be commenced as soon as possible unless there are any contraindications.

The first thrombolytic drug was streptokinase, derived from bacteria. This means the drug can only be used once as the body makes antibodies that render it ineffective when administered a second time.

Other genetically engineered alternatives, e.g. alteplase or tenecteplase are now more frequently used. Tenecteplase has the advantage of only needing one bolus dose.

Contraindications for the use of fibrinolytics include recent haemorrhage, trauma or surgery, history of cerebrovascular disease, severe hypertension, history of peptic ulceration and pregnancy.

It is important to observe for any signs of bleeding when the patient is on thrombolytics.

Cardiac markers of myocardial necrosis

These are substances that are released into the bloodstream by the damaged myocardium and may be measured by biochemical assays.

Examples are cardiac troponins I and T and creatinine kinase (CK).

They rise following cardiac damage and this may confirm the diagnosis of myocardial infarction.

CK is a relatively non-specific marker as it is also released by damaged skeletal muscle. It peaks within 24 hours of MI and falls back to baseline in 48 hours.

Troponins are highly specific to damaged cardiac muscle although they may be undetectable within the first 12 hours of the MI (see Table 2.4).

If troponin is within normal limits 18 hours after the onset of the chest pain, an acute myocardial infarction (either STEMI or NSTEMI) can be discounted.

Aspirin

Aspirin 75 mg daily has been shown to reduce mortality following an MI and also to work in an additive manner with thrombolytics in the prevention of a second MI.

Clopidogrel is another antiplatelet drug that is administered alongside low-dose aspirin in acute coronary syndrome. The drug is continued for up to 1 year.

Heparin

Heparin is an anticoagulant that works rapidly but has a short duration. It is used in the treatment of pulmonary embolism and deep venous thrombosis but may also be used in ACS.

Low-molecular-weight heparins (LMWHs) are usually used and they are admisistered once daily by subcutaneous injection. Examples include dalteparin (Fragmin®) and enoxaparin (Clexane®).

Cardiac arrhythmias

Cardiac arrhythmia is the commonest and most lethal complication of an MI. The most dangerous irregularity is ventricular fibrillation (VF) which constitutes a cardiac arrest. This is shown in Figure 5.1. Immediate treatment of VF using defibrillation (DC shock) may be lifesaving.

Fig. 5.1 Ventricular fibrillation.

From Hampton/The ECG Made Easy, Elsevier 2003, reproduced with permission.

Drugs used to treat cardiac arrhythmias include the following:

Amiodarone – used in atrial fibrillation and other supraventricular arrhythmias but also ventricular arrhythmias including non-responsive ventricular tachycardia. Amiodarone should be given by a central line if possible when given intravenously.

Lidocaine – used in ventricular arrhythmias, including ventricular tachycardia.

Digoxin – used in atrial fibrillation.

Adenosine – extremely short-acting drug useful in paroxysmal supraventricular tachycardia but often used as an aid to the diagnosis of broad or narrow complex supraventricular tachycardias.

Verapamil – a calcium antagonist that is occasionally used in supraventricular tachycardias. It must not be given to a patient who is being treated with a beta-blocker as both drugs reduce the force of cardiac contractions.

Beta-blockers – act mainly by decreasing the effects of the sympathetic nervous system on the heart. They may be used with digoxin to control the ventricular response in atrial fibrillation and are also useful in some forms of supraventricular tachycardia. Esmolol and sotalol are examples.

Atropine – used to treat bradyarrhythmias (slow rate), although a pacemaker may sometimes be needed.

There are many different cardiac arrhythmias which may follow an MI. When you work in CCU, collect the rhythm strips from several patients, label them correctly and point out their identifying features. Note the treatment of the arrhythmia.

Acute MI is commonly associated with fatal dysrhythmias and the detection and treatment of these was the primary reason for the creation of CCUs. Dysrhythmias may occur because of abnormal impulse formation, abnormal conduction or ectopic activity.

Following an MI patients invariably show overactivity of the autonomic nervous system. Parasympathetic overactivity is common after an inferior or posterior MI. Sympathetic overactivity (tachycardia and transient hypertension) may be present in nearly half of all patients (especially with anterior MI) and lowers the threshold for ventricular fibrillation.

Different cardiac arrhythmias and their causes are shown in Table 5.2.

Table 5.2 Causes of different cardiac arrhythmias

Abnormal impulse formation and ectopic beats	Conduction disturbances
At the sinus node Sinus arrhythmia Sinus bradycardia Sinus tachycardia Sinus arrest	In the sinus node SA block
In the atria Atrial ectopic beats Atrial tachycardia Atrial fibrillation Atrial flutter Wandering atrial pacemaker	In the AV node First- second- and third-degree AV block
In the AV node Nodal ectopic beats Junctional rhythm Junctional tachycardia	In the bundle of His Left bundle branch block Right bundle branch block Left anterior and posterior hemiblocks
In the ventricles Ventricular ectopic beats Idioventricular rhythm Ventricular tachycardia Ventricular fibrillation	Others Intra-atrial block Ventricular pre-excitation Atrioventricular dissociation

Consequences of cardiac dysrhythmias

Impairment of circulation or myocardial oxygenation has consequences that are extremely variable but are more pronounced in the presence of cardiac disease.

The healthy heart can withstand many abnormal rhythms. The diseased heart cannot and sustained tachycardias may lead to circulatory collapse or ischaemic pain.

Management of acute dysrhythmias aims:

To restore normal sinus rhythm.

To prevent recurrence of the dysrhythmia.

Establishment of sinus rhythm is not always possible (e.g. in atrial fibrillation) and treatment is then designed to slow the ventricular rate and improve cardiac output.

Sinus bradycardia

Sinus rhythm slower than 60 beats per minute during the day or 50 beats per minute in the night.

Bradycardia occurs in about 30% of patients following MI.

Normally indicates parasympathetic overactivity, with release of acetylcholine from autonomic fibres in the atria and AV node.

Afferent vagal fibres are more common on the inferior surface of the heart and inferior MI is complicated more by this. Slowing of the heart is useful and protective in that it limits myocardial work but may result in hypotension secondary to a reduced output. Coronary perfusion may also be reduced.

Usually symptomless but sudden onset of bradycardia may result in hypotension with dizziness or syncope.

Causes include:

Hypothermia, hypothyroidism, raised intracranial pressure.

Drug therapy with beta-blockers, digitalis or other antiarrhythmics.

Acute ischaemia and infarction.

Chronic degenerative causes.

Junctional bradycardia

If the sinus node fails to initiate an impulse and there are no other focuses in the atria, the AV junction takes over the pacemaker function.

Most commonly occurs after acute MI, particularly if the patient is hypoxic or acidotic.

Relatively slow (40–60 beats per minute) but sometimes may speed up and junctional tachycardia (>100) may occur.

Heart block

This is a block to the conduction of impulses and may occur at any point in the conducting system of the heart.

Atrioventricular block is a block either in the atrioventricular (AV) node or the bundle of His (atrioventricular bundle).

A block lower down in the conducting system is bundle branch block and this occurs in the bundle of His either in the right or left bundle branches. Various conduction disturbances can occur and are usually asymptomatic but some patients may present with syncope.

There are three forms of AV block:

First-degree AV block where there is prolongation of the PR interval to no more than 0.22 s and every atrial depolarization is followed by delayed conduction to the ventricles.

Second-degree heart block where some P waves conduct and some do not. There are several forms – Mobitz I block (Wenckebach block), Mobitz II block and 2:1 or 3:1 (advanced) block where every second or third P wave conducts to the ventricles. The reader is referred to one of the more advanced medical texts in the Further Reading for more detail.

Third-degree (complete) AV block where all atrial activity fails to conduct to the ventricles. The electrical activity from the atria and ventricles is completely unrelated.

Ventricular standstill and asystole

Occurs when impulses fail to reach the ventricles or impulse formation ceases.

If the problem is in the conduction system, atrial P waves may continue to occur.

There will be no ventricular activity unless a ventricular pacemaker takes over.

The ventricles are left without electrical stimulation and ventricular standstill occurs.

No cardiac output and cardiac arrest results.

More often, no electrical activity (either atrial or ventricular) is seen and the term asystole is used.

This form of arrest has a poor prognosis and has several causes:

Metabolic acidosis.

Electrolyte imbalance.

Hypoxia and drugs.

About 25% of arrests in hospital and 10% out of hospital are of this type. Mortality exceeds 90%.

Tachycardias

An increase in rate is the normal response of the heart to increased work. This occurs so that cardiac output will increase.

However, abnormal tachycardias are frequently associated with a diminished cardiac output.

Increase in heart rate is at the expense of diastole and the heart has less time to fill.

If ventricular filling is reduced, cardiac output will be reduced.

Coronary blood flow takes place in diastole and therefore ischaemia may result.

Symptoms provoked by tachycardia may include angina, dyspnoea, palpitations or syncope.

Most tachycardias are produced by re-entry or enhanced automaticity.

Narrow complex tachycardias include junctional tachycardias (SVTs), atrial flutter and atrial fibrillation.

Each may present as sustained or paroxysmal tachycardia.

Atrial flutter

Rate 220–350/min (usually about 300).

ECG shows flutter waves which have a saw-tooth appearance in the inferior leads.

There may be some AV blockade resulting in a ventricular rate of about 150 (i.e. 2:1 block).

Atrial flutter is always unstable and should be converted to sinus rhythm.

Atrial fibrillation

One of the commonest cardiac arrhythmias.

Affects approximately 1 in 20 of those over the age of 65 years in the UK.

Complicates 10–15% of MIs and is associated with a poor prognosis.

Normal atrial contraction is replaced by a series of irregular fibrillation waves (350–600/min) caused by multiple and changing micro re-entry circuits.

Myocardial contraction is ineffective for atrial emptying and the atria remain functionally in diastole.

Reduces cardiac output by 10–20%.

Although AF makes the heart less efficient, the most important consequence is thromboembolism, especially stroke.

Patients with chronic atrial fibrillation are usually prescribed the anticoagulant warfarin in an attempt to prevent embolism and stroke.

Sinus tachycardia

Sinus rhythm greater than 100 and commonly between 100 and 150.

P waves are normal and have a 1:1 relationship with the QRS.

Found in one-third of patients with MI – an attempt to maintain cardiac output when there is reduced stroke volume.

May be worsened by fear, pain or anxiety.

Adequate analgesia will often settle this post-MI.

Mortality for those with MI is higher in sinus tachycardia than for those with sinus bradycardia.

Atrial ectopic beats

Common in health and disease.

Seen as premature P waves on ECG.

Very common after an MI. May indicate sympathetic overactivity, hypoxia or anxiety.

Usually asymptomatic and cause no haemodynamic upset.

Ventricular dysrhythmias

These include ventricular ectopics, ventricular tachycardia, ventricular flutter and ventricular fibrillation.

Myocardial ischaemia predisposes to ventricular dysrhythmias as normal electrical conduction pathways may be disturbed.

Myocardial irritability following an MI is the commonest cause of ventricular arrhythmias.

Necrotic myocardial tissue is a focus for this ectopic activity.

Predisposing factors following an MI include potassium imbalances or drugs.

Ventricular ectopics

These are premature ventricular complexes which can occur at any time in diastole.

The QRS complex is premature and widened. Danger is progression to VT.

Beta-blockers post-MI seem to reduce serious dysrhythmias as well as limiting infarct size.

Ventricular tachycardia

This is a life-threatening re-entry dysrhythmia. QRS complexes are wide and regular at a rate of 100–220 beats per minute. The atria continue to beat and dissociated P waves may be seen. The atrial rate is usually slower as it arises from the SA node.

There are four types of ventricular tachycardia (VT):

The commonest is monomorphic VT and the complexes are of uniform appearance (monomorphic). Each episode of VT continues for a variable time and usually terminates in a long pause before sinus rhythm returns.

Polymorphic VT (torsades de pointes) is a dangerous dysrhythmia. The QRS undulates around the isoelectric line, with a marked change in amplitude every 5–30 beats. Episodes may be precipitated by drugs that prolong the QT interval or by electrolyte imbalances. Usually terminates spontaneously but may lead to VF.

Ventricular flutter is characterized by a rapid ventricular rate of about 180–250 beats. The ECG has been likened to a row of hairpins. It often precedes VF.

Accelerated idioventricular tachycardia is an escape rhythm which is slow, usually about 60 and not exceeding 120. After about 30 beats, sinus rhythm usually returns but may occasionally be replaced by sustained VT or VF.

Ventricular fibrillation

Electrically and mechanically, the heart is completely disorganized and cardiac arrest ensues.

The ECG shows fine and coarse waves of irregular size, shape and rhythm.

Fine VF may mimic asystole and produce an apparently flat line on the ECG.

About 90% of deaths following acute MI are due to VF. Nearly half occur in the first half hour.

Primary VF is that which occurs in the first 12 hours after MI. Usually associated with a good prognosis as the heart is usually still functioning well.

Reperfusional VF may occur following thrombolysis, but this probably reflects a good prognosis as the infarct-related artery has been re-opened.

Secondary or late VF occurs when function has been severely compromised by the infarct and prognosis is poor.

The Resuscitation Council (UK) has produced guidelines for the management of peri-arrest arrhythmias and these can be obtained from their website (www.resus.org.uk). They have been designed to allow the advanced life support provider to treat the patient effectively and safely in an emergency.

Sudden cardiac death

This is defined as death due to cardiac causes within 6 hours of the onset of symptoms. About 80% of cases in the UK are probably due to coronary artery disease and about 40% of deaths due to coronary artery disease occur this way. Most cases are due to fatal ventricular arrhythmias with myocardial ischaemia.

Cardiac failure

Heart failure occurs when the heart is no longer acting as an efficient pump and thus cannot respond to the demands made upon it.

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Tags: A Nurses Survival Guide to the Ward

Jun 15, 2016 | Posted by admin in NURSING | Comments Off

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