Cardiovascular Alterations and Management

Physical examination

Physical appearance varies and depends on the impact of pain, size and location of the infarction in the individual. Heart rate and blood pressure may be raised due to anxiety. Impaired left ventricular function may result in dyspnoea, tachycardia, hypotension, pallor, sweating, nausea and vomiting. Impaired right ventricular function may be indicated by jugular vein distension and peripheral oedema. Abnormalities in heart sounds may be present, including a muffled and diminished first heart sound due to decreased contractility. A fourth heart sound is common, whereas a third heart sound is uncommon. Many patients develop a pericardial rub after about 48–72 hours due to an inflammatory response to the damaged myocardium. Additional findings occur with complications, and these are discussed in that specific section below.

Electrocardiographic examination

Patients with chest discomfort should be assessed by an appropriately qualified person and have an ECG recorded within 5 minutes of arrival at a healthcare facility to determine the presence and extent of myocardial ischaemia, the risk of adverse events and to provide a baseline for subsequent changes.⁷ Most importantly, the ECG is essential to determine whether emergency reperfusion is required, and is recommended as the sole test for selecting patients for PCI or thrombolysis. Where ST segment monitoring is available, this should be continuous. Alternatively, if chest discomfort persists, ECGs should be repeated every 15 minutes. Even when chest pain resolves it is important to record a series of 12-lead ECGs during admission to determine changes over time. (The normal ECG is covered in Chapter 9, whereas this section addresses ischaemic changes in the ECG.)

Myocardial ischaemia, injury or infarction cause cellular alterations and affect depolarisation and repolarisation.¹⁰ Myocardial ischaemia may be a transient finding on the ECG. Ischaemia results in T wave inversion or ST segment depression in the leads facing the ischaemic area.¹¹ Ischaemic T waves are usually symmetrical, narrower and more pointed. ST segment depression of 1 mm for 0.08 seconds is indicative of ischaemia, especially when forming a sharp angle with an upright T wave.¹² These changes are reversible with reduction in demand (e.g. by rest, nitrates).

On acute presentation, myocardial injury (infarction) is most commonly associated with ST segment elevation on the ECG, although this is not universal. In addition, a typical pattern of ECG changes over time (evolution of the ST segments, Q wave development and T wave inversion) are often seen (described below), but these changes too are not universal. The distinction between the various acute coronary syndromes, including ST elevation acute coronary syndrome (STEACS), ST elevation myocardial infarction (STEMI) and non-ST elevation myocardial infarction (non-STEMI), is important for ensuring appropriate assessment and protocol-based treatment¹³ for the various presentations.

The location and extent of ischaemia or infarction may be evident on the ECG leads overlying the affected area, as follows:

Additional leads are needed to view the right ventricle and posterior wall. Chest electrodes can be placed on the right chest wall using the same landmarks as the left chest to view the right ventricle (see Chapter 9). Further electrodes, V7–V9, may be placed over the posterior of the left chest to view the posterior wall. Other indicative signs of posterior wall damage are a small r wave in V1 and/or ST depression in V3 and V4 as these may be reciprocal changes. The endocardial surface of the posterior wall faces the praecordial leads of the ECG so the signs of ischaemia and infarction are reversed or reciprocal such as ST depraession or a small r wave. If these signs are present a left-sided ECG, V7–V9, should be done to confirm or rule out a posterior infarction.

Continuous ECG monitoring is essential to detect arrhythmias, which often accompany AMI and are a common cause of death. The arrhythmia may be due to poor perfusion of the conduction tissue. More often, arrhythmias occur because ischaemic tissue has a lower fibrillatory threshold and ischaemia is not being managed. Arrhythmias also result from left ventricular failure.

Typical ECG evolution pattern

The initial ECG features of myocardial infarction are ST segment elevation with tall T-waves recorded in leads overlying the area of damaged myocardium. These changes gradually change, or evolve, over time, with ST segments returning to baseline (within hours), while Q waves develop (hours to days) and T waves become inverted (days to weeks). The time course for the evolutionary changes is accelerated by reperfusion, e.g. PCI, thrombolysis or surgery. Thus an almost fully-evolved pattern may be seen within hours if successful reperfusion has been undertaken (see Figures 10.2–10.4 for an example). Given the expected time course for evolution, it is possible to approximate how recently infarction has occurred, which is essential in determining management:

FIGURE 10.2 Acute inferoposterior infarction: ST elevation in indicative leads II, III and aVF. The ST segment depression in I and aVL is reciprocal to the inferior infarction. As well, ST depression in anterior leads (V1–V3) is reciprocal to posterior wall infarction. Posterior leads (not shown here) were recorded and revealed ST elevation in V7, V8 and V9. This patient had acute (100%) obstruction at the ostium of the right coronary artery.

FIGURE 10.3 The same patient as above, recorded only 1 hour later, after stenting of the right coronary artery with an evolving inferoposterior infarction. Note the ST segments in II, III and aVF are still elevated but returning to baseline. The reciprocal ST depression is likewise diminishing and can now be seen only in aVL, V1 and V2. Q waves have already developed in inferior leads.

FIGURE 10.4 The same patient again, recorded a further 21 hours later. An almost fully evolved pattern is now present. Note the ST segments inferiorly have almost completely returned to baseline (as have the reciprocal changes). The Q waves remain, and T waves have now inverted inferiorly.

FIGURE 10.5 Acute anterolateral infarction in a patient with left anterior descending coronary artery obstruction. Note the ST elevation and tall (hyperacute) T waves across the chest leads V1–V6. ECG recorded on admission.

Biochemical markers

Intracellular cardiac enzymes enter the blood as ischaemic cells die, and elevated levels are used to confirm myocardial infarction and estimate the extent of cell death. The cardiac troponins T and I (cTnT and cTnI) have been found to be both sensitive and specific measures of cardiac muscle damage.¹⁴ Troponin I is rapidly released into the bloodstream, so it is especially useful for the diagnosis and subsequent risk stratification of patients presenting with chest pain in the early stages. Troponin I is also a more appropriate marker to use in postoperative and trauma patients than creatine kinase–MB (CK-MB), as CK-MB levels will be affected by muscle damage. However, CK-MB is less costly and more readily available, and so is still often used, particularly in the presence of a non-diagnostic ECG. C-reactive protein assays may prove to be useful, as baseline and discharge levels are predictive of subsequent cardiac events. However, the laboratory facilities are not readily available.

Coronary angiography and left heart catheterisation

Coronary angiography gives a detailed record of coronary artery anatomy and pathophysiology. Specially designed catheters are advanced with the assistance of a guidewire into the ascending aorta via the femoral or brachial arteries and manoeuvred into the ostium of each coronary artery. Contrast media is then injected and images are taken from several views to provide detailed information on the extent, site and severity of coronary artery lesions and the blood flow into each artery. This flow is graded using the Thrombolysis in Myocardial Infarction (TIMI) studies system (see Table 10.2).¹⁵ Typically, a left ventricular angiogram is performed during the same procedure to assess the appearance and function of the left ventricle, mitral and aortic valves. If CHD is present, treatment is determined as appropriate according to the severity (PCI, coronary artery bypass grafting or medical therapy). The nursing care for coronary angiography is similar to PCI, and is covered under that section.

TABLE 10.2 Thrombolysis in Myocardial Infarction (TIMI) flow grades in coronary arteries¹⁵

Exercise test

Exercise testing with ECG monitoring forms part of the diagnostic screen for patients suspected of stable angina. The Bruce protocol is used most often and considered positive for CHD if there is 1 mm or more of reversible ST segment depression.¹⁶ False-positive tests are more common in populations with a lower incidence of CHD, including women.¹⁷

Chest radiography

An initial chest X-ray film is useful to exclude other causes of chest pain, such as pneumonia, pneumothorax and aortic aneurysm, and to assess whether heart failure and/or pulmonary congestion are present. If the diagnosis is clearly ACS or AMI, this step can wait until after thrombolysis or PCI.

Thrombolytic therapy

Thrombolytic therapy has been demonstrated to show a significant reduction in mortality in the high-risk group described above.²⁰ The greatest reduction in mortality occurs if the reperfusion occurs within the first ‘golden’ hour of presentation.²⁰ Thrombolysis can be delivered effectively in many settings where other methods of reperfusion are not available.

Clots formed in response to injury normally dissolve using the body’s fibrinolytic processes as tissue repair takes place. This requires the presence of the proenzyme plasminogen, which is converted into the enzyme plasmin when activated by macrophages and degrades the clot. Thrombolytic agents, including streptokinase and tissue-type plasminogen activator (tPA), have been developed that trigger conversion of plasminogen to plasmin and therefore break down clots. It is essential to screen patients for contraindications to thrombolysis quickly but thoroughly so that therapy can be commenced as soon as possible. Contraindications are given in the National Health Foundation of Australia (NHFA) Guidelines.

Streptokinase and tenecteplase are the most commonly prescribed thrombolytic agents. Streptokinase is prepared from beta-haemolytic streptococci and is a potent plasminogen activator.²¹ Streptokinase is not thrombus-specific, so plasmin is released into the general circulation that may break down any recent clot formed as a result of surgery, injection or healing, leading to a potential increase in haemorrhagic episodes. Streptokinase is bacterial in origin, so it is antigenic. Most individuals have been exposed to beta-haemolytic streptococci so antibodies are often present, which means a higher dose may be required owing to the destruction of some of the enzyme when administered. Occasionally an escalated allergic response will occur and will need urgent treatment. This is more likely if streptokinase has been administered in the previous 6 months. Streptokinase is given intravenously over 60–90 minutes, because it has a short half-life.

The drug tissue-type plasminogen activator (tPA) is available as alteplase, tenecteplase and reteplase. These agents are of human origin, made by recombinant DNA techniques.²² The drug activates only plasminogen present in blood clots, so the risk of haemorrhage is decreased. Unlike streptokinase, tPA can be given repeatedly without risk of anaphylactic reaction. However, tPA costs about 10 times as much as streptokinase, so it is occasionally still reserved for patients who have recently received streptokinase or are at risk of allergic reaction. Often patients with anterior ischaemic changes are treated with tPA (alteplase) based on the GUSTO-1 trial that showed improved outcomes in terms of reduction of ischaemia.²³ Alteplase is usually given by infusion, whereas reteplase, which has a longer half-life, can be given in two bolus injections.

Nursing management of patients post-thrombolysis focuses on monitoring and detection of bleeding complications and/or return of ischaemia. Care is as follows:

Coronary angioplasty

Coronary angioplasty (PTCA) procedures are being used about twice as frequently as coronary artery bypass graft surgery, with 155 PTCA procedures performed for every 100,000 population in Australia in 2008–09.² PTCA rates have grown dramatically in patients aged over 75 years. In this procedure, a catheter is introduced by the brachial or femoral artery into the coronary arteries and advanced into the area of occlusion or stenosis under the guidance of imagery and specifically designed catheters. A balloon attached to the end of the catheter is then inflated to widen the lumen of the artery by stretching the vessel wall, rupturing the atheromatous plaque and cracking the intima and media of the artery (see Figure 10.7).

FIGURE 10.7 PTCA procedure.¹⁰⁶

PTCA tends to be reserved for patients with single- or double-vessel disease as assessed on coronary artery angiograms. Angioplasty provides better symptom relief than medication alone, but there is no evidence of survival benefits.²⁴ Primary angioplasty results in a higher rate of patency of the affected artery in AMI (>90%), lower rates of CVA and reinfarction and higher short-term survival than thrombolysis.²⁵ PTCA is recommended in all patients presenting with chest pain who meet the indications for reperfusion when: (a) facilities are available and can be achieved within 60 minutes; (b) there are contraindications to fibrinolytic therapy described above; (c) ischaemia would result in large anterior AMI within 4 hours; or (d) haemodynamic instability or cardiogenic shock are present.

A stent is usually inserted to prevent abrupt closure and maintain patency for longer.²⁶ The structure of the stent within the vessel enlarges the lumen and prevents vessel stricture. Restenosis due to intimal hyperplasia is a relatively common complication, occurring 10–12 weeks postimplantation. In response to this problem, drug-eluting stents have been developed. The drug coatings include sirolimus, a macrolide antibiotic that has been demonstrated to effectively decrease hyperplasia and prevent reduction of flow.²⁷ Paclitaxel has also shown promise in a series of studies.²⁸ In addition to dactinomycin, these drugs are undergoing approval processes.

Nursing management of patients post-PTCA includes care of the puncture site to prevent bleeding and detect arterial changes (including clot and aneurysm).²⁹ The process used to create and maintain access for insertion of the catheters can damage the blood vessel(s) and alter perfusion to the limb. The sheath used to aid insertion and maintain access is usually maintained for 1–2 hours post-procedure for emergency access. Care is as follows:

Many patients find the PTCA procedure and confirmation of CHD diagnosis stressful.³² It is an important nursing role to provide patients with preparatory information about the procedure and care required during recovery. As family members provide valuable support and reminders about recovery, these people should be included in any information sessions. The patient and family need to be provided with information about the possibility of restenosis, mobility restrictions at home and the lifestyle changes needed to reduce the risk of worsening CHD.

Nursing care for thrombolysis

Patients receiving thrombolytics require constant observation, regular non-invasive blood pressure measurement for hypotension, and monitoring for allergic reactions to streptokinase. Continuous ECG monitoring for arrhythmias and ST segment changes is essential. Some arrhythmias, particularly idioventricular arrhythmias, are associated with reperfusion and tend to be benign. ST segment monitoring and assessment of pain help evaluate the effectiveness of the thrombolysis. Thrombolysis is considered to have failed if the patient is still in pain and the ST segment has not resolved within 60–90 minutes.¹⁸ If thrombolysis fails, patients are at high risk for other interventions, so repeat thrombolysis is often the only treatment option. Salvage or rescue angioplasty may be undertaken if available at the site.

Medications

Provision of medications and assessment of the effectiveness of treatment is a major component of the nurse’s role in caring for the cardiac patient. Many of the medications are accompanied by side effects and interactions with other drugs, which the nurse must monitor. An array of medications is used to treat AMI patients, including aspirin, lipid-lowering agents, beta-blockers and organic nitrates (see Table 10.3).

Symptom control

Control of anginal symptoms with medication usually includes sublingual glyceryl trinitrate (GTN) for immediate symptom control and one or more antianginal medications for sustained symptom management.¹⁸ Beta-blockers are usually commenced unless contraindicated. Calcium channel blockers may be used in patients who do not have cardiac failure or heart block. (These medications are described in the next section.) The choice of medication may depend on how acceptable the patient finds the reduction in symptoms and the presence of side effects. Patients need to take antianginal agents continuously, regardless of symptoms. Patients should also be encouraged to take sublingual GTN prophylactically.

Angina may also be managed by avoiding situations that trigger angina. Education needs to be directed at awareness of symptoms and management of unstable angina and AMI symptoms, and the need for emergency care. Although these patients are at low risk of further cardiovascular events in the short term, in the medium to long term, risk may accumulate. Patients with angina are encouraged to attend cardiac rehabilitation programs to learn how to deal with symptom management.⁴¹

Angiotensin-converting enzyme (ACE) inhibitors have been recommended for all post-AMI patients while in hospital, with review of prescription at 4–6 weeks postdischarge. Patients with left ventricular failure should be maintained on ACE inhibitors. Similarly, diuretics provide the mainstay of the management of left ventricular failure if it is present (see Chapter 19). Diabetic patients have a higher mortality after AMI in both acute and long-term phases. Provision of an insulin-glucose infusion for BSL >11 mmol/L during the acute phase, followed by subcutaneous injections for at least 3 months, has been demonstrated to significantly reduce mortality up to 3 years post-AMI.⁴²

Transfer to a step-down unit or general ward usually occurs when the patient is pain-free and is haemodynamically stable. Stability means that patients are not dependent on IV inotropic or vasoactive support and have no arrhythmias. Discharge home after AMI varies, but usually occurs at day 3 for low-risk patients.¹⁸

Emotional responses and patient and family support

ACS or AMI is usually accompanied by feelings of acute anxiety and fear, as most patients are aware of the significant threat posed to their health.¹⁸ For many patients it may also be the first experience of acute illness and associated aspects such as ambulance transport, emergency care and hospitalisation, so they may experience shock and disbelief as well. Fast-track processes require patients and their families to process a large amount of information and make decisions quickly, and this, added to an alien environment, full of unfamiliar technology and personnel, can be quite distressing. However, the environment can also promote a feeling of security for patients and their families. Patients’ perceptions of the CCU environment have been linked to recovery.⁴³

Anxiety is a common response to the stress of an acute cardiac event and leads to important physiological and psychological changes.⁴⁴ The sympathetic nervous system is stimulated, resulting in increased heart rate, respiration and blood pressure. These responses increase the workload of the heart and therefore myocardial oxygen demand. In an acute cardiac event, these demands occur when perfusion is already poor and may lead to worse outcomes, including ventricular arrhythmias and increased myocardial ischaemia. Therefore, staff working in emergency and coronary care should employ strategies to reduce a patient’s anxiety.

Increasing a patient’s sense of control, calm and confidence in care reduces the patient’s sense of vulnerability, whether it is realistic or not.⁴⁴ This can be achieved by:

Nurses need to monitor patients for signs of excessive anxiety, including facial expressions and behavioural changes. However, overt behaviours may be controlled by the patient, so careful conversation and/or use of specific assessments may be necessary to detect anxiety. The move to the step-down or general ward may also be stressful to the patient and family. This move needs to be planned and discussed, and promoted as a sign of recovery.

Cardiac rehabilitation

Coronary heart disease is a chronic disease process, which often presents with acute events such as ACS or AMI. Like all chronic illnesses, it has implications for patients in terms of lifestyle change, uncertainty of long-term outcomes, functional changes and social and economic alterations. Cardiac rehabilitation aims to address these issues. The World Health Organization describes cardiac rehabilitation as ‘the sum of activities required to influence favourably the underlying cause of the disease, as well as to ensure the patients the best possible physical, mental and social conditions so that they may, by their own efforts, preserve, or resume when lost, as normal a place as possible in the life of the community’.⁴⁶Systematic, individualised rehabilitation and secondary prevention need to be offered to all AMI patients. Participation in well-structured, multidisciplinary programs has been demonstrated to reduce mortality by up to 30%.⁴⁷ Additional benefits have been shown for improvements in exercise tolerance, symptoms, serum lipids, psychological wellbeing and cessation of smoking.^48–50

Cardiac rehabilitation is structured around four phases, beginning with phase I, during admission.⁵⁰ The components of phase I include:

The phases that follow, from II to IV, are managed in the outpatient setting and begin with assessment, liaison with multidisciplinary professionals and health education. Phase II occurs in the immediate postdischarge period and includes liaison with community-based carers and services and further assessment. In phase III, tailored, supervised exercise programs are usually conducted and there is a range of psychosocial interventions, such as support sessions and stress management. Finally, in phase IV the focus is on chronic disease management and maintaining risk modification behaviours. All phases require incorporation of the principles of adult learning to maximise learning and behaviour change. These principles include recognition of ‘readiness to learn’.⁵⁰ Adults are ready to learn most effectively when they are physically and emotionally stable and are aware of the problem or need to learn. Nurses, because of their expertise and continual presence, are best placed to assess and provide education at optimal times.

Cardiogenic shock

Cardiogenic shock occurs as a complication of MI in about 5–10% of patients and is the most common cause of death in hospitals.⁵⁰ It arises from loss of contractile force, and generally occurs when ventricular damage is more than 40% and ejection fraction less than 35%. Cardiogenic shock and the related management are described in more detail in Chapter 12.

Arrhythmias

Arrhythmias often occur in ACS and AMI and are often the cause of death in the prehospital phase. Management of the prehospital phase centres on community education and an effective, rapidly responsive ambulance service, as exemplified in Seattle in the USA.⁵¹ Arrhythmias may be generated by poorly perfused tissue and electrolyte alterations, and increased sympathetic tone during infarction, but are more often due to a failing left ventricle. They may also complicate reperfusion after successful revascularisation.⁵² It is essential to rapidly and effectively treat arrhythmias in the ACS and AMI context. The goal of treatment is to maintain cardiac output while reducing workload. Arrhythmias and management are described in Chapter 11.

Pericarditis

Pericarditis is an inflammation of the visceral and parietal layers of the pericardium that cover the heart. This inflammation occurs in approximately 20% of AMI patients within the following 2–3 days.¹⁰ The patient experiences chest pain, which may be confused with ischaemic pain. This confusion with an ischaemic event may be compounded by the additional presence of ST segment elevation on the ECG. However, pericardial pain increases with deep inspiration and a pericardial rub is often present. Electrocardiographically, the elevated ST segments of pericarditis are typically concave upwards (saddle-shaped) and often widespread, contrasting with convex ST segment elevation limited to the distribution of a single coronary artery in infarction.⁵³ Pericarditis normally responds to anti-inflammatory treatment by aspirin, indomethacin and/or corticosteroids. Approximately 1–5% of AMI patients develop pericarditis as a late complication, 2 weeks to a few months post-AMI.¹⁸ Usually this late-onset pericarditis is associated with Dressler’s syndrome and may be an autoimmune response to myocardial injury. This is a chronic condition requiring systemic corticosteroid treatment.

Structural defects

Myocardial tissue death may be catastrophic if it is extensive or results in rupture of ventricular or papillary muscle. These conditions are rare and symptoms develop rapidly. Intraventricular septal rupture is usually associated with anterior MI. The patient develops progressive dyspnoea, tachycardia and pulmonary congestion, as well as a loud systolic murmur associated with a thrill felt in the parasternal area. If a pulmonary artery catheter is present, blood samples from the right atrium and right ventricle will reveal a higher than usual oxygen content. Diagnosis must be confirmed by cardiac catheterisation, and urgent surgery is required.

Papillary muscle rupture most often occurs 2–7 days after MI. Patients experience a sudden onset of pulmonary oedema secondary to pulmonary hypertension and cardiogenic shock. Additional heart sounds and a systolic murmur will be heard. Urgent surgery is required, as the mortality rate for papillary muscle rupture is 95%.⁵⁴ Cardiac rupture most often occurs within 5 days of MI and is commonest in older women. The patient experiences continuous chest pain, dyspnoea and hypotension as tamponade develops. Symptoms may worsen rapidly and result in pulseless electrical activity (PEA) unless surgery is undertaken immediately.