Chest pain as a symptom can lead to over 400 eventual diagnoses. Up to one third of those patients admitted to an acute medical unit may have chest pain as a component of their presenting complaint. Chest pain is almost ubiquitous in patients admitted to the cardiothoracic intensive care unit (CICU). For example, the preoperative patient with ischaemic heart disease may experience the full range of associated symptoms from central crushing pain with radiation, to the silent myocardial infarction of a long-term diabetic with associated neuropathy. Once these same patients have undergone surgical revascularisation, this ischaemic pain will probably be substituted for the dull, central tenderness of a median sternotomy, or the pleuritic pain of a residual pneumothorax irritated by the intercostal chest drains. The evaluation and subsequent treatment of chest pain on the CICU is vital to enhance the clinical outcome of this patient population.
In this chapter we will endeavour to discuss the rapid yet thorough assessment of chest pain as a symptom, the initial examination and investigation strategy required, and outline the emergent therapeutic options required for each differential diagnosis.
As with all clinical encounters the greatest aid to formulation of an accurate differential diagnosis is a thorough clinical history. Several confounding factors exist in the ICU patient that make the history less reliable. The spectrum of confounders ranges from those patients that are sedated and ventilated, through the heavily narcotised and disorientated, to the patient with ‘distraction’ pains who may under-report symptomatic changes. These challenges can result in important delays in the detection of the pathology underlying chest pain.
Given the above issues a focused approach to history taking is required. The mainstays of site, character, radiation, onset, severity, exacerbating factors and timing all still apply although many of these will be very dependent on the preceding interventions and current therapy that the patient is undergoing. The new onset of a complaint of chest pain, therefore, requires a flexible approach to clinical assessment to rule out the most important and potentially life threatening causes in a systematic fashion.
The role of clinical examination in the CICU can often be overlooked. With all the intensive monitoring and real time data that are now available, including bedside transthoracic echocardiography and easy access computerised tomography, the stethoscope can become a vestigial appendage. However, this patient population with positive pressure ventilation and invasive procedures is particularly prone to complications such as tension pneumothorax that need to be rapidly assessed, diagnosed and treated to avoid unnecessary morbidity and potential mortality. Indeed, the CICU patient is at particular risk when transferred from the controlled environment of the unit to other departments for investigation, and the role of clinical assessment must not be forgotten.
The elective patient recovering on the CICU is likely to have been thoroughly investigated prior to admission. Many of the emergent admissions will also have a diagnosis underlying their chest pain by the time they arrive. However, these critically unwell and increasingly aged patients are prone to further, sometimes unrelated, pathologies. Thus a physician must have a widespread understanding of those conditions that most commonly occur in the CICU patient.
It is beyond the scope of this chapter to cover all of the differential diagnoses the CICU staff may encounter in the patient with chest pain. However, we will aim to discuss those that are most common, those that are less common but life threatening, and those that are rare but need highlighting to ensure they are not overlooked.
Most of the patients that arrive on the CICU are likely to have undergone some investigation into their coronary vasculature, be it an invasive coronary angiography or some form of non-invasive functional or anatomical test. In fact, the majority of such patients will be admitted to the CICU to recover from a procedure, performed either percutaneously or surgically, to improve the vascular supply of the myocardial bed. These patients are not, however, immune from further myocardial ischaemia.
Primary percutaneous coronary intervention is now the revascularisation method of choice for patients presenting with an ST elevation myocardial infarction. The admission rate to the CICU following this procedure is around 5% and has been rising steadily year on year. The majority of these patients are intubated and ventilated in the periarrest period in the community, although some will require ventilation during the PPCI procedure itself. If the cardiac arrest is prolonged then these patients will undergo a period of cooling, or at least avoidance of hyperthermia, to aid neurological recovery.
A particular challenge in the ventilated patient post PPCI is the administration and absorption of dual antiplatelet medication. The risk of acute stent thrombosis in this population is tenfold that of the spontaneously ventilating patient, with a mortality approaching 40%. It is, therefore, important to ensure that patients receive and are absorbing the dual antiplatelets as prescribed by the interventional cardiology team, and that premature cessation is avoided in all but life threatening bleeding. In those patients who are unable to absorb enterically, alternatives include administration per rectum or substitution for an intravenous agent, for example the glycoprotein IIb/IIIa inhibitors such as abciximab, eptifibatide and tirofiban.
Any chest pain with concomitant ECG changes in the post PCI cohort of patients should trigger an emergent cardiology consultation to rule out acute stent thrombosis requiring repeat intervention. The second most common cause of postprocedural chest pain in this group is a technical problem with the stent placement, either an inflow or outflow coronary artery dissection, or perhaps the obstruction of a side branch. Finally, the role of untreated bystander disease is important as lesions that remain in other vessels may well become symptomatic in the high catecholamine milieu that exists post PPCI.
The rate of postoperative myocardial infarction following coronary artery bypass grafting is estimated to be between 5 and 10%. The incidence of graft related ischaemia is thought to be approximately 3%. In the intubated patient the clues to infarction and ischaemia are persistent low cardiac output state, dysrhythmia, evolving ECG changes and new regional wall motion abnormalities on echocardiographic imaging. The routine use of biochemical markers of myocardial damage is unlikely to be useful in the diagnosis in this population. In the awake patient, the chest pain of myocardial ischaemia can be difficult to differentiate from the postoperative sternal wound pain although any patient describing their usual angina should be investigated further. Patients in whom early graft failure is suspected have a significant adverse outcome unless treated promptly.
A second form of postprocedural cardiac ischaemia is that induced by poor myocardial protection. This is difficult to diagnose and may present as a global reduction in left or right ventricular function with associated haemodynamic compromise requiring inotropic support.
Even in the patient with apparently unobstructed coronary arteries who undergoes cardiac surgery, for example for a valve replacement, there is a risk of both plaque rupture and importantly embolic obstruction of the coronaries. This is particularly prevalent in those patients with dilated atria and preoperative atrial fibrillation. One final consideration is the occlusion of the coronary ostia by the stent struts on a prosthetic aortic valve.
A further mechanism of potential coronary flow limitation is the phenomenon of coronary vasospasm. This is often difficult to diagnose and is particularly prevalent at the time of high catecholamine drive, such as during extubation. Intravenous vasodilators usually allow rapid resolution and prevent the lasting damage of infarction.
Acute aortic dissection is the most common life threatening pathology of the thoracic aorta and carries a mortality of 1% per hour in the early stages. In the simplest Stanford classification, type A aortic dissection involves the ascending aorta, whereas type B dissections are those that do not involve the ascending aorta. This classification is useful, as type A dissections benefit from emergent surgical repair, whereas type B aortic dissections are best managed medically unless they become complicated. Type A aortic dissections are more common in patients in their sixth and seventh decades, whereas type B dissections typically affect the elderly.
Although traditionally thought to be associated with the connective tissue disorders such as Marfan, Loeys–Dietz and Ehlers–Danlos syndromes, more common predisposing factors include hypertension and bicuspid aortic valve anatomy. In the CICU setting, the physician must always be cognisant of the postsurgical patient with sudden onset of intrascapular pain and haemodynamic instability. Any instrumentation of the ascending aorta, be that percutaneously with ostial coronary stent placement, or surgically during aortic cannulation for cardiopulmonary bypass or during aortic valve replacement, may subsequently cause separation of the layers of the aortic wall. Rarely, reports have been published of aortic dissection following cocaine use, during heavy lifting and during systemic inflammatory vasculopathy. Although perhaps the most feared complication of pregnancy, dissection during pregnancy is relatively uncommon.
The typical chest pain associated with aortic dissection is said to be a searing or tearing pain that starts in the chest and rapidly radiates to the intrascapular region. Immediate complications include right coronary artery occlusion and associated inferior ST elevation, cardiac tamponade, acute aortic valve insufficiency and neurological deficit. Atypical presentations include renal failure of uncertain aetiology due to loss of the renal arterial supply, and mesenteric ischaemia manifest by rising serum lactate, abdominal pain and frequently loose stools. The loss of a peripheral pulse was only present in 19% of patients recorded in the International Registry of Acute Aortic Dissection series. In 15% of patients with an acute aortic dissection the chest radiograph will fail to show the classic widened mediastinum, and contrast enhanced computed tomography has become the first line in investigation. In those centres with expertise in transoesophageal echocardiography, this imaging modality has the advantage of being both sensitive and specific, and also relatively rapidly performed.
Once diagnosed, type A aortic dissection is initially treated by stabilisation of the patient using intravenous beta blockade. Thereafter, emergent surgery to obliterate the false lumen and repair the ascending aorta using an interposition graft is required.
Postprocedural management requires tight blood pressure control with beta-blocker therapy providing the pharmacological mainstay. Various authors have reported survival rates of between 50 and 90% 1 year following acute type A aortic dissection.