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Cardiovascular Alterations and Management 243

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requiring admission to a critical care unit. Previous INFECTIVE ENDOCARDITIS
hypertension is not always present, but because of chronic
adaptive vascular changes may provide some level of pro- Infective endocarditis remains a potentially life-threatening
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tection against acute tissue injury. Symptoms may not disorder, with mortality remaining as high as 20–25%
develop until the blood pressure exceeds 220/110 mmHg, even in this era of relative rheumatic fever control. This
whereas in patients without previous hypertension, same era, however, sees other means of developing endo-
hypertensive emergencies may occur at levels of even carditis, with factors such as longer life, IV drug use,
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160/100 mmHg. When the diastolic pressure is persis- prosthetic valves, greater rates of cannulation during hos-
tently above 130 mmHg, there is risk of vascular damage pitalisation, cardiac surgery, resistant organisms, and
and must be treated. increased numbers of immunocompromised patients
from immunosuppressant drugs and HIV/AIDS. 99,100
Diagnosis Infection of the endocardium, often with involvement of
A thorough history is taken, including any hypertension the cardiac valves, occurs most commonly due to staphy-
management, known renal or cerebrovascular disease, lococcal, streptococcal and enterococcal bacteraemia. 99,100
eclampsia in previous pregnancies if gravid, or use of stim- The definition of infective endocarditis now also includes
ulants or illicit drugs such as cocaine. Patient assessment an infection of any structure within the heart such as
should include evidence of end-organ damage, such as prosthetic valves, implanted devices and chordae tendin-
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back pain (aortic dissection), neurological damage: head- eae. Infective endocarditis can be acute or subacute.
ache, altered consciousness, confusion, visual loss, stupor Acute infective endocarditis progresses over days to weeks
or seizure activity (encephalopathy); cardiac damage: chest with destruction of valves and metastatic infection. Sub-
pain, ST segment changes, cardiac enlargement, or the acute infective endocarditis occurs over weeks to months
development of heart failure or pulmonary oedema; and and is milder than acute infective endocarditis. Endothe-
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renal damage: oliguria and azotaemia. Serum urea, creati- lial damage occurs in the endocardium. Platelet-fibrin
nine, electrolytes, urinalysis, ECG and chest X-ray should deposits form and a lesion develops. Bacterial colonisa-
be performed. tion then occurs and vegetation adheres to the endocar-
dial lesion. Many of the signs and symptoms of infective
Management endocarditis are due to the immune response to the
microorganism. The patient presents with fever, and
More severe, or malignant, hypertension may cause retinal general features of febrile illness, which may include
haemorrhage or papilloedema, and emergency treatment septic shock. Joint pain is common and septic arthritis is
should immediately be instituted. Other contexts in sometimes seen. Cardiac symptoms develop when there
which there is a need for rapid treatment of severe hyper- is valvular involvement, which may manifest as erosion
tension include intracranial bleeding, acute myocardial through valve leaflets producing regurgitation, fusing of
infarction, phaeochromocytoma, recovery from cardiac valve leaflets or vegetations (outgrowths from valve struc-
surgery, and bleeding from vascular procedure sites. tures), producing valvular stenosis or regurgitation. The
100
Hypertensive emergencies in pregnancy threaten both the mitral valve is more commonly affected, but aortic valve
mother and the fetus. 95
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involvement carries a worse prognosis. Conduction
The aim of treatment is to acutely lower the blood pres- system involvement manifests as arrhythmias and con-
sure, but neither too quickly nor too dramatically. duction defects. Embolic complications are relatively
Recommendations vary, but an initial aim of 150/110– common and multifactorial. Septic emboli, embolisation
160/100 mmHg within 2–6 hours, or a 25% reduction in of atrial thrombi when atrial fibrillation is present, and
mean arterial pressure within 2 hours, has been fragmentation of vegetations may all give rise to pulmo-
described. 96,97 Continuous direct arterial pressure moni- nary and systemic emboli. These most often present as
toring should be in place during treatment. Intravenous splenic infarction, stroke, peripheral vascular occlusion
sodium nitroprusside, a rapidly acting arterial and venous and renal failure. 98
dilator, is most frequently used, at doses of 0.25–10 µg/kg/
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min. Weaning of nitroprusside is undertaken after the Diagnosis
later introduction of oral antihypertensives. Care is Diagnosis of infective endocarditis is based on the modi-
required to avoid hypotension during treatment, as well as fied Duke criteria. This is based on the presence of micro-
rebound hypertension as nitroprusside is withdrawn. organisms (identified in blood cultures), pathological
Rapidly acting beta-adrenergic blocking agents with short lesions (vegetation or abcess present), and clinical crite-
half-lives such as IV esmolol may be used at doses of 50– ria. The clinical criteria are based on two major criteria or
100 µg/kg/min (or higher) in patients without standard one major and three minor criteria or five minor criteria.
contraindications to beta-adrenergic blockers (asthma, Major clinical criteria are:
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heart failure). Glyceryl trinitrate infusions at 10–100 µg/ ● positive blood culture
min or higher are used for combined venous and arterial ● evidence of endocardial involvement (positive echo-
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dilation, especially if there is angina. Intravenous cardiography, abscess, partial dehiscence of a pros-
frusemide may be introduced during the acute phase. After thetic valve, or new valvular vegetation)
intravenous therapies have been established and progress
towards target pressures is made, oral agents are intro- Minor clinical criteria include:
duced. These include oral beta-adrenergic blockers, ● fever with body temperature ≥38°C
calcium channel blockers, ACE inhibitors and diuretics. ● predisposing heart condition or intravenous drug use