Hypertension is a commonly encountered clinical problem in the cardiothoracic critical care unit in both its chronic and acute forms. It is estimated that over one billion of the world’s population are affected by hypertension, many of whom may be undiagnosed or inadequately managed. Chronic hypertension is a risk factor for cardiovascular disease and is therefore seen with greater prevalence in the cardiothoracic patient population. Such patients are at greater risk of pre-existing left ventricular dysfunction, cerebrovascular disease and chronic kidney disease, factors which are independently associated with poorer outcomes. Acute hypertension in cardiothoracic critical care may represent undiagnosed chronic hypertension or arise as a complication of the presenting complaint. Acute hypertension can complicate cardiac surgery, leading to haemorrhage, end-organ damage, prolonged length of stay and poorer outcomes.
The aetiology of hypertension in the cardiothoracic critical care unit is often multifactorial and may resolve with management of the underlying precipitant alone. Identification of the exact cause requires a systematic approach as seen in Table 30.1.
|Central nervous system||Cerebrovascular accident|
|Postoperative cognitive dysfunction or delirium|
|Raised intracranial pressure|
|Alleviation of obstructed outflow with hypertrophied LV|
|Inappropriate or excessive vasopressor or inotropic support|
|Renal||Acute kidney injury|
|Blocked urinary catheter|
|Acute alcohol or nicotine withdrawal|
|Failure to reinitiate anti-hypertensive medication|
Before initiation of anti-hypertensive therapy, an underlying cause should be sought and corrected. This is particularly true in the case of raised intracranial pressure whereby mean arterial pressure is raised in order to maintain cerebral perfusion pressure.
Blood pressure or mean arterial pressure (MAP) is considered in simple terms as the product of the cardiac output (CO) and systemic vascular resistance (SVR). The cardiac output itself is determined by the product of the heart rate (HR) and stroke volume (SV) and can be summarised as follows:
MAP (mmHg) = (HR × SV) × SVR.
This simplification diminishes the contribution of other haemodynamic variables. For example, the stroke volume depends on the contractility of the left ventricle which itself depends on multiple factors including preload, afterload and sympathetic activation. Systemic vascular resistance is also influenced by the autonomic nervous system as well as precapillary sphincter tone. Hypertension can occur acutely with an increase in any of the above variables.
In chronic primary or essential hypertension, decreases in vascular compliance and endothelial cell dysfunction result in sustained elevations in blood pressure, which generally develop slowly over time. This is accompanied by compensatory changes in physiology which themselves have implications in managing chronically hypertensive patients on the cardiothoracic critical care unit.
In health, acute changes or swings in mean arterial pressure are sensed by baroreceptors found in the carotid sinus and aortic arch. An increase in blood pressure results in activation of a negative feedback reflex loop whereby both heart rate and systemic vascular resistance fall in response to increased parasympathetic tone. This results in a lowering of blood pressure. In chronic hypertension baroreceptors reset over time to a higher level of mean arterial pressure, a process which is reversed with initiation of anti-hypertensive therapy.
Additionally, organ blood flow, which is maintained at a near constant level by the process of autoregulation, is also adjusted to a higher level of perfusion pressure. Autoregulation allows blood vessels to adjust their calibre in response to metabolic, mechanical and neurogenic factors, and is particularly important in the maintenance of blood flow in cerebral, coronary and renal perfusion. Mechanical factors refer to changes in arterial pressure transmitted transmurally. Increases in arterial pressure lead to the compensatory response of vasoconstriction thereby preventing a sudden increase in flow. Autoregulation protects from the deleterious effects of acute hypoperfusion or hyperperfusion. However, this only occurs within a certain range of mean arterial pressures. The lower range of the autoregulation curve varies markedly between individuals and depending on acute care setting. Traditionally the lower limit is thought to be 60 to 70 mmHg in most individuals. The upper limit has never been clearly defined but it certainly is <110 mmHg in many individuals. Outside this range, blood vessels are either maximally dilated or constricted and flow therefore becomes directly dependent on perfusion pressure. In chronic hypertension, the autoregulation curve is shifted to the right for a given mean arterial pressure as shown in Figure 30.1. This explains why organ ischaemia may occur with rapid lowering of mean arterial pressure in patients with established chronic hypertension.
Figure 30.1 Cerebral blood flow autoregulation curve.
Chronic hypertension results in an increase in afterload, which leads to an increase in myocardial work. Over time this is maintained or compensated for by ventricular hypertrophy. In terms of coronary blood flow, unless the increase in demand can be met by an increase in supply, ischaemia may occur. Additionally, chronically elevated mean arterial pressure can lead to diastolic dysfunction due to failure of adequate ventricular relaxation and subsequent congestive heart failure can supervene.
The diagnosis and management of hypertension must be taken in the context of its presentation. The spectrum of hypertension includes an incidental finding in an asymptomatic patient to hypertensive crises with associated organ damage. In the context of the cardiothoracic unit this ranges from cautious reintroduction of preoperative anti-hypertensive medication postoperatively to rapid lowering of blood pressure in the situation of aortic dissection to limit further extension of the false lumen.
Preoperative hypertension is typically diagnosed in the primary care setting through routine screening. The traditional cut-off blood pressure is 140/90 mmHg or more. The blood pressure must be measured in both arms and replicated on two separate occasions. Further confirmation requires ambulatory or home blood pressure monitoring. Hypertension can be classified based on the severity of blood pressure.
Stage 1: Blood pressure of 140/90 mmHg or more AND an average blood pressure of 135/85 mmHg or more on home or ambulatory monitoring.
Stage 2: Blood pressure of 160/100 mmHg or more AND an average blood pressure of 150/95 mmHg or more on home or ambulatory monitoring.
Stage 3: Systolic blood pressure of ≥180 mmHg OR diastolic blood pressure ≥110 mmHg.
Whilst awaiting confirmation, further investigations looking for evidence of target organ damage should be performed. This includes fundoscopy, biochemistry for renal function and lipid profile, urinary protein levels and an electrocardiograph.
Stage 3 hypertension is also referred to as severe hypertension and is considered a hypertensive urgency. In these circumstances immediate initiation of treatment should be considered. In addition for patients with suspected accelerated hypertension, defined as severe hypertension with signs on fundoscopy of hypertensive retinopathy or papilloedema, a referral for immediate specialist advice and treatment should be made.
Hypertension can also be classified based on its aetiology. Primary or essential hypertension describes hypertension which occurs without an underlying identifiable cause. This represents over 90% of all cases. It typically arises in the elderly. The exact aetiology is unclear but is likely to be an interaction of environmental and genetic factors resulting in age-related decline in vessel compliance. Secondary hypertension on the other hand is hypertension as a consequence of an underlying disease process. This includes pathologies affecting the adrenal gland such as excess catecholamines as seen in phaeochromocytoma and aldosterone in Conn’s syndrome. Secondary hypertension is more common in the younger population and treatment targets the underlying disease in addition to traditional anti-hypertensive medication.
Acute hypertension can present in the critical care setting, the emergency department or primary care. Acute severe elevations in blood pressure are often classified based on the presence or absence of end-organ damage. End-organ damage has been quoted as being present in 19% of all presentations of acute severe hypertension. A hypertensive emergency describes when severe hypertension as defined by BP >180/110 is associated with end-organ damage. Examples of end-organ damage can be seen in Table 30.2. Under these circumstances, anti-hypertensive treatment should be initiated as a priority in a monitored environment. Severe hypertension in the absence of end-organ damage is considered a hypertensive urgency. Treatment should be offered immediately but does necessitate hospitalisation.
|Central nervous system||Cerebrovascular accident|
|Cardiovascular||Left ventricular hypertrophy|
The guidelines for the management of chronic hypertension are outlined by NICE. Patients with hypertension requiring cardiothoracic surgery should ideally be established on effective anti-hypertensive therapy in primary care. Current targets suggest an optimal BP of below 140/90 mmHg in those aged less than 80 years and below 150/90 mmHg in people aged over 80 years. Poorly managed or undiagnosed hypertension should be identified at surgical pre-assessment and appropriate treatment instigated. No specific cut-off values exist above which surgery should be cancelled based on the presence of hypertension alone. For non-cardiac elective surgery, a blood pressure above 180/110 mmHg would be an indication for cancellation and optimisation of blood pressure control prior to surgery.
Initiation of anti-hypertensive therapy is indicated in the following situations:
Stage 1 hypertension, less than 80 years of age and one of the following:
Target organ damage
Any cardiovascular disease
Predicted 10 year cardiovascular risk of more than 20%.
Stage 1 and less than 40 years of age.
Stage 2 or 3.
The choice of treatment subsequently depends on age, ethnicity and response to treatment. This is outlined in Table 30.3.
|Treatment step||Patient||Recommended therapy|
|CCB or thiazide-like diuretic|
|2||Combined ACE inhibitor and CCB|
|ARB (in preference to ACE inhibitor) combined with CCB|
|3||Triple therapy: combination of ACE inhibitor or ARB with CCB and diuretic therapy|
ACE angiotensin converting enzyme, ARB angiotensin II receptor blocker, CCB calcium channel blocker.
Before moving on to each step, compliance and optimal dosing should be ensured before the addition of a further agent. Additionally, hypertension which persists despite triple therapy is considered resistant hypertension and expert advice at this stage should be sought.
Presently beta-blockers are not recommended as initial therapy for hypertension except in certain circumstances such as women of child-bearing age and those intolerant of ACE inhibitors and ARBs. Extreme caution should be exercised with all of these agents in patients with aortic stenosis, impaired ventricular function or pulmonary hypertension.