CLINICAL SCENARIOS

CASE 1

A 56 year old male presents for inguinal hernia repair. PMHx NAD. On no medications. On examination his BP is 190/110, and his ECG shows LVH with strain.

How would you manage this patient?

CASE 2

A 61 year old female undergoes an anterior resection for rectal carcinoma. She has known hypertension, treated with Amlodipine 5mg daily. In the recovery room postoperative, her blood pressure rises to 195/100.

How would you manage this patient?

CASE 3

A 79 year old female is admitted through A&E following a stroke. She has fallen down the stairs and has a subcapsular fracture of her right femur. On examination, she has a left hemiparesis. Her GCS score is 12. Her blood pressure is 220/120. She has bilateral papilloedema. The orthopaedic team are anxious to repair her hip to prevent fat embolism.

How would you manage this patient?

CASE 4

A 64 year old female, who is awaiting CABG, undergoes right carotid endarterectomy for a 90% occlusion. Her regular medications are isosorbide mononitrate 60 mg daily, diltiazem 90 mg bd, aspirin 75 mg daily and metoprolol 50 mg daily. You are called to see her in the high dependency unit. Her blood pressure is 200/90; her heart rate is 88.

How would you manage this patient?

CASE 5

A 33 year old female undergoes a laparoscopic cholecystectomy. Apart from her history of gallstones, her only other complaint is migraine. She has no known allergies. Family history is non contributory. In the anaesthetic room, her pulse was 110 and her BP was 110/60. Anaesthesia was induced with fentanyl, propofol and vecuronium. She has had morphine 10mg and cyclizine 25mg, and is expiring 1.3% isoflurane in 70% nitrous oxide.Twenty minutes after incision, her blood pressure suddenly rises to 210/110, and her heart rate increases to 150 beats/min.

How would you manage this patient?

WHAT IS HYPERTENSION?

Joint National Committee on Detection, Evaluation and Treatment of High Blood Pressure Arch Intern Med 153:154, 1993

Diagnosis of hypertension (HTN) is made when two or more readings (on different visits), of diastolic blood pressure (BP) >90 mmHg, or systolic BP >140 mmHg.

Isolated systolic hypertension: SBP > 140 mmHg, DBP <90 mmHg.

Essential hypertension: no cause can be found (95% of cases).

Accelerated hypertension: markedly elevated HTN plus grade 3 retinopathy (haemorrhages and exudates).

Malignant hypertension: markedly elevated HTN (diastolic>140mmHg) plus papilloedema.

Complicated hypertension: HTN plus cardiovascular ("end organ") damage consequent to it: stroke, CCF, renal failure, MI, AAA.

White coat hypertension: BP only raised when examined by a health care professional.

CLASSIFICATION

Primary ["Essential"] hypertension.

Secondary hypertension:

• Aortic regurgitation
• Thyrotoxicosis
• Patent ductus arteriosus

1. Renal

• Glomerulonephritis (acute or chronic)
• Pyelonephritis
• Polycystic kidneys
• Renal artery stenosis
• Polycystic kidneys

2. Endocrine

• Cushing’s syndrome (excessive glucocorticoids)
• Congential adrenal hyperplasia
• Conn’s syndrome (primary hyperaldosteronism)
• Phaeochromocytoma
• Hypothyroidism
• Acromegaly

3. Neurogenic

• Raised intracranial pressure
• Psychological ("white coat hypertension")
• Acute porphyria
• Lead poisoning

4. Miscellaneous

• Coarctation of the aorta
• Polyarteritis Nodosa
• Hypercalcaemia
• Increased intravascular volume (PRV)

WHY IS HYPERTENSION IMPORTANT?

1. It is common (50 million Americans).
2. It is a risk factor for cardiovascular disease.
3. It causes end organ damage: heart, brain, kidneys
4. It may indicate the presence serious endocrine related disese: diabetes, thyrotoxicosis, phaeochromocytoma, Cushing’s, Conn’s, etc.
5. It may indicate the presence of serious renal disease.
6. It increases the risk of an adverse anaesthetic outcome.
7. Perioperatively it indicates:

Anxiety
Inadequate anaesthesia [awareness]
Inadequate analgesia.

TREATMENT OF HYPERTENSION

Diuretics

Sympathoplegics

1. Receptors: Beta blockers – reduce cardiac output initially, later ¯ PVR

Alpha blockers – useful in diabetics or as second line tx

2. CNS active agents: Methyldopa and clonidine, a 2 selective, decrease sympathetic outflow [mechanism unknown]. Salt retention. Rebound HTN.

3. Ganglion blockers: block sympathetic ganglia. Cause postural hypotension.

4. Post ganglionic sympathetic nerve terminal blockers. Drugs that deplete nerve terminal of NAD stores (reserpine), block release of NAD (guanethidine).

Vasodilators

1. Nitroprusside – vasodilatation secondary to nitric oxide activity.

2. Hydralazine – action unknown, acts on arterioles.

3. Calcium channel blockers – nifedipine, diltiazem, amlodopine.

4. Nitrates – vasodilation secondary to release of nitric oxide, dilate veins>arteries>arterioles.

Angiotensin Antagonists

Angiotensin converting enzyme inhibitors antagonise the conversion of Angiotensin I to Angiotensin II, and the metabolism of bradykinin. Angiotensin is a vasoconstrictor, which stimulated the release of aldosterone (conserves salt and water in the kidney). Bradykinin a vasodilator.

Others

Magnesium acts as a calcium channel blocker, thus vasodilating.

TREATMENT PROTOCOLS

Non urgent: Beta blocker +/- thiazide, or calcium channel blocker (asthmatics) or ACE inhibitor (diabetes / associated CCF).

Urgent: GTN, then nitroprusside or labetolol, then hydralazine. "Bring the BP down gently"

PATHOPHYSIOLOGY OF ESSENTIAL HYPERTENSION

PERIPHERAL BLOOD VESSELS

END ORGAN DYSFUNCTION

1. THE HEART

ECG shows left ventricular hypertrophy with strain

BP = CO X PR

PERIPHERAL RESISTANCE (PR): circulating blood volume, vascular tone (smooth muscle and local vasoactive agents) sympathetic nervous system activity, renin-angiotensin – aldosterone axis, antidiuretic hormone, atrial natiuretic peptide.

CARDIAC OUTPUT

CO = HR X SV

HEART RATE: depends on baroreceptor activity, sympathetic nervous system activity and vagal tone

STROKE VOLUME depends on Preload (LVEDV), Afterload (LV systolic wall tension and peripheral resistance), and contractility (Starling curve).

WALL TENSION: Laplace’s Law:

Wall tension = transmural pressure X ventricular radius / 2 X wall thickness

In order to cope with the increased afterload, the heart hypertrophies [increasing the denominator above]. This leads to increased myocardial O2 requirement, and endomyocardial fibrosis. Cardiac dilatation eventually follows, and subsequent heart failure.

Hypertension causes:

1. Acceleration of atheromatous disease.
2. Myocardial ischaemia in the absence of coronary artery disease.
3. Decreased myocardial compliance and an increase in the atrial contribution to diastolic filling and cardiac output.
4. Congestive cardiac failure / pulmonary oedema.

Fleisher and Barash: Anaesthesia and Analgesia 1992 74; 586 – 598

"The risk for perioperative myocardial ischaemia is increased in hypertensive patients with left ventricular hypertrophy."

2. BRAIN

Strandgaard S: Circulation 1976 53:720-27

Autoregulation of cerebral blood flow in hypertensive patients.

Lower limit of autoregulation was:

113mmHg in severe hypertension 73 mmHg in normotensive patients

Lowest limit of blood pressure tolerated without symptoms was:

65 mmHg in severe HTN, 53 mmHg in treated HTN, 43mmHg in normotensives

This return to the right occurs after 8 – 12 months, maybe longer.

We cannot measure cerebral autoregulation, so a good rule of thumb is:

• A 25% decrease in MAP reaches the lower limit of autoregulation.
• A 55% decrease in MAP reaches symptomatic brain hypoperfusion.
• Remember that these patients may also have cerebrovascular and carotid arterial disease. "Watershed" ischaemia may occur with even relative hypoperfusion.
• Treatment of hypertension significantly reduces the incidence of stroke.

3. RENAL

The kidneys are "sitting ducks" in hypertension.

• End organ damage to the kidneys from HTN: glomerular sclerosis, abnormal distribution of renal blood flow & decreased GFR.

"Prerenal" hypoperfusion due to a sudden and sustained decrease in BP (during anaesthesia for major surgery) leads to postoperative renal insufficiency.

PREOPERATIVE HYPERTENSION AND PERIOPERATIVE RISK

Determinants of risk:

• Level of blood pressure.
• Duration of treatment.
• Degree of end organ damage.
• Type of surgery.

Level of hypertension:

• Severe HTN increased risk: BP lability, myocardial ischaemia, MI, pulmonary oedema arrhythmias, renal failure and neurologic damage.

From Goldman and Caldera Anesthesiology 1979

• Patients with mild to moderate hypertension are not at increased risk of major morbid events.
• Patients with any form of preoperative hypertension, treated or untreated, have an increased risk of post op HTN.
• Prolonged increases or decreases in MAP by 20 mmHg or 20% increased risk of postoperative complications.

Type of surgery associated with increased risk:

Aortic surgery, carotid endarterectomy, CABG, craniotomies (aneurysm clipping), AVM, posterior fossa surgery. All at risk of postop HTN (Goldman).

METHODS TO REDUCE PERIOPERATIVE RISK

1. Adequate preoperative blood pressure control.

Continue all antihypertensives up to and including the day of surgery (except diuretics).

Delay elective surgery if SBP>200 mmHg, or if DBP >120 mmHg, until BP <190/110 mmHg, preferably lowered to 140/90 mmHg over several weeks.

Acute control within hours of surgery is inadvisable.

2. Antihypertensive therapy

Use of agents to attenuate the haemodynamic responses to intubation, incision and extubation:

• Opioids – Fentanyl, Alfentanyl.
• Antihypertensives – Esmolol, Labetalol, Atenolol, Metoprolol, clonidine, enalapril (one dose preop).
• Lignocaine

3. Hydration

Volume load the hypertensive patient prior to induction.

This helps to minimise the peaks and valleys that characterise the hypertensive patient.

4. Choice of agents

Consider using agents with minimal haemodynamic effects – fentanyl, thiopentone rather than propofol, pethidine rather than morphine, vecuronium or cis-atracurium rather than atracurium, sevoflurane induction etc.

5. Analgesia

Opioid and non steroidal anti-inflammatory agents prevent the hypertensive response to pain, intra- and post- operatively.

ACUTE POSTOPERATIVE HYPERTENSION

Differential diagnosis

Risk associated:

• Loss of vascular anastomoses
• Intracranial bleeding
• Myocardial ischaemia [particularly when associated with tachycardia]

Treatment

Depends on

• The clinical situation
• The aetiology
• The degree of hypertension
• Analgesia must be optimized
• Hypertension, where worrisome, should be treated with: GTN, Labetolol, Esmolol, Nitroprusside, Hydralazine etc. Avoid sublingual nifedipine.

• Antihypertensive drug withdrawal (e.g., clonidine)
• Autonomic hyperactivity
• Collagen-vascular diseases Drugs (e.g., cocaine, amphetamines)
• Glomerulonephritis (acute)
• Head trauma
• Neoplasias (e.g., pheochromocytoma)
• Preeclampsia & eclampsia
• Renovascular hypertension

The manifestations of hypertensive crises are those of end-organ dysfunction:

1. Hypertensive encephalopathy
2. Acute aortic dissection
3. Acute myocardial infarction
4. Acute cerebral vascular accident
5. Acute hypertensive renal injury
6. Acute congestive heart failure

It is important to recognize that the absolute level of BP may not be as important as the rate of increase. Patients with longstanding hypertension may tolerate systolic BPs of 200 mm Hg or diastolic BPs of up to 150 mm Hg without developing hypertensive encephalopathy, while children or pregnant women may develop encephalopathy with diastolic BPs 100 mm Hg.

Management

• What was the patient's blood pressure prior to presentation, does the patient have any prior or current complaints, and what medications, prescription and nonprescription, has the patient taken?
• Palpation of pulses in all extremities is necessary.
• A fundoscopic examination is mandatory
• FBC, urea, creatinine, urinalysis, chest x-ray, electrocardiogram (and head computed tomography are useful in patients with evidence of shortness of breath, chest pain, or neurological changes, respectively).
• These tests are performed simultaneously with the initiation of antihypertensive therapy.

KEY POINTS IN HYPERTENSION