Hypertension

Question 1

What is hypertension ?

Answer 1

sustained elevation of systemic arterial blood pressure

Can be caused by an increase in CO, total peripheral resistance, and vascular volume

Question 2

When is hypertension diagnosed?

Answer 2

• the mean of two or more BP measurements
  
  • made on two or more consecutive clinical visits
  • shows a diastolic pressure of ≥90 mmHg OR a systolic pressure of ≥140 mmHg.

Question 3

What are the known risk factors of hypertension?

Answer 3

Acute myocardial infarction (AMI), stroke, aneurysms and chronic renal disease

Question 4

What are the classifications of hypertension?

Answer 4

• Primary (idiopathic or essential hypertension)
	• Secondary
Other forms of abnormal BP include:
	• Isolated systolic hypertension
	• Orthostatic hypotension

Question 5

What is primary hypertension?

Answer 5

• Affects 90-95% of patients with no definable cause
  
  • May have a genetic predisposition and environmental influence - effects abnormal sodium transport or hyperactivity of the RAAS

Question 6

What is secondary hypertension?

Answer 6

• High BP associated with another cause and accounts for only 5-10% of cases
• Usually induced by a disease process (renal disease, Cushing’s disease, pheochromocytoma) orillicit drugs (phenylephrine in cold/cough preparation) which make up about 90% of these cases
Gestational hypertension makes up about 10% of secondary hypertension

Question 7

What is isolated hypertension?

Answer 7

systolic BP ≥140 mmHg and a diastolic blood pressure ≤90 mmHg

Question 8

What is orthostatic hypotension?

Answer 8

• Drop in BP (systolic and diastolic) when an individual stands up from sitting or lying down
  
  • Common in older people (≥65 years) and increases the risk of falls in this population
  • Can also be an effect of antihypertensive agents

Question 9

What are the modifiable risk factors to prevent hypertension?

Answer 9

• Overweight (BMI >25) and obesity (BMI >30)
• Physical inactivity
• Tobacco smoking
• Dietary salt (40-100 mmol/L or 0.5-1.0 teaspoon per day)
• Total cholesterol >6.5 mmol/L (treated)
• Stress (educational programs)
Alcohol (<2 drinks/day)

Question 10

What are the non-modifiable risk factors to prevent hypertension?

Answer 10

• Advancing age which is gender specific (males >55 years and women >65 years)
• Known family history of premature CVD
Ethnicity (Indigenous Australians and Torres Strait Islanders)

Question 11

What is the pathophysiology for primary hypertension?

Answer 11

Due to a trigger (genetics, environment) = inflammation, insulin resistance, dysfunction of the SNS, RAAS or related hormones = vasoconstriction and an increase in peripheral resistance and the possibility of renal salt and water retention which increases blood volume = sustained hypertension

Question 12

What are the clinical manifestations of hypertension?

Answer 12

• Early stages of hypertension exhibit no clinical signs (‘silent’)
• Most clinical manifestations are caused by complications that damage organs and/or tissues outside the CVS
*Chronic, untreated HTN leads to reactive changes in the smaller arteries and arterioles and cause variable wall thickness (arteriosclerosis) = decrease in the calibre of the vessel lumen = restricts the vessel’s capacity to dilate = possible heart and/or renal failure and stroke

Question 13

What are the diagnostic tests that should be performed for hypertension?

Answer 13

Before any diagnostic test can be performed, a detailed medical hx needs to be completed to identify and investigate risk factors:
• Needs to be documentation of increased BP on two or more different occasions
• Thorough physical assessment: auscultation for carotid, abdominal and femoral sounds
• Electrocardiogram (ECG)
• Lab tests (full blood examination (FBE) and urinalysis)
• 24-hour BP monitoring

*This will hopefully rule out any ‘white coat hypertension’ whereby the patient is stressed by a healthcare professional (HCP) to such a degree that there BP becomes elevated

Question 14

Pharmacological management of hypertension

Answer 14

“ABCD” approach

• Angiotensin Converting Enzyme (ACE) inhibitors (-pril)
• Angiotensin II Receptor Blockers (-artan)
• Alpha Blockers (-osin)
• Beta Blockers (-lol)
• Calcium Channel Blockers (-pine)
• Potassium-Sparing Diuretics

Question 15

What are the approaches to hypertensive management

Answer 15

• Depend on the presence of other coexisting conditions
  
  • Treatment of mild - moderate HTN usually starts with one drug (e.g. diuretic or a beta-blocker). If the BP remains above the target, consider other factors such as nonadherence. When one drug is only partially successful in lowering the BP, it is preferable to try a combination of drugs rather than a higher dose of the one drug

Question 16

Angiotensin Converting Enzyme (ACE) inhibitors

Answer 16

(-pril):
• Inhibits ACE = block conversion of angiotensin I to angiotensin II = relax BV and decrease force of cardiac contraction
• Decrease the release of aldosterone from the adrenal cortex leading to sodium loss and potassium retention and block breakdown of bradykinin
• Common adverse effects: dry persistent cough (10-20%); metallic taste (captopril), hyperkalaemia, confusion, restlessness, irregular HR, numbness and tingling of lips and limbs, muscle weakness and hypotension (common with the first dose). Administer at night to avoid dizziness and syncope
• Clinical considerations:
○ Avoid use with potassium supplements and spironolactone
○ When commencing treatment, start at the lowest dose
○ Renal function and electrolyte levels should be checked prior to administration and reviewed after 1-2 weeks
E.g. captopril, enalapril, perindopril and ramipril

Question 17

Angiotensin II Receptor Blocker

Answer 17

-artan):
• Block binding of angiotensin II to angiotensin (AT1) receptors = reduce vasoconstriction, block release of aldosterone from the adrenal cortex increasing sodium loss and potassium retention
• Common adverse effects: hypotension, dizziness, headache, hyperkalaemia and GI disturbances. The incidence of cough is less when compared to ACE inhibitors
• Clinical considerations are the same with ACE inhibitors
E.g. Losartan, candesartan and irbesartan

Question 18

Alpha Blocker

Answer 18

(-osin) • α1 and α2 medications: selective α1 blockers (antagonists) - prazosin and terazosin; and non-selective blockers (both) - phentolamine (pheochromocytoma)
• Block α1 receptors on arterioles and venules = reduce systemic vascular resistance, = decrease BP
• Some adverse effects include postural hypotension, nasal congestion, pupil constriction, fatigue and diarrhoea
• Hypotension is common on the first dose and in older patients; there may be fluid depletion and diuretics. The patient should rise slowly from a laying/sitting position to minimise postural hypotension. Medications should start at a low dose at bedtime to avoid this complication

Question 19

Beta Blockers

Answer 19

(-lol):
• β1 blockers: (cardio-selective) block β1 receptors = decreases heart rate and force of contraction; decrease renin release
E.g. atenolol, bisoprolol and metoprolol
• β2 blockers: block β2 receptors = bronchoconstriction, peripheral vasoconstriction and impaired insulin release (chronic use increases the risk of diabetes mellitus)
E.g. Non-cardio-selective (block both β1 and β2 receptors): carvedilol, pindolol and propranolol
• Adverse effects: bradycardia, hypotension, impaired peripheral circulation (cold extremities), vivid dreams and erectile dysfunction in males
• Contraindicated in asthma, COPD, bradycardia, cardiogenic shock, severe hypotension and diabetes
*May mask hypoglycaemic symptoms (palpitations, tremor, hunger) in diabetic patients
*Abrupt withdrawal can also cause rebound hypertension - If there is a need to reduce the dose, always do it slowly to prevent rebound hypertension
Administer dose in the morning to avoid vivid dreams (consider atenolol as it is less likely to enter the brain)

Question 20

Calcium Channel Blockers

Answer 20

(-pine):
• Block movement of calcium into cells (block L-type calcium channels)= relaxes muscle, cardiac contractility, cardiac conduction and vascular tone
• Some work on vascular smooth muscle (nifedipine) whereas others (diltiazem, verapamil) act on cardiac and vascular muscle
• Verapamil has a greater cardiac effect on AV node function when compared to diltiazem
• Adverse effects include headache, hypotension, dizziness, palpitations, facial flushing and skin rashes
• Contraindicated in cardiogenic shock
E.g. amlodipine, felodipine, nifedipine, diltiazem and verapamil

Question 21

Potassium-Sparing Diuretics

Answer 21

• Spironolactone: Blocks sodium channels and aldosterone (interferes with sodium/potassium exchange) = inhibits sodium absorption in the distal tubule = sodium excretion and a decrease in urinary potassium excretion
• Amiloride: (acts independently of aldosterone) inhibits sodium reabsorption in the distal convoluted tubule which decreases water retention
• Adverse effects for both diuretics: hyperkalaemia, gynaecomastia in men and postmenopausal bleeding in women. Avoid potassium supplements and ACE inhibitors
• Clinical considerations: monitor potassium levels
• Contraindicated in patients with hyperkalaemia
• A once-daily dose may prevent nocturia
E.g. spironolactone and amiloride