Hypertension

Page 2:

• Objectives:

  • Understand the significant public health concerns caused by hypertension

  • Review the physiology of factors affecting blood pressure

  • Define primary and secondary hypertension

  • Discuss modifiable & non-modifiable risk factors

  • Explain the pathophysiology and clinical manifestations of hypertension

  • Outline treatment measures

Page 3:

• Cardiovascular Disease:

  • Involves alteration in the heart and blood vessels, including the associated change in blood flow

  • The most common conditions are:

    • Hypertension

    • Coronary heart disease

    • Heart failure

    • Cerebrovascular disease

Page 4:

• Cardiovascular diseases:

  • Hypertension affects up to 1 in 5 NZers (bpac.org.nz).

  • One in 20 adults in NZ have been diagnosed with heart disease - >165,000 (Craft & Gordon 2019)

  • Causes 34% and 40% of deaths in New Zealand

  • Incidence increases with age

  • Rates of the disease in Maori exceed non-Maori

Page 5:

• Hypertension:

  • Many people are likely to have undiagnosed hypertension

  • Diagnosis is based on repeated measurements where systolic BP > 140 mmHg or diastolic BP > 90 mmHg

  • Blood pressures are classified into diagnostic categories with respective recommended interventions.

Page 6:

• Hypertension:

  • 90-95% of hypertension is primary

  • Risk factors causing hypertension:

    • Primary:

      • Family history

      • Age and gender

      • Abdominal obesity

      • Heavy alcohol intake

      • Glucose intolerance

      • High salt intake

      • Sedentary lifestyle

      • Low potassium, calcium, magnesium intake

    • Secondary:

      • Kidney disease

      • Endocrine imbalance, e.g. adrenocortical

      • Drugs, e.g. oral contraceptives, corticosteroids, antihistamines

Page 7:

• Revision:

  • Blood Pressure is the pressure that blood exerts on the blood vessel walls

  • This needs to be sufficient for adequate organ perfusion

  • Pressure within the arteries is maintained by contraction of the left ventricle, vascular resistance and volume of blood

  • BP = CO X PVR

  • CO is the product of HR and SV, and SV as mainly influenced by preload, contractility and afterload.

  • Cardiac Output = heart rate X stroke volume

  • CO = HR X SV

Page 8:

• Preload:

  • The work imposed on the heart

  • Preload → Stretch at the end of ventricle filling- Pressure in the left ventricle before contraction

  • Depends on adequate venous return to fill the heart with blood and adequate cardiac muscle stretch to promote a strong contraction.

  • The Frank Starling mechanism- the greater the stretch the greater the force of the contraction

Page 9:

• Afterload:

  • Afterload → Resistance

  • The force required taken to open the aortic valve and push blood against the vascular pressure

  • Affected by increased resistance from the aorta and pulmonary artery

  • ↑ peripheral vascular resistance, leads to lower blood output

  • → ↑ blood pressure

  • → ↑ workload for the heart

Page 10:

• Control of Blood Pressure:

  • Homeostatic neural and hormonal mechanisms work via the autonomic nervous system.

  • Baroreceptors detect pressure changes in the aorta and carotid arteries

  • When pressure drops they signal SNS to increase cardiac output, peripheral resistance and blood volume.

  • When pressure increases they activate the PNS and inhibit the SNS to reduce cardiac output, peripheral resistance and blood volume.

Page 16:

• Hypertension Clinical manifestations:

  • Early – none – a ‘silent’ condition

  • Later – symptoms arise due to associated damage of organs as well as vascular changes.

  • These include:

    • Heart disease

    • Renal insufficiency

    • Brain dysfunction

    • Impaired vision

    • Impaired mobility

    • Vascular occlusion and edema

Page 17:

• Increased peripheral vascular resistance causes:

  • Increased resistance to by ventricular ejection (afterload) causes

  • Increased workload for the left ventricle causes release of renin-angiotensin-aldosterone and sympathetic nervous system over time leads to stimulates

  • Hypertrophy release causes

  • Increased myocyte demand for oxygen (relative ischemia) eventually

  • Ventricular remodeling chronic long-term effect

  • Decreased contractility ( 1 cardiac output and underperfusion of vital tissues)

Page 18:

• Heart wall pathology - myocardium:

  • Remodeling of the heart occurs as a result of neural & hormonal responses hypertension

  • Categories:

    • Dilated (formerly congestive)

    • Hypertrophic

    • Restrictive

Page 19:

• Check eligibility for absolute CVD risk assessment:

  • Eligible

  • Not eligible

• Conduct absolute CVD risk assessment

• Define risk based on clinical assessment of target organ damage, relevant comorbidities or known vascular disease

• High risk >15%

• Moderate risk 10-15%

• Low risk <10%

• Provide lifestyle advice

• Any of the following?

  • Start immediate drug treatment

  • BP persistently >160/100mmHg

  • Manage associated conditions

  • Family history of >160/100 mmHg?

• Review according to clinical context

• Aboriginal or Torres Strait Islander

• Yes

• No

• Start drug treatment

• Review BP

• Start drug treatment

• If SBP - clinical context treatment 140-159 mmHg, review BP after 2 months of lifestyle advice

• SBP 140-159 mmHg

• SBP 130-139 mmHg or DBP 90-99 mmHg or DBP 85-90 mmHg

• Review BP in Start drug treatment 6 months

Page 20:

• Assessment of Hypertension:

  • Repeated measurement of high blood pressure

  • Family and previous history

  • Physical examination

  • Blood analysis of:

    • Na+, K+, Cl-, bicarbonate

    • Urea, creatinine, uric acid

    • Hemoglobin

    • Fasting glucose

    • Total cholesterol, LDL, HDL

  • Urinalysis

  • ECG

Page 21: Management of Hypertension

• Non-pharmacological lifestyle regimens

• Pharmacological treatment aims to:

  • Decrease Stroke Volume (preload)

    • Diuretics, ACE-inhibitors, angiotensin II blockers

  • Decrease Total Peripheral Resistance

    • ACE-inhibitors, angiotensin II blockers, calcium channel blockers, a1-blockers, direct-acting vasodilators

  • Decrease Heart Rate

    • β-blockers

Page 22: Medications A, B, C & D

• A: ACE & ARBs

• B: β-blockers

• C: Ca²+ Channel blockers

• D: Diuretics

Page 23: Where medications act

• Medications act on the Renin-Angiotensin-Aldosterone System (RAAS)

• Angiotensinogen is converted to Angiotensin I by Renin

• Angiotensin I is converted to Angiotensin II by Angiotensin Converting Enzyme (ACE)

• Angiotensin II acts on AT1 receptors to cause vasoconstriction and increase blood pressure

• Medications like ACE inhibitors and ARBs act on different points of the RAAS pathway to reduce blood pressure

Page 24: A- ACE inhibitors

• Reduce blood pressure by reducing blood volume

• No effect on heart rate, contractility, or electrical activity of the heart

• Act on the RAAS pathway to block the conversion of angiotensin I to angiotensin II

• Medications end in 'pril' (Cilazapril, Enalapril, Quinapril)

Page 25: A- ARB (Angiotensin receptor antagonists)

• Effectively the same clinically as ACE inhibitors

• Reduce blood pressure by reducing blood volume

• No effect on heart rate, contractility, or electrical activity of the heart

• Act on the RAAS pathway to block the action of angiotensin II and inhibit aldosterone release

• Medications end in 'sartan' (Lorsatan, Valsarten)

Page 26: B- β-blockers

• Decrease the rate of electrical conduction through the heart

• Decrease rate and force of contraction, reducing vasoconstriction

• Indirectly decrease blood pressure

• Medications end in 'olol' (Metoprolol, Propranolol, Carvedilol)

Page 27: C- Ca+ Channel Blockers

• Act on the heart and blood vessels to dilate arteries, reducing peripheral resistance

• Two types: Dihydropyridines (DHPs) and Non-Dihydropyridines (Non-DHPs)

  • DHPs block systemic vasoconstriction

  • Non-DHPs change heart rate, rhythm, and strength

• Medications end in 'pine' (Felodpine, Amlodipine) for DHPs and include Diltiazem and Verapamil for Non-DHPs

Page 28: D- Diuretics

• Decrease total blood volume by reducing fluid, reducing preload

• No effect on heart rate, contractility, or electrical activity of the heart

• Four classifications based on action and site of action:

  • Loop diuretics (Frusemide)

  • Thiazide diuretics (Bendrofluazide)

  • Potassium sparing diuretics (Spironolactone)

  • Osmotic diuretics (Monnitol for cerebral edema)

Page 29: Impact on Individual, Whanau, and Community: Hypertension

• Individual