Management and therapy of hypertension and heart failure Flashcards
Why should we detect, manage and treat hypertension?
Major risk factor for coronary disease and stroke
Predisposes to other target organ diseases e.g. renal disease, retinopathy, hypertensive heart disease and CHF
Hypertension is almost always asymptomatic until secondary disease is present»_space;> hypertension is a silent killer
Strategy for detection and treatment
Community based screening of population especially those statistically at greatest risk e.g. over 50s
Greater public awareness e.g. health education
Reliable diagnosis using agreed threshold BPs
Lifestyle management and treatment to target BPs to reduce life-time risk
Regular monitoring and review
Threshold BPs
Ideal: <120/80
Stage 1: >140-90 (135/85)
Stage 2: >160/100 (150/95)
Severe: SBP> 180 or DBP >110
Target BPs
Target BPs represent the desirable BP goals on treatment to minimise risk
Need to be realistic
Vary acording to age, 10 year CV risk, target organ disease and diabetic vascular complications
Mildly elevated BP
BP between the ideal value and stage 1 threshold may be managed by lifestyle changes
Key features of this approach are body weight reduction, increased physical exercise, smoking cessation, mental relaxation and stress management, sensible alcohol and caffeine intake
Dietary sodium restriction is widely advocated but unlikely to have much effect in most people
Stage 1 hypertension (not at risk)
If < 80 years and no target organ complications and 10 year CV risk <20%, advise lifestyle changes
Review annually
Target BP <140-90 mmHg
Stage 1 hypertension (at risk)
If <80 years and one or more of: target organ disease, established CV disease, renal disease, diabetes, 10 year risk >20%
Initiate drug treatment
Target BP <140-90 mmHg
<130/80 mmHg if diabetic or established CV disease
Stage 2 hypertension
Treat all patients to achieve target BP, regardless of age and other conditions
Target BP <140-90 mmHg
<130/80 mmHg if diabetic or established CV disease
General principles of drug treatment for hypertension
Selection of drug treatments for new cases should be according to current NICE guidelines (2011)
The general approach is stepwise, adding drugs from specific classes in a sequential manner according to the response
Evidence-based approach, founded on essential hypertension being of low renin or high renin types (i.e. less or more involvement of RAAS activation)
ACD algorithm step 1
If patient < 55 years with normal to high renin, treat with ACE inhibitor e.g. ramipril or AT1 antagonist (if not tolerated, use beta blocker)
If patient > 55 years or of African/ Caribbean descent of any age, with low to normal renin, treat with a calcium channel blocker e.g. amlodipine (if not tolerated, use thiazide-like diuretic e.g. indapamide)
ACD algorithm step 2
If patient < 55 years, add calcium channel blocker e.g. amlodipine (if not tolerated, use thiazide-like diuretic e.g. indapamide)
If patient > 55 years or of African/ Caribbean descent of any age, add ACE inhibitor or AT1 antagonist
ACD algorithm step 3
For any patient, A+C+D:
ACE inhibitor or AT1 antagonist
Calcium channel blocker
Thiazide-like diuretic
ACD algorithm step 4 (resistant hypertension)
A+C+D
Add additional diuretic e.g. spironolactone
If no response or not tolerated, add alpha 1 antagonist or beta blocker
Special cases and circumstances
A number of special conditions require particular approaches or have different target BPs Over 80s Isolated systolic hypertension Presence of diabetes Presence of target organ renal disease Pregnancy Severe hypertension
Hypertension in pregnancy
Gestational hypertension = after 20 weeks without proteinuria
Pre-eclampsia = after 20 weeks with proteinuria, can lead to eclampsia
In pre-existing or gestational hypertension, labetalol or methyldopa are used
Severe hypertension
Defined as BP >180/10 mm Hg
When acute end organ damage e.g. retinopathy treat as hypertensive emergency
Requires IV vasodilator treatment to reduce BP by ~25% within 2 hours to reduce risk of haemorrhagic stroke, subarachnoid haemorrhage etc. e.g. sodium nitride prusside
When no acute end organ disease, treat as hyertensive urgency
Lower BP over 24-48 hours with oral labetalol, amlodipine or felodipine
Management of chronic heart failure
Usually dealing with LV systolic dysfunction associated with reduced LV ejection fraction <45%
Where there is preserved EF e.g. diastolic heart failure or high output failure, optimal treatment is not clearly defined
Aims of treatment are: reduction in symptoms, increased exercise tolerance, decreased number of decompensation episodes, decreased mortality
Principles of drug treatment for chronic heart failure
Counteract the neurohormonal axis which drives progression of the condition
Renin-angiotensin-aldosterone system: ACE inhibitors, AT1 receptor antagonists, aldosterone antagonists
Sympathetic nervous system: beta-adrenoreceptor antagonists
Other drugs usually, as add-ons, may target other aspects
ACE inhibitors
e.g. enalapril, ramipril, lisinopril
Useful in all grades of LV dysfunction and there is a drug class effect
Low initial dose reduces risk of sudden rapid fall in BP, especially in patients already taking diuretics
Upward titration of dose over 2-3 weeks
With a loop or thiazide-like diuretic if oedema e.g. furosemide
Adverse effects of ACE inhibitors
Persistent dry cough should be monitored carefully in CHF patients on ACE inhibitors and possible pulmonary oedema excluded as a cause
Mild/insignificant reduction in renal fraction occurs after initiation of treatment in most patients
Monitor renal function (creatinine, urea) within first few weeks
Hyperkaleamia
AT1 receptor antagonists/ ARBs
e.g. losartan, valsartan, candesartan
If ACE inhibitor not tolerated, an AT1 antagonist may be used as an alternative
ARBs have essentially similar benefit as ACE inhibitor in CHF but high doses required
Possibility of additional benefit when ACE inhibitor and ARBs combined
Sacubitril potentiates natriuretic peptides; used in fixed combination with valsartan
Beta blockers
e.g. bisoprolol, carvedilol (A and B blocker), nebivolol are licensed in UK, metoprolol is used elsewhere
Recommended for all patients with stable CHF unless contraindicated or not tolerated
Introduce one ACE inhibitor or AT1 antagonist therapy is initiated
Effects of beta blockers
Benefit is related to blunting of sympathetic influences especially on heart rate
Slower HR- longer diastolic filling period- better filling- more output
May also stabilise electrical conduction (class 1 antiarrhythmic effect) reducing arrhythmia
May also blunt circulating RAAS directly by inhibiting renin release but probably minor effect since ACE inhibitors already used
Dosing of beta blockers
Low initial dose which may cause transient worsening of symptoms e.g. fatigue, poor exercise tolerance
As symptoms improve, gradually titrate over 8 weeks to target dose or maximum tolerated
Bisoprolol fumarate: 1.25 mg mane»_space;> 10 mg mane
Carvedilol: 3.25 mg bd»_space;> 25 mg bd
Ivabradine may be added under specialist supervision (funny current blocker)
Aldosterone antagonists (mineralocorticoid receptor antagonists)
e.g. spironolactone, eplerenone
Used as adjunctive therapies on top of maximum ACE inhibitor and beta blocker therapy
Usually a low dose is required
Beware of hyperkalaemia, especially with ACE inhibitor
Adjunctive/ alternative therapies
Loop and thiazide related diuretics may be added if patients remain symptomatic on first-line therapy
Digoxin- may produce symptomatic benefit in patients in sinus rhythm, but no mortality benefit
Ivabradine- funny current blocker, slows HR
Evidence of benefit for some patients with high HR despite beta-blockade
Hydralazine/ nitrate combination
Balanced venodilatation and arteriodilatation, reduced preload and afterload, increased CO
Mortality benefit but not as good as that seen with ACE inhibitor therapy
May be an alternative for patients who can not tolerate ACE inhibitor or ARB
Especially useful for African/ Caribbean patients
Symptoms of acute decompensation
Worsening peripheral oedema Pulmonary oedema Worsening dyspnoea with orthopnoea Cough, often frothy or blood-stained sputum Worsened fatigue and exercise tolerance Dizziness and confusion Decreased urine output Coldness and pallor
Management of acute decompensation
IV opiates e.g. morphine to reduce anxiety, high flow O2 to aid breathlessness, fluid offloading and haemodynamic stabilisation
Loop diuretic IV/IM e.g. furosemide, bumetanide to reduce pulmonary oedema and titrated to renal function
Nitrate IV e.g. glyceryl trinitrate to venodilate and reduce preload, titrated to systolic BP
Sympathomimetic inotrope IV e.g. dopexamine for short term inotropic effect
PDE-3 inhibitor IV e.g. milrinone, enoximone for short term inotropic effect
