5 - Hypertension and Heart Failure Flashcards
(26 cards)
define hypertension, and explain pathophys briefly
hypertension is a long term elevation in BP above normal that will lead to end organ damage and heart failure
an elevated BP will go on to cause
the vasculature will hypertrophy and thicken - increasing TPR and decrease compliance long term
this can cause renal damage, peripheral vascular disease, vasuclar dimentia, retionopahtys and LVH - heart failure
1st step of treatment is ?
recommend lifestyle changes
how do we diagnose hypertension - general idea, not specifics
Sitting, relaxed and arm is supported
• Both arms, >15 mmHg difference repeat measurement and use arm with higher reading
• Measurements over period of visits +/- ABPM/HBPM
- Aim – target BP and reduced CVD risk
- 140/90 < 80 years old inc. type II diabetes
- 150/90 > 80 years old
- 135/85 type 1 diabetes
outline the staging of hypertension
120/80 mmHg “desired” – minimise CVD risk
• Stage 1 hypertension
Clinic blood pressure ranging from 140/90 mmHg to 159/99 mmHg
• Stage 2 hypertension
Clinic blood pressure of 160/100 mmHg or higher but less than 180/120 mmHg
• Stage 3 or severe hypertension
Clinic sbp of 180 mmHg or higher or clinic dbp of 120 mmHg or higher.
what is prehypertension ?
what are some of the recommend advice and changes ?
>120/80 <140/90 mmHg • Promotion of regular exercise • Modified healthy/balanced diet • Reduction in stress and increased relaxation • Limited/reduced alcohol intake • Discourage excessive caffeine consumption • Smoking cessation • Reduction in dietary sodium • Contribute to CVD risk reduction
what are the primary hypertension therapeutic agents ?
• Angiotensin converting enzyme (ACE) inhibitors
(ACEi)
Angiotensin (AT1)receptor blockers (ARBs)
- Calcium channel blockers (CCBs)
- Diuretics – thiazide and thiazide-like
outline/draw the RAAS system, including where enzymes are made - use this to show where some of the drugs target
do it, then check against lec 5 - slide 17
outline how an ACEi works and the resulting effects it has
ACE - luminal surface of capillary endothelial cells, predominantly in the lungs
• ACE catalyses conversion of angiotensin-I to potent active vasoconstrictor angiotensin-II
• AT1 receptor subtype typical of classic angiotensin-II actions
- vasoconstriction, stimulation of aldosterone, cardiac and vascular muscle cell growth and vasopressin (ADH) release from posterior pituitary
Limit the conversion of Angiotensin-I to Angiotensin-II by inhibiting circulating and tissue ACE
• A reduction in Angiotensin-II effects, resulting in
• vasodilation (↓ PVR →↓afterload)
• reduction in aldosterone release (↑Na + H2O exc.)
• reduced vasopressin (ADH) release (↑ H2O exc.)
• reduced cell growth and proliferation
• Bradykinin also a substrate for ACE
• Use of ACEi therefore potentiates bradykinin
- vasodilatation via NOS/NO and PGI2
→ ACEi vasodilation in low-renin hypertensives
what are the side effects of an ACEi
what are the contraindications
Hypotension! Dry cough (10-15% - BK association) hyperkalaemia (low aldosterone ↑ K+)
renal failure (esp. renal artery stenosis where constriction of efferent arteriole needed)
AKD,
DONT TAKE - pregnant or breastfeeding - CKD
angioedema (BK more common in black population)
what are important DDI’s ?
↑K+ drugs
NSAIDs,
other antihypertensive agent
what are the two key ACEis
Lisinopril
Ramipril
the Prils
outline how ARB’s work (angiotension receptor blockers/antangonists)
AT1 and AT2 receptors - AT1 important in relation to
cardiovascular regulation
• no effect on bradykinin - less effective in low-renin hypertensives
↓ ↓ dry cough and angioedema
• Directly targeting AT1 receptors - more effective at inhibiting Ang-II mediated vasoconstriction
contraindications and DDI’s of ARB’s
X Renal artery stenosis, AKD, pregnancy, breastfeeding, (CKD - caution)
Δ ↑K+ drugs, NSAIDs, other antihypertensive agents
name the two key ARB’s
Candesartan
Losartan
the sartans
outline how CCB’s (calcium chanel blockers work)
LTCCs allow inward Ca2+ flux into cells – voltage
operated calcium channel (VOCC)
• Expressed throughout the body - inc. vascular
smooth muscle cells AND cardiac myocytes plus SA
and AV node
• CCBs target calcium initiated smooth muscle
contraction (in hypertension) - block ca entering smooth muscle - less contractile force and hence vasodilation of vessels
• 3 classes of CCB interact with different sites on (α1)
subunit of VOCC - selectivity for vascular smooth muscle or myocardium
what are the types of CCBs
when are they 1st choice over ACEi
- dihydropyridines
- non-dihyropyridine - phenylalkylamines and benzothiazapines
- dihydropyridines selective for peripheral vasculature, little chronotropic or inotropic effects (first line CCB for hypertension)
- Phenylalkyamine depresses SA node and slows AV conduction, negative inotropy - targets MYOCARDIUM
- Benzothiazapines - bit of both effects
CCBs – primary choice antihypertensive in low renin patients
what are the dihydropyridine class of CCB’s
name the three drugs
Side Effects
contras and DDI’s
amlodipine, nifedipine, nimodipine
the idipines
- Amlodipine has long half life others tend to be shorter
- Nimodipine selectivity for cerebral vasculature (sub arachnoid haemorrhage)
side effects: Ankle swelling, flushing, headaches (vasodilation)
Palpitations (compensatory tachycardia)
X Unstable angina, severe aortic stenosis - they need the higher TPR
Δ amlodipine + simvastatin (increased effect of statin), other antihypertensive agents
name the key benzothiazapine
diltiazem
outline the phenylalkylamines
one key drug
role and cases used for
side effects
contras + DDI’s
Verapamil
Class IV anti-arrhythmic agent/prolongs the action potential/effective refractory period
- Less peripheral vasodilatation, negative chronotropic and inotropic effects
- Used for: Arrhythmia, angina, (hypertension)
• Constipation, bradycardia (i.v.), heart block and cardiac failure
- X Poor LV function (caution), AV nodal conduction delay
- Δ β-blockers (cardiologist only), other antihypertensive and antiarrhythmic agents
outline the phenylalkylamines
two key drug
role
side effects
contras + DDI’s
thiazide - bendroflumethiazide
thiazide like - indapamide
• Inhibit N+/Cl- co-transporter in DCT
↓Na+ and H2O (RAAS compensates)
• Useful over CCB in oedema
- Hypokalaemia, hyponatraemia, hyperuricemia, arrhythmia
- ↑ glucose (especially with beta-blockers)
- ↑ cholesterol and triglyceride
X Hypokalaemia, hyponatraemia, gout,
Δ NSAIDs, ↑K+ drugs (monitoring)
describe the approach to treating primary hypertension
look at the diagram on lec 5 slide 28 - this is KEY ! so do it
why use ACEi or ARB for type 2 diabetics - the two pronged approach
↓ Diabetic nephropathy and CKD with proteinuria
dilation of efferent glomerular arteriole
So called “two pronged” approach
↓PVR→↓BP and dilation of efferent glomerular arteriole
→ reduced intraglomerular pressure – good for type II diabetes
what do we give extra if a patient is at stage 4 resistant hypertension ?
do DDI’s and Contras
- Spironolactone – aldosterone receptor antagonist
- X Hyperkalaemia, Addison’s
- Δ ↑K+ drugs inc. ACEi and ARBs (monitoring)
• α and β blockers if high K+
outline B blockers
3 key drug
mechanism
side effects
contras + DDI’s
labetalol, bisoprolol, metoprolol - lols
Decrease sympathetic tone by blocking NAd and reducing myocardial contraction → ↓ CO
↓ renin secretion β1
Bronchospasm, heart block, Raynaud’s (cold hands), lethargy, impotence
• Mask tachycardia – sign of insulin induced hypoglycaemia
X Asthma, (COPD), haemodynamic instability, hepatic failure (dose monitoring)
Δ non-dihydropyridine CCB – verapamil and diltiazem – asystole!
