Hypertension And Heart Failure Flashcards
What is blood pressure?
Driving force to perfuse organs with blood (force per unit area acting on vessels)
How to calculate resistance to flow
(8Xviscosity) X length / pie radius4 (to the power) = resistance to flow
Define hypertension, what are the three categories of causes?
An elevation in blood pressure associated with an increase risk of some harm
140/90 mmHg
Essential/ primary/ idiopathic (90%) Secondary to other pathology Pre- hypertensive Isolated systolic/ diastolic White coat/ clinic
Best practice for recording blood pressure
Sitting
Relaxed
Arm supported
Both arms >15mmHg difference repeat measurement and use arm with higher reading
Measurements over period of visits +/- ABPM/ HBPM
Emergency treatment required >180/ 120 + clinical signs
CVD risk and end organ damage should be assessed whilst waiting for hypertensive conformation
What are the blood pressure boundaries for diagnosing hypertension?
140/90 <80yrs
150/90 >80yrs
135/85 type 1 diabetes
Offer treatment
Target aim: 120/80 mmHg
What blood pressure categories hypertension as stage 1, 2 or 3/ severe?
Stage 1: clinic 140/90 - 159/99 mmHg
and subsequent ABPM daytime average or HBPM average 135/85 - 149/94 mmHg
Stage 2: clinic 160/100 mmHg or higher
And subsequent ABPM daytime average or HBpM average of 150/95 mmHg or higher
Stage 3/ severe: clinic systolic 180mmHg/ higher or diastolic 120mmHg/ higher
What categorises someone as prehypertension? How can you reduce their risk?
> 120/80 <140/90 mmHg
✅promotion regular exercise, modified healthy/ balanced diet, reduction in stress and increased relaxation, limited/ reduced alcohol intake, discourage Xs caffeine, smoking cessation, reduction dietary sodium
= CVD risk reduction
List the main primary hypertension therapeutic agents
Angiotensin converting enzyme inhibitors (ACEi)
Angiotensin (AT1) receptor blockers (ARBs)
Calcium channel blockers (CCBs)
Diuretics- thiazides and thiazides like
Other agents
Where is ACE found? How does angiotensin-2 cause its actions?
ACE - luminal surface of capillary endothelial cells predominantly in lungs
Catalysed conversion angiotensin 1 to angiotensin 2 vasoconstrictor
Angiotensin 2 binds to AT1 and AT2 receptors
AT1 - receptor subtype typical of classic angiotensin 2 actions (vasoconstriction, stimulations of aldosterone, cardiac and vascular muscle cell growth and vasopressin release from PP)
Why is there still some angiotensin 2 produced even with a high dose of ACEi?
Angiotensin 2 also produced from angiotensin 1 independently of ACE via chymases
What are the side effects of ACEi, explain why you get some of them? When shouldn’t you use ACEi? Give an example of one
Dry cough - build up of bradykinin (also substrate for ACE)
Hypotension - vasodilation by stopping production of angiotensin 2 and also from build up bradykinin (vasodilator via NOS/NO and PGI2)
Hyperkalaemia (low aldosterone)
Angioedema (more common black ppl)
Renal failure (renal artery stenosis where construction of efferent arteriole needed)
❌if person has renal artery stenosis, AKD, pregnant, breastfeeding
Be careful if: on drugs increase K, NSAIDs, other antihylertenisve agents
E.g. ramipril, lisinopril
Angiotensin 2 receptor blockers/ antagonists (ARBs): benefits, drawbacks, when to avoid, when to be cautious, examples
AT1 and AT2 receptors
No effect bradykinin ✅
Reduced angioedema✅
Less effective in low-renin hypertensives❌
directly target AT1 more effective at inhibiting Ang2 mediated vasoconstriction (chymase production too)
When to avoid: renal artery stenosis, AKD, pregnancy, breastfeeding
Be cautious: other K increasing drugs, NSAIDs, other antihypertensive agents
Candesartan or losartan
How do Calcium channel blockers work?
L-type calcium channels allow inward Ca flux (VOCC) expressed throughout body e.g. vascular smooth muscle cells, cardiac myocytes, SA and AV node
Calcium channel blockers target calcium initiated smooth muscle contraction (in hypertension) - 3 types interact with different sites on alpha-1 subunit of VOCC (selectivity for vascular smooth muscle or myocardium)
What are the 3 classes of Calcium channel blockers? Compare them briefly
- dihydropyridine
Selective for peripheral vasculature, little chronotropic or inotropic effects (first line CCB for hypertension) cerebral vs peripheral selectivity
Non-hydropyridines:
- phenyalkylamines
Depresses SA node and slows AV conduction, negative inotropy - benzothiazpines sit in middle
When are calcium channel blockers the first choice for antihypertenisve treatment?
In low renin patients
Compare different drugs in the dihydropyridine class. What do they do? Side effects, when are they unsuitable, drug reactions?
Amlodipine - longer half life
Nimodipine - selectivity for cerebral vasculature (sub arachnoid haemorrhage)
Selective for peripheral vasculature, little chronotropic or inotropic effects (first line CCB for hypertension) cerebral vs peripheral selectivity
❌ankle swelling, flushing, headaches (vasodilation), palpitations (compensatory tachycardia reflex)
Unsuitable: unstable angina, severe aortic stenosis
Drug reactions: amlodipine + simvastatin (increased effect of statin), other antihypertensive agents
How do phenylalkyamines work, example, uses, side effects, contraindications, drug interactions?
Class 4 anti-arrhythmic agent/ prolongs action potential/ effective refractory period
E.g. VERAPAMIL
Less peripheral vasodilation, negative chronotropic and inotropic effects
Used for: arrhythmia, angina, hypertension
❌constipation, bradycardia (I.v.), heart block, cardiac failure
Contraindicated: poor LV function (caution needed), AV nodal conduction delay
Interactions: beta blockers, other antihypertensive and antiarrhythmic agents
Example of a benzodiazepine
DILTIAZEM
Sit between other CCB classes
How do thiazides and thiazides-like diuretics work? Give examples. Side effects, contraindications, drug interactions
Inhibit Na/ CL co-transporter in DCT
Long term effects mediated by sensitivity of vascular smooth muscle to vasoconstrictors Ca/ Na
E.g. BENDROFLUMETHIAZIDE, Inadapamide (thiazides like)
❌hypokalaemia, hyponatraemia, hyperuricemia, Arrhythmia, increased glucose/ cholesterol/ triglyceride
Contraindicated: hypokalaemia, hyponatraemia, gout
Interactions: NSAIDs, K lowering drugs (monitoring)
Describe the steps to treatment of primary hypertension
Hypertension with type 2 diabetes or hypertension age <55 and not black Africans or African Caribbean-> ACEi / ARB -> + CCB / thiazide-like diuretic -> 3: ACEi / ARB + CCB + TLD -> 4: confirm resistant hypertension, discuss adherence, expert advice or add: low dose spironolactone if blood K 4.5
Hypertension >55yrs or black African or African Caribbean family origin -> CCB -> + ACEi / TLD -> steps 3 and 4 as above
When are diuretics used over CCBs?
In oedema
When do you need to seek expert advice in regards to antihypertensive medication?
If Bp is uncontrolled on optimal tolerated doses of 4 drugs
How do you treat resistant hypertension and what is it? Contraindications, drug interactions, when might you use a different treatment?
If BP not controlled after step 3 e.g. after ACEi / ARB + CCB + TLD
First thing to consider is:
SPIRONOLACTONE- aldosterone receptor antagonist
Not if: hyperkalaemia, Addison’s
Interactions: K+ increasing drugs e.g. ACEi and ARBs (monitoring)
Can give alpha and beta blockers if high K
Centrally acting drugs - labetalol (pregnancy, IV hypertensive emergencies) reduced sympathetic outflow
How do beta adrenoceptor blockers work? Give examples, side effects, contraindications, drug interactions
Decreased sympathetic tone by blocking NAd and reducing myocardial contraction, decreases renin secretion
E.g. LABETALOL, bisoprolol, metoprolol
❌ bronchospasm, heart block, Raynaud’s, lethargy, impotence Mask tachycardia (sign of insulin induced hypoglycaemia)
Contraindications: asthma, COPD, haemodynamic instability, hepatic failure (dose monitoring)
Drug interactions: non- dihydropyridine CCB - verapamil and diltiazem -> asytole
How do alpha adrenoceptor blockers work, example, side effects, contraindications, drug interaction
Selective antagonism of alpha 1 adrenoceptors, reduce peripheral vascular resistance
E.g. DOXAZOSIN
❌postural hypotension, dizziness, syncope, headache, fatigue
Don’t give if already have postural hypotension
- dihydropyridine CCBs
Definition of heart failure, symptoms
Abnormality in cardiac function which is responsible for the failure of the heart to pump blood at a rate commensurate with the requirements of metabolising tissues
Characterised by symptoms that may present and often in later stages - exercise intolerance, dyspnoea, fatigue, swelling
How does physiological response to reduced cardiac output sometimes lead to further pathology?
Cardiac output reduction detected
Neurohormonal response (sympathetic NS and RaAS)
Vasoconstriction
Increased preload and afterload
Increased cardiac workload
Ventricular dilation and remodelling (proliferating signalling) - increased myocardial O2 demand
Management of heart failure pathway
Chronic heart failure diagnosed -> diuretics (furosemide)
With preserved ejection fraction -> manage comorbidities, personalised exercise based cardiac rehabilitation programme unless unstable
With reduced ejection fraction -> offer *ACEi (lisinopril) and BB (bisoprolol) and MRA (spironolactone) if symptoms continue -> personalised exercise programme
*consider ARB (candersartan) if into,errant to ACEi
