3.1 Hypertension And Heart Failure Flashcards
How do you calculate mean arterial pressure?.
CO x TPR.
What is resistance to flow inversely proportional to?
Inversely proportional to the radius (to the 4th power)
So, Vacoconstiction = increased peripheral resistance = increased BP
What can hyperinsulinemia and hyperglycaemia lead to?
Endothelial dysfunction and reactive oxygen species, decreased NO
Why do you need to treat Hypertension?
Precursor to cardiovascular disease
Define hypertension
An elevation in blood pressure that is associated with an increase in risk of some harm
What are some causes of hypertension?
White coat/clinic
Isolated systolic/diastolic (only one is raised)
Prehypertensive
Secondary
How do you diagnose and treat hypertension?
- screening sessions
- increase public awareness of risk factors
- reliable diagnoses based on clinical guidelines
- promote appropriate lifestyle changes to limit risk
- regulate monitoring and refinement of medication.
What are the clinical methods of diagnoses of hypertension?
Measure BP with patient sat relaxed with a supported arm
Measurements in both arms should be similar, within 20mmHg
Severe = medical emergency, send to A&E
Patient management follows diagnoses
Cardiovascular risk and wend organ damage should be assessed whilst waiting for HT conformation
Normal BP?
<120/80 mmHg
Stage 1 hypertension measuring ?
140/90 mmHg or higher
Home - 135/80 mmHg
Stage 2 hypertension BP?
160/100 mmHg or higher
Home 150/95
Severe hypertension bp?
SYSTOLIC IS 180 mmHg or higher or diastolic is 110 mmHg or higher
What is prehypertension?
Elevated BP below stage 1 diagnoses with no end organ damage that can be treated in the first instance with lifestyle changes
What can lifestyle changes can treat elevated bp in prehypertension?
Regular exercise
Modified health/balanced diet
Reduction in stress and increased relaxation
Limited/reduced alcohol intake
Discourage excessive caffeine consumption
Smoking cessation
Reduction in dietary sodium
What are some primary HT therapeutic agents?
ACE inhibitors
Angiotensin receptor blockers
Calcium channel blockers
Diuretics
Where does ACE and Ang 2 act?
Luminal surface of capillary endothelial cells, predominantly in the lungs
Catalysts conversion of Ang 1 to And 2 which is a vasoconstrictor
Ang 2 acts through AT1 and AT2 receptors
Name 4 ACE inhibitors.
Captopril
Enalapril
Lisinopril
Ramipril
Why do ace inhibitors cause a dry cough?
ACE substrate = bradykinin
If ACE is inhibited, get a build up of bradykinin = dry cough
What side affects are associated with ACE inhibitors?
Dry cough
Angioedema
Renal failure
Hyperkalaemia
How do angiotensin 2 receptor blockers work?
Block AT1 receptors which carry out majority of angiotensin 2 functions (unlike AT2 receptor)
Directly targeting AT1 receptors means they’re more effective at inhibiting Ang 2 mediated vasoconstriction
What side effects do you get with ang 2 receptor antagonists?
Renal failure and hyperkalaemia
No dry cough as no effect on bradykinin
Name 4 ang 2 receptor antagonists
Losartan
Candesartan
Eprosartan
Irbesartan
What do calcium channel blockers target?
Calcium inhibiated smooth muscle contraction
There are three classes that interact with different sites on a1 subunit of VOCC selectivity for vascular smooth muscle cells or myocardium
What are the three classes of calcium channel blockers?
- Dihydropyridine
Non dihydropyridine
- Phenylalkamines and benzothiazapines
How do dihydropyridine CCB work and what are their properties?
More selective for peripheral vasculature, show little chronological or inotropic effect
- first line CBB for HT
- good oral absorption
- protein bound
- metabolised by liver
Name an example of a dihydropyridine CBB and name its adverse effects.
Amolodipine is an example
Adverse effects
- sympathetic NS activation = tachycardia (rare)
- palpitation
- flushing/sweating/throbbing headache
- oedema
What is the mode of phenylalkylamines CBB?
Depresses SA node and slows AV conduction, negative inotropy
Prolongs the AP and effective refractory period
Impede ca transport across myocardial and vascular smooth muscle cell membrane
Give an example of a phenylalkylamine and give it’s adverse effects
Verapamil
Effects include
- constipation
- bradycardia
- negative inotrope = can worsen heart failure, especially with a beta blocker
What are the properties of benzothiazapines CBB ?
Impede ca transport across ca and smooth muscle cell membrane
Prolong AP
Name a benzothiazapines CCB and give its adverse effects
Diltiazem
Effects
- risk of bradycardia
- negative inotropic effect less than verapamil = can worsen heart failure
What are some adverse effects of thiazides? Name an example
Example = bendroflumethiazide
Effects
- hypokalaemia
- increased urea and Uris acid levels
- impaired glucose tolerance especially with beta blockers
- cholesterol and triglycerides levels increase
- activates RAAS
Why is there no point in giving ARBs to a low renin patient?
Low activity in RAAS system anyway so no point in targeting it for treatment.
In pregnancy or a hypertensive emergency, what centrally acting drugs would you use?
Labetalol reduced sympathetic outflow
What is spironolactone?
Mineralocorticoid/ aldosterone receptor antagonists
What is amiloride?
A K+ sparing diuretic acting on distal tubule
What is the effect of alpha adrenoreceptors blocking agents? Name an example.
Doxazosin is an example
They antagonise the contractile effects of noradrenaline on vascular smooth muscle
Reduced peripheral vascular resistance
Benign effect on plasma lipids/glucose
Safe in renal disease
Adverse effects
- postural hypotension
- headache and fatigue
- oedema
What is the effect of beta adrenoreceptors blockers? Name an example
Bisoprolol is an example
Decreased sympathetic tone by blocking Nad and reducing myocardial contraction = decreased CO = decreased renin secretion
What are the adverse effects of beta adrenoreceptors blockers?
Adverse effects
- bronchoconstriction so don’t give in asthma, COPD and 2nd/3rd degree heart block
- mask tachycardia = sign of insulin induced hyperglycaemia = caution in diabeties
- lethargy and impaired concentration
- reduced excersise tolerance
- bradycardia
- raynauds
E.g bisoprolol
What are the aims of heart failure treatment?
Manage symptoms
Increase exercise tolerance
Decreased mortality
Address arrhythmia
NB: furosemide is typically used in most patients for symptoms but has little impact on survival
How can ace inhibitors and ARBs treat heart failure?
In LV dysfunction
Low initial dose reduces risk of sudden rapid fall in BP, especially in patients already taking diuretics
If ACE inhibitors not tolerated, use ARB as alternative
If not working can use both together
Make sure you monitor renal function
Why may a patient be given spironolactone with a ACE inhibitor or diuretic?
It maximises their effects.
NB: spironolactone is a aldosterone/mineralocorticoid receptor antagonist
What is the role of B adrenoreceptors antagonists?
Recommended for all patients with stable clinical heart failure
Introduced once ACE inhibitor or ARB therapy is initiated
Blunts sympathetic influences especially on HR = slower HR = longer diastolic filling period = better filling = more output
May stabilise electrical conduction reducing arrhythmia
May also blunt circulating RAAS by working on renin but probably minor since already on ACE
Low initial dose which may cause transient worsening of symptoms
