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Htn And Heart Failure Flashcards

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1
Q

How is resistance related to radius of vessels

A

Ss, Small changes on the radius have big changes in resistance and hence blood pressure (r^4)

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2
Q

Descrbe the pathophysiology of H&n

A
  • Elevated blood pressure (essential/primary/idiopathic) still not completely understood - debated
  • Leads to vascular changes inc. remodelling and thickening, hypertrophy
  • Increased vasoactive substances inc. ET-1, Nad, angII
  • Vascular remodelling as direct result of local salt sensitivity
  • Hyperinsulinemia and hyperglycaemia – endothelial dysfunction and reactive oxygen species (ROS) ↓NO
  • ….culminating in permanent and maintained medial hypertrophy of vascularture → ↑↑TPR and ↓↓compliance
  • End organ damage (renal, peripheral vascular disease, aneurysm, vascular dementia, retinal disease)
  • “Hypertensive heart disease” LVH → dilated cardiac failure
  • ↑ Morbidity and mortality
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3
Q

Why does H&n need to be treated

A

Increase above normal increases risk of chd and stroke. Needs to be treated. Precursor to cardiovascular diseases

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4
Q

Define Htn

A

• Labile, age, sex and population differences makes defining HT difficult
• “An elevation in blood pressure that is associated with an increase in
risk of some harm”
• “Significantly high to cause end organ damage”
• “An elevated blood pressure that treated will do more good than harm”
• NICE suggest that 140/90 mmHg defines hypertension - ≥ 40% population of England
• Reduction in BP – both SBP and DBP reduces CVD risk
• Essential/primary/idiopathic – 90% secondary
prehypertensive
isolated systolic/diastolic
white coat/clinic - is real phenomenon

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5
Q

Desribe the diagnosis and treatment of htn

A

• Screening those at risk
• Increasing public awareness of risk factors
• Reliable diagnoses based on clinical guidelines
• Promote appropriate lifestyle changes to limit risk – no immediate gain
• Regular monitoring and refinement of medication – resistant HT, increasing risk of CHD/stroke, adherence!
• SILENT KILLER!
• Current UK guidelines:
British hypertension society
SIGN No. 49 (Scotland)
NICE CG 127 and clinical evidence update 32

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6
Q

Describe th best practices for diagnosing htn

A
  • Measure blood pressure whilst patient is sitting, relaxed and arm is supported
  • Measurements in both arms, >20 mmHg difference repeat measurement and use arm with higher reading
  • diagnosis of stage 1 or stage 2 hypertension should follow elevated BP measurements made over several visits and or addition of ABPM. HBPM an alternative if ABPM not tolerated
  • If severe hypertension is observed, urgent or emergency treatment should be initiated
  • Cardiovascular risk and end organ damage should be assessed whilst waiting for HT confirmation
  • How patient will be managed following diagnosis will vary but aiming to achieve target BP and reduce risk of CVD is primary aim
  • Target BP will vary according to associated risk, age, end organ damage and complications of diabetes and other peripheral vascular disease
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7
Q

Define stage 1 2 and severe htn

A

1: 140/90 or 135/85
Clinic vs home
2: 160/100 C or 150/95 H
Severe: systolic 180 higher C do diastolic 110 or higher C
• Diabetic and renal compromise stage 1 >130/80 as a starting point
• Isolated systolic hypertension mild >140 SBP <90 DBP, moderate >160 SBP <90 DBP

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8
Q

What ispre hypertesion

A
  • Elevated BP below stage 1 diagnoses with no end organ damage can be treated in the first instance with lifestyle changes
  • 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
  • Should be promoted to all patient groups
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9
Q

What are primary htn therapeutic agents

A
  • Angiotensin converting enzyme (ACE) inhibitors Angiotensin (AT1) receptor blockers (ARBs)
  • Calcium channel blockers (CCBs) • Diuretics
  • Other agents used in specific circumstances
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10
Q

Describe the actions of ace and ang ii

A

• ACE - luminal surface of capillary endothelial cells, predominantly in the lungs
• ACE catalyses conversion of angiotensin-I to potent active vasoconstrictor angiotensin-II
• Angiotensin-II affords action through AT1 and AT2 receptors
• 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

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11
Q

What are ace inhibitor moas

A

Eg ramipril
•
• • • • •
• •
Limit the conversion of Angiotensin-I to Angiotensin-II by inhibiting circulating and tissue ACE
Thus a reduction in Angiotensin-II effects, resulting in vasodilation
reduction in aldosterone release reduced vasopressin (ADH) release reduced cell growth and proliferation
All can contribute to antihypertensive effects
NB. Angiotensin-II can also be produced from angiotensin-I independently of ACE via chymase interaction – (see ARB’s)

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12
Q

What are the side effects/contraindications to acei

A

Bradykinin (BK) also a substrate for ACE
• ACE is kininase-II – breaks down kinins - inc. BK
• Use of ACE inhibitors therefore potentiates BK - vasodilatation via NOS/NO and PGI2
- ACE inhibitor vasodilation in low-renin hypertensives (see later slides A/CD)
• Well tolerated but associated with persistent dry cough (10-15%) (BK), angioedema (more common in black population), renal failure (inc. renal artery stenosis) and hyperkalaemia.

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13
Q

Describe arbs

A

Eg losartan • AT1 and AT2 receptors - AT1 important in relation to cardiovascular regulation
• Confusing nomenclature – Angiotensin-II blockers, AT1-receptor blockers or ARB’s
• ARB’s have no effect on BK- less effective in low-renin hypertensives, but aren’t associated with dry cough
• Directly targeting AT1 receptors therefore more effective at inhibiting Ang-II mediated vasoconstriction (chymase production)
• As with ACE inhibitors: renal failure and hyperkalaemia are side effects

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14
Q

Describe ltccs and ccbs

A
  • LTCCs allow inward Ca2+ flux into cells – voltage operated calcium channel (VOCC)
  • Expressed throughout the body - inc. vascular smooth muscle cells AND cardiac myocytes
  • Large calcium flux into cell, further calcium from SR and activation of contractile proteins (myosin, actin)
  • CCBs target calcium initiated smooth muscle contraction
  • Three classes of CCB that interact with different sites on (α1) subunit of VOCC’s selectivity for VSMC or myocardium
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15
Q

Whar er the classes of ltccs and ccbs

A

• - Dihydropyridine class
- non-dihyropyridine - Phenylalkylamines and Benzothiazapines
• Dihydropyridine class more selective for peripheral vasculature, show little chronotropic or inotropic effects (first line CCB for HT)
• Phenylalkyamine depresses SA node and slows AV conduction, negative inotropy
• Benzothiazapines sit in the middle
• CCBs – primary choice antihypertensive in low renin hypertensives

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16
Q

What are the properties of dihydropyridines

A 
Eg amlodipine 
Properties:
• Good oral absorption
• Protein bound > 90%
• Metabolised by the liver
• Few have active metabolite
17
Q

What are the adverse effects of dihydropyridies

A

Adverse effects:
• Sympathetic nervous system activation – tachycardia - rare
• Palpitations
• Flushing, sweating, throbbing headache
• Oedema
• Amlodipine and simvastatin (increased Cp of simvastatin)

18
Q

Wha are the actions of phenylalkylamines

A

Eg verapamil
Phenylalkylamines
Action:
• Impedes calcium transport across the myocardial and vascular smooth muscle cell membrane
• Class IV anti-arrhythmic agent/prolongs the action potential/effective refractory period
• Less peripheral vasodilatation, negative chronotropic and inotropic effects
• Arrhythmia, angina, (hypertension)

19
Q

What are the adverse effects of penylalkylamines

A

Adverse effects:
• Constipation
• Risk of bradycardia
• Negative inotrope - can worsen heart failure - additive with beta blockers

20
Q

What are the properties of benzothiapines

A

Eg diltiazen
Properties:
• Impedes calcium transport across the myocardial and vascular smooth muscle cell membrane
• Prolongs the action potential/effective refractory period
• Sits between amlodipine et al. and verapamil in vascular and cardiac
effects
• Angina (hypertension)

21
Q

What are the adverse effects o benzothiazapines

A

Adverse effects:
• Risk of bradycardia
• Negative inotropic effect less than verapamil - can worsen heart failure

22
Q

Describe thiazides

A

Eg benxoflumethiazide
• Moderately potent, inhibit Na+ reabsorption in distal convoluted tubule
• Diuresis resulting in lower blood and extracellular volume ↓TPR
• Useful over CCBs in odema
• Long term effects mediated by sensitivity of VSM to
vasoconstrictors Ca2+/Nad – we think!

23
Q

What are the adverse elects o diazides

A

Adverse effects:
• Hypokalaemia
• Increased urea and uric acid levels
• Impaired glucose tolerance (especially with beta-blockers)
• Cholesterol and triglyceride levels increased
• Activates RAAS

24
Q

Describe the nice guidelines for treating 1o htn

A

S

25
Q

What are the other options

A

Spironolactone, labetalol
• If A, C or D are not effective or contraindicated then several other classes can be considered
• ACE inhibitor first line for hypertension in HF and DM patients
• Alpha-adrenoceptor blockers
• Beta-adrenoceptor blockers
• Spironolactone – mineralocorticoid/aldosterone receptor antagonist
• Amiloride – K+ sparing acting on distal tubule
• Direct renin inhibitor – aliskirin
• Other direct vasodilators – nitrates e.g. SNP (hypertensive emergency i.v.)
• Centrally acting drugs – labetalol (pregnancy, hypertensive
emergency i.v.) - reduce sympathetic outflow - not typically in primary practice but p.o. labetalol in pregnancy

26
Q

Describe alpha adrenoceptor blockers

A 
Eg doxazosin 
• Selective antagonism at post-synaptic α-1 adrenoceptors and antagonise the contractile effects of noradrenaline on vascular smooth muscle
• Reduce peripheral vascular resistance
• Benign effect on plasma lipids/glucose
• Safe in renal disease
27
Q

What are the adverse effects of alph blockers

A

Adverse effects:
• Postural hypotension………Dizziness
• Headache and fatigue
• Oedema (especially if combined with dihydropyridine)

28
Q

Describe beta blockers

A

Eg bishop roll
Decrease sympathetic tone by blocking Nad and reducing myocardial contraction → ↓ CO (↓ renin secretion) affording antihypertensive effects

29
Q

What are teh adverse effects of beta blockers

A
  • Can cause bronchoconstriction so contraindicated in asthmatics and COPD also in 2nd/3rd degree heart block
  • Also mask tachycardia – sign of insulin induced hypoglycaemia – caution in diabetics
  • Lethargy and impaired concentration
  • Reduce exercise tolerance
  • Bradycardia
  • Raynaud’s (cold hands)
30
Q

What is heart failure briefly

A

• Cardiac output (CO) ~ 5L/min in a typical adult
• CO varies in response to both physiological and pathological factors - preload – filling pressure (LVEDP – surrogate for sarcomere length) - afterload – “load” that ventricle must eject blood against
- contractility
- heart rate
• 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 of HF
- exercise intolerance, breathlessness, fatigue (swelling)
• Acute heart failure – the result of sudden circulatory collapse – haemorrhagic shock or cardiogenic shock during AMI, sepsis

31
Q

Describe teh aetiology of hf

A

• •
Usually, there is some form of cardiomyopathy
“disease of the myocardium associated with cardiac dysfunction” (WHO,
1995)
many causes of cardiomyopathy
-inherited
congenital hypertrophic CM arrhythmogenic RV CM
-acquired
ischaemic cardiomyopathy pressure overload
valve disease infection/inflammation/alcohol

32
Q

What is the self perpetuating @spiral”

A

Physiological neurohormonal response in its attempt to compensate will eventually lead to further pathology- ss

33
Q

Describe management of h

A

• 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
• Correct underlying cause (replace valve, angioplasty)
• Non pharmacological management – ↓↓salt intake, liquid reduction
~ 1.5L
AIMS of treatment are:
• reduction in symptoms (dyspnoea, fatigue, oedema)
• Managed increase in exercise tolerance
• decreased mortality
• address arrhythmias, hyperlipidaemia, diabetes
Diuretics, typically furosemide, are used in most patients symptomatically (congestive symptoms) but have little impact on survival
furosemide

34
Q

Describe acei and arb in hf

A

• 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
• monitor renal function within first few weeks
• if ACE inhibitor not tolerated, an AT1 antagonist (ARB) may be used as alternative
• ARBs have essentially similar benefit as ACE inhibitor in HF, typically
start with ACE inhibitor, if not tolerated then ARB (under close supervision of cardiologist can be used together)

35
Q

Desribe teh use of spironolactoe in hf

A
  • In some individuals refractory hyperaldosteronism occurs (RAAS gene polymorphism?) (sometimescalledaldosteroneescape)
  • Typically used as adjunct to max ACE inhibitor and diuretic
  • 1663 patients NYA class III/IV
  • LVEF ≤ 35%
  • ACE inhibitor, loop diuretic and digoxin (most)
  • 25 mg spironolactone SID
  • All cause mortality
36
Q

Describe the usage of beta antagonists in hf

A

• recommended for ALL patients with stable CHF unless contraindicated or not tolerated
• introduce once ACE inhibitor or AT1 antagonist (ARB) therapy is initiated
• 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 I antiarrhythmic effect) reducing arrhythmia
• may also blunt circulating RAAS directly inhibiting renin, but probably minor effect since ACE inhibitors already used
• LOW initial dose which may cause transient worsening of symptoms (e.g. fatigue, poor exercise tolerance)

Cpt (24 decks)

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