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_Sem 4. CPT NOTES > S3 L1 Hypertension and Heart Failure > Flashcards

S3 L1 Hypertension and Heart Failure Flashcards

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1
Q

What is blood pressure?

A

Driving force to perfuse organ with blood (force per unit area acting on vessels)
- Pressure needed to drive blood out of the heart- requires a pressure gradient

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2
Q

What are some of the features of BP?

A 
Not uniform throughout the body 
- Gravity has an impact 
Measure systolic and diastolic pressure 
Cyclical 
Physiologically regulated variable → changes
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3
Q

What affect the BP?

A

Mean Arterial Pressure (MAP)= Cardiac output (CO) x total peripheral resistance (TPR)
TRP also called systemic vascular resistance

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4
Q

How can the mean arterial pressure be calculated?

A

Diastolic blood pressure + ((systolic blood pressure - diastolic blood pressure)/ 3)
Time in systolic blood pressure is much smaller

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5
Q

How is the blood pressure regulated?

A

Autonomic sympathetic pathway and renin angiotensin-aldosterone system (RAAS)
Plus autacoid including bradykinin and NO (vasodilation)- action from the endothelium on vascular smooth muscle

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6
Q

How does the sympathetic activity regulate BP?

A

Decrease in BP
- ↑Activation of β1 adrenoreceptors on the heart → CO
- ↑ Activation of α1 adreno receptors on smooth muscle → ↑venous return
- ↑ Activation of β1 adrenoreceptor on kidney → ↑peripheral resistance and ↑renin release
Increase in Blood pressure

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7
Q

How does the renal blood flow regulate BP?

A

Decrease BP
↓ Renal blood flow → ↓ GFR → ↑Na+, H2O retention → ↑Blood volume → ↑CO → ↑BP
AND
↓ Renal blood flow→ ↑Renin → ↑Angiotensin II → ↑Aldosterone → ↑Sodium, water retention → ↑BV → ↑CO → ↑BP

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8
Q

How are resistance and increased mean arterial pressure related?

A

Resistance to flow = 8nL / πr^4
Radius of vessel main determinant of flow
Small change in radius = big change in resistance

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9
Q

How does the radius change?

A

Smooth muscle tone changes total peripheral resistance

Vasoconstriction causes ↑peripheral resistance require ↑BP to drive blood through systemic circulation to maintain CO

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10
Q

What is the pathophysiology of hypertension?

A
  1. Elevated blood pressure (essential/primary/idiopathic) still not completely understood
  2. Leads to vascular changes including remodelling, thickening and hypertrophy
  3. Increased vasoactive substances including ET-1 (endothelin-1), NA (noradrenaline) and AngII (angiotensin II)
  4. Vascular remodelling also occurs as a direct result of local salt sensitivity
  5. Hyperinsulinemia and hyperglycaemia lead to endothelial dysfunction and increased ROS - NO signalling reduced
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11
Q

What is the end results of hypertension?

A
  1. Permanent and maintained medial hypertrophy of vasculature with ↑↑TPR and ↓Compliance of vessels
  2. Results in end organ damage (renal, peripheral vascular disease, aneurysm, vascular dementia and retinal disease)
  3. Hypertensive heart disease- LVH → dilated cardiac failure
  4. Increased morbidity and mortality
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12
Q

Why should we treat hypertension?

A

Silent killer- often asymptomatic

Increases the risk of other diseases such a coronary heart disease, stroke

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13
Q

How is hypertension defined?

A

Labile, age, sex and population differences make it difficult to define
Elevation in blood pressure that is associated with an increase in risk of some harm
Significant to cause end organ damage
An elevated blood pressure that treated will do more good than harm

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14
Q

What is the NICE definition of hypertension?

A

140/90 mmHg= hypertension

Approx >40% population in England

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15
Q

What are the different types of hypertension?

A

Essential/ primary/ idiopathic - 90% of cases
Other 10%
- Secondary hypertension (secondary to another disease)
- Pre hypertension
- Isolated systolic/diastolic hypertension
- White coat/ clinic (real phenomenon- elevated BP in GP or hospital settings)

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16
Q

How is hypertension diagnosed?

A
  • Screening the at risk population
  • Increasing public awareness of risk factors
  • Appropriate lifestyle changes to limit risk- no immediate gain presence a challenge- don’t see or feel change so difficult to believe changes are working
  • Reliable measurements based on clinical guidelines
  • Regular monitoring and refinement of medication
  • SILENT KILLER
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17
Q

How should a BP be obtained?

A
  • Sitting, relaxed and arm is supported
  • Both arms >15mmHg difference repeat measurement and use arm with higher reading
  • Measurements over period of visits +/- Ambulatory BP measurement (ABPM) or Home BP measurement (HBPM)
  • Emergency treatment required (>180 SBP or 120 DBP + clinical signs)
  • CVD risk and end organ damage should be assessed whilst waiting for hypertension confirmation
  • Aim- target BP and reduced CVD risk
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18
Q

What is the target BP?

A

140/90 <80 year old including type II diabetes
150/90 >80 year old
135/85 type 1 diabetes

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19
Q

What are the different stages of hypertension?

A 
120/80 mmHg 'desired' minimise CVD risk 
Stage 1
- Clinical BP 140/90 - 159/99 mmHg and subsequent ABPM daytime/ HBPM average blood pressure ranging from 135/85 mmHg to 149/94 mmHg
Stage 2
- Clinical BP 160/100 - 180/120 mmHg
- ABPM/HBPM 150/95mmHg or higher 
Stage 3
- Clinical systolic BP of 180mmHg or higher OR clinical diastolic BP of 120mmHg or higher
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20
Q

What is prehypertension?

A

Slippery slop to hypertension >120/80 <140/90 mmHg

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21
Q

How can you prevent progression of hypertension?

A
  1. Promotion of regular exercise
  2. Modified healthy/balance diet
  3. Reduction in stress and increased relaxation
  4. Limited/ reduced alcohol intake
  5. Discourage excessive caffeine consumption
  6. Smoking cessation
  7. Reduction in dietary sodium
    - All contribute to CVD risk reduction
    These should be promoted to all patient groups not just pre pharmacological groups
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22
Q

What are the classes of drugs that are used to treat hypertension?

A

Angiotensin converting enzyme inhibitors (ACEi)
Angiotensin (AT1) receptor blockers (ARBs)
Calcium channel blockers (CCBs)
Diuretics- thiazide and thiazide-like
Other agents

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23
Q

What is ACE?

A

Angiotensin converting enzyme
Found on the luminal surface of capillary endothelial cells, predominantly in the lungs
Catalyses the conversion of AngI to AngII (active vasoconstrictor)

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24
Q

What is angiotensin II?

A

Afford action through AT1 (and AT2 receptors)
AT1 receptor subtype typical of classic angiotensin II action
- Vasoconstriction
- Stimulation of aldosterone (DCT)
- Cardiac and vascular muscle cell growth
- Vasopressin (ADH) release from posterior pituitary
BP↑ through combination of vasoconstriction and ↑circulating blood volume

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25
Q

What do ACEi do?

A

Limit the conversion of AngI to AngII by inhibiting ACE
Reduction in AngII activity
- Vasodilation ↓peripheral resistance → ↓afterload
- Reduction in aldosterone release ↑Na+ and H2O excretion
- Reduce vasopressin (ADH) release (↑H2O excretion)
- Reduce cell growth and proliferation
All can contribute to antihypertensive effects
AngII can also be produced from AngI independently of ACE via Chymases (additional pathway)

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26
Q

What are some of the common ACEi?

A

‘-pril’

  1. Lisinopril
  2. Ramipril
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27
Q

What are the adverse effects of ACEi?

A

Hypotension
Dry cough (10-15% bradykinin association)
Hyperkalaemia (low aldosterone ↑K+)
Cause or worsen renal failure (especially renal artery stenosis where constriction of efferent arterioles are needed)
Angioedema (more common in Afro-Caribbean patients)

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28
Q

What are the warning/contraindications of using ACEi?

A
  • Renal artery stenosis
  • AKD
  • Pregnancy
  • CKD- cation
  • Idiopathic angioedema
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29
Q

What are the important drug interactions of ACEi?

A

↑K+ drugs
NSAIDs
Other antihypertensive agents

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30
Q

How do ACEi affect bradykinin?

A

ACE also needed for bradykinin breakdown into peptide fragments
Use of ACEi potentiate bradykinin
- Vasodilation via NOS/NO and PGI2
→ ACEi vasodilation in low-renin hypertensives

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31
Q

What are the Angiotensin receptors blockers (ARB)?

A

‘-sartan’
Candesartan
Losartan

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32
Q

Where are the main mechanisms of action of ARBs?

A

AT1 and AT2 receptors
AT1 are important in relation to cardiovascular regulation
Confusing nomenclature- AngII blockers - block angiotensin II, AT1-receptors blockers- act at T1 receptor or ARBs
No affect on bradykinin as act further down in the pathway - less effective in low-renin hypertensive patients dry cough and angioedema much less likely

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33
Q

What are the adverse effects of ARBs?

A

Hypotension
Hyperkalaemia (low aldosterone ↑K+)
Cause or worsen renal failure

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34
Q

What are the warnings/contraindications of ARBs?

A

Renal artery stenosis
AKD
Pregnancy
CKD

35
Q

What are the important drug interactions of ARBs?

A

↑K+ drugs

NSAIDs

36
Q

Which are more effective the ACEi or ARBs?

A

ARBs- Directly targeting AT1 receptors
More effective at inhibiting AngII mediated vasoconstriction than ACEi
(chymase production AngII- block further downstream in the pathway)

37
Q

How do ARBs work?

A

Bind to AT1 receptor preventing AngII binding
Prevents:
- Arterial vasoconstriction
- Tubular Na+, Cl- and H20 reabsorption and K+ excretion
- Aldosterone release from adrenal cortex
- Posterior pituitary gland ADH release

38
Q

What are L-type calcium channels

A
  • Stimulated → Allow inward flux of Ca2+ ions into cells- VOCC→ calcium induced calcium release from SR → Contraction
  • On smooth muscles cells and cardiac myocytes plus SA and AV node
  • Calcium initiate smooth muscle contraction
39
Q

How do calcium channel blockers work?

A

Bind to LTCC/VOCC inhibit influx of Ca2+
Inhibit Ca2+ initiated smooth muscle contraction
Different CCB bind to different subunit (α1)
Different selectivity for vascular smooth muscle or myocardium

40
Q

What are the classes of calcium channel blockers?

A

Dihydropyridines

Non-dihydropyridines → Phenylalkylamines and benzothiazapines

41
Q

What are the dihydropyridines?

A

Selective for peripheral vasculature
Little chronotropic or inotropic effects
Used in hypertension
Primary choice in low renin patients

42
Q

What do the non-dihydropyridines do?

A

Phenylalkyamines- depress SA node and slow AV node conduction, negative inotrophy
Benzothiazapines- In the middle, some cardiac effects, some peripheral vasculature effects

43
Q

What are some of the dihydropyridine CCB?

A

‘-ipine’
Amlodipine - longer half life
Nifedipine
Nimodipine - selective for cerebral vasculature

44
Q

What are the adverse effects of dihydropyridine CCBs?

A

Ankle swelling, flushing, headaches → vasodilation

Palpitations → compensatory tachycardia

45
Q

What are the contraindications of dihydropyridine CCBs?

A

Unstable angina, severe aortic stenosis

46
Q

What are the drug-drug interactions?

A

Used with simvastatin → Increases the effects of simvastatin so reduced dose maybe necessary

47
Q

What are the phenylalkylamines used for?

A

Class IV anti-arrhythmic agent/ prolongs the action potential/ effective refractory period
Less peripheral vasodilation
More action on cardiac tissue- negative chronotropic and inotropic effects
Treat: Arrhythmias, angina, sometime hypertension

48
Q

How do the phenylalkylamines have an effect on cardiac tissue?

A

?

49
Q

What are the adverse effects of phenylalkylamines?

A

Constipation
Bradycardia
Heart block
Cardiac failure

50
Q

What are the contraindications of phenylalkylamines?

A

Poor LV function - use with caution

AV nodal conduction delay

51
Q

What are the important drug-drug interactions of phenylalkylamines?

A

β-blockers

Other antihypertensives and antiarrhythmic agents

52
Q

What is the benzothiazapine

A

Diltiazem

53
Q

What is the benzothiazapine?

A

Diltiazem

54
Q

How do the thiazide and thiazide-like diuretics work?

A

Inhibit the Na+/Cl- cotransporter in the DCT
↓Na+ and H2O reabsorption
(RAAS compensated with time- further down tubule increase Na+ uptake through ENaC)
Also helps cause vasodilation

55
Q

What are some of the thiazide ad thiazide-like diuretics?

A

Thiazide- bendroflumethiazide

Thiazide like- indapamide

56
Q

What are the adverse effects of thiazide and thiazide like diuretics?

A 
Hypokalaema 
Hyponatraemia 
Hyperuricemia (gout) - competition at OATs
Arrhythmias 
↑glucose 
↑cholesterol ad triacylglyceride
57
Q

What are the contraindications of thiazide and thiazide-like diuretics?

A

Hypokalaemia
Hyponatraemia
Gout

58
Q

What are the important drug-drug interactions with thiazide and thiazide like diuretics?

A

NSAIDs

↓K+ such as loop diuretics

59
Q

How is primary hypertension treated?

A

Step 1 → ACEi or ARB or CCB
Step 2 → Add on ACEi or ARB or CCB (depending on what’s already been prescribed) or thiazide-like diuretic
Step 3 → Combination of all of them (ACEi or ARB and CCB and thiazide-like diuretic)
Step 4 → Confirm resistant hypertension - add in spironolactone, α blocker or β blocker

60
Q

How do you decide what to give in step 1?

A

Hypertension w/o type 2 diabetes

  • Age 55 or + or black African or African-Caribbean family origin → CCB
  • Age <55 and not black African or African-Caribbean family origin → ACEi or ARB
61
Q

How are patients with hypertension and type 2 diabetes treated?

A

ACEi or ARB
Help to ↓diabetic nephropathy and CKD with proteinuria by dilation of efferent glomerular arteriole → ↓pressure in the glomerulus
Two pronged approach
1- ↓peripheral vascular resistance → ↓BP
2- Dilation of efferent glomerular arteriole → ↓glomerular pressure

62
Q

What things should be considered in Step 4 for resistant hypertension before adding another drug?

A

Need to consider patient adherence, compliance, check drugs are being taken in the correct way

63
Q

What is spironolactone?

A

Aldosterone receptor antagonist
- Aldosterone mineralocorticoid released from the adrenal cortex
Adverse effects→ hyerkalaemia, gynaecomastia (males develop breast tissue)
Contraindications→ hyperkalaemia and Addisons (too little cortisol and aldosterone
Drug-drug interactions→ ↑K+ drugs, pregnancy

64
Q

What is considered instead of spironolactone in pregnancy?

A

Labetalol - reduced sympathetic outflow

65
Q

What are beta adrenoreceptor blockers?

A
  • Decrease sympathetic tone by blocking NA and reducing myocardial contraction → ↓CO
  • ↓Renin secretion β1
66
Q

What are the adverse effects of beta blockers?

A

Bronchospasm
Heart block
Raynaud’s
Lethargy
Impotence
Mask tachycardia- sign of insulin induced hypoglycaemia
- think about β1 (heart) and β2 (lungs) selectivity when considering side effects

67
Q

What are the contraindications of beta blockers?

A

Asthma, COPD, haemodynamic instability, hepatic failure

68
Q

What are the important drug-drug interactions with beta blockers?

A

Non-dihydropyridine CCBs verapamila and diltiazem causes asystole (heart stops)

69
Q

What are examples of the β-adrenoreceptor blockers?

A

‘-lol’
Labetalol
Bisoprolol
Metoprolol

70
Q

What are the α-adrenoreceptor blockers?

A

Selective antagonists of α1 adrenoreceptors
Reduce peripheral vascular resistance
- Also affect urinary tract → bladder neck and prostate- benign prostatic hyperplasia
Relatively safe in renal disease

71
Q

What are the adverse effects of α-blockers?

A

Postural hypotension
Dizziness
Syncope
Headache and fatigue

72
Q

What are the contraindications of α-blockers?

A

Postural hypotension

73
Q

What are the important drug-drug interaction of α-blockers?

A

Dihydropyridine CCB - oedema

74
Q

What is an example of α-blocker?

A

‘-osin’

Doxazosin

75
Q

What is heart failure?

A

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 tissue
- Reduced CO

76
Q

What can affect the CO?

A

CO= HR x SV
Varies in response to physiological and pathological factors
- Preload- filling pressure
- Afterload- load the ventricle must eject
- Contractility
- Heart Rate

77
Q

What are the characteristic symptoms of HF?

A

Exercise intolerance
Dyspnoea
Fatigue (swelling)

78
Q

What is meant by the self perpetuating spiral of HF?

A

Phsyiological neurohormonal response attempts to compensate
Eventually will cause further pathology
1. Compromised cardiac function
2 ↓Arterial BP
3. Baroreceptor reflex
4. ↑Sympathetic outflow → α1- vasoconstriction and β1- ↑renin
5. ↑renin → ↑AngII → ↑aldosterone and vasoconstriction → Na+ retention → Intravascular volume expansion → ↑preload → ↑myocardial demand
6. Vasoconstriction → ↑afterload → ↑myocardial demand
7. Worsening HF

79
Q

How if HF managed?

A
  • Usually caused by LV systolic dysfunction and associated LV ejection fraction (<45%)
  • Correct underlying cause
  • Non pharmacological management- ↓ salt intake, liquid retention - 1.5L- keep BP ↓ - ↓pressure on heart
  • Addition of diuretic plus other therapeutic agents
80
Q

What are the aims of HF treatment?

A
  • Reduction in symptoms (dyspnoea, fatigue, oedema)
  • Managed ↑exercise tolerance
  • Address arrhythmias, hyperlipidaemia and diabetes
  • ↑quality of life and slow morbidity
81
Q

What treatments would you give?

A

1- Furosemide - loop diuretic → reduced BP and signs of volume overload
2- Lisinopril/ Ramipril - ACEi, Spironolactone- mineralocorticoid receptor antagonist (if symptoms continue), candesartan/losartan- ARB → reduce sympathetic output, vasodilation, reduced Na+ and H2O water retention, ↑bradykinin
3- Bisoprolol - β-blocker → Reduce remodelling and ↑systolic function

82
Q

When would spironolactone be used to treat HF?

A

Refractory hyperaldosteronism occurs

- Aldosterone escape- excessive RAAS despite ACEi and ARB and diuretic

83
Q

When are β-blockers used?

A 
Counterintuitively 
Negative inotropic effect 
Reduce contractions- slow the heart 
- reduce damage caused by sympathetic activity 
- reduce β1 activity of renin 
- limit remodelling of cardiac tissue

_Sem 4. CPT NOTES (26 decks)

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