CPTP

Offer ANTI-HYPERTENSIVE drug treatment to people:

who have stage 1 hypertension, are aged under 80 and meet identified criteria
who have stage 2 hypertension at any age

If aged <40 with stage 1 hypertension and w/o evidence of target organ damage, CVS disease, renal disease or diabetes,
consider:

specialist evaluation of secondary causes of hypertension

further assessment of potential target organ damage

Target BPs

>80 yo, 150/90

<80 yo, 140/90
Doesnt apply to diabetics [130-135 mmHg systolic blood] - guidance remains same.

DIURETICS

CARDIAC GLYCOSIDE

HPT and HF

Mechanism of Action

DIGOXIN

Thiazide;
HYDROCHLOROTHIAZIDE,

Antiarrhythmic: vagolytic effect reduces

rate and conduction velocity in sinus
and AV nodes
Inotropic - increases intracellular Ca++
Enhance cardiac muscle contractility
hence, increase cardiac output

Increasing sodium and water excretion

(reduce Na+ and H2O retention) =>
decrease in extracellular volume, resulting
in a cardiac o/put and renal blood flow.
Act mainly in the cortical region of the
ascending loop of Henle and the distal
tubule.

Adverse effects
(A) CARDIAC
Heart block
Supraventricular and
ventricular arrhythmias
(B) NON-CARDIAC
Nausea, vomiting,
constipation
Confusion
Visual disturbances
uricaemia => GOUT
K+, Mg+ (blood), Ca2+
(urine)
Should be monitored when
using with digoxin

Indications

Interaction/CI

SVT arrhythmias
Chronic AF
Heart failure

Thiazides
decreased potassium
level

HF
Possible: elderly with
isolated systolic HPT

Gout, renal failure

[use loop d.]

CPTP

Loop
FUROSEMIDE,

B- BLOCKER

K+ sparing
Aldosterone antagonist:
SPIRONOLACTONE
Amiloride
Prototype: Propranolol
Non-selective: Atenolol
Selective: BISOPROLOL
(asthma with HPT)
LEBATOLOL PREGNANT

Inhibit the co-transport of Na+/K+/2CL- in

the luminal membrane in the ascending
limb on loH. It could cause decreased renal
vascular resistance and increased renal
blood flow.

ACEi

Acute P Oedema

Gastric upset, peptic

ulcers.
Gynaecomastia,
amenorrhea

HPT (usually in
combination with
thiazide)

Renal dysfunction
bcause increased risk
of hyperkalaemia.

Hypotension
Bradycardia
Fatigue, Insomnia,
hallucinations
Sexual dysf(x) + libido
Disturb serum lipid
patterns; HDL, plasma
TGA

Angina, post-MI,
tachycardias

Asthma, COPD, heart

block

Dry cough
Altered taste
K+ (potassium level
should be monitored)
Skin rash
Hypotension
Fever

HPT, post MI
LV dysfunction
Diabetic nephropathy
(with ARB, ACEi slows
the progression of
diabetic nephropathy)
CRF, and for pt with
increased risk of CAD

Pregnancy foetal
malformations
Hyperkalaemia
Bilateral renal artery
stenosis

Altered taste
K+ (potassium level
should be monitored)
Skin rash
Hypotension
Fever

Pts cant tolerate ACEi

Pregnancy foetal
malformations

Acts on C tubules to inhibit Na+

reabsorption and K+ excretion.

1.

activation of b1 adrenoceptors on
the heart
2. renin => angiotensin ->
aldosterone -> Na, H2O retention
3. Na, H2O retention

LISINOPRIL
RAMIPRIL

Ca2+ content of the urine

Ototoxicity
uricaemia => GOUT
K+, Mg+ (blood), Ca2+
(urine)

Decrease both preload and after load.

Block the ACE that cleaves angiotensin I
to form potent vasoconstrictor
angiotensin II.
ACEi inhibits breaks down of bradykinin
which also increases the prod. Of NO
and prostacyclin by the BV.
angiotensin II and bradykinin

ARB

Losartan

Competitive antagonists of the

angiotensin type 1 receptor.

CPTP

CCB

AMLODIPINE
Diltiazem
Verapamil

A-BLOCKER

Hydralazine, Minoxidil,
Diazoxide, Fenaldopam

CENTRAL
CYMPAT
HOLYTIC

Doxazosin

P. VASO

Methyldopa, Clonidine,
Moxonidine, Rilmendine

Block the inward of the ca2+ by binding

to the L-type Ca channels in the heart
and in smooth muscle of the coronary
and peripheral arteriolar vasculature.
This causes the smooth muscles to
relax, dilating mainly arterioles.
Competitive block of alpha1
adrenoceptors. Synthetic steroids
They decrease peripheral vascular
resistance and lower arterial BP by
causing relaxation of both arterial and
venous smooth muscle.

Activation of potassium channels

Increase in K+ conductancehyperpolarisation- relaxation of
vascular smooth muscle

Decrease sympathetic outflow from

vasopressor center in brainstem

Constipation
Fatigue, flushing
Hypotension
Headache, dizziness

Useful for HPT pts with

asthma, DM, angina
and/or peripheral
vascular disease

Little interaction with

other CVS drugs

Reflex tachy and first-dose

syncope

Prostatism

Urinary incontinence

Reflex stimulation to heart

May prompt angina
pectoris, MI

Pregnant pt with HPT

PREGNANT
SAFE

Labetalol - beta blockers

Methyldopa - alpha-adrenergic agonist
Nifedipine - calcium channel blockers

CHD risk reduction

Reduces relative risk (given) x probability of developing CHD (get from the calculator in the net)

Stroke risk reduction

Reduces relative risk (given) X prob got from the calculator ->

Number needed to treat (NNT)

Numbers needed to treat = 100 / Absolute risk reduction

UNSAFE
Beta blocker - growth retardation
Thiazides - oligohydramnios
ACE Inhibitors - cleft palate
Alpha blockers - cleft palate

CPTP

Acute HF

First line
Sit patient up, give high flow oxygen, iv access
Diamorphine 2.5-5mg i.v. (in-dwelling i.v. cannula)
Furosemide 40-120mg i.v. (lower dose with diuretic nave patient)
Buccal GTN 5mg if BP >100 systolic
Second line (not better within 2 hrs)
GTN 1-2mg/min i.v. infusion, increasing as tolerated by BP
Dobutamine 2.5-7.5microg/kg/min infusion, higher dose if hypotensive
Nebulised salbutamol 2.5-5mg 4hrly, as tolerated by heart rate
Third line (consider occasionally)
Mechanical ventilation (tired patient, inability to maintain oxygenation)
Intra-aortic balloon pump (generally only if there is a reversible cause for the heart failure)
Dialysis/CVVH