CVD treatments

Karo
Mind Map by Karo, updated more than 1 year ago
Karo
Created by Karo almost 7 years ago
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pham1008 Mind Map on CVD treatments, created by Karo on 04/29/2013.
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Resource summary

CVD treatments
1 hypertension
1.1 thiazide diuretics
1.1.1 bendroflumethiazide 2.5mg OM
1.1.2 inhibit Na reabsorption in the early diluting segment of the distal tubule
1.1.2.1 inhibit the Na/Cl co-transporter
1.1.3 side effects: hypokalemia, hyponatremia, hypomagnesaemia, hypercalcemia, hyperuricaemia, hyperglycemia,hyperlipidaemia, impotence(reversible)
1.2 beta blockers
1.2.1 cardioselective: bisoprolol, atenolol; nonselective: propranolol
1.2.2 decrease HR and contractile force thus decrease CO
1.2.3 vasodilation
1.2.4 decrease Na and water retention
1.2.5 SE:bradycardia, tiredness, fatigue, lipids, broncospasm, cold hands and feet, lipid soluble-nightmares, masking hypoglycaemia symp in insulin dep DM
1.3 ACE inhibitors
1.3.1 lisinopril 10mg od
1.3.2 inhibit the formation of A2 form A1
1.3.2.1 A2 is a potent vasoconstrictor and promotes aldosterone release
1.3.3 SE: hyperkalaemia(check U&E), acure renal failure(U&E), first dose hypotension, dry cough, skin rash and angioedema, alter sense of taste
1.4 angiotensin II receptor antagonists
1.4.1 losartan
1.4.2 SE: same as ACE inhibitors minus cough and angioedema
1.5 calcium channel blockers
1.5.1 dyhydropyridines: amlodipine&nifedipine
1.5.1.1 vasodilation of coronary and peripheral arteries
1.5.2 phenylalkamines: verapamil
1.5.2.1 slow AV nodal conduction
1.5.2.1.1 reduces HR & CO
1.5.2.2 causes constipation
1.5.3 benzothiazipine derivatives: diltiazem
1.6 alpha 1 antagonists
1.6.1 doxazosin up to 16mg od
1.6.2 dilate blood vessels and reduce PVR
2 dyslipidaemia
2.1 HMG Co A Reductase Inhibitors (statins)
2.1.1 simvastatin max 80mg od
2.1.2 partially block HMG Co A reductase
2.1.3 inhibit biosynthesis in liver
2.1.4 metabolised by CYP3A4
2.1.5 rhabdomylosis
2.1.6 SE: skin reactions, headaches, GI, myalgia
2.2 fibrates

Annotations:

  • CI in gallbladder disease
2.2.1 benzafibrate 400mg/day
2.2.2 bind to PPAR alpha on hepatocytes
2.2.2.1 increases VLDL clearance
2.2.3 also decrease hepatic TG secretion
2.2.4 SE: gi, headache, skin reactions, fatigue
2.2.5 increace warfarin conc by binding to albumin
2.3 bile acid binding agents

Annotations:

  • ionic exchange resins insoluble in water mix with water and take with meal take other meds 1hr before or 4-6hrs after the resin
2.3.1 cholestyramine 4-36g/day
2.3.2 not absorbed! bind to bile acid in intestine
2.3.2.1 increase bile excretion
2.3.3 reduced absorption of fat sol vit & many drugs eg digoxin
2.3.4 SE: significant GI
2.4 cholesterol binding agents
2.4.1 ezetimibe 10mg od
2.4.2 inhibits absorption of endogenous and biliary cholesterol in the GI

Annotations:

  • this is done using transporter protein NPC1L1
2.4.3 SE: headache, abdo pain, diarrhoea
2.5 nicotinic acid and derivatives

Annotations:

  • poor side effects profile
2.5.1 inhibits hepatic TG production and VLDL secretion
3 IHD
3.1 stable angina

Annotations:

  • -symptoms usually precipitate by exercise, cold environment and relieved by rest -burning sensation over the sternum, often radiates to the left jaw, shoulder and arm -chest tightness & shortness of breath -30s to 30min
3.1.1 modification of disease
3.1.1.1 Antiplatelets
3.1.1.2 ACE inhibitors
3.1.1.3 Statins
3.1.2 symptomatic therapy
3.1.2.1 nitrates

Annotations:

  • -dilate veins more then arteries -they reduce cardiac workload (angina) -low oral bioavailability need nitrate free period - 8-12 hours
3.1.2.1.1 orally: *isosorbide dinitrate 30-120mg daily in 2-3 doses *isosorbide mononitrate 20-120mg daily in 1-2 doses
3.1.2.1.2 GTN - sublingual glyceryl trinitrate

Annotations:

  • every 5 mins, up to 3 doses in total, if chest pain persists
3.1.2.2 beta blockers

Annotations:

  • reduce myocardial O2 demand and prevent symptoms
3.1.2.3 calcium channel blockers

Annotations:

  • dyhydropyridines - vasodilation & improve coronary blood flow - prevent symptoms verapamil & diltiazem - decrease AV node conduction - reduce cardiac workload
3.1.2.4 potassium channel blockers
3.1.2.4.1 nicorandil

Annotations:

  • -ATP dependent K channel activation & nitrate like activity -arterial and venous vasodilation may be used as monotherapy or with beta blockers or calcium channel blockers
3.1.2.5 ivabradine

Annotations:

  • HR lowering drug use if beta blockers CI
3.1.2.6 ranolazine

Annotations:

  • adjunctive therapy in patients who are inadequately controlled or intolerant of beta-blockers or calcium channel blockers -reduces calcium overload in ischaemic myocytes through inhibition of the late sodium current
3.1.3 surgical procedures
3.1.3.1 Percutaneous transluminal coronary angioplasty (PTCA)
3.1.3.2 coronary artery bypass grafting (CABG)
3.2 STEMI

Annotations:

  • -burning or chest discomfort even at rest, severe new onset angina or increasing angina that lasts >20 min -pain may radiate to jaw, shoulder and down left arm -may also present with nausea, vomiting, shortness of breath
3.2.1 immediate care

Annotations:

  • to remove pain, prevent deterioration, prevent complications and improve cardiac function
3.2.1.1 ECG monitoring
3.2.1.2 oxygen
3.2.1.3 slow IV diamorphine

Annotations:

  • reduce pain and anxiety
3.2.1.4 metoclopramide 10mg IV

Annotations:

  • antiemetic
3.2.1.5 SL or IV nitrate

Annotations:

  • for ischaemic pain
3.2.1.6 clopidogrel 300mg & aspirin 300mg

Annotations:

  • antiplatelet to limit further extension of thrombus
3.2.1.7 restoring patency of the occluded artery
3.2.1.7.1 percutaneous coronary intervension
3.2.1.7.2 thrombolytic agent

Annotations:

  • lyse thrombus and restore blood flow + anticoagulant
3.2.2 secondary prophylaxis

Annotations:

  • prevent further infraction/death; modification of risk factors
3.2.2.1 antiplatelets
3.2.2.1.1 eg aspirin, clopidogrel, prasugrel, ticagrelor
3.2.2.1.2 aspirin inhibits COX enzyme irreversibly by acetylation
3.2.2.1.2.1 reduces thromboxane, prostaglandins, and prostaglandins synthesis
3.2.2.1.3 clopidogrel inhibits platelet aggregation by irreversibly blocking ADP pathway
3.2.2.1.3.1 SE: thrombotic thrombocytopenia purpura
3.2.2.1.4 if patients can't tolerate antiplatelets give warfarin INR 2-3 for up to 4 years
3.2.2.2 Beta-blockers
3.2.2.3 race limiting calcium channel blockers
3.2.2.4 ACE inhibitors
3.2.2.5 Aldosterone antaginists - Eplerenone
3.2.2.6 nitrates
3.2.2.7 lipid lowering treatment
3.2.3 initial management - drug therapy
3.2.3.1 glycoprotein IIb/IIIa
3.2.3.2 antiplatelets
3.2.3.3 anticoagulant
3.2.3.4 thrombolytic drugs

Annotations:

  • to break up thrombus and restore blood flow
4 HF
4.1 diuretics
4.1.1 loop
4.1.2 thiazide
4.1.3 K sparing
4.2 ACE inhibitors
4.3 Angiotensin II antagonists
4.4 Aldosterone antagonists
4.5 Beta-blockers
4.6 Cardiac glycosides
4.7 other vasodilators
5 thrombosis
5.1 Heparin

Annotations:

  • ADR: haemorrage - most common Major bleeding is less common in LMWH thank UFH
5.1.1 UFH

Annotations:

  • mixtures of sulfated mucopolysaccharides of variable lengths
5.1.1.1 MOA: prevents the growth and propagation of a formed thrombus

Annotations:

  • -binds to antithrombin: causes conformational change. activation of heparin-antithrombin complex accelerates certain activated clotting factors (9a.10a,11a,12a,thromnin(2a)) -also binds directly to thrombin
5.1.2 LMWH

Annotations:

  • more expensive then UFH show similar efficacy
5.1.2.1 MOA: enhance and accelerate the activity of antithrombin on factor Xa. Prevents growth and propagation of formed thrombi.
5.1.2.2 eg enoxaparin, deltaparin, tinzaparin
5.2 Heparinoids

Annotations:

  • a mixture of low molecular weight sulfated glycosaminoglycans
5.2.1 MOA: promotes inhibition of factor Xa by antithrombin but it does not prolong the APTT
5.2.2 danaparoid
5.3 Hirudins

Annotations:

  • eg lepirudin
5.3.1 MOA: they bind to the active site on thrombin
5.4 Fondaparinux
5.4.1 MOA: bind to antithrombin and accelerates antithrombin activity factror Xa
5.5 Vit K antagonists
5.5.1 warfarin
5.5.2 MOA: bind to the hepatic reductase enzyme that converts vit K to the active form. Inhibits hepatic synthesis of vit K dependent clotting factors
5.6 Thromobolitycs

Annotations:

  • only indicated in life-thretening acute massive pulmonary embolus
5.6.1 MOA: activate plasminogen, thus promote the breakdown of fibrin to fibrinogen
6 AF
6.1 Proxymal AF

Annotations:

  • Recurrent, self terminating episodes of AF. Episode <7 days (most resolve within 24h)
6.1.1 rhythm control
6.1.1.1 rate control (if rhythm fails)
6.2 Persistent AF

Annotations:

  • Sustained AF that terminates with cardioversion
6.2.1 rate or rhythm control
6.2.1.1 try other if previous fails
6.3 Permanent AF

Annotations:

  • AF that is long standing, cardioversion failed of not attempted
6.3.1 rate control
6.3.1.1 rhythm control (if rate fails)
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