treatment Flashcards
Vagal manoeuvers
induce vagal firing from the cardiovascular control centre in the medulla, in order to slow the heart rate, and interrupt the rapid ventricular rate in a supraventricular tachycardia.increase in transmural pressure in the aorta, and the initial baroreceptor reflex causing an initial slowing of the heart, through afferents to the medulla and a reduction in sympathetic outflow and increased vagal firing.
Cardioversion
cardioversion is the delivery of electrical energy that is synchronised with the QRS complex in an attempt to revert an abnormal rhythm
defibrillation is the non-synchronised delivery of electrical energy and is used in unstable rhythms (pulseless VT or VF)
benefits and risks need to weighed
may be monophasic or biphasic
high success rates in SVT and atrial flutter
100,150,200
Adenosine
CLASS 5
short acting anti-arrhythmic
naturally occurring purine nucleoside
MECHANISM OF ACTION
depression of SA & AV nodal activity
antagonises cAMP-mediated catecholamine stimulation of ventricular muscle
Adrenaline
adrenaline is a naturally occuring catecholamine acts on alpha and beta adrengic receptors. the receptors cause in heart rate increase (B1), increase force of contraction (B1), Bronchodilation (B2) and peripheral constriction (A1) 20mcg-50mcg intervals of a minute NO MAX
Atropine
Atropine is a competitive muscarinic antagonist, used to treat drug-induced bradycardia. It block ACHL on the vagus nerve to stimulate SA node activity to fire more concentrations and blocks adrenal gland activity 600 mcg
Amiodarone
CLASS
class III anti-arrhythmic
MECHANISM OF ACTION
Prolongs action potential of the refractory period of atrial, nodal and venticular tissues.Reduces conduction
prolongs cardiac action potential & delaying refractory period
Delays K+ efflux
Depresses Na+ influx
Depresses Ca2+ influx
Partial antagonism of alpha & beta receptors buy reducing number of receptors or uncoupling adenyl cyclase
Defibrillation
200, 300,360
shace ,not wet , 360 access ,
Frusemide
a loop diuretic that acts by inhibiting sodium and chloride absorption in the ascending loop of Henle
Use for congestive heart failure
Do not use for cardiogenic pulmonary oedema QAS
Aspirin
irreversible acetylation of cyclooxygenase -> blocks the production of prostaglandins from membrane phospholipids -> inactivation of platelet aggregation by arachidonic acid and collagen.
USE- ACS and cardiogenic pulmonary odema
DONT - allergy , psychostimulant use, suspected bleed, peptic bleed, patients <18
300 mg
GTN
Vasodilator that decreases preload by increasing venous capcity ,pooling venous blood in veins reducing venticular pressure and after load, vasodilation of coronary arteries decreasing spasms
attaches to nitric oxide on smooth muscle then converts GTP to cgmp promoting decrease in Ca+ reducing myosin activity for increasing blood pressure
USE ACS, odema
don’t 150< or <50 systolic <100 ,Head trauma
GTN dangers
Patients with RV infarction are very preload sensitive (due to poor RV contractility) and can develop severe hypotension in response to nitrates or other preload-reducing agents.
Hypotension in right ventricular infarction is treated with fluid loading, and nitrates are contraindicated.
Clopidogrel
anti-platelet agent
MECHANISM OF ACTION
inhibition of the ADP platelet receptor and subsequent ADP-mediated activation of the glycoprotein IIb/IIIa complex -> inhibits platelet aggregation on PY12 recpetor
Tenecteplase
CLASS
thrombolytic
MECHANISM OF ACTION
selectively binds to fibrin and converts plasminogen -> plasmin -> degradation of fibrin matrix
Enoxaparin
Anticoagulant, the inhibition of thrombin through clotting cascade of inhibit of 10
IPPV
Intermittent positive pressure ventilation, With intermittent positive pressure ventilation, the lungs are expanded by actively blowing air into them. to improve and promote the cough mechanism, (2) to improve distribution of ventilation, and (3) to enhance delivery of inhaled medications.