CVS - HR , Antiarrhythmic Drugs Flashcards
explain Heart failure , DF,Classification , Clinical manifestation
—Df: its progressive clinical syndrome in which either structural or functional abnormalities impair the ability of the heart to meet the metabolic demands of the body
—Classification: they are 2
1-Anatomical:
1.1 Anatomical left-sided : usually duo to systemic hypertension
1.2 Anatomical right-sided : caused by to many things such as pre load , left-sided HF cause Pulmonary Conjation which lead to fail of the right side
1.3 in both sided
2-Pathophysiological :
2.1 systolic : ventricle cant pump the blood through systolic phase which is bcs the muscle are week Ex> ischemic heart disease
2.2 diastolic : duo to hypertrophy the heart cant pump the required amount if the blood in the filing phase
—Clinical manifestation:
decrease Cop leads to following mechanism:
1-sympathetic over activity duo to decreased oxygen to brain leading tachycardia
2-renal ischemia : increase of RAAS ( renin angiotensin aldosterone system) lead to V.C and aldosterone lead to salt and water retention which lead to increase after load and preload and more heart failure
explain the drug therapy of HF
1-Positive Iontropic
- Cardiac glycosides > digoxin
- Debutamine ( for short term only )
- phosphodiestrase inhibitor > Milrinone
2-ACE inhibitors
3-V.D
4-B.Blockers
explain the Glycosides Drugs , chemical structure , molecular mechanism,Autonomic effect , pharmacological effect , uses , Contraindications,
—Drugs :
1-Digoxin Tab
2-Strophanthin K Amp
-Chemical structure: it consists of :
1-Steroid nucleus : lipophilic and essential for activity
2-Lacton ring : hydrophilic and essential for activity
3-Series of sugar : linked to C 3 of steroid and isn’t essential for activity , changing in the glucose would lead to changes in the pharmacokinetics
—molecular mechanism:
its inhibit Na+K+ atapse enzyme , Entering of the sodium to the cell is Passive action so we dont need The
Na+/K+atapes pump so accumulation of the Sodium inside the cell and K+ extracellular, Accumulation of intercellular Sodium leads to :
1-increase the Calcium release from the Sarcoplasmic reticulum
2-Displacement of intercellular Calcium from binding site
3-increases intercellular Sodium prevent Calcium explosions from the cell by inhibition of Na+/Ca+ exchanger
—Autonomic effect :
1-increase Vegal activity > bradycardia
2-decrease sympathetic activity duo to better Oxygenation
—Pharmacological effect :
1-increase Contractility duo to accumulation of Calcium
2-decrease RAAS secretion
3-relief of lung conjation
4-decrease HR duo to vegal increase of vegal tone
5-Normalization of of the Bp
—Uses :
1- chronic HF> digoxin
2- Acute HF > Strophanthin K
3-Arterial fibrillation
—Contraindications
1-sever bradycardia
2-AV block
3-CNS: fatigue ,insomnia , change in the color of vision
4-GIT : Anorexia , Vomating, nausea
5- decrease Duress
explain the differences between Digoxin and Strophanthin-K
—Digoxin
1-lipophcity: moderate
2-Absorption: 60-80%
3-Biotransformation in liver : less then 40%
4-execration : kidney 80%
5-Half life : 1.5 days
6-Accumulation: more then strophanthin
7-ROA: orally and IV
—Strophanthin K
1-lipophcity: low
2-Absorption: 50-70%
3-Biotransformation in liver : Non
4-execration : kidney 70%
5-Half life : 1 day
6-Accumulation: less then digoxin
7-ROA: only IV
explain the Phosphodieastrase inhibitor drugs in HF ( Bipyradins )
-Drug : Milrinone Amp
-mechanism: they inhibit PDE enzyme type 3 which lead to increase cAMP and cAMp leads to Increase Calcium influx in myocardial cells which results of increase the strength of Contraction
—Adverse effect :
1-Thrombocytopenia
2-increase liver toxicity
-uses :
1-they are used IV only for short term treatment of CHF for patient who digoxin doesn’t affect on them
2-For acute AHF ( Acute Atrium Failure)
Explain the Calcium Sensitizer Drug For HF
-Drug : Levosimendan Falcon 0,25%-5ml
-mechanism:
1-increase the sensitivity of Cardiomyocytes to Calcium by increasing myofilment Calcium by binding to Cardiac troponin in the calcium dependent manner
2- also its selective of Phosphodiestrase enzyme type 3 inhibitor which lead to Accumulation of cAMP which lead to
1-improve contractility
2-and vascular smooth muscle relaxation
—pharmacological effect :
1-V.D
2- decrease pre load and after load
3-Arrhythmoginc effect
-uses :
1-Acute HF
2-Acute decomposition CHF
explain the Dobutamine in HF
- drug : Dobutamine Amp
- its synthatic and has caticol ring
-mechanism of action : stimulate B1 in the cardiac which lead to increase the cardiac out put - uses or treatment : to treat
Cardioginc shock ، increase the systolic Bp in the HF
-Roa: IVi ( intravenous infusion) in salain or glucose
Explain the Df , AP of Cardiac and its Phases , differences between Phase 4 in Atrium and ventricular, pathophysiology of Arrhythmia
-DF of AP : in the resting state K+ ions is found mainly intracellular while Na+ and Ca+ extracellular making the intracellular is negative
-phases :
Phase 0 : rapid depolarization of the cells duo to rapid influx of Na+
Phase 1 : short period of Redepolazation duo to slow influx of K+
Phase 2 : Plateu delay in repolarization duo to slow influx of Ca
Phase 3 : second period of Rapid repolarization duo to rapid out influx of K+
Phase 4 : the resting state is restored , Na is extracellular , K+ back to intracellular by Na/K+ pump
- Difference between Phase 4 in Atrium and ventricular : is the slop the atrium consist of Slop duo to pre entering of Ca+ to the cells in this phase
—Pathophysiology of Arrhythmia:
-Df : its disturbance in the normal heart rhythm and its results from :
1-Abnormal impulse generation
2-abnormal impulse conduction
Classification of Arrhythmia, and its drugs
- Classification of arrhythmia:
1-Bradyarrhythmia AV block : drugs > Atropin , Adrenaline , isoprenaline
2-tackyarrhythmia : consist of 4 classes
Explain Class 1A in arrhythmia
—its increase the APD by inhibition of Na channel
-Drugs :
1-Quinidine tab
2-Disopyramide tab
3-Procainamide tab
—mechanism:
1-they block Na+ channel leading to decrease the Rate of Phase 0 depolarization which lead to increase The APD
2-decrease the exitibality on the atrial side slop which lead to decrease the firing of SA nodes
—pharmacological effect :
1- Arropine like action duo to blocked of muscranic receptor
2-hypotension duo to block of à receptor
-side effect :
1-Atropin like action
2-hypotension
3-small doses cause increase AV conduction
4-negative Iontropic effect
- uses :
1-Supraventrecular Arrhythmia
2-ventricular tachyarrhytmia
—NB : the difference between Procainamide and Quinidine is that Procainamide cause SLE like
Explain Class 1C in Arrhythmia
—they have no effect of the APD
-Drugs : Propafenone amp ,Ethacyzin tab
-mechanism: by slowing the influx of sodium ions into the cardiac muscles cells causing decrease im excitability of the cells
-uses :
1-Supraventrecular
2-ventricular Arrhythmia
Explain Class 1B
—they are also Na channel blocker and the decrease the APD
-drugs :
1-Lidocaine Amp ,
2-Mexiletine Caps
3-Phenytoin tabs
—mechanism: it decrease the APD by increasing K+ in the 3rd phase ( repolarization) and inhibition of sodium in phase 4
—uses :
1-ventricular tachyarrhythmia
2-Acute MI > lidocaine
3-Arrhythmia with over dose of cardiac glycosides > phenytoin
explain class 2 in arrhythmia
— class 2 are B.Blockers
-Drugs :
1-selective : B1> metoprolol ,Atenolol
2-nonselective : Propranolol tabl
-mechanism: they block Sodium, Potassium, Calcium , channel’s which lead to inhibition of phase 4 and depress Autmoticity and prolong Av conduction , also increase HrR, and decrease conductivity
—Side effect :
1-CVS : decrease conductivity, bradycardia , AV block , hypotension
2-Respiratory: bronchispasm
3-GiT : dyspipsia
4- CNS : inly lipophlic drug such as Atenolol > depression
-Uses :
1-Supraventrecular
2-And ventrecular tachyarrhythmia
Explain Class 3 in arrhythmia
—They are K+ channel blocker
-Drugs :
1- Amiodarone
2-Sotalol
-mechanism: inhibition of K+ channel in phase 3 which prolongate The Apd also inhibit Na+ and Ca+ , also casue Cornary V.D
-side effect :
1-Bradycardia
2-Arterial hypotension
3-tachyarrhythmia
4-Pulmonary fibrosis
5- photo sensitivity
6-hyperthyroidism
-uses : most type of arrhythmia
-contraindication: Arrhythmia duo to thyrotoxicosis
Explain Class 4 in arrhythmia
-They are clacium channel blocker
-Drugs :
1-Verapamil
2-diltiazem
-mechanism:its prolongate the APD through inhibation of Ca+ in phase 2 pleatue , also inhibit the AV conduction
—Side effect :
1- Decrease conductivity
2-bradycardia
—uses : superventercular tachyarrhythmia
