Cardiovascular Flashcards

1
Q

Vaughen- Williams

A
I - Na channel blockers
II - Beta blockers
III-  Potassium channel blockers
IV- Calcium channel blockers
V- other substances (Digoxin , atropine)
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2
Q

Class I: Na channel blockers

A

Class IA:

  1. Quinidine - PO,IV vegal+ direct effect , negative inotropic+chronotropic effect. Dog: vomiting , Eq: laminitis , swelling of nasal mocus, supraventricular arrhythmia
  2. Procainamide: arrhythmic short HL , negative inotropic -don’t use im heart failure! Ventricular arrhythmias (refractory to lidocaine)

Class IB:

  1. Lidocaine: Immediate treatment of life threatening VA. No negative inotropic effect- safe in cardiac faliure.no supraventricular effect, Short HL - sick sinus symdrome, check K (hypokalemia reduces the effect), no PO
  2. Mexiletine - PO , at home ventricular arrhythmia treatment.
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3
Q

Class III: K channel blockers

A

Increase ERP (used in re-entry)

  1. Sotalol - good in Boxer cardiomyopathy,B-blocker effect.
  2. Amiodarone - I-IV effect (not in cardiac patients, both types of arrhythmia) - best for decreasing blood pressure
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4
Q

Class IV: Ca channel blockers

A

Dec ca= dec. Contraction + vasodolation.
Inotropic+chronotropic effect , can cause bradycardia, supraventricular arrythmmia
1. Dihydropyridine type (vesseles): amlodipine, nifedipine
2. Non-dohydropyridine type (heart) - Verapamil (- inotropic) , diltiazem (antiarrhythmic)

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5
Q

CHF treatment

A
  1. Increasing contractility ( digitalis glycosides)
  2. Decreasing preload and afterload (ACE inhibitors)
  3. Inodilator (1+2) : PDE inhibitors
  4. Vasoactive substances: A+V vasodolators (2)(nitroglycerine)
  5. Diuretics - dec. Preload
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6
Q

Acute heart faliure drugs

A

Epinephrine (B+a1)

Dobutamine (+ inotropic)

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7
Q

Chronic heart faliure

A

Digoxin

Pimobendane (PDE)
Inc. IC Ca = +Ve inotropic -

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8
Q

Digoxin

A

NA/K ATPase inhibition=> IC Na accumilation=> negative feedback for Na/Ca pump=> no Ca comes in

  • positive inotropic effect + conductance stabilizing effect , inc. vegal tone bradycardia
  • Improves renal blood flow!(vasodilation of the kidney) (More Na + water excretion)
  1. Digoxin: Low TI ,PO, protein binding interaction, accumilates, plasma measuring after 3-5 days , effect inc. by hypokalemia.
    SE: , arrythmia , bardycardia , vomiting
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9
Q

PDE Inhibitor

A
  • Phosphodiesterase inhibition => inc. cAMP accumulation => inc. IC Ca => positive inotropic effect
  • Vasodilation of both arteries and veins (without inc. in oxygen consumption)

Pimobendane (Vetmedin) - inc. Ca , PO (1h before feeding to prevent vomiting)

Contraindicated: outflow obstruction (HCM, stenosis) = rupture, extensive binding.

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10
Q

How to manage cardiac faliure?

A
  1. Increase contractility - positive inotripic effect (digoxin)
  2. Decrease preload - diuretics
  3. Decrease afterload- vasodilators
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11
Q

ACE inhibitors

A

Physio:Dec. CO => Dec. Renal blood flow => renin release in kidney

Angiotensin II: aldosterone, vasovinstriction, ADH -inc.BP
Drug VASODILATOR - dec. Preload+afterload
*safe,prodrug,Used in hypertension, heart faliure dog, cat renal faliure hypertension, PROTEINURIA (detection sulfosalisylic test + = milky)
*dec. both preload+afterload , not effect on the heart (contractility), inc. GFR
*be careful of azotaemia (check blood after 1 week)
*Hypotension
*Pril - prilat
Enalarpril , Benazepril , Ramipril , Lisinopril (not prodrug, safe for renal/heart)
*Benazepril - 50% excretion via kidney , 50% via bile (no lower dose in case of chronic renal)

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12
Q

Angiotensin II Antagonist

A

Reduce BP and angiotensin II effect, (reduced GFR proteins can’t leave)
*TELMISARTAN- 1st choice for proteinuria
Valsartan, losarten ,

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13
Q

Diuretics classification

A

Decrease preload

  1. Cardiac diuretics (digoxin, xanthine derivatives, ACE inhibitors)
  2. Osmotic douretics (mannitol)
  3. Natriuretic (carboanhydrase, loop, thiazides, potassium sparing)
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14
Q

Cardiac diuretics

A
  1. Digoxin -mild diuretics
  2. Xanthine derviatives (caffeine , theophylline , theobromine) - effects on heart and urination - polyuria
  3. ACE inhibitor - mild diuretics
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15
Q

Osmotic Diuretics

A
  • Mannitol: LIFE SAVING DRUG, Filtered but not reabsorbed, cannot cross biological membranes (PO= diarrhea. Only IV .
  • Life threatening edemas , acute renal faliure, acute glaucoma
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16
Q

Natriuretics

A

Decrease Na reabsorption - water follow

  1. Carbohydrase inhibition: ~20% prox. Convoluted tubule (mild). Inc. urine Na+ Hco3 , GLAUCOMA (inhibits production ). SE: Urine alkalosis (uroliths)
    * Acetozolamide (cysteine stones)
    * Dorozolamide (glaucoma)
  2. Loop diuretics: ~70% Na/K/2Cl inhibition (no reabsorption, most effective) , excretion of Ca, Mg
    * FUROSEMIDE, torsemide, etacrinic acid.
    * indication: Heart faliure , oligouria, edemas
    * SE: hypokalemia, hypomagnesimia, metabolic alkalosis
    * Aldosterone escape

3.Thiazides: distal tubules ~20% , inhibits Na/Cl cotransporter , K excretion inc . Ca excretion dec! *Chlorothiazide , Hydrochlorothiazide (dec BP)
Indications: heart faliure , hypertension, uroliths
SE: hypokalemia, alkalosis

  1. Potassium sparing Diuretics: collecting duct 4%
    A group: Amiloride , Triamterene - inhibits Na/K pump
    B group: Aldosterone antagonists -Spironolactone (contraindicate furosemide, K)
    dec. Na/K ATPase, inc Na,K excretion.. used in CHF, preventing aldosterone effect, hyperaldosteronism.
17
Q

Combined treatment fir CHF

A
  1. Dog: Furosemide+ pimobendane+ sporolactone

2. Amlodipine (most active)+ ACE inhibitor:(leadt active) / angiotensin II antagonist (2nd)

18
Q

Vasodialators

A

Contraction mechanism: Ca+ Calmodulin => activates MLCK => Myosin LC- P (active) => contraction => vasovinstriction

  1. Ca blockers: dihydropyridines , non-dohydropyridine
  2. Organic nitrates: (NO: cGMP MLCP) nitroglycerin - pronounced V+A dilatation, (mesentery, coronary), dec preload + afterload, sublingually, IV, patch
  3. other substances: A1 antagonists (prasozin, doxazosine) , PDE inhibitors , RAAS blockers