ANTIARRHYTHMIC DRUG

SODIUM CHANNEL BLOCKER

IV BOLUS FOR VPC'S & VENTRICLULAR ARRHYTHMIAS

W/O EPINEPHRINE

TOXICITY: CNS SEDATION, ATAXIA-> SEIZURES-> D/C

CAUTION IN CATS

NO ORAL D/T 1ST PASS & GI UPSET

ORAL SODIUM CHANNEL BLOCKER

GI & CNS SIDE EFFECTS POSSIBLE

ANTIARRHYTHMIC 

ORAL SODIUM CHANNEL BLOCKER

WORKS FOR SUPRAVENTRICULAR ARRHYTHMIAS

ORAL SODIUM CHANNEL BLOCKER

NOT COMMONLY USED

β-BLOCKER

SLOW HEART= NEGATIVE CHRONOTROPE

DECREASE STRENGTH OF CONTRACTION= NEGATIVE INOTROPE

INDERAL®

NONSELECTIVE β-BLOCKER (β1 & β2 ACTIVITY)

SIDE EFFECT: BRONCHCONSTRICTION

TIMOLOL, ATENOLOL, NADOLOL, CAREDILOL, METOPROLOL

MORE SELECTIVE BUT STILL HAVE SOME β2 ACTIVITY

PROBLEM W/ BETA BLOCKERS

DEPRESS AUTOMACITY OF SA NODE, SLOW CONDUCTION OF AV NODE

ATRIOVENTRICULAR BLOCK

ELECTRICAL IMPULSE DELAYED @ AV NODE, NOT GETTING FROM ATRIA TO VENTRICLES

1ST DEGREE- INCREASE P=R INTERVAL; 2ND DEGREE- OCC MISSED QRS COMPLEX; 3RD DEGREE- AV DISSOCIATION

"I DON'T WANT TO SLOW DOWN- WANNA SPEED UP!"

"YOUR BLOCKING MY β1 RECEPTORS I'M GOING TO ADD MORE" 

HAPPENS WHEN GIVING ANTAGONIST

CARDIAC MUSCLE INCREASES THE # OF β1 RECEPTORS -> MORE SENSITIVE TO CATECHOLAMINE STIMULATION

ANIMAL BECOMES RESISTANT TO EFFECTS OF β-BLOCKER

NEED TO DECREASE DOSE SLOWLY B/C NOW HAVE LOTS BETA1 RECEPTORS NOT BEING BLOCKED

BLOCK CA²+ FROM ENTERING CARDIAC CELL

SLOW CONDUCTION

SLOW AUTOMATICITY

NEGATIVE INOTROPES

IE:VERAPAMIL

DILTIAZEM- CATS W/ HYPERTROPHIC CARDIOMYOPATHY OTHERWISE NOT COMMON

EPINEPHRINE, NOREPINEPHRINE, DOBUTAMINE, DOPAMINE

POSITIVE INOTROPES

USE LIMITED -SHORT PERIODS (IV)

D/T DOWN REGULATION (DON'T WANT TO BE HYPER- WILL DECREASE # RECEPTORS

POSITIVE INOTROPE (STRENGTHENS MYOCARDIAL CELL CONTRACTION BY INCREASING Ca AVAILABILITY) & NEGATIVE CHRONOTROPE (ENHANCES PARASYMPATHETIC EFFECT @ SA & AV NODES-> SLOWS HEART)

VERY SMALL THERAPEUTIC INDEX

TOXICITY= (EARLY)ANOREXIA, VOMITING, DIARRHEA; (LATE)BRADYCARDIA, HEART BLOCK

D/C IMMEDIATELY, LONG 1/2LIFE

VASODILATOR

DILATES ARTERIES ONLY

EASIER FOR HEART TO MOVE BLOOD BY DECREASING ARTERIAL RESISTANCE-> LOWERS BLOOD PRESSURE LEADS TO ↓ BP TO CONSTRICTION OF RENAL ARTERIES-> ↓RENAL PERFUSION-> STIMULATE RENIN-ANGIOTENSION CASCADE-> H2O RETENTION IN BODY 

BEING REPLACED BY ACE INHIBITORS

VASODILATOR

INHIBIT ANGIOTENSION- CONVERTING ENZYME (ACE)

BLOCK RENIN-ANGIOTENSIN CASCADE

INHIBIT WATER RETENTION

VERY COMMON

ENALAPRIL (ENCARD®,VASOTEC®)

BENAZEPRIL (LOTENSIN®)

LISINOPRIL (PRINIVIL®, ZESTRIL®)

START WITH LOW DOSE THEN INCREASE

VASODILATOR

VENOUS DILATOR

SELECTIVE CORONARY ARTERIOLE DILATOR

CREAM OR PATCH

CAUTION: ABSORBED THRU SKIN- WEAR GLOVES, VARY SITE

PREVENT RENAL REABSORPTION OF EITHER Na+ or K+

INCREASE URINE FORMATION

H2O LOSS IN URINE-> DECREAS FLUID IN BLOOD-> DECREASE BLOOD PRESSURE

THERAPEUTIC DEHYDRATION

"LOOP DIURETIC" 

INHIBITS LOOP OF HENLE FROM PULLING Na+ OUT OF FILTRATE

CAN'T CONCENTRATE URINE

DCT RECLAIMS Na+ & EXCHANGES FOR K+

MAY CAUSE HYPOKALEMIA

CHF, PULMONARY EDEMA, DIURESIS IN TOXICOSIS

MOST FREQUENTLY USED

POTASSIM-SPARING DIURETICS

SPIRONOLACTONE- COMPETITIVE ANTAGONIST OF ALDOSTERONE

RARELY USED SINCE ACE INHIBITORS 

OSMOTIC DIURETIC

CARBOHYDRATE THAT PHYSICALLY RETAINS H20 IN THE RENAL TUBULE VIA OSMOSIS-> H20 LOSS VIA URINE'EMERGENCY DRUP ONLY

DECREASE PLATELET AGGREGATION-> DECREASES CLOT FORMATION

THROMBOEMBOLI (CRITTERS)