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What composes the cardiovascular system?
3 components
1. HEART
2. VASCULATURE
3. AUTONOMIC NERVOUS SYSTEM (parasympathetic and sympathetic)
In tlEAhe sympathetic nervous system, how do the preganglionic neurons function/ synapse?
3 DIFFERENT WAYS TO SYNAPSE WITH POSTGANGLIONIC NEURONS
1. PASS UP OR DOWN SYMPATHETIC CHAIN & SYNAPSE AT HIGHER OR LOWER GANGLION.
2. LEAVE THE GANGLION BY WAY OF A CORD LEADING TO SPECIAL GANGLIA IN THE VISCERA = SYNAPSING WITH POSTGANGLIONIC SYMPATHETIC NEURONS RUNNING TO THE SMOOTH MUSCULAR WALLS OF THE VISCERA.
3. PASS THRU GANGLION AND INTO ADRENAL MEDULLA SYNAPSING WITH HIGHLY-MODIFIED POST GANGLIONIC CELLS THAT MAKE UP THE SECRETORY PORTION OF THE ADRENAL GLAND
Presynaptic Neurotransmitter in the sympathetic system is the ------------------ and postsynaptic is -------------.
1.ACETYLCHOLINE
2. POST SYNAPTIC IS NOREPINEPHRINE
The sympathetic innervation is located in the
Thoracic and Lumbar spines:
T1-L2
, thevascular smooth muscle blood vessel contractions occur in -/-/-/- and is via which receptors?
Contraction of blood vessels in the SKIN, SPLANCHNIC, SKELETAL MUSCLE AND RENAL occur by the
ALPHA-1 ADRENERGIC RECEPTORS
ALPHA-1 (VASOCONSTRICTION)
Relaxation of blood vessels in the sympathetic NS occurs by action of the .....?
BETA ADRENERGIC RECEPTORS
WHAT IS THE SYMPATHETIC RESPONSE IN THE HEART AND WHAT CONTROLS THIS?
SYMPATHETIC RESPONSES INCLUDE INCREASES IN
1. CHRONOTROPY (BETA 1 RECEPTORS INCREASE HEARTRATE)
2. INOTROPY (BETA 1&2 INCREASE CONTRACTILITY)
3. DROMOTROPY (CONDUCTION INCREASES)
What happens in the kidneys?
INCREASE RENIN RELEASE VIA BETA 1 ADRENERGIC RECEPTORS
THE MAJOR SOURCE OF CARDIAC STIMULATION IS WHAT? HOW IS IT FORMED?
THE STELLATE GANGLIA. FORMED WITH THE INFERIOR CERVICAL AND 1ST THORACIC GANGLIA.
THE RIGHT AND LEFT STELLATE GANGLIA ARE RESPONS?IBLE FOR WHAT
THE RIGHT AND LEFT STELLATE GANGLIA STIMULATE THE HEART. RIGHT INCREASES HEARTRATE.
LEFT INCREASES CONTRACTILITY
IN THE SNS, WHAT OCCURS IN THE LUNGS?
BRONCHIOLAR SMOOTH MUSCLE RELAXATION VIA THE BETA 2 ADRENERGIC RECEPTORS
IN THE SNS WHAT OCCURS IN THE LIVER.... CONTROLLED BY WHAT?
INCREASED GLUCOSE METABOLISM (GLYCOGEN STORES ARE CONVERTED TO GLUCOSE); BETA 2 CELLS
IN THE SNS, WHAT OCCURS IN THE GI TRACT?
DECREASED PERISTASIS AND MOTILITY VIA THE BETA 2 ADRENERGIC RECEPTORS.
THE MAIN NERVE IN THE PNS IS -------; CN ---?
VAGUS NERVE; CN 10
OTHER PREGANGLIONIC PARASYMPATHETIC NEURONS ARISE FROM THE ---------- AND ENTER ---?
ARISE FROM THE MEDULLA OBLONGATA AND THEY ENTER THE THORAX WITH BRANCHES OF THE RECURRENT LARYNGEAL AND THE THORACIC VAGUS NERVE.
IN THE SNS, WHAT OCCURS IN THE LUNGS?
BRONCHIOLAR SMOOTH MUSCLE RELAXATION VIA THE BETA 2 ADRENERGIC RECEPTORS
IN THE SNS WHAT OCCURS IN THE LIVER.... CONTROLLED BY WHAT?
INCREASED GLUCOSE METABOLISM (GLYCOGEN STORES ARE CONVERTED TO GLUCOSE); BETA 2 CELLS
IN THE SNS, WHAT OCCURS IN THE GI TRACT?
DECREASED PERISTASIS AND MOTILITY VIA THE BETA 2 ADRENERGIC RECEPTORS.
THE MAIN NERVE IN THE PNS IS -------; CN ---?
VAGUS NERVE; CN 10
OTHER PREGANGLIONIC PARASYMPATHETIC NEURONS ARISE FROM THE ---------- AND ENTER ---?
ARISE FROM THE MEDULLA OBLONGATA AND THEY ENTER THE THORAX WITH BRANCHES OF THE RECURRENT LARYNGEAL AND THE THORACIC VAGUS NERVE.
THE VENTRAL AND DORSAL CARDIO-PULMONARY PLEXUS ARE LOCATED WHERE?
BTW THE AORTIC ARC AND THE TRACHEAL BIFURCATION AND RECEIVE BOTH SYMPATHETIC AND PARASYMPATHETIC STIMULATION. THE PREGANGLIONIC PARASYMPATHETIC NEURONS ALSO EXTEND FOM THE BRAIN AND LOWER TIP OF SPINAL CORD AND CONVERGE AT THIS PLEXUS ALSO.
Each preganglionic parasympathetic neuron synapse with--------, that are located where?
They synapse with just a few post-ganglionic neurons which are located near- or in- the effector organ, muscle or gland.( THE POSTGANGLIONIC PARASYMPATHETIC NERVES ARE VERY SHORT)
THE 3 CARDIAC NERVES OF THE VENTRAL/DORSAL CARDIOPULMONARY PLEXUS ARE?
RIGHT CORONARYCARDIAC NERVE
LEFT CORONARYCARDIAC NERVE
LEFT LATERAL CARDIAC NERVE
THE MOST ABUNDANT PARASYMPATHETIC NERVES ARE LOCATED WHERE?
1. CORONARY SINUS
2. SUPERIOR VENA CAVA (svc)
THE PRE AND POST GANGLIONIC NEUROTRANSMITTER IN THE PNS ARE? ARE THERE ANY OTHER NEUROTRANSMITTORS?
ONLY ACETYLCHOLINE; However, a few postganglionic neurons also release NITRIC OXIDE as their neurotransmitter.
The parasym postganglionic neurons nearest the heart are generally further away from the structures they innervate (TRUE/FALSE)
FALSE; THEY ARE VERY CLOSE TO THE STRUCTURES THEY INNERVATED AND ARE THEREFORE VERY SHORT.
What activates the muscarinic receptors?
STIMULATION from the nicotinic receptors and the release of the acetylcholine at the neuroeffector junction activates the muscarinic receptors.
The muscarinic receptor is ---?
It is the main END-RECEPTOR that is stimulated by ACETYLCHOLINE released from postganglionic PNS junctions of the cardiac and smooth muscles.
In the PNS the M2 receptors are responsible for?
Decreasing INOTROPY, CHRONOTROPY AND DROMOTROPY.
M3 receptors in the PNS are responsible for ?-----via what? and what is this used interchangeably with?
SMOOTH MUSCLE RELAXATION via THE EDRF (ENDOTHELIAL DERIVED RELAXING FACTOR)- EDRF is used interchangeably with Nitric-Oxide b/c it has vasodilatory properties.
Carbon Monoxide formation has what effect on smooth muscle? CO formation is stimulated by what in the blood?
Causes smooth muscle relaxation.
Proteins can stimulate formation of CO.
Identify the valves in the heart
ATRIOVENTRICULAR:MITRAL (LEFT) ; TRICUSPID (RIGHT)
SEMILUNAR VALVES (AORTIC AND PULMONARY VALVES)
Corornary circulatory flow is regulated by what?
OXYGEN DEMAND-
The coronaries vasodilate when more oxygen is needed and the heart gets perfused.
RCA arises from where?
RIGHT ANTERIOR AORTIC SINUS (AKA SINUS OF VALSALVA)
LCA arises from where?
LEFT ANTERIOR AORTIC SINUS (AKA SINUS OF VALSALVA)
WHERE IS THE AORTIC SINUS LOCATED? WHAT ARE THE COMPONENTS?
IT IS ON E OTHE ANATOMIC DILATIONS OF THE ASCENDING AORTA; OCCURING JUST ABOVE THE AORTIC VALVA (DISTAL TO THE VALVE)
THERE ARE 3 AORTIC SINUSES- THE RIGHT; LEFT AND POSTERIOR.
WHAT IS THE POSTERIOR AORTIC SINUS CALLED AND WHY?
THE NON-CORONARY SINUS ; B/C NO VESSEL ARISE FROM IT
HOW DOES THE LCA DIVIDE?
INTO THE LAD (LEFT ANTERIOR DESCENDING) AND THE LEFT CIRCUMFLEX BRANCH.
WHAT IS THE WIDOW MAKER?
A HIGHLY STENOTIC LEFT MAIN CORONARY ARTERY OR PROXIMAL LAD ARTERY OFTHE HEART.
TRACE THE PATTERN OF FLOW IN THE LAD
Goes down the ANTERIOR LEFT VENTRICLE- through the INTERVENTRICULAR GROVE to supply the DIAGONAL AND CEPHALPERFORATIOG BRANCHES.
OCCLUSIVE DISEASE OF THE LAD WILL BE SEEN IN WHICH LEADS
V3,V5,V6, AVL AND LEAD1
HOW IS CORONARY ARTERY DOMINANCE DETERMINED?
BASED ON WHICH ARTERY CROSSES THE CRUX TO SUPPLY THE POSTERIOR DESCENDING ARTERY (AKA THE POSTERIOR INTERVENTRICULAR ARTERY)
DECRIBE THE FREQUENCY OF CORONARY ARTERY DOMINANCE.
50% RIGHT DOMINANCE (SUPPLY BY THE RCA)
20% LEFT DOMINANCE (SUPPLIED BY THE CIRCUMFLEX ARTERY)
30% CODOMINANCE - SUPPLIED BY BOTH RCA AND L.CX.
IN THE CV SYSTEM, THE ACTIVITIES OCCURING IN NORMAL CORONARIES IN THE PNS INCLUDE:
1. EXOGENOUS ACETYLCHOLINE
2. ELECTRICAL VAGAL STIMULATION
3. REFLEX ACTIVATION VIA RECEPTORS (BARO/CHEMO AND VENTRICULAR RECEPTORS)
REFLEX ACTIVATION IN THE PNS INCLUDE WHICH RECEPTORS:
BARORECEPTORS, CHEMORECEPTORS AND VENTRICULAR RECEPTORS.
WHERE DO VAGAL FIBERS END IN THE PNS
IN THE ADVENTIA OF CORONARY VESSELS.
IN NORMAL CORONARIES, PARASYMPATHETIC RESPONSE IS?
VASODILATION
IN THE PNS, ATHEROSCLEROTIC CORONARIES RESPOND BY?
VASOCONSTICTING
IN THE CV SYSTEM, DURING SYMPATHETIC RESPONSE, WHAT OCCURS IN THE CORONARIES IN RESPONSE TO ALPHA STIMULATION?
VASOCONSTRICTION IN RESPONSE TO ALPHA-1 AND 2 STIMULATION (ALPHA-1 in LARGER VESSELS) (ALPHA-2 IN SMALLER VESSELS)
BETA STIMULATION RESULTS IN WHAT IN THE SNS IN THE CV-SYSTEM?
CORONARY VASODILATION (MOSTLY IN SMALLER CORONARY ARTERIES)
WHAT CARDIAC NERVES EMERGE FROM THE CARDIOPULMONARY PLEXUS?
RIGHT AND LEFT CARDIAC NERVES AND THE LEFT LATERAL CARDIAC NERVES EMERGE
TRUE OR FALSE:
GANGLIA OCCUR WITHIN THE HEART, NEAR THE STRUCTURE INNERVATED BY LONG POSTGANGLIONIC NEURONS.
FALSE: THE POST GANGLIONIC NEURONS ARE SHORT- THE REST IS TRUE.
THE RIGHT DORSAL MEDIAL AND LATERAL CARDIAC NERVES ARE NORMALLY PARASYMPATHETIC OR SYMPATHETIC? THEY FOLLOW WHAT TO WHERE?
THE DORSAL MEDIAL AND LATERAL CARDIAC NERVES ARE SYMPATHETIC AND THEY FOLLOW THE LEFT MAIN CORONARY TO THE LAD AND CX ARTERIES.
IN THE HEART, THE SYMPATHETIC SYSTEM INVOLVES WHICH STRUCTURES/NERVES?
STELLATE GANGLION AND CAUDAL CERVICAL SYMPATHETIC TRUNK
RIGHT DORSAL MEDIAL
LEFT CARDIAC NERVES
IN CV PHYSIOLOGY, THE PARASYMPATHETIC SYSTEM FLOW IS FROM THE....?
MEDULLA OBLONGATA TO THE THORAX VIA RECURRENT LARYNGEAL AND VAGUS NERVES.
THE GREATEST CONC OF THE PARASYMPATHETIC NERVES IS IN THE ?
SA NODE
WHAT ARE THE PERCENTAGES OF BETA 1 AND 2 IN THE RA AND THE VENTRICLES.
BETA 1 AND BETA 2 ARE THE SYMPATHETIC NERVES IN THE HEART.
RIGHT ATRIUM: 74% BETA1; 26% BETA 2
VENTRICLES: 86% BETA 1; AND 14% BETA 2
THE ELECTRICAL PATHWAY OF THE HEART FOLLOWS WHICH FLOW?
SA NODE
AV NODE
BUNDLE OF HIS
RIGHT BUNDLE
LEFT BUNDLE
PURKINJE FIBERS
ENDOCARDIUM
EPICARDIUM OF THE VENTRICLES
WHAT IS THE PUMPING EFFICIENCY OF THE HEART?
THE ENERGY REQUIRED TO PUMP A GIVEN BLOOD VOLUME.
WHAT AFFECTS THE PUMPING EFFICIENCY?
AC CAMP
AFTERLOAD
CONTRACTILITY
CONDUCTION ABNORMALITIES
ANATOMICAL ABNORMALITIES
MYOCARDIUM/COMPROMISED
PRE-LOAD
WHAT AFFECTS THE MYOCARDIAL OXYGEN CONSUMPTION?
LOVE(lvedp)-PARIS

PRELOAD (lvedp)
AFTERLOAD
RATE (HEARTRATE-TACHY)
INOTROPIC STATE (strength of squeeze)
STROKE VOLUME (wall tension)
FACTORS THAT AFFECT THE CARDIAC PERFORMANCE.
C- IPAD
CHRONOTROPHY (rate)
INOTROPY
PRELOAD
AFTERLOAD
DROMOTROPY
THE FRANK-STARLING LAW STATES THAT...
THE FORCE OF CONTRACTION OF THE CARDIAC MUSCLE IS PROPORTIONAL TO ITS INITIAL LENGTH.
THE EQUATION FOR STROKE VOLUME IS ?
EDV - ESV = SV
NORMAL STROKE VOL IS .......? AND NORMAL LVEDP IS .........?
STROKE VOL: 70-130 ML

LVEDP IS 5-13
How does the pulmonary circulation differ in pressure and resistance from that of the Systemic Circulation.
The Pulmonary circ has
LOW PRESSURE AND RESISTANCE

SYSTEMIC CIRCULATION: HIGH PRESSURE AND HIGH RESISTANCE

THE CIRCULATORY SYSTEM IS AFFECTED BY THE AUTONOMIC NERVOUS SYSTEM
HOW IS THE CIRCULATORY SYSTEM CLASSIFIED?
BY SIZE, FUNCTION AND LOCATION.
LIST THE ORDER OF THE VESSELS
ARTERIES
ARTERIOLES
CAPILLARIES
VENULES (HIGHLY DISTENSIBLE)
VEINS
CIRCULATORY STOP COCKS AREA?
THE ARTERIOLES
THE PRIMARY RESISTANCE VESSELS ARE?
THE ARTERIOLES
THE RESISTANCE VESSELS ARE CONTROLLED BY
THE SYMPATHETIC NERVOUS SYSTEM
THE CAPACITANCE VESSELS ARE?
VEIN AND VENULES- CONTAIN 50% OF TOTAL BLOOD.
FLOW OF THE CAPACITANCE VESSELS IS CONTROLLED BY?
SYMPATHETIC AND HUMORAL FACTORS.
SYMPATHETIC AND HUMORAL FACTORS CONTROL ----------- AND ------.
FLOW OF CAPACITANCE VESSELS AND PERMEABILITY.
SHORT TERM REGULATION IN THE CV SYSTEM TAKES.....?
SECONDS TO MINUTES
THE LONG TERM REGULATION IN THE CV SYSTEM TAKES: ...
DAYS TO WEEKS
MAP IS DETERMINED BY THE ...
BARORECEPTORS IN THE AORTIC ARCH AND CAROTID ARTERIES. AND BY THE REFLEX PATHWAYS (FEEDBACK LOOPS)
SHORT TERM REGULATION IS COMPRISED OF/CONTROLLED BY?
1. ANS
2. MAP CHANGES SENSED BY BARORECEPTORS
3. VASOMOTOR CENTERS INTHE MEDULLA
4. SYMPATHETIC AND PARASYMPATHETIC OUTPUT.
DURING SHORT TERM REGULATION, A DROP IN THE MAP ELLICITS WHAT ACTIVITIES?
1. SENSED BY THE BARORECEPTORS
2. INCREASE IN SYMPATHETIC TONE
3. DECREASE IN VAGAL TONE (PARASYMPATHETIC)
4. DECREASE NEURONAL ACTIVITY TO THE MEDULLARY CENTER (PARASYMPATHETIC)
DURING SHORT TERM REGULATION, A RISE IN THE MAP ELLICITS WHAT ACTIVITIES?
INCREASED BARORECEPTOR ACTIVITY
INCREASED VAGAL TONE
DECREASE IN SYMPATHETIC TONE
DECREASE IN VAGAL TONE DENOTES .....
INCREASING THE HR
INCREASING SYMPATHETIC T HONE DENOTES INCREASES IN WHAT?
V- HIP

VENOUS TONE
HEARTRATE
INOTROPY
PVR
WHAT MEDIATES LONG TERM REGULATION, AND WHAT IS CONTROLLED?
HUMORAL FACTORS MEDIATE LONG TERM REGULATION AND
BLOOD VOLUME
SODIUM REGULATION AND WATER RETENTION ARE ALL CONTROLLED (BLOOD, WATER, SODIUM)
THE RAS SYSTEM IS INVOLVED IN WHICH REGULATION (LONG OR SHORT-TERM)?
LONGTERM
RENIN FROM LIVER CONVERTS ANGIOTENSINOGEN TO ANGIO-1 ; THAT BY ACE TO ANGIO-2; ALDOSTERONE PRODUCTION AND SUBSEQUENT WATER RETENTION AND INCREASED BLOOD VOLUME.
CHANNELS AFFECTED BY DRUGS ACTING DIRECTLY ON CARDIAC TISSUE INCLUDE?
K, NA, CA CHANNELS
DRUGS ACTING ON VASCULATURE INCLUDE?
NOREPINEPHRINE (ALPHA-1 ADRENORECEPTOR)
AND EPINEPHRINE (BETA-2 VIA cAMP LEADING TO VASORELAXATION)
NAME THE FOUR DRUGS IDENTIFIED AS ACTING ON THE CARDIAC VASCULATURE.
ADENOSINE
NITRIC OXIDE
ENDOTHELIN
ERGONOVINE
WHAT KIND OF SYSTEMIC EFFECT DOES ADENOSINE HAVE? HOW IS IT DOSED?
NONE.
6MG/1SEC WAIT TO SEE IF CONVERTS; GIVE 12MG/1SEC. CAN STOP THE HEART TRANSIENTLY.
HOW DOES NITRIC OXIDE WORKS?....OVERALL EFFECT IS?
WORKS ON ENDOTHELIUM OF BLOOD VESSEL. STIMULATES cGMP = CAUSES DEPHOSPPHORYLATION OF MYOSIN CHAIN = SMOOTH MUSCLE RELAXATION.
MOST POTENT VASOCONSTRICTOR IS?
ENDOTHELIN
USED FOR DIAGNOSIS OF VARIANT ANGINA:...? THIS DRUG CAN CAUSE------ & -----?
ERGONOVINE.
CAN CAUSE INFARCTION AND DEATH. CAUSES BETA CONSTRICTION BY STIMULATING ALPHA.
VAUGHAN WILLIAMS/HARRISON CLASSIFICATION OF ANTIARRHYTHMIC DRUGS: CLASSES ARE?
CLASS 1: NA CHANNEL BLOCKERS (1A;1B;1C)
CLASS 2: BETA BLOCKERS
CLASS 3: K BLOCKERS
CLASS 4: CALCIUM CHANNEL BLOCKERS
THEN THE UNCLASSIFIED.
HOW DO SODIUM CHANNEL BLOCKERS WORK.
DEPRESS PHASE 0 DEPOLARIZATION.
HOW DO CLASS 1A DRUGS WORK......NAME 3
HAVE INCREASED POTENCY AT HIGH HEART RATE. PROLONG TIME TO NEXT ACTION POTENTIAL.
MODERATE DEPRESSION OF DEPOLARIZATION AND PROLONGS REPOLARIZATION. (BLOCK K CHANNELS ALSO) QUINIDINE AND PROCAINIMIDE (PQ)
HOW DO CLASS 1B WORK?
Block ONLY Sodium channels at high heart rates- selectively. WEAK DEPRESSION AND SHORTENS REPOLARIZATION. (LP) LIDOCAIN AND PHENYTOIN)
HOW DO CLASS 1C WORK?
EQUALLY BLOCK SODIUM CHANNELS AT ALL/ANY HEART RATE. HAVE STRONG DEPRESSION OF DEPOLARIZATION WITH LITTLE EFFECT ON REPOLARIZATION. (
FLECANIDE/ ENCAINIDE)
CLASS TWO DRUGS WORK BY?
ANTAGONIZING BETA RECEPTORS THEY INDIRECTLY BLOCK CALCIUM CHANNELS BY ATTENUATING ADRENERGIC ACTION AND BLOCK THE PROARRHYTHMIC EFFECTS OF CATECHOLAMINES) PROPANOLOL AND DL SOTALOL (remember DL is 2 letters so DL Sotalol belongs to CLASS II DRUGS)
CLASS III DRUGS WORK BY?
BLOCKING THE OUTFLOW OF POTASSIUM FROM THE CELLS: AMIODARONE ; DOFETILIDE AND IBUTILIDE
AMIODARONE BELONGS TO CLASS ...........BUT HAS CLASS ............AND ........ ACTIONS.
CLASS III BUT HAS CLASSES 1 AND 4 ACTION
CLASS 4 DRUGS ARE....AND HOW DO THEY WORK
DILTIAZEM AND VERAPRAMIL....WORK BY BLOCKING L TYPE VOLTAGE GATED CALCIUM CHANNELS
UNCLASSIFIED CLASS INCLUDES..... THEY WORK BY MIMICKING WHICH ACTIVITY?
THEY HAVE PARASYMPATHETIC LIKE ACTION AT THE SA NODE AND AV NODE
TERMINATE RE-ENTRANT PHENOMENON IN AV NODE. DIGOXIN (INCREASES VAGAL NERVE ACTIVITY AND SLOWS AV CONDUCTION) AND ADENOSINE
WHAT HAPPEN IN PHASE 4?
NA/K PUMP DEPENDENT
SODIUM IS PUMPED OUT AND K PUMPED IN (3 TO 2)
WHAT HAPPENS IN PHASE 0
NA INFLUX INTO THE CELL INTRACELLULAR CONTENT MORE POSITIVE BY 20mV
what happens in phase I
fast sodium channels close
what happens in phase II
CA ENTRY VIA SLOW CHANNELS...HENCE THE PLATEAU.
WHAT HAPPENS IN PHASE III?
POTASSIUM LEAVES THE CELLS
WHAT IS CLASS 1A EFFECT ON PHASE 0; DEPOLARIZATION; REFRACTORY PERIOD; CONDUCTION,; CALCIUM CHANNELS?
PHASE 0 DEPRESSED
PROLONGS DEPOLARIZATION
INCREASES REFRACTORY PERIOD
DECREASES CONDUCTION; NO EFFECT ON CALCIUM CHANNELS
THE ARRYTHMIAS BEST TREATED WITH CLASS IB DRUGS ARE...?
VTACH
PVC
VFIB
BY LIDOCAINE AND PHENYTOIN
CLASS IB DRUGS DO WHAT TO
AP
REFRACTORINESS
SHORTEN ACTION POT.
REDUCE REFRACTORINESS
CLASS I -C DO WHAT TO PHASE 0
CONDUCTIVITY
AND ARE GOOD FOR TREATING WHAT ARRHYTHMIAS
DEPRESSES PHASE 0 STRONGLY
DEPRESSES CONDUCTIVITY
GOOD FOR LIFE THREATENING VTACH AND SVT (FLECAINIDE AND PROPAFENONE)
BB SLOW CONDUCTION THROUGH WHICH NODE
AV NODE
WHAT EFFECT DO CLASS III HAVE ON
K CHANNELS
REPOLARIZATION
NA CHANNELS
CONDUCTION
ACTION POTENTIAL AND DURATION
REFRACTORY PERIOD
RE-ENTRY PHENOMENON
BLOCK K CHANNELS
PROLONG REPOLARIZATION
NO AFFECT ON NA CHAN
DO NOT SLOW CONDUCTION
PROLONG ACTION POTENTIAL
PROLONG REFRACTORY
PREVENT RE-ENTRANT PHENOMENON (AMIO- BRETYLIUM, SOTALOL)
NAME THE FATAL ARRHYTHMIAS ASSOCIATED WITH CLASS 1 DRUGS
1A & 1C: QT, PR, QRS PROLONGATION
1A AND III- TORSADES
DIGOXIN TOXICITY
AV BLOCK ARE ASSOCIATED WITH WHICH DRUGS
CLASS I
MORE WITH 2 AND 4
CV DEPRESSION IS ASSOCIATED WITH WHICH CLASSES
BB (CLASS II); CLASS 4 AND CLASS 1 (1A/1C)
(1- AC; 2; 4)
ATROPINE-LIKE SIDE EFFECTS ARE..........ASSOCIATED WITH WHICH CLASS?
1A
CONFUSE, HOT, FLUSHED, TACHY, DRY
BETA BLOCKER SIDE EFFECTS ARE
BRONCHOSPASM, BRADY, CLAUDICATION; CLASS II DRUGS
NAUSEA AND VOMITING ASSOCIATED WITH...
CLASS 1A AND DIGOXIN
PARESTHESIAS AND SEIZURES ASSOCIATED WITH
CLASS 1B
DOPAMINE BETA-HYDROXYLASE IS AKA......AND IS RESPONSIBLE FOR WHICH REACTION?
ASCORBATE
CONVERTS DOPAMINE TO NOREPINEPHRINE
DESCRIBE THE ORDER OF CATECHOLAMINE PRODUCION
TYROSINE (TYROSINE HYDROXYLASE) = LDOPA (L-AMINO ACID DECARBOXYLASE) = DOPAMINE (DOPAMINE HYDROXYLASE) = NOREPINEPHRINE (N-METHYLTRANSFERASE) =EPINEPHRINE
THE NATURAL CATECHOLAMINES ARE?
EPINEPHRINE
NOREPINEPHRINE
DOBUTAMINE
SYNTHETIC CATECHOLAMINES ARE
DOBUTAMINE
ISOPROTERENOL
INDIRECT ACTING SYNTHETIC CATECHOLAMINES ARE?
AME (AMPHETAMINES, METARAMINOL, EPHEDRINE)
DIRECT ACTING CATECHOLAMINES ARE
PHENYLEPHRINE
METHOXAMINE
(think- a act directlly at night- PM)
PHENYLEPHRINE: SAY THE EFFECT ON-
CORONARY PERFUSION (WHY)?
EFFECT ON ALPHA?
CONSTRICTION GREATER ON ARTERIES OR VEINS?
MIMICS WHICH DRUG...
POTENCY AND DURATION COMPARED TO THE ABOVE DRUG.
INCREASES CORONARY PERFUSION B/C IT INCREASES PRELOAD
STIMULATES ALPHA-1 DIRECTLY
GREATER CONSTRICTION ON VEINS THAN ARTERIES
MIMIC LEVO
LESS POTENT AND LONGER LASTING THAN LEVO.
PHENYLEPHRINE DOSE
CHRONOTROPIC EFFECT
REFLEX BARORECEPTORS ;
EFFECT ON MAP, CO AND SVR
GOOD FOR PTS WITH AI OR AS
BAD FOR AI OR AS
DOSE- 25-200 MCG IVP
NO DIRECT CHRONOTROPY
REFLEX BRADY- AS BP INC, HR DECREASES
INCREASE MAP AND SVR
DECREASES CO AND HR
GOOD FOR AS
BAD FOR AI
PHENYLEPHRINE EFFECT ON
PAP
BLOOD FLOW TO CUTANEOUS BEDS
RENAL AND SPLANCHNIC BLOOD FLOW
ORAL CLONIDINE
PAP INCREASED
DECREASES BLOOD FLOW TO CUTANEOUS, RENAL AND SPLANCHNIC.
ORAL CLONIDINE POTENTIATES IT'S PRESSOR EFFECT
EPHEDRINE EFFECT:
DOSE
CORRECTS WHAT?
RESTORES ?
SIMILAR TO ........BUT LESS INTENSE?
..........X DURATION OF ABOVE DRUG.
AFFECTS WHICH RECEPTORS
MORE SELECTIVE ALPHA WHERE
5-25MG IV
CORRECTS HYPOTENSION ESP W/SPINAL OR REGIONAL
RESTORES BP AND UTERINE BLOOD FLOW
SIMILAR TO EPI
10 X THE DURATION BUT LESS INTENSE
A AND B RESPONSES BUT MORE A ON PERIPHEAL VESSELS
EPHEDRINE: EFFECT ON
NOREPINEPHRINE;
INDIRECT OR DIRECT
ALPHA OR BETA
INTERACTION WITH...
HYPERGLYCEMIA OR NOT
MYDRIASIS OR MIOSIS
CAUSES ENDOGENOUS RELEASE OF NE
INDIRECT ACTING ON BOTH ALPHA AND BETA
MAOI INTERACTION
NO HYPERGLYCEMIA
CAUSES MYDRIASIS
COMMON PHENOMENA WITH EPHEDRINE
RAPID TACHYPHYLAXIS
PERSISTENT BINDING OF ALPHA RECEPTORS
PERSISTS AFTER BP RETURNS TO NORMAL
NOREPINEPHRINE;
BEGINS WHERE...?
STORED WHERE?
RELEASE REQUIRES?
REUPTAKE REQUIRES ?
WHAT PHENOMENA CAN OCCUR WITH HIGH OUTPUT?
BEGINS IN CYTOPLASM
STORE IN SYNAPTIC VESCICLES
RELEASE REQUIRES CALCIUM
REUPTAKE REQUIRES MAGNESIUM AND ATP
TACHYPHYLAXIS CAN OCCUR
WHAT ARE THE DIFFERENT ROUTES OF TERMINATION OF ACTION?
FROM PRE TO POST SYNAPTIC
1. REUPTAKE VIA FEED BACK LOOP
2. DIFFUSION FROM RECEPTORS (GETS TAKEN UP)
3. MAO METABOLISM IN THE CYTOPLASM
4. COMT METABOLISM IN THE LIVER
NOREPINEPHRINE
DOSE:
RECEPTOR (S) IT ACTS ON:
=POTENT TO..... AT .....
VASCULAR BED EFFECT
EFFECT ON MAP, BP, HR, SVR, SBP AND DBP
CAN CAUSE......2DARY TO .....
GOOD TO USE IN ......?
DOSE 1-20MCG/KG/MIN
POTENT ALPHA AGONIST
WEAK B-2 RECEPTOR ACTIVITY
VASOCONSTRICTS ALL VASCULAR BEDS
INCREAES SVR, HR, BP, MAP (ALL)
METABOLIC ACIDOSIS 2DARY TO TISSUE HYPOPERFUSION
GOOD FOR SEPSIS
EPINEPHRINE EFFECT:
ACTIVATES WHICH RECEPTORS?
MOST POTENT ACTIVATOR OF....
....TO... TIMES MORE ACTIVE THAN.......
..... TIMES MORE POTENT THAN ......
ORAL ADMIN: GOOD/BAD
CAN BE GIVEN VIA:
LIPID SOLUBLE?
BOTH BETA 1&2
MOST POTENT ACTIVATOR OR ALPHA-ADRENERGIC RECEPTORS
2-10 TIMES MORE ACTIVE THAN LEVO
100X MORE POTENT ISOPROTERENOL
POOR ORAL ADMIIN
GIVE IV, SC, ETT
POORLY LIPID SOLUBLE
EPINEPHRINE
DOSE:
WHICH RECEPTOR PREDOMINATES IN RENAL AND CUTANEOUS VASCULAR BEDS?
1-2 MCGS/MIN BETA-2
4 MCG/MIN BETA2 DROPS AND B1 STIMULATED
10-20MCG/MIN (ALPHA AND BETA STIMULATION)
ALPHA PREDOMINATES IN RENAL AND CUTANEOUS BEDS- NOT IN SPLANCHNIC
EPINEPHRINE EFFECT ON:
BP, SBP, DBP, HR MAP
INCREASES SBP, HR, MAP
DECREASES DBP 2DARY TO B2 SMOOTH MUSCLE STIMULATION
EPINEPHRINE EFFECT ON:
BRONCHI SMOOTH MUSCLE
GLYCOGEN
ADIPOSE TISSUE
INSULIN SECRETION
PLASMA LACTATE
IRIS RADIAL MUSCLE
INCREASES WHICH ELECTROLYTE
CARDIAC EFFECT
URINE OUTPUT
BRONCHIAL SMOOTH MUSCLE RELAXED
GLYCOGENOLYSIS
LIPOLYSIS
INHIBITS INSULIN RELEASE
INCREASES LACTATE
CONTRACT RADIAL MUSCLE
INCREASE POTASSIUM LEVELS
DYSRHYTHMIAS ASSO WITH EPI
URINARY RETENTION
Dopamine effect:
activated by......
stimulates.....
at renal doses can cause.....
inhibits release of what?...
ACTIVATION BY ADENYLATE CYCLASE
STIMULATES D1 POSTSYNAPTICALLY
VASODILATION IN RENAL, MESENTERY, CORONARY AND CEREBRAL AT RENAL DOSES;
BLOCK NE RELEASE VIA D2 PRESYNAPTICALLY
Dopamine effect:
activated by......
stimulates.....
at renal doses can cause.....
inhibits release of what?...
ACTIVATION BY ADENYLATE CYCLASE
STIMULATES D1 POSTSYNAPTICALLY
VASODILATION IN RENAL, MESENTERY, CORONARY AND CEREBRAL AT RENAL DOSES;
BLOCK NE RELEASE VIA D2 PRESYNAPTICALLY
DOPAMINE EFFECT:
METABOLISM
DISSOLVE ONLY IN... WHY?
DOSES:
WARNING WITH ADMINISTRATION?
RAPIDLY METABOLIZED
DISSOLVE IN D5W B/C LESS BREAKDOWN
DOSE: 0.5 - 3 MCG/KG/MIN (D1)
3-10 (B1- CATECHOLAMINE EFFECT)
>10MCG/KG/MIN ALPHA RECEPTORS
EXTRAVASATION CAN OCCUR
DOPAMINE CONT'D:
USE IN.....
CAUSES CONTRACTILITY OF .....
ASSUMED TO IMPROVE.....AND ..... AT RENAL DOSES.
EFFECT ON SODIUM?
U/O?
AFFECT ON RHYTHM?
EFFECT ON HYPOXIC RESPONSE? IS VIA.....
USE IN LOW CO AND MAP
MYOCARDIAL CONTRACTILITY
GFR AND RENAL BLOOD FLOW BETTER AT RENAL DOSES
EXCRETION OF SODIUM
INCREASES U/O
LESS ARHYTHMIAS THAN EPI.
POOR VENTILATORY RESPONSE TO HYPOXIA (DETECTION IS VIA CAROTID BODIES)
DOBUTAMINE:
RECEPTOR (S);
DISSOLVE IN .....
DOSE.....
IN PTS WITH CHF, IMPROVES...;
EFFECT ON HR, SVR, PVR,MAP
NE RELEASE
CONDUCTION VELOCITY ...
B1 RECEPTOR ADRENERGIC RECEPTOR
DISSOLVE IN D5W
2-10 MCG/KG/MIN (POOR RESPONSE WITH >10)
IMPROVES CO IN PTS WITH CHF
INCREASES HR (DOSE DEPENDENT); MAP
DECREASES SVR AND PVR
NO DIRECT RELEASE OF NE
INCREASE IN AV NODE CONDUCTION VELOCITY
INCREASES MAP VIA HYPERDYNAMIC STATE
FIRST LINE DRUG FOR LOW CO IS ....?
DOBUTAMINE
PDE INHIBITORS ARE.....?
MILRINONE AND AMRINONE
PDE INHIBITORS WORK BY?
PREVENTING INACTIVATION OF cAMP AND cGMP - THUS ALLOWING THE SECOND MESSENGER TO EXECUTE SIGNALS INTO THE NUCLEUS.
MILRINONE:
ACTIVATES WHAT?
ADENYLATE CYCLASE cAMP SYSTEM BEYOND THE B RECEPTOR.
cAMP IN THE MYOCARDIUM AND Cgmp IN VASCULAR SMOOTH MUSCLE
WHAT SHOULD YOU ABSOLUTELY NOT DO WITH MILRINONE ADMINISTRATION
BOLUS THE PT.
CAN CAUSE HYPOTENSION AND CARDIAC ARREST
MILRINONE DOSE:
AFFECT ON TRANSPULMONARY PRESSURE GRADIENT?
AFFECT ON PVR?
BEST FOR WHICH PATIENTS?
DO NOT BOLUS MILRINONE
DOSE IS 0.125-1MCG/KG/MIN
NO AFFECT ON PULM PRESS GRADIENT
DECREASE PVR BY INCREASE IN CO WHICH RECRUITS COLLATERALS
GREAT FOR PTS WITH DIASTOLIC DYSFUNCTION AS SEEN WITH PTS AFTER BYPASS
WHAT FACTORS AFFECT OXYGEN SUPPLY?
HEART
OXYGEN SUPPLY AND SATURATION
PaO2
HGB
CORONARY BLOOD FLOW (CPP IS = DP-LVEDP)
WHAT FACTORS AFFECT OXYGEN DEMAND
HEARTRATE
PRELOAD
AFTERLOAD
WALL TENSION
CONTRACTILITY
THE 3 MAIN AREAS OF CARDIOVASCULAR ACTIONS OF NITRODILATORS ARE...
THE SYSTEMIC VASCULATURE
CARDIAC (HEART)
CORONARIES
WHAT IS THE EFFECT OF NITRODILATORS ON THE HEART?
REDUCES PRELOAD AND AFTERLOAD- DECREASING WALL STRESS
DECREASES OXYGEN DEMAND
WHAT IS THE EFFECT OF NITRODILATORS ON THE CORONARIES?
VASODILATE (ESP EPICARDIAL CORONARIES)
PREVENT VASOSPASMS
IMPROVE SUBENDOCARDIAL PERFUSION
INCREASE OXYGEN DELIVERY
WHAT IS THE EFFECT OF NITRODILATORS ON THE SYSTEMIC VASCULATURE?
VASODILATION (VENOUS>ARTERIAL)
DECREASE VENOUS AND ARTERIAL PRESSURE (SMALL EFFECT ON ARTERIAL PRESSURE)
INITIAL THERAPY FOR ALL TYPES OF ISCHEMIA WARRANTS THE USE OF ...
NITRATES
WHAT BE USED WITH NITRATES SHD HYPOTENSION OCCUR WITHOUT RESOLUTION OF ISCHEMIA
PHENYLEPHRINE AND NITROGLYCERINE = CHEMICAL IABP; CAN VASODILATE AND INCREASE CORONARY PERFUSION AT THE SAME TIME
What is the mechanism of smooth muscle relaxation with nitrates?
NITRATE CONVERSION TO NITRIC OXIDE WHICH STIMULATES GUANYLATE CYCLASE METABOLISM TO PRODUCE cGMP
NITROGLYCERIN:
AT LOWER DOSES WHAT HAPPENS?
THIS RESULTS IN WHAT?
AT HIGHER DOSES WHAT HAPPENS? WHAT SHD YOU ADD AS A RESULT?
VASODILATION OF THE PULMONARY SYSTEM RESULTS IN WHAT?
PROMINENT VENODILATION = LOWER DOSES.
BLOOD POOLS IN SPLANCHNIC CIRC
HIGHER DOSE = SMALL ARTERIOLES AND RESISTANCE VESSELS DILATE = DECREASE IN AFTERLOAD AND BP (ADD PHENYLEPHRINE)
THE RAP,PAP AND PCWP ALL DECREASE WITH PULM VASODILATION
WHAT CAN OCCUR WITH HIGH NITROGLYCERIN ADMIN? WHAT IS THE DOSE TO AVOID
METHEMOGLOBINEMIA
5MG/KG/DAY OR HIGHER
WHAT CAN OCCUR WITH HIGH NITROGLYCERIN ADMIN? WHAT IS THE DOSE TO AVOID
METHEMOGLOBINEMIA
5MG/KG/DAY OR HIGHER
CONTRAINDICATED IN PTS USING WHAT?
VIAGRA, LEVITRA, CIALIS WITHIN 24-48HOURS- CAN CAUSE REBOUND HYPOTENSION
WHEN IS THE USE OF NITROGLYCERINE WARRANTED?
IN ACUTE LEFT HEART FAILURE WITH NORMAL BP
WHAT HAS REPLACED NITROPRUSSIDE ?
INODILATORS
NITROPRUSSIDE
CAUSES FORMATION OF ....
IS CONVERTED TO ....
WHERE?
EXCRETED BY ....
TOXICITY CAUSES...?
INHIBITS WHAT?...
FORMATION OF cGMP IN VASCULAR TISSUE
CONVERTED TO FREE CYANIDE THEN THIOCYANATE IN THE LIVER
EXCRETED BY KIDNEYS
CAUSES HISTOTOXICITY
INHIBITS CELLULAR OXIDATIVE PHOSPHORYLATION (CAN'T USE OXYGEN AT THE TISSUE LEVEL)
NITROPRUSSIDE
DOSE:
SE INCLUDE?
DOSE: 0.5 - 10 MCG/KG/MIN
SE INCLUDE: HYPOTENSION (DIASTOLIC)
CYANIDE TOXICITY
IF OVERDOSE OF NITROPRUSSIDE OCCURS, USE?
SODIUM THIOSULFATE AS ANTIDOTE - BINDING AGENT 150-200MG/KG
WHAT ARE SPECIFIC INDICATIONS FOR USE OF NITROPRUSSIDE?
1. SEVERE ACUTE OR CHRONIC HEART FAILURE
2. HTN CRISIS (USE W/ESMOLOL)
3. DISSECTING ANEURYSM
4. CONTROLLED HYPOTENSION ESP IN OR
5. POST BYPASS HTN CRISIS
BETA BLOCKERS ARE INDICATED IN
HTN
ANGINA
MI
ARRYTHMIAS
HEART FAILURE
CARDIAC EFFECT THAT CAUSES AN INCREASE IN RELAXATION STATE IS CALLED?
LUSITROPY
THE CARIOSELECTIVE BB INCLUDE?
E- BAMA
ESMOLOL
BISOPROLOL
ACEBUTALOL
METOPROLOL
ATENOLOL
NONCARDIOSELECTIVE BB ARE?
NP - STP
NADOLOL
PROPANOLOL
SOTALOL
TIMOLOL
PINDOLOL
WHAT DETERMINES CARDIOSELECTIVITY
DOSE DEPENDENT- THE HIGHER THE DOSE THE MORE CARDIOSELECTIVE
BB BINDING IS ..... BY AGONIST.
THERE IS A SHIFT TO THE .............OF THE CURVE FOR AGONIST> WHAT DOES THIS MEAN?
CHRONIC ADMINISTRATION ASSOCIATED WITH ?
WHAT IS THE #1 EFFECT IF BB ARE HELD ABRUPTLY?
BINDING IS REVERSIBLE BY AGONIST
THERE IS A RIGHT SHIFT IN THE DOSE RESPONSE CURVE FOR AGONIST
(THE HIGHER THE BB DOSE THE MORE AGONIST YOU NEED TO REVERSE IT)
CHRONIC ADMIN= UP REGULATION
REBOUND HYPERTENSION IF HELD
METOPROLOL:
DOSE; ORAL AND IV
PREVENT WHAT?
REVERSIBLE?
ASTHMA AND COPD EFFECTS?
DOSE: ORAL50-400MG
IV 5-20MG
PREVENT INOTROPY AND CHRONOTROPY
READILY REVERSIBLE WITH B AGONIST
AFFECT ASTHMA MORE THAN COPD (BRONCHOCONSTRICTION)
ESMOLOL
ONSET: SLOW/RAPID?
DURATION?
DOSE; IVP OR INFUSION.
ONSET RAPID
DURATION 10-30MIN AFTER D/C'D
DOSE: 0.5MG.KG IV OVER 60 SECS IVP;
50-300 MCG/KG/MIN
INDICATION FOR ESMOLOL?
USED TO BLUNT RESPONSE TO ET INTUBATION
WHAT IS THE PH OF ESMOLOL?
WHAT IS THE ELIMINATION HALF LIFE?
HOW IS IT METOLYSIS
PH IS 4.5 TO 5.5 - ACIDIC
PAIN ON INJECTION
ELIMINATION HALF TIME IS 9MINS
PLASMA ESTERASES RAPIDLY HYDROLYSE IT.
LABETALOL:
WHICH RECEPTORS?
WHICH ARE SPARED?
RATIO OF BETA TO ALPHA
WHAT DOES THE DRUG DO
BETA AND ALPHA BLOCKADE
SPARE ALPHA 2 RECEPTORS
B TO ALPHA 7:1
LOWERS BP AND SVR
WHAT IS UNCHANGED WITH LABETALOL
CO AND SV UNCHANGED
LABETALOL CAN CAUSE WHAT...... ESP WITH CCB.
CHF
WHAT IS THE ADDITIVE EFFECT OF LABETALOL AND CCB?
HEART BLOCK
SUDDEN WITHDRAWAL =

ANY CNS EFFECTS?
HYPERTENSIVE CRISIS.
YES
CALCIUM CHANNEL BLOCKER ARE INDICATED IN ?
HTN
ANGINA
ARRHYTHMIAS
cardiac effect of CCB INCLUDE
DECREASE CONTRACTILITY, HR, AND CONDUCTION VELOCITY
VASCULAR EFFECTS OF CCB INCLUDE
VASODILATION
CCB - MECHANISM OF ACTION
THEY BLOCK L TYPE CHANNELS (MAIN CHANNELS BLOCKED) T TYPE CHANNELS AND ION INFLUX VIA L CHANNELS
L TYPE CHANNELS FACILITATE WHAT
THEY SUSTAIN SLOW ENTRY OF CALCIUM
T TYPE CHANNELS ARE ASSOCIATED WITH WHAT?
VASCULAR SMOOTH MUSCLE CELL MEMBRANE
ION INFLUX VIA L CHANNELS CAUSE
EXCITATION AND CONTRACTION COUPLING
THE FOUR CLASSES OF DRUGS THAT INTERACT WITH L TYPE CCB ARE?
DD-BP
DIHYDROPYRIDINE (DHP) DERIVATIVES
DIARYLAMINOPROPYLAMINE
BENZODIAZEPINES
PHENYLALKYL-AMINES
1,4 DYHYDROPYRIDINE DERIVATIVES ARE WHICH DRUGS
NIFEDIPINE
NIMODIPINE
NICARDIPINE
ISRADIPINE
AMLODIPINE
FELODIPINE
THE MOST POTENT CORONARYVASODILATOR IS
NIFEDIPINE (ESP IN EPICARDIAL VESSELS)
DILTIAZEM:
INDICATIONS....
SE PROFILE....HIGH OR LOW
RASH (RATE CONTROL-AFIB, AFLUTTER- ANGINA, SVT, HTN

LOW SE PROFILE
EXAMPLE OF PHENYLALKYLAMINE IS ...
VERAPRAMIL (THINK VP)
EXAMPLE OF BENZOTHIAZEPINES INCLUDE?
DILTIAZEM
EXAMPLE OF DIARYLAMINOPHROPYLAMINE ETHER IS ?

WHO IS THIS DRUG CONTRAINDICATED IN?
BEPRIDIL- ANTIANGINAL/ANTIARRHYTHMIC-
LOWERS HR AND CAUSES DILATATION- B/C IT SLOWS CONDUCTION DO NOT USE IN SICK SINUS SYNDROME, PROLONGED QT, 2-3RD DEGREE HEART BLOCK
NIMODIPINE:
IMPORTANCE IN SOLUBILITY?
WHAT DOES IT PREVENT
WHAT IS IT EFFECTIVE IN REVERSING?
HIGHLY LIPID SOLUBLE- ENTERS BBB AND CNS
PREVENT CEREBRAL VASOSPASMS
REVERSES CEREBRAL HYPOXIA.
IN LARGE CEREBRAL ARTERIES, NIMODIPINE DOES WHAT?
BLOCKS EXTRACELLULAR CALCIUM IONS.
UNIQUE PROPERTY OF NIFEDIPINE IS THAT ...
ITS INTRISIC INOTROPY IS OFFSET BY POTENT ARTERIAL DILATION = DECREASED BP AND INCREASED CO
USE NIFEDIPINE WITH CAUTION IN WHICH PTS?
PTS WITH DECREASED LV FXN
THE BESST VASODILATOR OF THE CCB IS?
BEST FOR .....
NICARDIPINE
BEST FOR RESIDUAL HTN AFTER BB
WHICH CCB HAS LOCAL ANESTHETIC AFFECT?
VERAPRAMIL
VERAPRAMIL:
ACTS ON......CHANNELS?
POTENCY COMPARED TO DHPS?
GREAT FOR .....?
EFFECT ON HR, SV, CO
USE WITH CAUTION IN
ACTS ON FAST NA CHANNELS
LESS POTENT THAN DHP'S
GREAT FOR SVT
NO SIGNIFICANT CHANGE IN HR, SV, CO
CAUTION IN PTS WITH VENTRICULAR DYSFXN- CAN POTENTIATE VENTRICULAR DYSFXN.
DILTIAZEM
POTENCY COMPARED TO VERAPRAMIL...
ATTENTUATES BAROREFLEX WHEN?
LESS POTENT AND FEWER INOTROPIC EFFECTS THAN VERAPRAMIL.
ATTENUATES BAROREFLEX IN HIGH HR DUE TO NTG
ATTENUATES BAROREFLEX IN LOW HR DUE TO PHENYLEPRINE
DILTIAZEM
POTENCY COMPARED TO VERAPRAMIL...
ATTENTUATES BAROREFLEX WHEN?
LESS POTENT AND FEWER INOTROPIC EFFECTS THAN VERAPRAMIL.
ATTENUATES BAROREFLEX IN HIGH HR DUE TO NTG
ATTENUATES BAROREFLEX IN LOW HR DUE TO PHENYLEPRINE
DILTIAZEM;
DOSING......
SE INCLUDE.....
0.25MG/KG OVER A FEW MIN.....IF NO RESPONSE GO TO 0.35MG/KG OVER 2 MIN . INFUSION TO FF CAN BE A 5-15MG/HR

SE = BAHA
BRADY
ASYSTOLE
HYPOTENSION
AV BLOCK 3RD DEGREE
DILTIAZEM;
DOSING......
SE INCLUDE.....
0.25MG/KG OVER A FEW MIN.....IF NO RESPONSE GO TO 0.35MG/KG OVER 2 MIN . INFUSION TO FF CAN BE A 5-15MG/HR

SE = BAHA
BRADY
ASYSTOLE
HYPOTENSION
AV BLOCK 3RD DEGREE
DILTIAZEM BLOCKS ........VASOCONSTRICTION DUE TO WHAT FOUR THINGS?
CORONARY VASOCONSTRICTION.....DUE TO PASA (PROSTAGLANDINS, SEROTONIN, ALPHA AGONISTS),
WHAT WAS AN IMPORTANT NOTE OF INTEREST WITH DILTIAZEM USE IN POST INFARCT PTS WITH LOW EF?
HAVE HIGHER MOTALITY IF TREATED WITH DILTIAZEM THAN WHEN NOT TREATED.
WHAT ARE THE THERAPEUTIC EFFECTS OF BEPRIDIL?
AAA
ANTIANGINAL
ANTI-HTN
ANTIARRYTHMIC (TYPE 1 = INHIBITS SLOW AND FAST INWARD CA++ CURRENT
AMIODARONE:
REFRACTORY PERIOD
CARDIAC TISSUE AND ACCESSORY TRACTS EFFECT?
ANTIADRENERGIC EFFECT?
EFFECT ON CORONARIES
WHAT CARDIAC EKG SIGN SEEN.....
SE WITH PROLONG USE....
PROLONGS REFRACTORY
WORKS ON ALL CARDIAC TISSUES AND ACCESSORY TRACTS
BLOCKS ALPHA AND BETA
DILATES CORONARIES
INCREASES CORONARY BLOOD FLOW
QT PROLONGATION AND YELLOW CORNEAL DEPOSITS.
AMIODARONE:
1/2 LIFE;
PB:
PLASMA VERSUS MYOCARDIAL MED CONCENTRATION;
EFFECT ON PULM;
MORTALITY:
PROLONGED 1/2 LIFE 31 HOURS
PB EXTENSIVE
10-50TIMES MORE IN MYOCARDIUM THAN PLASMA
SYSTEMIC AND PULM VASODILATATION
PULM ALVEOLITIS OR FIBROSIS
MORTALITY 5-10%
FREE OXYGEN RADIALS
AMIODARONE:
1/2 LIFE;
PB:
PLASMA VERSUS MYOCARDIAL MED CONCENTRATION;
EFFECT ON PULM;
MORTALITY:
PROLONGED 1/2 LIFE 31 HOURS
PB EXTENSIVE
10-50TIMES MORE IN MYOCARDIUM THAN PLASMA
SYSTEMIC AND PULM VASODILATATION
PULM ALVEOLITIS OR FIBROSIS
MORTALITY 5-10%
FREE OXYGEN RADIALS
AMIODARONE
USE FOR:
EFFECT ON HR
INDICATED IN WHICH ARRHYTHMIAS.- .....
USE AS ADJUNCT TO....
PROLONGED QT
V-TACH DYSRHYTHMIAS
SLOW HR RESISTANT ATROPINE
TX FOR POLY VT, SHOCK REFRACTORY VT, OR PULSELESS VT
ADJUNCT TO ELECTRICAL CONVERSION FOR SVT AND NSSVT (150MG -SHOCK; 300MG SHOCK)
AMIO DOSE:
150mg iv over 10 mins
may repeat in 10mins
then, 1mg/min x 6hours
0.5mg/min for maintenance
terminal elimination is over 40 days