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216 Cards in this Set
- Front
- Back
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What composes the cardiovascular system?
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3 components
1. HEART 2. VASCULATURE 3. AUTONOMIC NERVOUS SYSTEM (parasympathetic and sympathetic) |
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In tlEAhe sympathetic nervous system, how do the preganglionic neurons function/ synapse?
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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 |
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Presynaptic Neurotransmitter in the sympathetic system is the ------------------ and postsynaptic is -------------.
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1.ACETYLCHOLINE
2. POST SYNAPTIC IS NOREPINEPHRINE |
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The sympathetic innervation is located in the
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Thoracic and Lumbar spines:
T1-L2 |
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, thevascular smooth muscle blood vessel contractions occur in -/-/-/- and is via which receptors?
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Contraction of blood vessels in the SKIN, SPLANCHNIC, SKELETAL MUSCLE AND RENAL occur by the
ALPHA-1 ADRENERGIC RECEPTORS ALPHA-1 (VASOCONSTRICTION) |
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Relaxation of blood vessels in the sympathetic NS occurs by action of the .....?
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BETA ADRENERGIC RECEPTORS
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WHAT IS THE SYMPATHETIC RESPONSE IN THE HEART AND WHAT CONTROLS THIS?
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SYMPATHETIC RESPONSES INCLUDE INCREASES IN
1. CHRONOTROPY (BETA 1 RECEPTORS INCREASE HEARTRATE) 2. INOTROPY (BETA 1&2 INCREASE CONTRACTILITY) 3. DROMOTROPY (CONDUCTION INCREASES) |
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What happens in the kidneys?
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INCREASE RENIN RELEASE VIA BETA 1 ADRENERGIC RECEPTORS
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THE MAJOR SOURCE OF CARDIAC STIMULATION IS WHAT? HOW IS IT FORMED?
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THE STELLATE GANGLIA. FORMED WITH THE INFERIOR CERVICAL AND 1ST THORACIC GANGLIA.
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THE RIGHT AND LEFT STELLATE GANGLIA ARE RESPONS?IBLE FOR WHAT
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THE RIGHT AND LEFT STELLATE GANGLIA STIMULATE THE HEART. RIGHT INCREASES HEARTRATE.
LEFT INCREASES CONTRACTILITY |
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IN THE SNS, WHAT OCCURS IN THE LUNGS?
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BRONCHIOLAR SMOOTH MUSCLE RELAXATION VIA THE BETA 2 ADRENERGIC RECEPTORS
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IN THE SNS WHAT OCCURS IN THE LIVER.... CONTROLLED BY WHAT?
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INCREASED GLUCOSE METABOLISM (GLYCOGEN STORES ARE CONVERTED TO GLUCOSE); BETA 2 CELLS
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IN THE SNS, WHAT OCCURS IN THE GI TRACT?
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DECREASED PERISTASIS AND MOTILITY VIA THE BETA 2 ADRENERGIC RECEPTORS.
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THE MAIN NERVE IN THE PNS IS -------; CN ---?
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VAGUS NERVE; CN 10
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OTHER PREGANGLIONIC PARASYMPATHETIC NEURONS ARISE FROM THE ---------- AND ENTER ---?
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ARISE FROM THE MEDULLA OBLONGATA AND THEY ENTER THE THORAX WITH BRANCHES OF THE RECURRENT LARYNGEAL AND THE THORACIC VAGUS NERVE.
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IN THE SNS, WHAT OCCURS IN THE LUNGS?
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BRONCHIOLAR SMOOTH MUSCLE RELAXATION VIA THE BETA 2 ADRENERGIC RECEPTORS
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IN THE SNS WHAT OCCURS IN THE LIVER.... CONTROLLED BY WHAT?
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INCREASED GLUCOSE METABOLISM (GLYCOGEN STORES ARE CONVERTED TO GLUCOSE); BETA 2 CELLS
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IN THE SNS, WHAT OCCURS IN THE GI TRACT?
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DECREASED PERISTASIS AND MOTILITY VIA THE BETA 2 ADRENERGIC RECEPTORS.
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THE MAIN NERVE IN THE PNS IS -------; CN ---?
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VAGUS NERVE; CN 10
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OTHER PREGANGLIONIC PARASYMPATHETIC NEURONS ARISE FROM THE ---------- AND ENTER ---?
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ARISE FROM THE MEDULLA OBLONGATA AND THEY ENTER THE THORAX WITH BRANCHES OF THE RECURRENT LARYNGEAL AND THE THORACIC VAGUS NERVE.
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THE VENTRAL AND DORSAL CARDIO-PULMONARY PLEXUS ARE LOCATED WHERE?
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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.
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Each preganglionic parasympathetic neuron synapse with--------, that are located where?
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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)
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THE 3 CARDIAC NERVES OF THE VENTRAL/DORSAL CARDIOPULMONARY PLEXUS ARE?
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RIGHT CORONARYCARDIAC NERVE
LEFT CORONARYCARDIAC NERVE LEFT LATERAL CARDIAC NERVE |
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THE MOST ABUNDANT PARASYMPATHETIC NERVES ARE LOCATED WHERE?
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1. CORONARY SINUS
2. SUPERIOR VENA CAVA (svc) |
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THE PRE AND POST GANGLIONIC NEUROTRANSMITTER IN THE PNS ARE? ARE THERE ANY OTHER NEUROTRANSMITTORS?
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ONLY ACETYLCHOLINE; However, a few postganglionic neurons also release NITRIC OXIDE as their neurotransmitter.
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The parasym postganglionic neurons nearest the heart are generally further away from the structures they innervate (TRUE/FALSE)
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FALSE; THEY ARE VERY CLOSE TO THE STRUCTURES THEY INNERVATED AND ARE THEREFORE VERY SHORT.
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What activates the muscarinic receptors?
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STIMULATION from the nicotinic receptors and the release of the acetylcholine at the neuroeffector junction activates the muscarinic receptors.
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The muscarinic receptor is ---?
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It is the main END-RECEPTOR that is stimulated by ACETYLCHOLINE released from postganglionic PNS junctions of the cardiac and smooth muscles.
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In the PNS the M2 receptors are responsible for?
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Decreasing INOTROPY, CHRONOTROPY AND DROMOTROPY.
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M3 receptors in the PNS are responsible for ?-----via what? and what is this used interchangeably with?
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SMOOTH MUSCLE RELAXATION via THE EDRF (ENDOTHELIAL DERIVED RELAXING FACTOR)- EDRF is used interchangeably with Nitric-Oxide b/c it has vasodilatory properties.
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Carbon Monoxide formation has what effect on smooth muscle? CO formation is stimulated by what in the blood?
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Causes smooth muscle relaxation.
Proteins can stimulate formation of CO. |
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Identify the valves in the heart
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ATRIOVENTRICULAR:MITRAL (LEFT) ; TRICUSPID (RIGHT)
SEMILUNAR VALVES (AORTIC AND PULMONARY VALVES) |
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Corornary circulatory flow is regulated by what?
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OXYGEN DEMAND-
The coronaries vasodilate when more oxygen is needed and the heart gets perfused. |
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RCA arises from where?
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RIGHT ANTERIOR AORTIC SINUS (AKA SINUS OF VALSALVA)
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LCA arises from where?
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LEFT ANTERIOR AORTIC SINUS (AKA SINUS OF VALSALVA)
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WHERE IS THE AORTIC SINUS LOCATED? WHAT ARE THE COMPONENTS?
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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. |
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WHAT IS THE POSTERIOR AORTIC SINUS CALLED AND WHY?
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THE NON-CORONARY SINUS ; B/C NO VESSEL ARISE FROM IT
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HOW DOES THE LCA DIVIDE?
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INTO THE LAD (LEFT ANTERIOR DESCENDING) AND THE LEFT CIRCUMFLEX BRANCH.
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WHAT IS THE WIDOW MAKER?
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A HIGHLY STENOTIC LEFT MAIN CORONARY ARTERY OR PROXIMAL LAD ARTERY OFTHE HEART.
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TRACE THE PATTERN OF FLOW IN THE LAD
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Goes down the ANTERIOR LEFT VENTRICLE- through the INTERVENTRICULAR GROVE to supply the DIAGONAL AND CEPHALPERFORATIOG BRANCHES.
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OCCLUSIVE DISEASE OF THE LAD WILL BE SEEN IN WHICH LEADS
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V3,V5,V6, AVL AND LEAD1
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HOW IS CORONARY ARTERY DOMINANCE DETERMINED?
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BASED ON WHICH ARTERY CROSSES THE CRUX TO SUPPLY THE POSTERIOR DESCENDING ARTERY (AKA THE POSTERIOR INTERVENTRICULAR ARTERY)
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DECRIBE THE FREQUENCY OF CORONARY ARTERY DOMINANCE.
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50% RIGHT DOMINANCE (SUPPLY BY THE RCA)
20% LEFT DOMINANCE (SUPPLIED BY THE CIRCUMFLEX ARTERY) 30% CODOMINANCE - SUPPLIED BY BOTH RCA AND L.CX. |
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IN THE CV SYSTEM, THE ACTIVITIES OCCURING IN NORMAL CORONARIES IN THE PNS INCLUDE:
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1. EXOGENOUS ACETYLCHOLINE
2. ELECTRICAL VAGAL STIMULATION 3. REFLEX ACTIVATION VIA RECEPTORS (BARO/CHEMO AND VENTRICULAR RECEPTORS) |
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REFLEX ACTIVATION IN THE PNS INCLUDE WHICH RECEPTORS:
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BARORECEPTORS, CHEMORECEPTORS AND VENTRICULAR RECEPTORS.
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WHERE DO VAGAL FIBERS END IN THE PNS
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IN THE ADVENTIA OF CORONARY VESSELS.
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IN NORMAL CORONARIES, PARASYMPATHETIC RESPONSE IS?
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VASODILATION
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IN THE PNS, ATHEROSCLEROTIC CORONARIES RESPOND BY?
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VASOCONSTICTING
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IN THE CV SYSTEM, DURING SYMPATHETIC RESPONSE, WHAT OCCURS IN THE CORONARIES IN RESPONSE TO ALPHA STIMULATION?
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VASOCONSTRICTION IN RESPONSE TO ALPHA-1 AND 2 STIMULATION (ALPHA-1 in LARGER VESSELS) (ALPHA-2 IN SMALLER VESSELS)
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BETA STIMULATION RESULTS IN WHAT IN THE SNS IN THE CV-SYSTEM?
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CORONARY VASODILATION (MOSTLY IN SMALLER CORONARY ARTERIES)
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WHAT CARDIAC NERVES EMERGE FROM THE CARDIOPULMONARY PLEXUS?
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RIGHT AND LEFT CARDIAC NERVES AND THE LEFT LATERAL CARDIAC NERVES EMERGE
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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.
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THE RIGHT DORSAL MEDIAL AND LATERAL CARDIAC NERVES ARE NORMALLY PARASYMPATHETIC OR SYMPATHETIC? THEY FOLLOW WHAT TO WHERE?
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THE DORSAL MEDIAL AND LATERAL CARDIAC NERVES ARE SYMPATHETIC AND THEY FOLLOW THE LEFT MAIN CORONARY TO THE LAD AND CX ARTERIES.
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IN THE HEART, THE SYMPATHETIC SYSTEM INVOLVES WHICH STRUCTURES/NERVES?
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STELLATE GANGLION AND CAUDAL CERVICAL SYMPATHETIC TRUNK
RIGHT DORSAL MEDIAL LEFT CARDIAC NERVES |
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IN CV PHYSIOLOGY, THE PARASYMPATHETIC SYSTEM FLOW IS FROM THE....?
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MEDULLA OBLONGATA TO THE THORAX VIA RECURRENT LARYNGEAL AND VAGUS NERVES.
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THE GREATEST CONC OF THE PARASYMPATHETIC NERVES IS IN THE ?
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SA NODE
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WHAT ARE THE PERCENTAGES OF BETA 1 AND 2 IN THE RA AND THE VENTRICLES.
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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 |
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THE ELECTRICAL PATHWAY OF THE HEART FOLLOWS WHICH FLOW?
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SA NODE
AV NODE BUNDLE OF HIS RIGHT BUNDLE LEFT BUNDLE PURKINJE FIBERS ENDOCARDIUM EPICARDIUM OF THE VENTRICLES |
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WHAT IS THE PUMPING EFFICIENCY OF THE HEART?
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THE ENERGY REQUIRED TO PUMP A GIVEN BLOOD VOLUME.
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WHAT AFFECTS THE PUMPING EFFICIENCY?
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AC CAMP
AFTERLOAD CONTRACTILITY CONDUCTION ABNORMALITIES ANATOMICAL ABNORMALITIES MYOCARDIUM/COMPROMISED PRE-LOAD |
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WHAT AFFECTS THE MYOCARDIAL OXYGEN CONSUMPTION?
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LOVE(lvedp)-PARIS
PRELOAD (lvedp) AFTERLOAD RATE (HEARTRATE-TACHY) INOTROPIC STATE (strength of squeeze) STROKE VOLUME (wall tension) |
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FACTORS THAT AFFECT THE CARDIAC PERFORMANCE.
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C- IPAD
CHRONOTROPHY (rate) INOTROPY PRELOAD AFTERLOAD DROMOTROPY |
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THE FRANK-STARLING LAW STATES THAT...
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THE FORCE OF CONTRACTION OF THE CARDIAC MUSCLE IS PROPORTIONAL TO ITS INITIAL LENGTH.
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THE EQUATION FOR STROKE VOLUME IS ?
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EDV - ESV = SV
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NORMAL STROKE VOL IS .......? AND NORMAL LVEDP IS .........?
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STROKE VOL: 70-130 ML
LVEDP IS 5-13 |
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How does the pulmonary circulation differ in pressure and resistance from that of the Systemic Circulation.
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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 |
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HOW IS THE CIRCULATORY SYSTEM CLASSIFIED?
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BY SIZE, FUNCTION AND LOCATION.
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LIST THE ORDER OF THE VESSELS
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ARTERIES
ARTERIOLES CAPILLARIES VENULES (HIGHLY DISTENSIBLE) VEINS |
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CIRCULATORY STOP COCKS AREA?
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THE ARTERIOLES
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THE PRIMARY RESISTANCE VESSELS ARE?
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THE ARTERIOLES
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THE RESISTANCE VESSELS ARE CONTROLLED BY
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THE SYMPATHETIC NERVOUS SYSTEM
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THE CAPACITANCE VESSELS ARE?
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VEIN AND VENULES- CONTAIN 50% OF TOTAL BLOOD.
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FLOW OF THE CAPACITANCE VESSELS IS CONTROLLED BY?
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SYMPATHETIC AND HUMORAL FACTORS.
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SYMPATHETIC AND HUMORAL FACTORS CONTROL ----------- AND ------.
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FLOW OF CAPACITANCE VESSELS AND PERMEABILITY.
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SHORT TERM REGULATION IN THE CV SYSTEM TAKES.....?
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SECONDS TO MINUTES
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THE LONG TERM REGULATION IN THE CV SYSTEM TAKES: ...
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DAYS TO WEEKS
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MAP IS DETERMINED BY THE ...
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BARORECEPTORS IN THE AORTIC ARCH AND CAROTID ARTERIES. AND BY THE REFLEX PATHWAYS (FEEDBACK LOOPS)
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SHORT TERM REGULATION IS COMPRISED OF/CONTROLLED BY?
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1. ANS
2. MAP CHANGES SENSED BY BARORECEPTORS 3. VASOMOTOR CENTERS INTHE MEDULLA 4. SYMPATHETIC AND PARASYMPATHETIC OUTPUT. |
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DURING SHORT TERM REGULATION, A DROP IN THE MAP ELLICITS WHAT ACTIVITIES?
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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) |
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DURING SHORT TERM REGULATION, A RISE IN THE MAP ELLICITS WHAT ACTIVITIES?
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INCREASED BARORECEPTOR ACTIVITY
INCREASED VAGAL TONE DECREASE IN SYMPATHETIC TONE |
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DECREASE IN VAGAL TONE DENOTES .....
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INCREASING THE HR
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INCREASING SYMPATHETIC T HONE DENOTES INCREASES IN WHAT?
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V- HIP
VENOUS TONE HEARTRATE INOTROPY PVR |
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WHAT MEDIATES LONG TERM REGULATION, AND WHAT IS CONTROLLED?
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HUMORAL FACTORS MEDIATE LONG TERM REGULATION AND
BLOOD VOLUME SODIUM REGULATION AND WATER RETENTION ARE ALL CONTROLLED (BLOOD, WATER, SODIUM) |
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THE RAS SYSTEM IS INVOLVED IN WHICH REGULATION (LONG OR SHORT-TERM)?
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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. |
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CHANNELS AFFECTED BY DRUGS ACTING DIRECTLY ON CARDIAC TISSUE INCLUDE?
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K, NA, CA CHANNELS
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DRUGS ACTING ON VASCULATURE INCLUDE?
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NOREPINEPHRINE (ALPHA-1 ADRENORECEPTOR)
AND EPINEPHRINE (BETA-2 VIA cAMP LEADING TO VASORELAXATION) |
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NAME THE FOUR DRUGS IDENTIFIED AS ACTING ON THE CARDIAC VASCULATURE.
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ADENOSINE
NITRIC OXIDE ENDOTHELIN ERGONOVINE |
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WHAT KIND OF SYSTEMIC EFFECT DOES ADENOSINE HAVE? HOW IS IT DOSED?
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NONE.
6MG/1SEC WAIT TO SEE IF CONVERTS; GIVE 12MG/1SEC. CAN STOP THE HEART TRANSIENTLY. |
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HOW DOES NITRIC OXIDE WORKS?....OVERALL EFFECT IS?
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WORKS ON ENDOTHELIUM OF BLOOD VESSEL. STIMULATES cGMP = CAUSES DEPHOSPPHORYLATION OF MYOSIN CHAIN = SMOOTH MUSCLE RELAXATION.
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MOST POTENT VASOCONSTRICTOR IS?
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ENDOTHELIN
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USED FOR DIAGNOSIS OF VARIANT ANGINA:...? THIS DRUG CAN CAUSE------ & -----?
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ERGONOVINE.
CAN CAUSE INFARCTION AND DEATH. CAUSES BETA CONSTRICTION BY STIMULATING ALPHA. |
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VAUGHAN WILLIAMS/HARRISON CLASSIFICATION OF ANTIARRHYTHMIC DRUGS: CLASSES ARE?
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CLASS 1: NA CHANNEL BLOCKERS (1A;1B;1C)
CLASS 2: BETA BLOCKERS CLASS 3: K BLOCKERS CLASS 4: CALCIUM CHANNEL BLOCKERS THEN THE UNCLASSIFIED. |
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HOW DO SODIUM CHANNEL BLOCKERS WORK.
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DEPRESS PHASE 0 DEPOLARIZATION.
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HOW DO CLASS 1A DRUGS WORK......NAME 3
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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) |
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HOW DO CLASS 1B WORK?
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Block ONLY Sodium channels at high heart rates- selectively. WEAK DEPRESSION AND SHORTENS REPOLARIZATION. (LP) LIDOCAIN AND PHENYTOIN)
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HOW DO CLASS 1C WORK?
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EQUALLY BLOCK SODIUM CHANNELS AT ALL/ANY HEART RATE. HAVE STRONG DEPRESSION OF DEPOLARIZATION WITH LITTLE EFFECT ON REPOLARIZATION. (
FLECANIDE/ ENCAINIDE) |
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CLASS TWO DRUGS WORK BY?
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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)
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CLASS III DRUGS WORK BY?
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BLOCKING THE OUTFLOW OF POTASSIUM FROM THE CELLS: AMIODARONE ; DOFETILIDE AND IBUTILIDE
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AMIODARONE BELONGS TO CLASS ...........BUT HAS CLASS ............AND ........ ACTIONS.
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CLASS III BUT HAS CLASSES 1 AND 4 ACTION
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CLASS 4 DRUGS ARE....AND HOW DO THEY WORK
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DILTIAZEM AND VERAPRAMIL....WORK BY BLOCKING L TYPE VOLTAGE GATED CALCIUM CHANNELS
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UNCLASSIFIED CLASS INCLUDES..... THEY WORK BY MIMICKING WHICH ACTIVITY?
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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 |
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WHAT HAPPEN IN PHASE 4?
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NA/K PUMP DEPENDENT
SODIUM IS PUMPED OUT AND K PUMPED IN (3 TO 2) |
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WHAT HAPPENS IN PHASE 0
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NA INFLUX INTO THE CELL INTRACELLULAR CONTENT MORE POSITIVE BY 20mV
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what happens in phase I
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fast sodium channels close
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what happens in phase II
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CA ENTRY VIA SLOW CHANNELS...HENCE THE PLATEAU.
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WHAT HAPPENS IN PHASE III?
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POTASSIUM LEAVES THE CELLS
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WHAT IS CLASS 1A EFFECT ON PHASE 0; DEPOLARIZATION; REFRACTORY PERIOD; CONDUCTION,; CALCIUM CHANNELS?
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PHASE 0 DEPRESSED
PROLONGS DEPOLARIZATION INCREASES REFRACTORY PERIOD DECREASES CONDUCTION; NO EFFECT ON CALCIUM CHANNELS |
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THE ARRYTHMIAS BEST TREATED WITH CLASS IB DRUGS ARE...?
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VTACH
PVC VFIB BY LIDOCAINE AND PHENYTOIN |
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CLASS IB DRUGS DO WHAT TO
AP REFRACTORINESS |
SHORTEN ACTION POT.
REDUCE REFRACTORINESS |
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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) |
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BB SLOW CONDUCTION THROUGH WHICH NODE
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AV NODE
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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) |
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NAME THE FATAL ARRHYTHMIAS ASSOCIATED WITH CLASS 1 DRUGS
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1A & 1C: QT, PR, QRS PROLONGATION
1A AND III- TORSADES DIGOXIN TOXICITY |
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AV BLOCK ARE ASSOCIATED WITH WHICH DRUGS
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CLASS I
MORE WITH 2 AND 4 |
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CV DEPRESSION IS ASSOCIATED WITH WHICH CLASSES
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BB (CLASS II); CLASS 4 AND CLASS 1 (1A/1C)
(1- AC; 2; 4) |
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ATROPINE-LIKE SIDE EFFECTS ARE..........ASSOCIATED WITH WHICH CLASS?
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1A
CONFUSE, HOT, FLUSHED, TACHY, DRY |
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BETA BLOCKER SIDE EFFECTS ARE
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BRONCHOSPASM, BRADY, CLAUDICATION; CLASS II DRUGS
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NAUSEA AND VOMITING ASSOCIATED WITH...
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CLASS 1A AND DIGOXIN
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PARESTHESIAS AND SEIZURES ASSOCIATED WITH
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CLASS 1B
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DOPAMINE BETA-HYDROXYLASE IS AKA......AND IS RESPONSIBLE FOR WHICH REACTION?
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ASCORBATE
CONVERTS DOPAMINE TO NOREPINEPHRINE |
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DESCRIBE THE ORDER OF CATECHOLAMINE PRODUCION
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TYROSINE (TYROSINE HYDROXYLASE) = LDOPA (L-AMINO ACID DECARBOXYLASE) = DOPAMINE (DOPAMINE HYDROXYLASE) = NOREPINEPHRINE (N-METHYLTRANSFERASE) =EPINEPHRINE
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THE NATURAL CATECHOLAMINES ARE?
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EPINEPHRINE
NOREPINEPHRINE DOBUTAMINE |
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SYNTHETIC CATECHOLAMINES ARE
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DOBUTAMINE
ISOPROTERENOL |
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INDIRECT ACTING SYNTHETIC CATECHOLAMINES ARE?
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AME (AMPHETAMINES, METARAMINOL, EPHEDRINE)
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DIRECT ACTING CATECHOLAMINES ARE
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PHENYLEPHRINE
METHOXAMINE (think- a act directlly at night- PM) |
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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. |
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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 |
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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 |
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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 |
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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 |
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COMMON PHENOMENA WITH EPHEDRINE
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RAPID TACHYPHYLAXIS
PERSISTENT BINDING OF ALPHA RECEPTORS PERSISTS AFTER BP RETURNS TO NORMAL |
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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 |
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WHAT ARE THE DIFFERENT ROUTES OF TERMINATION OF ACTION?
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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 |
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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 |
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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 |
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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 |
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EPINEPHRINE EFFECT ON:
BP, SBP, DBP, HR MAP |
INCREASES SBP, HR, MAP
DECREASES DBP 2DARY TO B2 SMOOTH MUSCLE STIMULATION |
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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 |
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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 |
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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 |
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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 |
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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) |
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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 |
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FIRST LINE DRUG FOR LOW CO IS ....?
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DOBUTAMINE
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PDE INHIBITORS ARE.....?
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MILRINONE AND AMRINONE
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PDE INHIBITORS WORK BY?
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PREVENTING INACTIVATION OF cAMP AND cGMP - THUS ALLOWING THE SECOND MESSENGER TO EXECUTE SIGNALS INTO THE NUCLEUS.
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MILRINONE:
ACTIVATES WHAT? |
ADENYLATE CYCLASE cAMP SYSTEM BEYOND THE B RECEPTOR.
cAMP IN THE MYOCARDIUM AND Cgmp IN VASCULAR SMOOTH MUSCLE |
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WHAT SHOULD YOU ABSOLUTELY NOT DO WITH MILRINONE ADMINISTRATION
|
BOLUS THE PT.
CAN CAUSE HYPOTENSION AND CARDIAC ARREST |
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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 |
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WHAT FACTORS AFFECT OXYGEN SUPPLY?
|
HEART
OXYGEN SUPPLY AND SATURATION PaO2 HGB CORONARY BLOOD FLOW (CPP IS = DP-LVEDP) |
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WHAT FACTORS AFFECT OXYGEN DEMAND
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HEARTRATE
PRELOAD AFTERLOAD WALL TENSION CONTRACTILITY |
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THE 3 MAIN AREAS OF CARDIOVASCULAR ACTIONS OF NITRODILATORS ARE...
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THE SYSTEMIC VASCULATURE
CARDIAC (HEART) CORONARIES |
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WHAT IS THE EFFECT OF NITRODILATORS ON THE HEART?
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REDUCES PRELOAD AND AFTERLOAD- DECREASING WALL STRESS
DECREASES OXYGEN DEMAND |
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WHAT IS THE EFFECT OF NITRODILATORS ON THE CORONARIES?
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VASODILATE (ESP EPICARDIAL CORONARIES)
PREVENT VASOSPASMS IMPROVE SUBENDOCARDIAL PERFUSION INCREASE OXYGEN DELIVERY |
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WHAT IS THE EFFECT OF NITRODILATORS ON THE SYSTEMIC VASCULATURE?
|
VASODILATION (VENOUS>ARTERIAL)
DECREASE VENOUS AND ARTERIAL PRESSURE (SMALL EFFECT ON ARTERIAL PRESSURE) |
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INITIAL THERAPY FOR ALL TYPES OF ISCHEMIA WARRANTS THE USE OF ...
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NITRATES
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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
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What is the mechanism of smooth muscle relaxation with nitrates?
|
NITRATE CONVERSION TO NITRIC OXIDE WHICH STIMULATES GUANYLATE CYCLASE METABOLISM TO PRODUCE cGMP
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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 |
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WHAT CAN OCCUR WITH HIGH NITROGLYCERIN ADMIN? WHAT IS THE DOSE TO AVOID
|
METHEMOGLOBINEMIA
5MG/KG/DAY OR HIGHER |
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WHAT CAN OCCUR WITH HIGH NITROGLYCERIN ADMIN? WHAT IS THE DOSE TO AVOID
|
METHEMOGLOBINEMIA
5MG/KG/DAY OR HIGHER |
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CONTRAINDICATED IN PTS USING WHAT?
|
VIAGRA, LEVITRA, CIALIS WITHIN 24-48HOURS- CAN CAUSE REBOUND HYPOTENSION
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WHEN IS THE USE OF NITROGLYCERINE WARRANTED?
|
IN ACUTE LEFT HEART FAILURE WITH NORMAL BP
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WHAT HAS REPLACED NITROPRUSSIDE ?
|
INODILATORS
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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) |
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NITROPRUSSIDE
DOSE: SE INCLUDE? |
DOSE: 0.5 - 10 MCG/KG/MIN
SE INCLUDE: HYPOTENSION (DIASTOLIC) CYANIDE TOXICITY |
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IF OVERDOSE OF NITROPRUSSIDE OCCURS, USE?
|
SODIUM THIOSULFATE AS ANTIDOTE - BINDING AGENT 150-200MG/KG
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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 |
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BETA BLOCKERS ARE INDICATED IN
|
HTN
ANGINA MI ARRYTHMIAS HEART FAILURE |
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CARDIAC EFFECT THAT CAUSES AN INCREASE IN RELAXATION STATE IS CALLED?
|
LUSITROPY
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THE CARIOSELECTIVE BB INCLUDE?
|
E- BAMA
ESMOLOL BISOPROLOL ACEBUTALOL METOPROLOL ATENOLOL |
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NONCARDIOSELECTIVE BB ARE?
|
NP - STP
NADOLOL PROPANOLOL SOTALOL TIMOLOL PINDOLOL |
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WHAT DETERMINES CARDIOSELECTIVITY
|
DOSE DEPENDENT- THE HIGHER THE DOSE THE MORE CARDIOSELECTIVE
|
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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 |
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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) |
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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 |
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INDICATION FOR ESMOLOL?
|
USED TO BLUNT RESPONSE TO ET INTUBATION
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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. |
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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 |
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WHAT IS UNCHANGED WITH LABETALOL
|
CO AND SV UNCHANGED
|
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LABETALOL CAN CAUSE WHAT...... ESP WITH CCB.
|
CHF
|
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WHAT IS THE ADDITIVE EFFECT OF LABETALOL AND CCB?
|
HEART BLOCK
|
|
|
SUDDEN WITHDRAWAL =
ANY CNS EFFECTS? |
HYPERTENSIVE CRISIS.
YES |
|
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CALCIUM CHANNEL BLOCKER ARE INDICATED IN ?
|
HTN
ANGINA ARRHYTHMIAS |
|
|
cardiac effect of CCB INCLUDE
|
DECREASE CONTRACTILITY, HR, AND CONDUCTION VELOCITY
|
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VASCULAR EFFECTS OF CCB INCLUDE
|
VASODILATION
|
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CCB - MECHANISM OF ACTION
|
THEY BLOCK L TYPE CHANNELS (MAIN CHANNELS BLOCKED) T TYPE CHANNELS AND ION INFLUX VIA L CHANNELS
|
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L TYPE CHANNELS FACILITATE WHAT
|
THEY SUSTAIN SLOW ENTRY OF CALCIUM
|
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T TYPE CHANNELS ARE ASSOCIATED WITH WHAT?
|
VASCULAR SMOOTH MUSCLE CELL MEMBRANE
|
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ION INFLUX VIA L CHANNELS CAUSE
|
EXCITATION AND CONTRACTION COUPLING
|
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THE FOUR CLASSES OF DRUGS THAT INTERACT WITH L TYPE CCB ARE?
|
DD-BP
DIHYDROPYRIDINE (DHP) DERIVATIVES DIARYLAMINOPROPYLAMINE BENZODIAZEPINES PHENYLALKYL-AMINES |
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|
1,4 DYHYDROPYRIDINE DERIVATIVES ARE WHICH DRUGS
|
NIFEDIPINE
NIMODIPINE NICARDIPINE ISRADIPINE AMLODIPINE FELODIPINE |
|
|
THE MOST POTENT CORONARYVASODILATOR IS
|
NIFEDIPINE (ESP IN EPICARDIAL VESSELS)
|
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DILTIAZEM:
INDICATIONS.... SE PROFILE....HIGH OR LOW |
RASH (RATE CONTROL-AFIB, AFLUTTER- ANGINA, SVT, HTN
LOW SE PROFILE |
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EXAMPLE OF PHENYLALKYLAMINE IS ...
|
VERAPRAMIL (THINK VP)
|
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EXAMPLE OF BENZOTHIAZEPINES INCLUDE?
|
DILTIAZEM
|
|
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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 |
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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. |
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IN LARGE CEREBRAL ARTERIES, NIMODIPINE DOES WHAT?
|
BLOCKS EXTRACELLULAR CALCIUM IONS.
|
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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
|
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|
THE BESST VASODILATOR OF THE CCB IS?
BEST FOR ..... |
NICARDIPINE
BEST FOR RESIDUAL HTN AFTER BB |
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WHICH CCB HAS LOCAL ANESTHETIC AFFECT?
|
VERAPRAMIL
|
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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. |
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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 |
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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 |
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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 |
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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 |
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DILTIAZEM BLOCKS ........VASOCONSTRICTION DUE TO WHAT FOUR THINGS?
|
CORONARY VASOCONSTRICTION.....DUE TO PASA (PROSTAGLANDINS, SEROTONIN, ALPHA AGONISTS),
|
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|
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. |
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|
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 |
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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) |
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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 |
