Cardio Quiz 1b

eem8u's version from 2016-12-04 23:04

ANS drugs

Review of ANS
Question Answer
sympathetic system & metabolismincreased gluconeogenesis, glycogenolysis, lipolysis
sympathetic and PS working in tandem - 2 examplesmale sex organ, uterus in labor
baroreflex- explain1) decreased BP sensed in baroreceptor *** 2) DOWN BR activity to medulla 3) UP sympathetic and DOWN PS activity in medullary centers 4) vasoconstriction and UP cardiac output 5) **increase in BP
3 outcomes of baroreceptor reflex in decreased BP1) increased BP 2) increased HR 3) increase contractility
2 homeostatic mechanisms of CV fxautonomic (BR) / hormonal (renal: renin-angiotensin-aldosterone)


ANS neurotransmitters & receptors
Question Answer
Ach receptors- location (3)1) all preganglionic (nicotinic receptors) of PS and SYmp 2) all PS post (muscarinic) ***3) sweat glands (sympathetic)
NE - locationmost sympathetic PGang neurons
Dopa- locationsympathetic fibers of RENAL vasculature
Epi -locationreleased by adrenal medulla (a sympathetic ganglia)
a1 receptor - location & typevasculature, sympathetic
b1 receptor - location & typeheart, sympathetic
b2 receptor - location & typevasculature (and also in the heart, minor effect), sympathetic
d1 receptor - location & typerenal, sympathetic
****m2 receptor - location & typeHEART - *atria, PS
m3 receptor - location & typevasculature *NON-innervated (but affected by medication), PS
****current drugs & muscarinic subtypesdrugs do not distinguish
pheochromocytoma releasesEpi and NE (tumor of the adrenals


Receptor mechanisms & effects
Question Answer
M3 receptor - mechanism(and other m-odd number) couple to Gq > activate phospholipase C > increase Ca@ release > stimulate protein kinase C (stimulates M3 vasodilation via production of N.O.)
Nicotinic receptor - mechanismligand-gated
****M2 receptor - mechanism(and other m-even number) couple to Gi/Go (2 has 2) >> adenylyl cyclase inhibited / inhibit V-gated Ca2+ channel / hyper polarize GIRK channels (by increased K conductance
****a1 receptor - mechanismcouple to Gq (postsynaptically) >> ca2+ release (intracellularly), activate PKC
a2 receptor - mechanismcouple to Gi/Go (Presynaptic, inhibit transmitter release)
a1 receptor - effect (2)contract smooth muscle (arterioles in skin/viscera/salivary glands) / pupillary mydriasis (dilation via radial muscle contraction)
****b1 & b2 receptor mechanismGs >> adenylate cyclase >> increase cAMP level >> PKA >>> regulate L-type calcium channels/conduction/contraction
****b1 > b2 - location & effect (2)heart (UP chronotropy, isotropy, dromotropy, lusitropy) / ****JG cells (release renin)
b2 > b1 - location & effect (2) bronchial sm muscle DILATION / skeletal & coronary arteriole/veins DILATION
****d1 receptor - mechanismGs > increase cAMP
****d1 receptor - effectvasoDILATION in renal vasculature (and elsewhere)


Sympathetic effects on CV system
Question Answer
define-chronotropyheart rate
define-inotropycontractility of heart
define-dromotropyrate of conduction
define-lusitropyrate of relaxation
vascular sympathetic responses are mediated by ____ NTNE (plus EPI from adrenals)
****2 main vascular effects1- increased TPR (a constriction >> b dilation // decreased venous capacitance 2-redistribution of blood flow (away from alpha vessels towards b2 vessel) but **RENAL flow preserved b/c of D1 receptors***
2 main effects @ ventriclesPositive inotropy & lusitropy (mediated by b1)
b1 vs b2 in heart failureb1 down regulated — role of b2 more important
2 main effects @ atriapositive chronotropy & dromotropy (mediated by b1 mostly)


Drugs - Sympathetic Agonists
Question Answer
Epinephrine (adrenaline) - target receptorsALL a, b agonist
Epinephrine - vasculature effects (2)1- moderate BP increase (a1>b2) 2- redistribute blood flow (towards coronary/skeletal muscle)
Epinephrine- heart effects1- positive chrontropic / 2-positive inotropic (contractile force) / 3- increase C.O.
Epinephrine & vagal reflexWEAK vagal reflex response >> decrease HR and sympathetic tone (counteracted by Epi sitting directly in receptors)
****Epinephrine- clinical uses (2)1- cardiac arrest (to increase automaticity) 2- inotropic support
Norepinephrine - receptorsa, b1 agonist
Norepinephrine - vasculature effects1- increase in BP (**MORE THAN EPI)
****Norepinephrine - heart effects (2)1- direct b1 on chronotropy **but*** effect REVERSED by strong vagal reflex >> decrease HR / 2- positive inotropic (contractility)
****Norepinephrine - sides effects (3)severe hypertension / risk of reduced flow to kidney and intestines (worry about stroke) / necrosis of nearby tissue due to ****SEVERE extravasation (look for blanching)
Norepinephrine - uses (2)SHOCK 1- cardigenic / 2-septic/hypovolemic (if hypotension persists after fluid replenishment
isoproterenol - receptorsall beta AGONIST!
isoproterenol - vasculature effectsb2 dilator (bp down)
isoproterenol - heart effects (3)positive chronotropy and inotropy >> increase C.O. (while decreases MAP)
isoproterenol - vagal reflexreflex in same direction as direct effects on heart = LARGE increase in HR
****isoproterenol - uses (2)bradycardia / arryhtmias
****isoproterenol - SE’spalpitations, ***arrhythmias, angina pectoris, flushing (skin redness)


Drugs - Sympathetic Agonists
Question Answer
****dobutamine - receptorsb1
****dobutamine - effectspositive inotropic and chronotropic (ino > chrono)
****dobutamine - usecardiac decompensation (short-tern tx)
****dobutamine - SE’s (2)ectopic ventricular activity / in patients w a fib, may increase ventricular rate
albuterol - receptorsb2 agonist
albuterol - mechanism(bronchodilator for asthma) — cAMP —> relaxation of bronchial smooth muscle and stabilization of mast cells
b2 is gs
****albuterol - SE’stachycardia, agitation, ****hypokalemia >>> hypotension, arrhythmia, seizure
****why does albuterol cause tachycardiareflex response to drop in BP
dopamine - receptorsd1 > b1 > a1 agonist
dopamine - low dose effectactivates d1 >> increase renal blood flow & urine output
****dopamine - med dose effectactivates d1 (renal blood flow) and b1 (cardiac effects)
dopamine - high dose effectsvasoconstriction w/ ***renal flow spared***
dopamine - CV uses (3)1-cardiogenic shock (esp w/ low TPR) 2- heart block 3-bradycardia
dopamine - SE’s(related to b1) tachycardia, hypotension / (related to d1) nausea & vomitting
****fenoldopam - receptorsd1 (selective)
****fenoldopam - usetx severe hypertension (can use at high doses, unlike dopa) in patients w/ LOW RENAL fx
****fenoldopam - contraindicationglaucoma (increase intraocular pressure)


Drugs - Sympathetic Agonists
Question Answer
phenylephrine - receptorsa (slight a1 > a2) agonist
**** clonidine - receptorsa2 agonist (autoreceptors, inhibitory)
**** clonidine- mechanism**only sympatholytic adrenal agonist ** —> a2 (inhibitory) decreases sympathetic outflow
**** clonidine- uses (2)hypertension mgmt, hypertensive crisis (also: pain management, opiate withdrawal)
****clonidine-adverse effectsdrowsy, fatigue, xerostomia (dry mouth)
phenylephrine-usenasal decongestant
phenylephrine-adverse effectshypertension, exacerbation of Raynaud’s syndrome, bronchoconstriction
which drug’s effects change at low doses? why?Epinephrine - more potent @ b2 — see lower BP at beginning of infusion


Drugs - Beta-Blockers, general
Question Answer
****mechanism in reducing HTNreduced renin release (not first line due to SE’s)
**** first line for HTN in what patients? (3)Angina, A-fib, A-flutter, excessive sympathetic activity (Otherwise NOT first line)
****black box warningwithdrawal can exacerbate angina // can be cause of M.I. ---> angina = heart pain due to reduced blood flow to heart
****contraindication**asthma** // other bronchospastic diseases — due to possibility of b2 blockade (even if it is a b2 selective)
2 considerations in diabetes1- can induce hypoglycemia (b2 mediate gluconeogenesis, etc.) / 2 - mask b-receptor mediated symptoms of hypoglycemia (tremor/tachycardia/nervousness)
CV adverse effects (4)bradycardia, fatigue, worsened raynauds, erectile dysfunction
non-CV adverse effectCNS symptoms (nightmares, hallucinations), esp older adults


***Drugs - Beta-Blockers, specifics
Question Answer
propanolol - receptorsnon-selective B-antagonist --- "pro B"
****metoprolol - receptorsb1 antagonist
****carvedilol - receptorsa, b1, b2 (ALPHA and BETA blocker)
**** labetalol - receptors*mixed* a1 and b1 ANTAGONIST / b2 AGONIST
****labetalol - mechanism in ISA(ISA = high intrinsic sympathetic activity) will act as b2 antagonist (not agonist) b/c intrinsic affinity is higher
****beta blocker preferred in diabetescarvedilol (less effect on glucose metabolism
********shows improved outcome in HFcarvedilol
used in hypertensive emergency (esp. due to excess sympathetics)labetalol
possible causes of hypertensive emergency****b-blocker withdrawal, tyramine-MAOI interaction, pheochromocytoma, methamphet overdose… (recall which drug should be used…..)
****labetalol-adverse effectcould exacerbate HTN if B-receptors get blocked before alpha (because beta are vasodilatory) ***need to establish alpha blockade first!!!****


Drugs - PS
Question Answer
PS effect on vasculaturefew vessels have PS innervation, ALL have M3 receptors >> vasodilation w/ agonist
PS effects on heart - location and conditions**atria / more when there is HIGH sympathetic activity >> 1- SA node = negative chronotropy 2- AV node = negative dromotropy (potential for AV block)
PS effect on sweat glandNONE (but note that the receptors are MUSCARINIC with sympathetic innervation
Acetylcholine - receptorsfull agonist at ALL muscarinic and nicotinic receptors
Acetylcholine - effect (small vs large dose)small - short drop in BP w/ reflex tachycardia / large - BP drop accompanied by BRADYCARDIA (b/c of SA node effects)
Acetylcholine - therapeutic uselocal admin during eye surgery
atropine - receptors / BBB?muscarinic ANTAGONIST (DOES NOT cross BBB)
scopolamine - receptors / BBB?muscarinic ANTAGONIST (crosses BBB)
****atropine - therapeutic use (2)acute sinus bradycardia / A-V block (and pre-op to prevent salivation/secretions)
PS antagonist - adverse effectstachycardia, urinary retention, dry nasal passages, constipation, sedation/disorientation or delusion

ECG // Electrocardiogram


ECG Leads
Question Answer
Lead placementv1/v2 - 4th IC parasternal / v4 - 5th ic mid clavicle / v6 horizontal @ mid axilla
leads current flow is in WHAT directionnegative to positive
Lead I measures / degreesR arm —> L arm (one L) at 0 degrees
Lead II measures / degreesR arm —> L Leg (two L’s) at +60 degrees
Lead IIII measures / degreesL arm —> L leg at + 120
avF degrees+ 90 (from central pole)
avR degrees-150 (from central pole)
avL degrees-30 (from central pole)
normal location of driving current in heart (degrees)between -30 (aVL) and +120 (III)
3 leads measuring inferior portion of heartII, avF, III
5 leads measuring lateral Left heartI aVL IV-VI


ECG graph basics
Question Answer
****x axis / unitstime (.04 s or 40 ms / box) — big box = .2 seconds / 200 ms
****y axis /unitsvoltage (.1mv / box ) — big box = .5 mV
definition of R wave**first postive deflection after P wave** — can happen w/ or w/o Q
definition of S wavenegative deflection ***after R wave**
P waveatrial depolarization (L + R)
QRS- definition, normal timeventricular depolarization (L + R) = < 120 ms duration (<3 small squares) look in v1
T waveventricular Depolarization
PR interval- location, definition and normal time(from the beginning of the P wave to the beginning of the QRS) - from onset of atrial depol. to onset of ventr. depol. (usually 3-5 sm boxes = 120ms -200 ms)
QT interval - location, definitionbeginning of QRS to end of T // duration of ventricular depolarization and repolarization


Reading the ECG
Question Answer
3 step process for reading the ECG1- rate (sinus?) 2- rhythm 3- axis
normal P wave - sizewidth <3 small squares // height <2.5 small squares
****QT normal timing[< 460 ms] total / MALES - <420 males / FEMALES < 440 [11 sm squares]
****normal QRS duration (and **what lead**)V1—should be negative — < 120 ms duration (<3 small squares)
HR calculation, hard way1500 / # of small squares (1500 = 25 mm/sec  60 sec/min, paper is read at 25 mm/sec)
****QT interval, eyeball normalityT wave ends BEFORE halfway point b/t TWO ARS
****HR calculation, eyeballing300 [ 1 big square]

150 [2 big squares]

100 [ 3 big squares]

75 [4 big squares]

60 [ 5 big squares]
Determine sinus rhythm, stepwise 1- P-waves (I/II should be up & aVR down) 2- P waves vowed by QRS 3- rate 60 - 100 bpm with < 10% variation with respiration
***cheat method for HR300-150-100-75-60 ***(counting BIG SQUARES!!!)
cheat for axis determinationI and avF should be uPRIGHT


Basic EKG Abnormalities to know:
Question Answer
****peaked p wave indicatesright atrial enlargement (>2.5 small squares)
stretched/biphasic P wave indicatesLeft atrial enlargement
****Long PR interval, definition & indication> 220 ms —> FIRST degree AV block (slowed impulse
QRS > 120 msBUNDLE BRANCH block
****QRS > 120 ms AND upright in V1RBBB (shifts TOWARDS v1)


Question Answer
change in HR w/ inspiration vs expirationSPEED w/ INSPIRATION / slow with expiration
early/abnormal P-wave + normal QRS complexPremature Atrial Contraction (PAC) — not from SA node
reverse R wave progression indicates(in precordial, usually see getting progressively larger) dextrocardia (8.48)
early beat (QRS) w/o P wavePVC [ premature ventricular contraction]
describe QRS in PVC [ premature ventricular contraction]early, wIDERS (b/c inefficient)
sinus bradycardia/tachycardia defined as< 60 / min vs > 100 / min (with **normal p waves**
sinus bradycardia/tachycardia results fromproblem w/ SA node
I and avF in R-axis deviationI down / avF up “right always meets”
R-axis deviation range+90 to 180 (lower left quadrant)
I and avF in L-axis deviationI up /aVF down “eft always disagrees
L-axis devotion range0 to -90 (upper R quadrant)