SILVERSTEIN

ARRHYTHMIA LARGE GROUP [9Q]

1. A-FIB: most common sustained arrhythmia. irregularly irregular. no discrete P waves. mult wandering reentrant circuits. Risk of Stasis @
LEFT ATRIAL APPENDAGE-->Stroke.
2. A-FIB Tx: (1) CONTROL RATE @ AV node: DILTIAZEM (class IV), DIGITALIS (+vagal output), B-BLOCKERS (dec rate phase 4
depol); (2) RHYTHM CONTROL: SOTALOL (III, prolong QT) or PROPAFENONE (IC, dec phase 0 slope)
3. SVT: MOST COMMON PAROXYSMAL SVT CAUSED=AV NODE REENTRANT TACHYCARDIA (AVNRT)--> Responds to Vagal
maneuvers (Carotid massage, Valsalva, Coughing, Gagging); or ADENOSINE (blocks AV node)
4. CAROTID MASSAGE (only breaks AVNRT & AVRT circuits) baroreceptor reflex--INCR VAGAL OUTPUT: (1) decr If channel openings
(2) decr Ca chann openings (incr threshold) (3) incr ACh K chann openings (hyperpolarizes)
5. AVRT+WPW Syndrome: ACCESSORY PTHWY (faster) in addn to normal AV path. 2 ways to tx: (1) prolong refractory of distal
myocardium; (2) impair retrograde conduction
6. WPW: DELTA WAVE-some impulses SKIP AV node, travel down Accessory path --> EKG lacks PR segment (normal atria to vent impulse),
shows up as DELTA which is a little ramp leading up QRS (will appear WIDE).
7. Young Pt w irreg irreg, WIDE+NARROW QRS's = WPW + A Fib. Responds to vagal maneuvers. Rx = PROCAINAMIDE (IA) or
AMIODARONE (III)
8. VT: more QRS's than P's, independent rates via AV dissociation.
9. Monomorphic Ventricular Tachycardia- WIDE QRS in VT + hx of old MI. Old myocardial SCAR = reentry over fixed ANATOMIC circuit.
Tx: Amiodarone (III)
TACHYCARDIA [3Q]
1. ATRIAL FLUTTER: "sawtooth" Rate 180-350. Often 2:1 block w/ ventricular rate of EXACTLY 150 bpm. Re-entry along cavotricuspid
isthmus (unidir block+slowed conduction). Dx w Adenosine, Tx w heart cath ablation
2. PREMATURE ATRIAL CONTRACTION: look @ PR interval, see early beat w change in P wave morphology (but normal QRS); causes:
abn automaticity, re-entry, catecholamines. Tx symptomatics w B-Blockers
3. Irregularly Irreg w 3 diff P morphologies, due to intracell Ca2+ overload w/ underlying condition (eg COPD) = Multifocal Atrial Tach (MAT,
>100 bpm); or Wandering Atrial Pacemaker (WAP, <100 bpm).
BRADYCARDIA [3Q]
1. SLOWED SA node: (1) Decr If current; (2) more neg max diastolic potential; (3) increase threshold potential
2. Sensitivity to vagus stimulation: SA & AV > Atrial > Ventricular.
3. EXHALATION INCReases vagal firing, SLOWS HR. also: athletes, hypothyroidism, sleep, age, cardiomyopathy, HYPERkalemia,
HYPOglycemia, HYPOthermia
4. Escape Rhythms (when not overdrive-suppressed): Atria=60-80 bpm, Junctional=40-60; Ventricles=30-40
5. INVERTED P wave (or no P wave at all), normal QRS (40-60 bpm) = JUNCTIONAL RHYTHYM.
6. 1st Degree AV Block: slowed AV node conduction; constantly prolonged PR interval > 1 big box. (age-related degeneration, commonly)
7. 2nd Degree Mobitz type 1 (wenchkebach) block: PROGRESSIVE lengthened PR interval until dropped QRS. Asymptomatic.
8. 2nd Degree Motitz type 2 block: dropped QRS complex due to impaired conduction AFTER AV node (in His bundle or Purkinjes). better w
vagal. Tx: Pacemaker placement.
INTRODUCTION TO AXIS EKG [3Q]
1. ISOELECTRIC Rule: Axis is 90 degrees from isoelectric limb lead (perpendicular)
2. leads I and aVF to tell u which quadrant axis is in. If upper Left Quadrant, use lead II to tell u if true left axis deviation (versus normal)
3. NORMAL AXIS: -30 degrees (aVL) to +90 degrees (aVF)
AXIS WORKSHOP [3Q]
1. R-Wave Progression in Precordial Leads: V1-V2 (@ septum)=NEGATIVE; V3-V4 (@ anterior)="Transition zone"/isoelectric; V5-V6 (@
Lateral wall)=POSITIVE.
2. TALL R WAVES in V1 and V2 can be due to POSTERIOR WALL MYOCARDIAL INFARCTION or RIGHT VENTRICULAR
HYPERTROPHY
3. [EKG PIC] figure out axis
EKG BASICS OF READING [3Q]
1. SMALL BOX = 1 mm = 0.1 mV = 0.04 sec. BIG BOX = 0.2 sec, 5 mm, 5mV.
2. Wave of depolarization is a progressive wave of POSITIVE charges towards the POSITIVE electrode = UPWARD deflection on EKG.
3. P wave (0.08 to 0.11 sec) = Atrial depolarization (SA node fires @ start of P wave); PR interval = depol traveling from SA to Ventricles
(indicates AV node function)
4. QT Interval = all events of ventricular systole

EKG WORKSHOP [3Q]

1. NORMAL SINUS RHYTHYM: (1) P for every QRS (& vice versa); (2) Identical P waves; (3) Normal & consistance PR intervals; (4) P
waves UPRIGHT in II, III and aVF.
2. P wave should be POSITIVE in lead I, POSITIVE in inferior leads and NEGATIVE in aVR.
3. EKGs are only diagnostic for RATE and RHYTHYM (need more info to diagnose a pathology)
HEART IMAGING/ECHOCARDIOGRAM [3Q]
1. Parasternal LONG axis view: Top=RV. Left=LV. Right=AORTA. Bottome=LA
2. Parasternal SHORT axis view: shows 3 leaflets of AORTIC VALVE. turn probe around 90 degrees & tilt up or down..
3. Apical 4 chamber view: all 4 chambers + symmetric view of the 2 AV valves
4. Apical 2 chamber view: LV & LA. Mitral valve sitting close to base of heart (top). ("The left side of the heart is on the right side of the
screen")
5. Subcostal View: good view of IVC. Use for PFOs and ASDs dx (bc allows visualization of septum & any holes that may be present)

SORWEIDE
INTRO TO EKG [3Q]
1. P=0.08 to 0.11 sec. PR interval = 0.12 to 0.2 sec. QRS Complex = 0.06 to 0.11 sec.
2. J point = point where ST segment begins. ST elevation in symptomatic Pt = should be considered an MI.
3. Absolute refractory period = early part of T wave.
RHYTHYM STRIPS [3Q]
1. JUNCTIONAL BRADYCARDIA: SLOW ~40. Regular. no P's present (normal QRS's).
2. PVC: normal rate, regular rhythm. but wait, abnormal "extra" beat=EARLY, no P, wide QRS= normal sinus w PVCs.
3. TORSADES DE POINTES: Fast rate ~300. Regular rhythm. Ventricular origion-no P's, wide QRS's with some form. (special type of VTach)
LIPID LARGE GROUP [6Q]
1. 75% cholesterol comes from LIVER; 25% comes from diet. Removed from body in stool.
2. STATIN THERAPY AHA/ACC Guidelines: (1) known ASCVD (2) LDL>= 190 mg/dL (3) DIABETES age 40-75 with LDL 70-189 mg/dL
(4) LDL 70-189 mg/dL with 10 year risk > 7.5%
3. HIGH DOSE ATORVASTATIN 40-80mg or ROSUVASTATIN 20-40mg. Pt's should be treated with the "maximum appropriate intensity of
statin" and there is NO GOAL for tx. Labs: Lipids, LFTs, CK
4. TYPE II HYPERLIPIDEMIA expected labs: total cholesterol 300-600 mg/dL; LDL >200 mg/dL. LOF mutation at LDL receptors. Tx:
HIGH DOSE Statins bc Pt is very HIGH RISK for ASCVD.
5. Statin Adverse: GI upset, RASH (scratching until they bleed), liver irritation, RHABDOMYOLYSIS, DRY SKIN/EYES, myalgia
6. reasons to lower statin dose: (1) If they experience adverse reactions; (2) If the statin isn't very effective; (3) If patient is GETTING OLDER

JUNKINS
CONGENITAL HEART DEFECTS [6Q]
1. FETAL CIRCULATION SHUNTS (1) Ductus Venosus-Umblical V to IVC (50% of blood-bypasses liver); (2) Foramen Ovale-right to left
atrium; (3) Ductus Arteriosus-from Pulmonary Artery to descending aorta
2. TRANSITIONAL CIRCULATION: lungs inflate->decr resistance to blood flow thru lungs->incr O2 tension (causing decr PGE1 levels,
closure of ductus arteriosus). Cord is clamped, systemic vascular resistance increases -> CLOSURE of fetal shunts.
3. ACYANOTIC (Left to Right): ASD (mostly missing septum secundum, assoc w DOWN SYNDROME); AORTIC STENOSIS (4x more
common in males, exercise intol when older)
4. COARCTATION OF AORTA (acyanotic-left to right)-assoc w TURNER SYNDROME (45, X0) & Bicuspid Aortic Valve. WEAK
FEMORAL/LE pulses, HTN in UEs. higher SYSTOLIC BP in right arm. CXR show RIB NOTCHING. Tx: give PGE2 until surgery.
5. VSD (Left to Right) MOST COMMON!-if large=early CHF/cardiomegaly. may cause pulmonary vasc disease if uncorrected-->
dyspnea/cyanosis (reversal of shunt R->L Eisenmenger)
6. PATENT DUCTUS ARTERIOSUS (LEFT TO RIGHT): maternal rubella, premie.late cyanosis in LEs: Tx=Indomethocin to end patency of
ductus arteriosus.
7. TRANSPOSITION OF GREAT ARTERIES: CYANOSIS R to L. Egg-on-String XCR. Infant ONLY SURVIVES IF SHUNT is present to
allow blood mixing (tx: give PROSTAGLANDIN and OPERATE "arterial switch" Rashkind procedure). ASSOC W MATERNAL DIABETES!
8. TRICUSPID ATRESIA: absent Tricuspid valve, hypoplastic RV. req both ASD and VSD for viability. PALPABLE THRILL, digital clubbing
& JVD. Assoc w asplenia or right sided aortic arch.

9. TOTAL ANAMOLOUS PULMON VENOUS RTRN (TAPVR): "SNOWMAN SIGN" on CXR.

LARGE GROUP: CHD [6Q]
1. TETRALOGY OF FALLOT (RIGHT TO LEFT): 22q11 DiGeorge. abn cephalad displacement of outflow tract. (1) Pulm Stenosis (2) RVH
(3) Overriding Aora (4) VSD. BOOT SHAPE on XCR. Early Cyanotic "spells", clubbing of digits. SQUATTING incr TPR-> decreases r to l
shunt -> improves cyanosis. SURGICAL TX.
2. UNTREATED TOF: 90% mortality by age 10 versus 90-95% survival at 10 yrs IF SURGICALLY REPAIRED. Prognosis depends on how
soon TOF is repaired, residual RV dysfunction is common, 10% pts req re-operation within 20 yrs.
3. DOWN SYNDROME (Trisomy 21) 40% have heart defects: ASDs, VSDs, PDAs.
4. CYANOSIS in general: refers to blueish discoloration, caused by deoxy Hb concentration. at least 4g/dL. Arterial O2 saturation (spO2) of
between 80 to 85%.
5. EISENMENGER SYNDROME: uncorrected L to R shunt increases Pulm blood flow -> increases Pulm vasc resistance -> REVERSAL OF
SHUNT TO CYANOTIC, R to L. Exercise intol, hyperviscosity/stroke, hemoptysis. Pt must avoid activity/altitude/pregnancy/vasodilators.
6. PFO: paradoxical embolism from venous side crosses thru PFO to arterial side --> stroke. Co-morbid w A-Fib. Only becomes significant
when increased RA pressure.

KRAATZ
CV EMBRYOLOGY [3Q] <-- half assed
1. HEART TUBE: Mesenchymal angioblast clusters (blood islands) @ CRANIAL end of embryo (VENTRALLY)--moves caudally during
lateral folding--then fuses w inflow tract caudal.
2. 3rd Aortic Arch: CCA and L & R ICAs. 4th Aortic Arch: RCA & AORTIC ARCH. 6th Aortic Arch: L & R Pulm A & Ductus Arteriosus.
3. Vitelline System (Yolk Sac, Digestion) later forms Celiac trunk & SMA. but drains into Sinus venosus as fetus.
4. Septum Primum-on LEFT, grows bottom to top, leaving hole near top. (opposite for secundum). Foramen Ovale flap allows flow of blood
RIGHT to LEFT
5. S/I Endocardial Cusions fuse to bring ant/post parts together, Lateral endocardial cushions expand to form L and R sides of heart & allow
excavation for AV valve formation (?)
ANATOMY [3Q]
1. Upper limit pericardium=2nd ICS. Upper limit Heart=3rd ICS. Lower limit heart=xiphisternal junction. note: aortic arch courses LEFT,
behind manubrium, then DESCENDS at T4 IVD.
2. Transverse pericardial sinus (between inflow & outflow tracks)- can separate during surgery. Oblique Pericardial Sinus-site of fluid/infection
accumulation behind heart in pericardial sac.
3. LEFT Coronary A --> (1) circumflex A; (2) LAD/Anterior interventricular A *most of blood to IV septum!; (3) L marginal A. (note: SA
nodal branch varies b/w which Coronary A it comes off of)
4. DRAINS INTO RA: (1) IVC; (2) SVC; (3) Coronary Sinus; (4) Ant Cardiac V; (5) Great Cardiac V. note: thebesian veins = smallest cardiac
v
5. Mesocardium: connects heart to posterior body wall. dorsal mesocardium-connects all veins; visceral mesocardium- connects the two major
arteries leaving the heart.

AL-TIKIRITI
HISTO [3Q]
1. TUNICA INTIMA (endothelium, subendothelium, internal elastic lamina); TUNICA MEDIA; TUNICA ADVENTITIA
2. ELASTIC ARTERY; MUSCULAR ARTERY; ARTERIOLE; CAPILLARY; METARTERIOLE; VENULE; MUSCULAR VEIN; VALVE;
LYMPHATIC
3. PERICARDIUM (1) OUTER fibrous pericardium; (2) INNER serous parietal pericardium; (3) INNER serous visceral pericardium
4. HEART VALVE parts (1) Fibrosa (@ core); (2) Spongiosa (@ atrium/BV); (3) Ventricularus (ventricular)
5. in an ARTERY: tunica Media has Thinner external elastic lamina
...look @ pics.

KANDPAL
LIPOPROTEIN METABOLISM [3Q]
1. LPL deficiency or apoC II (Type I hyperlipoproteinemia or Familial LPLase deficiency): INCREASE CMs & TAGS in plasma. note:
Chylomicrons are from exogenous/dietary lipids.

2. Corneal arcus+tendon xanthoma: Type II hyperlipoproteinemia (familial hypercholesterolemia)-AUTO DOM mutation @ LDL receptor:
INCR plasma Cholesterol (300-600) & LDL > 200. Tx: bile depletion+Statin.
3. Tangier Disease: deficiency of ABCA1 --> near absence of HDL. (bad bc HDL is reservoir for apoCII & apoE-needed for CM and VLDL
metabolism; nascent HDL+ABCA1 mediates REVERSE CHOLESTEROL TRANSPORT)
4. TYPE III LIPOPROTEINEMIA: abnormal ApoE-> increases CM and IDL-> increases TAGs & Cholesterol. Tx: Gemfibrozil (fibric acid
derivative; OATP1B1 path, messes w Statin uptake/metab via glucoronosyl)
CHOLESTEROL METABOLISM [3Q]
1. Smith-Lemli-Opitz syndrome (SLOS)- Auto rec. Deficiency of 7-dehydrocholesterol reductase (last step in synth) --> congenital
malformations due to decrease cholesterol.
2. Control @ Rate-limiting/HMG-CoA reductase-(1) transcriptnl via SREBP; (2) Proteolytic degred (ubiquit if incr sterols); (3) covalnt mod
(inactive=phosphorylated); (4) Hormone (glucagon INHIBITS)
3. SITOSTEROLEMIA-Auto rec. mutat @ ABCG5 or ABCG8 (impaired excess cholest/sterol removal). Tendon/tuberous xanthomas. INCR
cholesterol & STEROL levels (phytosterol 50x higher than normal) =premature CAD.
4. NPC1L1 shuttles cholesterol into cell (TARGET of Ezetimibe/Zetia to reduce cholest absorption); ABCG5 and ABCG8 are in charge of
removing excess sterols from cells.
5. Cholesterol in LDL: DOWNREGULATES synthesis of LDL Receptors @ liver, DECREASING cellular uptake of LDL/cholesterol. It also
inhibits HMG CoA reductase to inhibit cholesterol synthesis.
6. Bile acids:

ISSAR
ANTIHYPERLIPIDEMIA DRUGS [6Q]
1. STATINS inhibit cholesterol synthesis (inhib HMG CoA reductase) --> INCR LDL Receptors --> REMOVAL of circulating LDL (via
recognition of apoB-100 on IDL & LDL; apoE on VLDL). Monitor: Lipid levels, AST/ALTs, CK
2. STATINS: anti-inflamm, Preg category X. LOVA & SIMVA=PRODRUGS. Risk=Rhabdo. INCR myopathy risk w antibiotics, Ca blockers,
grapefruit. INCR Bleeding w coumarin.
3. Bile Acid Sequest RESINS ("col-"): bind neg charge bileacids, incr excretion-->decr amnt of bile acids recycled to liver->more hepatic
cholestrl synth/incr LDL receptors->decr plasma LDL & cholest. CAUTION: Stool Compaction!
4. NIACIN: (1) binds HM74A receptors-> inhibits HSL-> decr TAG catab->decr FFAs to liver-> DECR TAGs and LDL. (2) incr Apo-A1->
incr HDLs (3) incr LPL activity-> decr TAGs
5. SIDE EFFECTS of NIACIN: Vasodilation (HA/Flushing/pruritis/Reflex tachycardia[..antidote=aspirin]), Hepatotoxicity, Hyperglycemia,
Gout (incr uric acid)
6. FENOFIBRATE + GEMFIBROZIL (FIBRIC ACID DERIVs): activate PPARa (1) incr LPL -> degrades TAGs (2) decr apo-CIII (3) incr
VLDL clearance (4) incr HDL via incr txn apo-AI and AII.
7. Lovaza and OMTRYG = Omega3 lipid regulator -> reduces TAG biosynthesis & increases FA oxidation @ liver. fishy burps. only approved
use for Pts w VERY HIGH TG levels.
8. LOMITAPIDE (Microsomal transfer protein inhibitor)-makes it so apoB cant be added to lipoproteins -> decreased CM and VLDL ->
decreased LDLs. BBW!!! Hepatotoxicity
9. MIPOMERSEN (oligonucleotide inhibitor)-promotes degredation of apoB-> decr LDL and VLDL-> ADJUNCT to other meds for pt's w FH.
BBW!!! Hepatotoxicity & injection site pain

FOLEY
PHYS OVERVIEW [3Q]
1. Circulatory system generally arranged IN PARALLEL, so Left ventricular ouput gets divided up (less resistance); in contrast, pulmonary
circulation is IN SERIES.
2. Q= deltaP (pi*r^4/8nL). Small changes in radius will be magnified because it is raised to the 4th power
3. CO=SV*HR. Cardiac output is the volume of blood pumped by EACH VENTRICLE per MINUTE.
4. SV= volume of blood pumped by EACH VENTRICLE per HEARTBEAT.
CARDIAC APs [3Q]
1. FAST RESPONSE APs= non-nodal/non pacemaker myocardial cells of atrium/ventricle and purkinje fibers.
2. SLOW RESPONSE APs=SA and AV nodal action potentials: slower rates of depolorization during phase 0; spontaneous phase 4 depol (If
channels)
3. Slow Inward (L-type) Ca+ channels (responsible for PHASE 2 plateau of the FAST RESPONSE AP)
4. DROMOTROPY/conduction velocity is DIRECTLY PROPORTIONAL TO (1) local ion currents; (2) Amplitude of AP; (3) Cell Diameter
5. Positive Dromotropy=FASTER conduction VELOCITY from atria to ventricles thru AV node (shortens PR interval, increases HR) =
sympathetics, catecholamines.

CARDIAC CYCLE & FUNCTION [4Q]

1. R ATRIAL PRESSURE: a wave = atrial contraction; c wave = rapid ventric contraction causes AV valve to bulge back into atria (also S1
sound & JVP); v wave = slow venous flow into atria @ beginning of diastole (also S2 sound)
2. Relationship of PRELOAD (EDV), AFTERLOAD, SV [graph]
3. Larger PRELOAD: incr ventricular filling (exercise, venous constriction, increased blood volume) --> incr vent filling pressure --> increased
shortening of fibers --> Increased Stroke Volume.
4. Larger AFTERLOAD: incr aortic/systemic pressure (HTN), pulm A HTN, Aortic/Pulm valve stenosis, coarctation of aorta --> vent must
eject against higher pressure--> DECREASED STROKE VOLUME --> increased end-systolic volume.
5. GREATER CONTRACTILITY: ventricle creates greater tension than usual during systole --> INCREASED STROKE VOLUME-->
decreased end-systolic volume. (but still same afterload and preload).
6. Ejection Fraction is index of contractility (normal=55-80%). EF=SV/EDV
7. SYMPATHETICS: Positive chronotropy (rate), positive dromotropy (conduction velocity), positive inotropy (contractility), positive
lusitropy (relaxation rate)
CARDIAC PUMP FUNCTION [4Q]
1. incr Blood Vol-> increased EDV (preload)-> incr STRETCH of cardiac mm fibers ->incr FORCE of contraction -> incr Blood Ejected from
ventricle
2. Cardiac Output = whole body O2/(arterial O2 - venous O2)
3. Cardiac Index = CO/body surface area
4. isometric contraction
BP & HTN [6Q]
1. FLOW VELOCITY is highest in Arteries and LOWEST in Capillaries (because capillaries have greatest TOTAL cross sectional area)
2. TURBULENT FLOW thru vessel--> most likely when velocity is HIGH, viscosity is LOW & at branchpoints in vasculature. Increases
resistance, produces heat and sound.
3. VENULES & VEINS store 60% of blood volume at any time (blood reservoire)--able to do so because venous system has highest compliant
properties (compliance=V/P)
4. GREATEST TOTAL PERIPHERAL RESISTANCE @ systemic ARTERIOLES.
5. MAP=CO*TPR = 2/3*diastolic + 1/3*systolic
6. BARORECEPTOR REFLEX: Decr MAP --> decr firing @ baroreceptors --> INCREASES sympathetics-> Incr arteriolar
tone/vasoconstriction/contractility/SV/HR (but decreases capillary pressure) --> INCREASES TPR --> brings MAP back up.
7. Vasoconstrictors= Endothelin, EDCFs, High NE/Epinephrine (stimulate alpha1), ADH/Vasopressin, ACE (RAAS system). Note: neural
vascular tone is maintained by NE!

BARNES
LARGE GRP HTN [9Q]
1. Lifestyle Mods: (1) wt reduction; (2) DASH diet; (3) decr dietary Na; (4) Physical activity; (5) Smoking/EtOH cessation
2. INCREASE TPR via: alpha1 activation, H+ ions (?), high viscosity (Hct), catecholamines, Endothelin, RAAS cascade, digitalis etc
3. Goal of JNC 7: (1) uncomplicated HTN <140/90. (2) DM or CKD <130/80. (3) Renal Disease and proteinuria <125/75 mmHg.
4. Goal of JNC 8 ALL Pts DIASTOLIC <90. SYSTOLIC GOALS: young, DM, CKD <140 mmHg. If just old < 150 mmHg.
5. AFRICAN DESCENT without CKD = CCBs or Thiazides!
6. SECONDARY HYPERTENSION: Age <30 or >55 with abrupt onset HTN. Refractory HTN to >3 antihypertensives, white males.
7. Liddle's Syndrome: Auto Dom. Upregulation of ENaC, greater Na retention --> HTN and Hypokalemia. Treatment: Amiloride (sodium
channel blocker)
8. HTN URGENCY: subacute increase BP >180/110. Manage within 24-48 hrs, orals: Captopril, Nicardipine/Nifedipine, Labetalol.
9. HTN EMERGENCY: ACUTE increase BP >180/120 mmHg. Retinal hemorrhages, papilledema, Acute pulm edema, left vent failure, CHF,
HA, N/V. Acute kidney injury 2' to thrombotic microangiopathy.
10. Etiology of 2' HTN: Renovasc HTN (Renal A stenosis/atherosclerosis), Polycystic Kidney Dz, Pheo, primary hyperaldosteronism,
mineralocorticoid excess, liddle's syndrome, aortic coarctation, sleep apnea, cushings, hyperthyroid.

FUCHS
ANTI-HYPERTENSIVES [6Q]
1. HYDRALAZINE: oral arterial vasodilator, decr PVR. (also incr CO, HR, SV, RAAS, Na reabsorption!) uses: HTN, pre-eclampsia (OK for
pregnants). SIDES: REFLEX TACHYCARDIA, LUPUS-LIKE SYNDROME
2. MINOXIDIL: SIDES-Reflex Tachy. use in COMBO w B-Blocker or LOOP DIURETIC due to Na+ and H2O retention. Uses: severe HTN.
Hair growth
3. NITROPRUSSIDE: for HTN CRISIS. SIDES: metabolic acidosis, arrhythmia/death, CYANIDE poisoning--antidote=thiosulfate.
4. CLONIDINE: centrally acting a2 agonist, decre HR & PVR. SIDES: drymouth/sedation, constip, ED. *CAUTION! WITHDRAWAL after
high dose Tx= HTN CRISIS!
5. RISK FETAL Hypotension, renal fail, fetal kidney malformation, death = ACE inhibitors and ARBs! (CONTRAINDICATED IN
PREGNANCY!)
6. Prazosin/Terazosin/Doxazosin: alpha 1 agonists @ art&ven. assoc w Na and H2O retention. co-administer B-blocker or diuretic. For Pts w
HTN & BPH or bladder obstruction.
ANTI-ARRHYTHMICS [6Q]
1. QUINIDINE, PROCAINAMIDE, DISOPYRAMIDE (IA); LIDOCAINE, MEXI, PHENYTOIN (IB); FLECAINIDE, PROPAFENONE (IC)
2. CLASS II: BETA BLOCKERS
3. CLASS III: AMIODARONE, DRONEDARONE, SOTALOL, DOFETILIDE, IBUTILIDE
4. CLASS IV: DILTIAZEM, VERAPAMIL
5. ADENOSINE, very quick agonist @ A1 purine receptor, opens K+ channel, inhibits Ca channel, inhibits If (neg chronotropy), inhibits NE
release. for SVT! side: AV Block.
6. DIGOXIN Use: A-Fib rate control, increases contractility (indirectly) and decreases HR thru vagal stimulation. SIDES: AV block, atrial tach,
yellow vision. CONTRAIND: WPW, pt's w hypokalemia or AV blocks.
7. DIGOXIN TOXICITY can be reversed by giving (1) immune Fab (DIGIBIND); (2) Mg2+ or (3) K+ (if the toxicity is related to incorrect use
in a Pt w hypokalemia)