Angina Types

• Stable: assoc with fixed coronary stenosis > 70%; responds well to NTG and rest
• Prinzmetal/variant: angina occurs at rest and assoc with coronary vasospasms (not atherosclerosis), usually responds promptly to NTG, Ca channel blockers
• Unstable (pre infarction): assoc with > 90% stenosis

Vascular Ectasis

• birthmarks, port wine stains, spider telangiectasia
• not true neoplasms, neither is bacillary angiomatosis
• Nervus flammeus: birthmark, flat, usually regress with age
• Port wine stain: does not regress with age, thickens the skin; may be associated with Stuge-Weber syndrome; CNS angiomas, Retardation, seizures

Capillary Hemangioma

• has small vascular spaces, some regress
• Juvenile/strawberry: a birthmark that initially grows with the child but spontaneously regresses by age 7
• Cherry: usually small, inc w/ freq with age and does not regress (no treatment except cosmetic)
• Pogenic Granuloma (involves skin and oral mucosa): lobular capillary hemangioma, small vessels, inflamation, looks like granulation tissue; assoc w/ pregnancy and trauma; polypoid, often ulcerated, may bleed, surgery is curative, may regress spontaneously

Cavernous Hemangioma

Coronary Vasospasms

• causes angina (can be stable but usually variant)
• narrowing of coronary artery lumen in absence of plaque
• may be idiopathic or drug induced(cocaine, triptans, vasoconstrictors)
• vasoconstrictors also increase afterload which is bad 
• can be aggravated by alcohol or smoking
• often experienced at rest, and ealry in the morning
• patients may lack the typical risk factors for coronary artery disease

Organic Nitrates

• useful in chronic stable, unstable and variant angina
• all nitrates led to release of NO, inc cGMP and smooth muscle relaxation
• reduces preload, stroke volume and cardiac output
• short acting and long acting
• all have tolerance (tachyphylaxis) so need nitrate free period
• adverse effects: headaches and hypotension (severe hypotension if taken with sildenafil or vardenafil or tadalafil)

Beta Blockers

• drug of choice for chronic stable angina
• reduces symptoms and improve exercise tolerance
• prevents secondary MIs and improve survival post MI
• has anti arrhythmic properties and hypotensive effects
• avoid in variant angina (may cause vasospasms)

Calcium Channel Blockers

• drug of choice for variant angina
• alternative option fo pts intolerant to beta blockers
• add on therapy for uncontrolled patients despite beta blocker therapy (typically dihydro to avoid excess bradycardia

Ranolazine

• one of the newer anti-anginal agents
• inh late Na current, reducing intracell Ca and Na (calcium and sodium overload in ischemic cells leads to cell injury and death)
• no impact on HR, contractility, coronary blood flow or BP
• usually reserved for refractory ps already on or not tolerating agents discused above
• more costly
• reduce symptoms of ischemia, but has no benefit on rates of MI, recurrent ischemia or cardiovasc death
• contraindicated in pts with concomitant strong CYP3A4 inducers or inhibitors (rifampin, st johns wort, azole fungals
• adv eff: dizziness, constipation, GI upset, QT prolongation (though no evidence it causes arrhyth

Short Acting Organic Nitrates

• used for all pts with stable angina to treat acute sx
• may be used monotherapy if pt has very infrequent or predicatble symptoms (prophylaxis)
• sublinqual NTG use 3 doses, rapid onset; persistant pain suggestive of ACS
• IV NTG reserved for inpatients w/ unstable angina, MI, or hypertensive emergenc

Beta Blockers Specifics

• dec HR, contractility, inc diastole, leads to better coronary blood flow
• sudden discontinuation can lead to rebound angina sx
• interactions agents w/ hypotensive or bardycardic effects
• avoid use in severe or decompensated asthma (may worsen) (use selective cardio ones)
• appear to be safe in COPD

Calcium Channel Blockers (CCBs)

• all of them block L type Ca channels, causing smooth muscle relaxation
• DHPs: mostly smooth muscle effecs, coronary arterioialtion and peripheral dilation
• NonDHPS: mostly cardiac muscle effects, decreased HR and contractility
• DHP: amlodipine, felodipne nifedipine
• NonDHPs: verapamil and diltiazem
• amlodipine may inc lvls of sivastatin
• adv eff DHPs: hypotension, peripheral edema, reflex tachycardia
• adv eff nonDHPs: constipation, bradycardia, hypotension, worsening of systolic CHF

Heparins

• catalyzes antithrombin activity (inh II, IX, X et all)
• UF greatly selective for factor X and thrombin, requires monitoring, elim by reticulendothelial system
• LWH (enoxaparin, dalt-): effects more predectable, renally excreted, outptient adm
• Fondaparinux: not selective for thrombin, Renally excreted, prevention of DVT in surgeries or heparin intolerance
• adv eff: bleeding (antidote sulfate that neut heparin), osteoporosis, hyperkalemia

Direct Thrombin Inhibitors

• Hirudin: irreversible thrombin inh in leeches
• Lepirudin: inhibit clot bound and circ thrombin, risk of inc bleed and Ab formation
• Bivalirudin, desirudin: reversible, RE
• Argatroban: small molc thrombin inh, reversible, alt to lepirudin in HIT, hepatically metab so use caution in liver disease
• short half lifes so use as alt to heparin in Heperain intolerance (HIT)

Dabigatran, Etexilate

• direct thrombin inhibitor (competitive inh)
• for Afib, risk for stroke or embolism
• renally eliminated and monitoring not necessary
• adverse effects, bleed and dyspepsia, CI in pregnancy

Rivaroxaban and apixaban

• competitive inh of factor Xa
• VTE prevention after HIP/knee surgery (DVT)
• also atrial fibriliation, RE a nd HM
• fixed doseses
• adverse effects, bleeding, CI in pregnancy

Clopidogrel and Ticlopidine

• purinergec rec antagonist (P2Y12): irrev inh of ADP binding to prevent expression of glycoprotein IIb/IIIa -> prevents platelet aggregation and activation
• prevents stroke, MI in combo w/ o in place of aspirin
• Adv eff: bleeding, neutropenia (ticlopidine)
• Clopidogrel is a pro drug act by CYP2C19 (risk of Heart attack, stroke, death in poor metabolizers (2-14% of pop in US)
• clodiogrel can be usd in conjuntion with aspirin, hepari for UA/NSTEMI

Dipyridamole

• PDE inhibitor - prevents breakdown of cAMP
• inc cAMP inh  platelet aggregation
• effective in combo w/ aspirin in prevent of stroke
• also used in combo with warfarin in prevention of thromboembolism

Cilostazol

• PDE inh type III inh, also a vasodilator
• used primarily to Tx intermittent claudication
• other uses currently under investigation

GpIIb/IIIa Antagonists

• Abciximab: monoclonal Ab against GpIIb/IIIa, use in stent placement and coronary angioplasty, limted by expense
• Eptifibatide, tirofiban: competitive rev antagonist of fibrinogen at the gpIIb/IIIa rec, prevention of thrombosis in acute coronary syndrome (ACS)

Aprotinin

• serine protease inhibitor
• direcet inhibitor of plasmin
• used in surgeries involving large blood loss

Ramipril

• ACE inh, used to reduce early MI mortalitiy, ossible limit of infarct size
• possible increase in collateral flow to the peri-infarct ischemic area
• therapy initiated after 6 hrs when the pt is stable and other therapies have been initiated
• used also with congestive heart failure and large infarcts

CVD Risk factors for women

• all the following impact women more
• Smoking 2x
• DM has 3x inc
• HTN  has 1x inc
• Obesity
• Depression has 3x inc 

CAD Gender Differences

• CAD leading cause of death in women and more women die of it than men
• Post MI prognosis worse in women 
• different risk factors men vs women
• women with atypical or NO prodromal symptoms

Radiopharmaceutical Agents

• Thallium 201: enter viable mocardial cells (by diffusion and active transport), can redistribute (one must initially image w.i 10-20 mins), half life 72 days
• Technetium 99m labelled agents: sestamibi, enters viable myocardial cells by passive diffusion (and binds to mitochondria), negligible redistribute and slow clearance (one may image up to 6 hr after inj), half life of six hrs

Perfusion

• Reversible: present on stress portion of examination  but not on resting portion of examination
• Fixed: present on stress and resting portions of the examinaiton (similar on both)
• Partially reversible: present on stress portion of examinatino: but less apparent on resting portion

Non-ST Elevation

• symptoms similar to unstable
• sufficient vscular occlusion to result in tissue damage and mild myocardial necrosis 
• ST depression and/or T wave inversion on EKG
• Elevated cardiac enzymes 

ST Elevation Myocardial Infarction

• symptoms similar to unstable angina
• may have associated severe pain/pressure, shortness of breath, diaphoresis and nausea
• caused by complete vessel occlusion resulting in myocardial necrosis
• ST elevation on EKG
• Elevated cardiac enzymes

Characterize the Chest Pain

• Typical Angina: substernal chest discomfort of char quality and duration, provoked by emotional strss or exertion, reduced with rest, NTG
• Atypical Chest Pain: 2 or fewer of above
• Non-Cardiac Chest Pain: 1 or fewer of above

Left Bundle Branch

• Intraventricular conduction disturbance
• associated with: ischemia, HTN, cardiomyopathy
• Obscures accurate interpretation of ST-T segment changes
• manage like STEMI

Aspirin

• irreversible blockage of platelet aggregation
• Plaque stabilization and arrest of thrombus formation
• indicated for full psectrum of ACS
• 23% reduction in mortality for pts with STEMI
• evidence of IA: anti thrombotic therapy with aspirin 

Percutaneous Coronary Intervntion (PCI)

• guide wire recanalizatino
• balloon angioplast
• intracoronary stent
• indications: recurrent angina at rest, elevated troponin or new ST segment depresion, recurrent angina with CHF symptoms, decreased LV functino
• benefits: minimally invasive, prompt vessel opening, reduced mortality and morbidity, lesens ventricular remodeling

Cardiac CT Angiographic Exam

Summary

• cardiac CT angio allows non invasive evaluation of noncalcified atherosclerotic plaque with clinically diagnostic detail 
• limited by motion, calc and paient size
• Positive predictive value of cardiac ct angio is steadily improving
• cardiac ct angio has high negative predictive value in pts w/ chest pain and low coronary risk profile
• value for patients wiht non diagnostic stress studies and need to avoid an in procedure
• CT angio is the preferred procedure to evaluate bypass grafts

Cardiogenic Shock

• leading cause of death in hospitalized pts
• severe LV dysfunction (most common) also RV dys, acute MR, VSD, free wall rupture
• STEMI w/ pulmonary edema: 20-40% in hospital mortality
• Patho: dec in BP, peripheral hypoperfusion, LV fails as pump, tachycardia, fluid retention and pulmonary edema
• Clinical pres: respiratory distress, mental status change, rales, s3 gallop, hypotension
• labs: inc in PCW, lactic acidosis, inc BUN/creatinine
• Treatment: intraaortic balloon pump, inotropic agents, diuretics, repurfusion therapy

Management of Cardiogenic shock

Low cardiac output and elevated PCWP

• vasopressors: dobutamine, dopamine and NE
• Increase intravascular volume: blood, crystalloids
• Increase HR: chronotropes (dopaine and dobutamine), temporary pacemaker
• PReload reduction (a BP tolerates): diuresis, nitroglycerin 
• also work to have reduce afterload (nitroprusside, ACE inh), positive pressure ventilation, intra aortic balloon pump and revascularizaiton

Papillary Muscle Rupture

• life threatening complication, accoutns for 5% of deaths
• occurs 2 to seven days post MI
• may be partial or complete
• because of blood supply posteriomedial papillary rupture occurs 5-12x more frequent than anterolateral papillary muscle 82% of these occur in first MI; may be STEMI or nonSTEMI
• presents with severe hypotension, tachypnea
• harsh, loud holosystolic murmur; may not be pansystolic but will end with a sudden drop off in intensity because of high end diastolic presure
• on echo will see a flail valve leaflet wiht an attached mass (papillary muscle head)
• may show tall V waves?

Rupture of Interventricular 

• nearly always a complication of a transmural MI
• Typically occurs 3-5 days after the acute event
• predictors of ventricular septal defect (VSD) ar eage, female gender, hypertension, nonsmokers, and anterior infarction, tachycardia and worse Killip class at admission
• VSD is assoc with 74% 30 day mortality
• pts develop hypotension, CHF and new harsh, loud and holosystolic murmur beats beard at the lower left sternal boreders
• key to management of these pts is rapid stabilization and prompt surgery
• simple: discrete defect and direct rhough communication across the septum, antieor MI, usually apical
• COmlex: inferior MI, basal interior posterior septum

Potentional Cumulative impact of 1st degree prev

of CAD

• Smoking cessation: 1/3 reduction
• BP reduction 20mm Hg: 1/4 reduction
• LDL rduction 1mmol/L: 1/4 reduction
• Cumulative Prevention: 5/6 reduction

TG Drugs

• omega 3 fatty acids and niacin and fibrates dec TG about 25-50%
• Statins dec TG 10-35%
• Ezetimibe dec TG 5-10%
• Bile Acid resins inc TG 0-20%
• TG reduction shifts the atherogenic lipid trial (dec TG which dec VLDL which increases HDL and de csdLDL)

Hypertrophy

• in overload, heart hypertrophies to make stronger pump at cost of greater myocardial O2 demand and vulnerability to ischemia
• Pressure overload (hypertension or valve stenosis) adds sarcomeres in parallel (myocytes get fatter)
• volume overload: (shunt, valve regurg) causes dilation, adds sarcomeres in series (myocytes get longer)
• because they get longer in volume overload, we use weight not wall thickness to measure hypertrophy

Micro in Hypertrophy

• increased myocyte diameter
• nuclear enlargement, hyperchromasia, boxcar rhomboidal nuclei
• Interstitial fibrosis
• fibrosis looks different then in healling of AMI: more so wispy finger  of collagen surounding viable myocytes

Myocarditis Causes

• Infections(viral, chagas, bacterial, toxo): most cmmon involves mononuclear inflam
• Immune (hypersensitivity, rheumatic, lupus): hypersensitivity invovles eosinophils, mononuclear inflam
• Unknown(sarcoid, giant cell): Giant cells (mononuclear infalm and giant cells)
• Myocarditis can affect young folks and be responsible for sudden cardiac death in this age group
• Chagas: see trypanosomes in cardiac myocye, endemic to south america (Reduviid bug), screen blood for, parasite with mixed inflam

Acute Decompensated HF (ADHF) 

Subsets

• Warm and Dry: normal: oral supportive therapy
• Warm and Wet: Pulmonary Congestion: decrease preload and inc O2
• Cold and Dry: hypoperfusion: increase CO
• Cold and WEt: hypoperfusion and Pulmonary congestion: goal is to find balance

Loop Diuretics

• Furosemide, torsemide, bemetanide
• for Heart failure
• blockk reabs of Na, Cl, K, in the loop
• effect: extreme diuresis, reduces morbidity
• FYI:inc dose not frequency and ceiling effect

Vasodilators

• very beneficial for pts with dyspnea, end up lowering BP overall
• can only be used on pts who have normal to high BP to start with
• Sodium nitroprusside: has cyanide metabolite (cleared by kidney), for Pulmonary congestion HF, or Hypoperfusion and pulmonary congestion HF
• Nesiritide: guanylate cyclase rec and for same as first
• NTG: for pulmonary congestion HF, mimics NO (cGMP inc) causing relaxation

Heart Failure Staging

• Stage A: at risk but w/o structural heart dz or symptoms:control HTN with ACE-I or ARB
• Stage B: Structural heart dz w/o signs or symptoms: use ACE-I (ARB)and add beta blocker
• Stage C: structural heart dz with prior or current sypmtoms: Pharm reduced ejection fraction (systolic failure) or pharm preserved ejection fraction (diastolic failure)
• Stage D: Refractory HF: fluid restriction, inotropic therapy or bridge therapies and advanced care measures

Structural Heart Disease with prior or current symptoms

of HF

• pharm reduced ejection fraction (systolic heart failure): Fluid retention (give diuretics), ACE-I, beta blocker, spironolactone, Hydralazine/nitrates, digoxin
• Pharm preserved ejection fraction (diastolic failure): fluid overload (give diuretics), hypertension (ACE-I and beta blockers)

Loop diuretics

• furosemide, torsemide, bumetanide
• increase excretion of H2O, Na, Cl, Mg, Ca and K
• durg interacitnos: fluid balance, K balance

Thiazide Diuretics

• Hydrocholorothiazide, chlorothiazide, chlorthalidone, indapamide, metalazone
• block Na Cl reabs in the distal tube
• effectsL inc excretion of H2O, Na, Cl, and K and dec excretion of Ca
• Adverse: hypovolemia, hypotension
• warnings: gout, parathyroid, renal impairment
• FYI: renal stones, osteoporosis, ineffective CrCL <30mL/min 

Aldosterone Blockers

• spironolactone and epleronone
• competes with aldosterone in distal tubule, heart, arteriolar smooth muscle
• effects: dec K and Mg secretion and dec Na retention
• stops catecholamine potentiation
• blocks direct fibrotic actions on myocardium
• adv effects: hyperkalemia, impotence amenorrhea
• epleronone can cause painful gynecomastia

Digoxin

• inhibits Na/K ATPase in myocardial cells: inc intracell Na which promotes Na/Ca exchange, leads to inc intracell Ca, improved isolated myocyte contractility and improved LV systolic function
• Renal Cells: dec Na reabs and dec renin available
• inc symptom control and exercise tolerace
• adv: bradycardia, fatigue, visual changes, N/V, hyperkalemia
• caution: WPW, AV locks, hypokalemia, renal impairment 
• Drug interactions: mycins, amiodarone, verapamil

Vegetative Endocarditis

• acute: staph auresu; subacute (s viridans), prosthesis (staph epi) and fungi 
• bacteremia is a must for infectious vegetative endocarditis
• vegetations can throw emboli, causing splinter hemorrhages in nail bed or: janeway lesions (nontender on sole or palm), osler nodes (tender fingertip or toe), roth spots (Retinal hemorrhage), or septic infarcts

Duroziez's Sign

• found in Aortic Regurg
• systolic murmur when compresssed proximally and diastolic murmur when compressed distally 
• also extremity edema in chronic decompensated

Indications for Mitral valve Surgery

• dyspnea with activities of daily living
• dilation of the left ventricle and a drop in the ejection fraction
• flail tip of mitral leaflet with attached portion of a papillary muscle
• atrial fibrillaiton (controversial)
• most cases of endocarditis do not require surgery

Ewart's Sign

• caused by large pericardial effusions
• dullnes to percussion, bronchial breath sounds, egophony below the angle of the left scapule

Echo and Doppler Features

of Cardiac Tamponade

• abnormal resp changes in vent dimentsions, right atrial compression, right vent diastolic collapse
• abnormal resp variation in tricuspid and mitral flow velocities, 
• dilated inferior vena cava with lack of inspirator collapse,
• left atrial compression, left vent diastolic compression 
• swinging heart

Triggered Automaticity 

DADs

• impuse initiation that is dependent on after-depolarization; membrane voltage oscillatations that occur
• DADs follow an action potention (delayed after depol)
• intracellular Ca overload
• inhibitor of Na-K ATPase by digitalis, catecholamines, ischemia
• due to digitalis toxicity

Triggered Automaticity

• impulse initiation that is dep on after depolarization
• EADs happen during an action potential (early after depol)
• do not depend on rise in intracellular Ca
• AP prolongation and reactivation of depolarizing currents fundamental
• reactivation of L type Ca
• QT prolongation, hypokalemia, hypomagnesemia, drugs

Class I Antiarrhythmics

• Na channel blockers
• group 1a, 1b and 1 c
• Na channels determine how fast membrane depolarizes (phase o) so these reduce phase 0 slope and peak of action potential
• reduce conduction velocity in non-nodal tissue
• specific binding/unbinding characteristics
• some alter APD and ERP by acitons on K channels (phase 3)
• depression of automatic properties in abnormal (non nodal) Na dependent pacemaker cells
• decreased slope of phase 4 depolarizaiton or elevate threshold

Group Ia Antiarrhythmics

• Na channel blockers
• Disopyramide, quinidine, procainamide (lupis like side effects)
• Intermediate on-off binding char: moderate slowing of conduction velocity and treat supraventricular and ventricular arrhythmias
• increase ERP (increase QT interval)

Group Ib Antiarrhythmics

• Na channel blockers
• lidocaine (neuro side effects) and mexilentine
• Fast on-off binding char: slight slowing of conduction velocity (least potent
• low pH accenuates activity (ischemic cells) and greatest effect at fast HR
• treat ventricular arrhythmias
• decrease ERP (decrease QT interval)

Group Ic

• Na channel blockers
• flecainide and propafenone
• slow on off binding char: marked slowing of conduction velocity (most potent), proarrhythmia related to strong Na blockade, treat supraventricular and ventricular arrhythmias
• no effect on ERP

Class II Antiarrhythmics

• Beta blockers
• useful in tachycardias where SA/AV nodes are abnormally automatic or part of reentry loops (SA/AV node blockers)
• inhibits sympathetic activity that nromally precipitates arrhythmias
• SA/AV tissue action-depolarization in response to slower Ca
• B blockers interfere with Ca influx
• decrease ventricular response in atrial tachycardias (like in atrial fibrilation)

Class III Antiarrhythmics

• K channel blockers
• Amiodarone (also dofetilidine, dronedarone, ibutilide, sotalol)
• k channels determine how fast membrane repolarizes (phase 3)
• slows/delays repolarization,QT prolongation, has proarrhythmia potential
• greatest effect at slow HR
• no effect on conduction on conduction velocity and automaticity
• used for supraventricular and ventricular arrhythmias

Amiodarone

• K channel blocker (Class III antiarrhythmic)
• most common antiarrhythmic
• treat chronic supravent and ventricular arrhythmias
• extremely long half life and large VD (lipophillic)
• many drug interactinos (classic is it and warfarin)
• I, II, III, and IV characteristics
• requires monitoring - thyroid problems, corneal microdeposits
• dronedarone is similar, but without iodine component (no thyroid dysfunction)

Class IV Antiarrhythmics

• CCBs (calcium channel blockers
• Verapamil and Diltiazem (non DHPs)
• slow Ca influx, SA/AV nodes depolarize
• CCBs reduce pacemaker firing rate (SA/AV node blockers
• useful for automatic or re-entrant tachycardias which arise form SA/AV nodes
• decrease ventricular response in atrial tachycardias (like atrial fibrilation)
• Decrease conduction velocity, QT prolongation, decrease automaticity

Digoxin (antiarrythmic)

• anti adrenergic-inhibit symp flow
• improves isolated myocyte contractility
• improves LV systolic function
• side effects: arrhythmias, visuals, hyperkalemia
• Caution: WPW syndrome, AV blocks, hypokalemia

Adenosine

• drug of choice (90-95% success rate)
• inhibits AV node conduction, increases AV node refractory period
• activate inward rectifier K current
• inhibits Ca current
• Extremely short half life (10 seconds, for acute)
• side effects: induction of short-duration high grade AV block, flushing, diaphoresis, dyspnea, nausea, chest heaviness
• side effect of bronchospasm (avoid in asthma patients)

Use of antiarrhythmics in HF

• avoid class I, II, III, IV drugs
• negative inotropic effects
• proarrhythmias
• amiodarone and dofetilide are neutral

Atrial Arrhythmias

• sinus tachycardia
• atrial tachycardia
• atrial flutter: impulse travel in circular course in atria, setting up regular, rapid flutter waves without any isoelectric baseline
• Atrial fibrilation: impulses take chaotic, random pathways in atria

Atrial Fibrillation

• cause: mitral valve diseae, CAD, LV dysfunctino, chronic lung disease, hyperthyroidism, pericarditis, PE, hypertrophic cardiomyopathies, idiopathic
• Therapies: control of ventricular rate (digoxin, beta, non DHP), prevent thromboembolism, restore sinus rhythm (electrical, ibutilide IV bolus, amiodarone)
• Maintenence of sinus rhythm (amiodarone, flecainide(best drug, horible if CAD or scar tho))
• hemodynamics of Afib: loss of atrial kick, shortening of diastolic filling time, decreased CO, dec coronary artery flow

Claudication Drug therapy

• Cilostazol only really efficacious med, most effective drug for tx of claudication
• phosphodiesterase inh with vasodilator and antiplatelet properties
• improves ambulatory distance and fatigue by 50% cannot be used in history of CHF
• alternative - pentoxifylline (subs xanthine deriv which dec blood viscosity and inc RBC flexibility but not as effective)

Ankle Brachial Index (ABI)

• right ankle brachial index = highest righ ankle preassure/highest right arm pressure (both systolic)
• ABI < 0.9 for mild to moderate obstruction
• ABI < 0.4 severe obstruction and severe ischemia
• > 1.3 vesel calcified and noncompressible
• Exrecise ABI (ABI >0.9, dec by 20% following exercise = PAD
• normal is .9-1.3

Fibromuscular Dysplasia (FMD)

• hyperplastic disorder affecting medium and small arteries -> intimal fibroplasia, medial dysplasia and periadventitial hyperplasia
• usually involves renal and carotid arteries but can affect extremity vessels (iliac and subclavian)
• predominantly in females 'string of beads' on angiogram
• PTA or surgical reconstruction if debilitating symptoms or threatened limbs

Thromboangiitis obliterans

Buerger's Disease

• Inflammatory occlusive vascular disorder of medium and small size arteries in distal and upper and lower extremities
• most frequent in men under age 40
• definitive relationship to smoking
• triad: claudication of affected extremitiy, Ranaud's phenomenon and migratory superficial phlebitis
• smooth tapering segmental lesions of distal vessels
• no specific treatment except abstention from tobacco: prognosis worse if continues to smoke

DeBakey Classification of 

Aortic Dissection

• Type I: Entry tear in AA, extent is AA, arch and Descending aorta
• TYpe II: Entry tear in AA, extent is confined to AA
• Type III A: entr tear in DA with proximal extension
• Type IIIB entry tear in DA and stays in DA
• Type I is most commen
• Standford classification: Type A is Types I, II, and IIIA; type B is IIIB

Single Gene Syndrome

• Holt-Oram Syndrome: limb abnormalities (ASD or VSD) and mutation in TBX5 gene 
• Noonan Syndrome: Short stature, webbed neck, pulmonary stenosis, mutaiton in one of 4 RAS signaling pathway (PTPN11, KRAS, SOS1, RAF1)

Coarctation of the Aorta

• narrowing at proximal protion of the descending aorta
• in infants it lies after aortic arch but before PDA
• associated turner syndrome and presents in infants wiht lower extremity cyanosis, weak/absent peripheral pulses, respiratory distress, acidosis and shock
• Adults have weak pulses in lower extremities, and enlargement collateral circulation leads to rib notching
• associated with bucuspid aortic valve

Tricuspid Atresia (cyanotic)

• tricuspid valve orfice fails to develop (no blood goes through); right ventricle becomes hypoplastic
• often assoc with ASD, resulting in right to left shunt; presents with early cyanosis
• syndromes: trisomy 21, cats eye, asplenia, christmas disease

Hypoplastic Left Heart Syndrome

• under development of LV
• under development/absence of mitral valve, aortic valve and aortic arch
• mostly males and assoc wiht turners, noonans and trisomies

Dromotropic Effects

• produce changes in conduction velocity, primarily in AV node
• NEgative effect: dec conduction velocity through AV node, increasing the PR interval (dec inward Ca current and inc outward K current)
• Positive effect: inc conduction vel through AV node, dec PR interval (inc inward Ca current 

Coronary Blood Flow

• Right coronary flow is highest during systole
• Left coronary flow is highest during diastole but has spike during systole
• left ventricle does a lot more work during diastole than right ventricle does
• O2 extraction is maximal at rest
• autoregulation helps maintain perfusion
• vasodilator reserve is 5 fold (normal as low as 3 fold)
• 3 is 50% stenosis and 1 is 90% stenosis

Types of Cyanosis

• Central cyanosis: right to left intracardiac shunt or pulmonary hypoxemia
• Peripheral cyanosis: cool, dark skin with diaphoresis due to vasoconstriction to compensate for a low cardiac output

Jugular Venous Pulsations

• A wave: atrial contraction
• C wave: Bulging of tricuspid leaflets into the right atrium during RV isovolumeic contraction 
• V wave: filling of right atrium during ventricular systole
• A and V normally about the same pressure and c is much smaller
• tricuspid regurg: causes inc V wave
• Tricuspid stenosis: causes prominant A wave and Small V wave 

Cardiac Auscultation

• S1: mitral-Tricuspid Closure
• S2: Aortic -Pulmonic closure
• S3: impaire drapid diastolic filling
• S4: atrial contraction (gallop if ventricle is not compliant
• Ejection click: opening of a calcified or fibrotic aortic valve
• Opening snap: opening of a calcified or fibrotic mitral valve

Pharmacologic Stress Testing

• Inotropic: dobutamine (beta 1 agonist): inc HR, BP, contractility, same effect as exercise
• Vasodilator (primarily used): adenosine: coronary dilaiton due to inc cAMP, contraindicated in patients with AV block and bcronchospasms (asthma)
• can use Adenosine A2A Agonists: inc coronary blood flow, reduced side effects, less AV block, can be used in asthmatics