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HEMODYNAMICS & CARDIAC ADAPTATION
- Myocardium histology review a. Striated muscle with branching, eccentric nuclei, intercalated disks b. Also collagen, glycogen-rich conducting tissue, caps, coronaries in epicardial fat, SR/T-tubules impt for Ca release/continuation of AP c. H band and I band shorten in contraction , A band does not
- Normal cardiac cycle a. LV > aortic valve > systemic circulation > RA > tricuspid > RV > pulm valve > pulm a > lungs > pulm v > LA > mitral valve > LV b. AV valves have papillary muscles w/chordae tendinae attached, semilunar valves lack both c. Mitral valve is the only one that has 2 cusps, the rest have 3
- Definitions a. Preload i. volume (or pressure load) of blood present at start of contraction, basically the EDV ii. clinical: increases in preload cause eccentric hypertrophy b. Afterload i. pressure the contracting LV has to push against during systole, basically the SBP ii. clinical: increases in afterload cause concentric hypertrophy c. Contractility i. intrinsic capacity of myocardium to contract, independent of preload/afterload, due to increased velocity of shortening ii. clinical: increased by exercise, catecholamines, ionotropes ; decreased by ischemia, acidosis d. Compliance i. distensibility, directly impacts preload (i.e. more distensible = easier to fill = higher EDV) ii. clinical: decreases compliance – hypertrophy (HTN), fibrosis (pericarditis), ischemia (MI), edema (pulm congestion) e. Frank-Starling i. normal : increase in preload increase sarcomere stretch increase energy of contraction increase CO ii. heart failure : lower contractility/flatter slope, need to find balance btw increasing preload (which would increase CO and thus maintain good perfusion) and preventing pulm edema iii. athlete : higher contractility/steeper slope iv. if preload is too low hypotension ; if preload is too high pulm edema f. LaPlace i. wall stress = ½ Pwall x radiuswall / thicknesswall (think: balloon pops when filled) ii. clinical: chronic stress induces hypertrophy decrease stress via increase wall thickness (BUT decreases compliance) g. Ejection Fraction i. % of EDV that is actually pumped out each beat, EF = SV / EDV, normal is 55-70% h. Stroke Volume i. Volume of blood pumped with each systole, SV = EDV – ESV, normal is 70-90 mL ii. Regulated by preload, afterload, contractility i. Cardiac Output i. Volume of blood pumped by heart per minute, CO = SV x HR, normal is 5 L/min ii. Measure via:
- Fick’s Method a. CO = O2 consumption (estimated @ 125) / AV oxygen difference (O2Pul a – O2Pul vein) b. Use for low output states, a-fib
- Indicator Method a. CO = rate of temperature inc of cold saline from RA > pulm a, or rate of dilution of dye b. Use for high output states (hyperthyroidism)
- Doppler a. Actually gives you SV by measuring outflow at aortic valve (that x HR = CO) b. Use for beat-to-beat and for determining severity of valvular dz j. Cardiac Index i. Normalizes CO to a persons size, CI = CO x Body Surface Area
- Pressures a. during diastole, pressures in the atria/ventricles should be equal, since the AV valves are open i. RA – 5, RV – 25/ ii. LA (aka PCWP) – 10, LV – 120/ iii. Pulm a – 25/ b. O2 sat should be about 75% in RA/RV/pulm a and 100% in PCWP/pulm v/LA/LV (important when determining shunts)
- Resistance a. SVR = (Mean arterial pressure – RA pressure) / CO, normal is 900-1300 and at least 10x the PVR i. HI = vasoconstricted / LO = vasodilated (ex: hi CO state, anemia, AV fistula) b. PVR = (PA pressure – PCWP) / CO, normal is 40- 6. Shunts a. If LR, see increase in O2 in right heart ; if R>L, see decrease in O2 in left heart. b. ASD causes LA RA shunt c. VSD causes LV RV shunt d. Patent ductus arteriosus causes aorta > pulm a shunt e. Eisenmengers i. LR shunt causes pulm congestion which eventually right sided hypertrophy and reversed R>L shunt
- Hypertrophy a. An increase in myocyte volume (more sarcomeres/mito) in response to chronic abnormalities of wall stress b. Reactive hypertrophy is non-pathological i. Athletes, or any appropriate response, i.e. surrounding healthy myoctes near MI c. Concentric – increased thickness:vol ratio i. Due to increase in afterload, (ex) HTN, aortic stenosis ii. Sarcomeres laid in parallel to increase thickness decrease wall stress (good) + decrease compliance (bad) iii. Cardiac work is maintained at elevated level, thus compensatory increase preload to maintain higher CO d. Eccentric – normal thickness:vol ratio i. Due increase in preload (ex) aortic/mitral regurgitation ii. Sarcomeres laid in series to dilate chamber increase compliance (good) + increase wall stress (bad)
iii. Higher wall stress = stimulus for concentric hypertrophy sarcomeres in parallel too dilated chamber with normal wall thickness (seen as enlarged heart on xray) e. Clinical consequences of hypertrophy i. Increase in collagen decrease in compliance ii. Hypertrophy faster than capillary growth perfusion deficit iii. Decreased myosin ATPase activity impaired contractility
- Failure a. Circulatory failure – insufficient oxygen delivery to tissues b. Heart failure – insufficient pump function c. Myocardial failure – insufficient myocardial contractile function i. Not every pt in m-failure is in h/c-failure, b/c of compensation , usually by increasing preload to maximize CO
1. If h/c-failure results despite adaptive measures like hypertrophy/dilation = decompensation
ii. Hallmark is low SV despite high preload + poor response to increasing afterload
- Aging a. Normal changes: lipofuscin, protein x-linking, oxidative damage, decrease VO2max/max HR/AV02 diff, decrease SV (thus an increase preload to maintain CO), impaired b-adrenergic fxn (higher levels of catechols but less sensitivity to them) b. CV aging alters the substrate i. Arteries become rigid, dilated, filled w/ plaques ii. Elastic collagen is replaced w/ rigid collagen iii. Hi glucose x-links proteins > reduced elasticity iv. Earlier return of reflected pressure wave adds resistance (i.e. increases afterload) to LV > hypertrophy and stiffening c. Age related changes of the LV : hypertrophy/myocyte enlargement, fibrosis, impaired relaxation (can > LA hypertrophy/ a-fib ) d. Aging and HTN : increase arterial stiffness > increase BP/aortic impedance > increase afterload > LV hypertrophy > (1) increase in LVEDP > increase LA size > a-fib, (2) increase in 02 demands > ischemia, (3) impaired diastolic fxn > CHF
EKGs
1. Four phases of cardiac AP a. Phase 0 – Na+ channels open (massive Na influx depolarization) b. Phase 1 – Na+ channels close, K+ channels open (K efflux slight repolarization) c. Phase 2 – Ca+ channels open, K+ channels stay open (Ca influx balances K efflux plateau) d. Phase 3 – Ca+ channels close, K+ channels stay open (hyperpolarization) e. Phase 4 – ATP-Na/K Pump re-establishes resting membrane potential i. Fast response = atrial/ventricular myoctyes, Purkinje fibers ii. Slow response = SA/AV node 1. SA node is intrinsic pacemaker (60-100) due to overdrive suppression of slower automaticity foci 2. AV node is sole structure capable to conduct depolarization to ventricles f. Depolarization is a wave of positive charges contraction, repolarization is a wave of negative charges relaxation 2. Logistics a. Paper i. Horizontal measures time, small sq = 0.04s, large sq = 0.2s, 5 large sq = 1s ii. Vertical measures deflection, small sq = 1mm (amplitude) or 0.1mV (voltage) b. Limb Leads i. Measures the frontal plane ii. LI/aVL – lateral leads, LII/LIII/aVF – inferior leads iii. Bipolar leads (Einthoven’s Triangle) 1. LI: L arm positive, R arm negative (+0°) 2. LII: L foot positive, R arm negative (+60°) 3. LIII: L foot positive, L arm negative (+120°) iv. Unipolar Leads 1. AVL – L arm positive (-30°) 2. AVF – L foot positive (+90°) 3. AVR – R arm positive (-150°) c. Chest Leads i. Measures the transverse plane ii. V1/V2 – R leads, V3/V4 – septal leads, V5/V6 – L leads d. Vectors i. (+) charges toward (+) electrode = (+) deflection ii. (+) charges away from (+) electrode = (-) deflection iii. (+) charges perpendicular to (+) electrode = biphasic (+/-) deflection iv. Repolarization (= (-) charges) is the exact opposite 3. Atrial Depolarization = P wave (<0.8s) i. Reflects SA AV node, vector = leftward, downward, forward ii. Look for +P in LII (max amplitude normally) and biphasic in V b. PR interval time btw atrial contraction and ventricular contraction (<0.2s) i. Since AV node is slow response, conduction is slowed delay (shown as PR segment) which allows for ventricular filling 4. Ventricular Depolarization = QRS complex (<0.1s) i. First (-) deflection always = Q wave, first (+) deflection always = R wave ii. Q wave – septal depolarization, vector rightward, downward, forward 1. Traditionally represented as negative, thus, look for in LI, aVL, V5-V iii. R wave – “early” ventricular depol toward ventricular apex, vector leftward, downward, forward 1. Positive deflection except in LIII, avR iv. S wave – “late” ventricular depol toward ventricular bases, vector leftward/upward (since L heart bigger) 1. Traditionally represented as negative, thus, deep in avF , V1-V6 (gets smaller) b. R wave progression - becomes more positive from V1V6 (vs S wave becoming less negative from V1V6) c. Transition Zone - when +/- deflection of R wave is equal, usually at V3/V d. ST segment: represents plateau phase of fast response, elevated in STEMI/depressed in NSTEMI, angina 5. Ventricular Repolarization = T wave a. vector rightward/upward i. opposite direction and opposite sign of R wave, thus P and T waves look similar
b. PAB: P’ wave (or too-tall T wave) + normal QRS + pause i. SA node is depolarized by PAB and resets in step w/ it, thus a pause before the next cycle ii. PAB w/ aberrant ventricular conduction: usually ventricles are able to be depol by PAB, but if one of the bundle branches has not completely repol, there will be non-simultaneous depol of ventricles slightly widened QRS c. PJB: no P wave (or inverted P’ wave if it produced retrograde atrial depol) + normal QRS + pause d. PVC: no P wave (hidden) + huge QRS + pause, DUE TO ISCHEMIA i. SA node discharges on schedule, so P-P intervals are regular ii. Pause has nothing to do w/ resetting of SA node, it’s b/c ventricles are not repol yet when normal stimulus arrives iii. Unifocal or multifocal (many foci producing different QRS morphologies) iv. 3+ PVC in a row is called ventricular tachycardia, >30s is called sustained VT v. R on T = when PVC falls on middle of T wave, this is really bad b/c ventricle is vulnerable here to developing VT vi. MVP produces benign PVCs (papillary m stretched during prolapse local ischemia activation of irritable foci e. Any of the premature beats can occur in bigeminy/trigeminy
7. Tachyarrhythmias (sudden series of very fast beats) a. Paroxysmal Tachycardia = rate 150- i. Paroxysmal Atrial Tachycardia: P’ wave followed by QRS-T ii. PAT w/ AV Block: two P’ waves followed by QRS-T, think digitalis toxicity iii. Paroxysmal Jxn’al Tachy: no P wave (or inverted P’ if retrograde atrial depol) followed by QRS-T, may involve reentry iv. PAT/PJT (aka supraventricular tachy) w/ aberrant ventricular conduction: above + wide QRS (<0.14s) v. WWP: bundle of Kent is accessory pathway which connects atria/ventricles shortened PR interval aka delta wave vi. LGL: James bundle is the accessory pathway no PR interval w/ P-QRS-T right in a row vii. Paroxysmal Ventricular Tachy: no P wave (hidden) + huge QRS (>0.14s) , basically a run of PVCs
- SA node continues to pace normally and occasionally, an atrial depol ventricular depol, seen as normal QRS within all the crazy PVCs = capture/fusion beat b. Flutter (single foci) = rate of 250- i. Atrial flutter: still get complete atrial depol, seen as series of P’ waves (sawtooth) , some of which depol vent ii. Ventricular flutter: still get complete vent depol, seen as series of smooth sine waves
- Despite depol, the rate is too high to eject blood decreased coronary perfusion ischemia multiple irritable foci ventricular fibrillation c. Fibrillation (multiple foci) = rate of 350- i. Atrial fibrillation: no identifiable P waves, jagged baseline w/ a few QRS ii. Ventricular fibrillation: totally erratic 8. Blocks a. Sinus block: temporarily fails to fire dropped beat w/ pause (maybe escape beat) i. Sick Sinus Syndrome: SA node dysfxn + failure of all supraventricular automaticity foci bradycardia b. AV Block: slow/eliminate conduction from atria to ventricles i. 1°: prolonged PR interval >0.2s, usually benign ii. 2°: 1. Wenckebach: progressively lengthening PR interval until P wave is not followed by a QRS complex, then restarts 2. Mobitz: not progressive, some P waves just don’t make it to ventricles
a. conduction ratio - # of P attempts:# of conducted beats; ex: 3:1 means 2 blocked Ps with 1 conducted
b. pathological, must tx w/ pacemaker (vs Wenke, which is benign)
iii. 3°: complete block of SA impulse (tho P waves still regular!), escape rhythm is either jxn’al or ventricular iv. Bundle Branch Blocks: block localized in either R or L bundle branch ventricles depolarize asynchronously
1. Two QRS complexes are recorded a wide QRS complex with **R-R’ spike
- RBBB** complexes (NOT pathological) seen in V1/V2 , LBBB complexes are seen in V5/V
HEART SOUND/MURMURS
NORMAL HEART SOUNDS
Sound Cause How to hear it Notes S1 Mitral/tricuspid valve closure
Diaphragm, over entire precordium
S2 Aortic/pulmonic valve closure
Diaphragm, over entire precordium
Normal splitting of P heard only over pulm valve*
Physiologic splitting : pulmonic closes later due to ↑ RV ejection time b/c of ↑ venous return during inspiration (single during expiration) Pathologic splitting : wide fixed = ASD, narrow fixed = pulm HTN*, reverse split = left BBB, aortic stenosis (closes so late its after P2)
*with pulm HTN, can hear elsewhere S3 Sudden distention of ventricles during rapid filling
Use bell, at apex
Early diastole “Ken-tuc- ky ”
Considered normal in young, healthy pt Always abnormal if pt >50, assoc w/ heart failure, mitral regurg, VSD (high flow across open valve)
ABNORMAL HEART SOUNDS
Sound Cause How to hear it Notes
S4 Forceful atrial kick in an effort to overcome a stiff ventricle
Use bell , at apex
Late diastole “ Ten -nes-see”
Common, as hear if hypertrophied LV Assoc w/ HTN, aortic stenosis, hypertrophic cardiomyopathy
S4 S1 S2 S3 S4 S
EC MS OS
Clicks
Ejection Opening of stenotic or deformed semilunars
Over involved valve Directly after S
Assoc w/ bicuspid aortic valve or aortic stenosis
Opening snap Opening of stenotic mitral valve
Diaphragm, at apex Directly after S
Assoc w/ mitral stenosis
Mid-systolic Sudden tensing of deformed mitral valve
At apex @ start of murmur
Assoc w/ mitral valve prolapse
Knocks Sudden tensing of the pericardium during rapid filling
At apex Early diastole (same as S3)
Assoc w/ constrictive pericarditis or restrictive cardiomyopathy
Bruits Turbulent flow due to stenosis
Heard over affected blood vessels
Assoc w/ vascular stenosis
Rubs Pericardial Inflamed serosal surfaces rubbing together
At apex Assoc w/ pericarditis Described as to-and-from “squeaky leather” (WTF??)
MURMURS BY TIMING
Sound Causes Notes Systolic Aortic/pulmonic stenosis Mitral/tricuspid regurgitation
Between S1S
holocystolic Mitral regurgitation VSD
Blowing (w/ mid-systolic click if also MVP) Best heard w/ diaphragm at apex radiating to axilla early Tricuspid regurgitation Heard best along L sternal border mid-systolic Aortic stenosis (most common) Harsh crescendo-decresendo w/ ejection click Best heard w/ diaphragm in 2 nd^ RICS radiating to neck
late Mitral valve prolapse Starts once the valve collapses back aka mid-systolic click Best heard w/ diaphragm at apex Diastolic Aortic/pulmonic regurgitation Mitral/tricuspid stenosis
Between S2S
early Aortic regurgitation High-pitched decrescendo (sounds like someone breathing out hard) Best heard w/ bell in 2 nd^ RICS as pt leans forward holding exhalation mid-diastolic Mitral stenosis Rumbling following opening snap Best heard w/ bell at apex w/ pt in left lat decubitus continuous Aortopulmonary connections Arterio-venous connections (AV fistula)
From uninterrupted flow of high P/R to low P/R w/o phasic interruption Extremely loud murmurs
MURMURS BY CAUSE
- Aortic Stenosis a. Etiology: bicuspid valve (congenital) > rheumatic (usually w/ MS) > degenerative (>65y) b. Pathology: bicuspid = that + heavy Ca, rheumatic = commissural/chordal fusion, degenerative = nodular stenosis c. Hemodynamic: pressure overload (as LV tries to push blood through narrowed valve) increased LV wall stress compensatory concentric LV hypertrophy decreased LV wall stress at expense of decreased LV compliance LA hypertrophy extra kick to (1) help get blood into a stiff ventricle & (2) increase preload so that CO can be maintained d. Heart sound: ejection click followed by harsh, crescendo-decrescendo systolic murmur + S e. Clinical: i. Sx: angina (hypertrophy increased O2 demand but decreased O2 supply due to loss of coronary perfusion pressure gradient), effort syncope (systemic VD w/ exercise + limited CO hypoTN), long latent period ii. Dx: pulsus parvus et tardus (pulse is slow and bounding due to dampened ejection into aorta) + murmur iii. Tx: no sx = no limitations, pressure gradient >50 but no sx = exercise limitations/ avoid diuretics , pressure gradient
50 w/ sx = surgery (balloon valvuloplasty, only palliative)
- Mitral Stenosis a. Etiology: rheumatic heart dz b. Pathology: commissural fusion , chordal shortening (both are dx of rheumatic), neovascularization of valve (H&E) c. Hemodynamic: pressure/vol overload (LA tries to push blood through narrowed valve) (1) LA dilation/hypertrophy d. a-fib stasis/THB (2) pulm congestion R heart failure & (3) LV underloading and loss of CO i. LV is normal in pure MS. e. Heart sound: opening snap followed by rumbling diastolic murmur + S2 split i. Longer the murmur, the longer the valve is open = higher gradient and more severe the stenosis ii. NO S3 b/c rapid diastolic filling not possible through stenotic valve
f. Clinical: iii. Sx: dyspnea (due to pulm congestion), rales, fatigue (due to decrease in CO), JVD/peripheral edema (due to right heart failure), infective endocarditis (due to deformed valve, uncommon once valve is really rigid), thromboembolus (due to stasis in dilated LA), hemoptysis, Ortners syndrome iv. Dx: EKG = p mitrale (biphasic p waves LII) + inverted p waves V1, CXR = dilated apical pulm vessels, ECHO = “hockeystick” valve leaflets v. Tx: prophylaxis for rheumatic fever/endocarditis, diuretics (reduce volume overload), digoxin (control a-fib), anti- coagulation (prevent stroke), surgery if indicated (think: balloon valvuloplasty in pregnant woman w/ MS)
- Aortic Regurg a. Etiology: rheumatic heart dz, congenital bicuspid, degenerative Ca, root dilation (i.e. Marfans), endocarditis, syphilis b. Pathology: rheumatic = retraction, Marfans = abnormal collagen, acute endocarditis = perforation c. Hemodynamic changes:
i. Kawasakis Disease – childhood acute febrile illness cardiac complications (? due to autoAb), present w/ 5 classic sx: fever, non-purulent conjunctivitis, palm/sole erythema, desquamation
- Aneurysms = abnormal dilation of vessel, usually artery a. Atherosclerotic – most common, fusiform type, M>40 w/ subrenal AAA , rupture = death, tx by graft b. Syphilitic – ischemic destruction of elastic tissue of thoracic aorta (aka tree barking) w/ assoc root dilation aortic regurg c. Dissecting – intimal tear in proximal aorta blood-filled channel dissection of blood down laminar plane = death w/o surgery i. Either 50y M w/ HTN or pt w/ CT abnormality (Marfans/Ehlers Danlos) w/ acute onset excruciating chest pain ii. Cystic medial degeneration more common if CT abnormality
- Venous Disorders – skipped in lecture, due to the self-assessment questions though… a. SVC syndrome due to pulm tumor, IVC syndrome due to renal tumor b. Varicose v. are NOT a risk for PE, but heart failure/bed rest/cancer/burns/post-op pts are
- Vascular Tumors a. Hemangioma – benign, =blood filled caps, red/blue spongy lesions that often spon regress b. Hemangioendothelioma – intermediate, =prolif of endoth cells, don’t metastasize c. Angiosarcoma – malignant, assoc w/ PVC/Thorotrast, vascular channels absent d. Kaposi’s sarcoma – classic/endemic/epidemic forms, epidemic in immunosuppressed pt w/ nodular lesions
CORONARY PHYSIOLOGY
- Blood supply of the heart a. RCA: supplies inferior/right heart, courses in right AV groove b. LCA: branches into… i. Left anterior descending (LAD) – supplies anterior/apical heart, courses in anterior IV groove 1. Gives rise to diagonal a which supply anterior LV 2. Gives rise to anterior septal a which supply anterior 2/3 of IV septum ii. Left circumflex (LCF) – supplies posterior/lateral heart, courses in left AV groove
- Gives rise to marginal a which supply lateral LV c. Dominance defined by which artery (RCA or LCF) gives rise to posterior descending artery /supplies the AV node (SA ½:½) i. PDA supplies posterior 1/3 IV septum ii. 90% people are right dominant d. Anterior papillary m = LAD/LCF, posterior papillary m = LCF/RCA i. postero-medial papillary m of mitral valve only supplied by PDA, thus, MI involving PDA can lead to mitral regurg
- Myocardial O2 consumption a. Coronary blood flow (O2 supply) is directly proportional to myocardial oxygen consumption (O2 demand) i. Supply/demand must be linked since anaerobic metabolism is insufficient and extraction is near-maximal b. Increased heart rate, preload/afterload, contractility will increase demand c. Increased coronary perfusion pressure/decreased resistance will increase supply (remember: Q = P/R)
- Factors which regulate coronary blood flow: a. Anatomic: pressure drop occurs as epicardial coronaries branch and pierce myocardium decrease in flow i. Collateral vessels can provide additional routes for flow in atherosclerosis b. Hydraulic: most coronary flow occurs during diastole when heart is relaxed and not squeezing vessels shut i. Sub-endocardium contracts more than epicardium greater restriction of blood flow during systole ii. To make up for that + increased wall stress due to EDV + increased O2 demand VD of sub-endo vessels iii. VD in sub-endo allows for homogenous blood flow but decreases VD reserve = increased risk of ischemia c. Autoregulation: maintenance of flow despite changes in perfusion pressure i. Vessels decrease resistance via VD using “vasodilatory reserve” ii. In fixed stenotic lesion (pressure <60 ), vessels already maximally dilated and autoregulation not possible ischemia d. Metabolic: adenosine is the most important mediator of VD in autoregulation e. Neural: net effect sympathetic tone is VD (b2 outweighs alpha) f. Humoral: intact endothelium helps regulate vascular tone and coagulant state i. NO will VD normal endothelium, nitroglycerine will work even if it’s damaged ii. ACh will VD normal endothelium but VC if it’s damaged (i.e. in HTN/atherosclerosis)
- Ischemia (inadequate perfusion low O2 angina) a. Atherosclerosis pressure gradient across the lesion (lower P distally) decreased flow compensatory VD increased flow i. Eventually vessels are max VD, so in periods of high O2 demand, perfusion pressure is insufficient ischemia ii. Fixed stenotic lesion >70% = ischemia w/ exercise , if >90% = ischemia at rest b. Metabolic consequences: decreased HEP stores, activation of anaerobic glycolysis (tho insufficient), production of lactate c. Fxn’al consequences: decreased systolic contraction, decreased diastolic relaxation ( lower coronary perfusion gradient) i. Myocardial stunning: reversible loss of fxn due to acute ischemia that returns days after reperfusion ii. Myocardial hibernation: reversible loss of fxn due to chronic ischemia that returns immediately upon reperfusion iii. <15-20m of ischemia is normally reversible
CORONARY ARTERY DISEASE
1. Disease of epicardial vessels, characterized by endothelial dysfxn, vascular inflamm, and intimal buildup of lipids/chol/Ca/debris
plaque formation, luminal obstruction, abnormal blood flow, and target organ ischemia
- Risk Factors a. Non-modifiable: age, gender, family hx are most powerful predictors (age, gender, FMx, genetics) b. Modifiable: high LDL, low HDL, HTN, DM, smoking, sedentary, high CRP - have independent effects on risk, not synergistic
- Pathophysiology a. Fatty streak more lipid accumulation + smc prolif fibrous cap overlying core of foam cells/chol luminal narrowing i. Endothelial injury due to oxidized LDL ( NO inactivation and impaired VD), which is taken up by MΦ and accumulates b. Repeated cycles of acute changes (rupture, erosion, intra-plaque hemmorage) risk of thrombus and partial/full occlusion c. Tends to occur in regions of branching/curvature where there is turbulent flow (ipso facto, the coronaries)
- Chronic Stable Angina a. Clinical syndrome characterized by chest pain with exertion (pain sensation due to adenosine ) b. 1˚ caused by fixed stenotic lesion in an epicardial coronary artery i. Vessels are maximally VD to increase perfusion (see above), but plaque prevents match of O2 supply/demand ii. Other causes: anemia, Prinzmetal (focal vasospasm angina at rest + ST elevation), microvascular abnormalities, increased extravascular forces (LV hypertrophy, AS, hypertrophic cardiomyopathy)
c. Sx: i. Retrosternal chest discomfort/heaviness that is relieved by rest/NTG ii. Sx vary between pts, but are always the same for an individual pt
- If sx significantly worsen, change, or occur more frequently, or have angina at rest = unstable angina d. Dx: i. EKG: about half of pts will have a normal resting EKG, otherwise look for ST depression >1mm (or elevation w/ Prinz) ii. Stress test: reproduces the angina sx via exercise, yet not very specific/sensitive iii. Imaging: complement stress test and help localize areas of ischemia
- Coronary angiography is gold standard for identifying vessel narrowings
- Radioisotope uptake (or echo) demonstrates aerobic metabolism e. Tx: i. Goal is to relieve sx and more importantly, prevent progression of CAD
- Sx relief from sL NTG
- Dz modifiers include b-blockers, stents, tx of modifiable risk factors (ex: statins to lower chol, BP meds) ii. 2˚ prevention is ASA ASA ASA. All pts should be on aspirin! (unless they have a bleeding disorder/allergy, obvi)
ACUTE CORONARY SYNDROMES
- Spectrum of diseases which includes unstable angina, NSTEMI, STEMI, and sudden death a. Rupture of an atherosclerotic plaque is the underlying etiology in nearly all cases b. Exposure of plaque elements coagulation/thrombus formation + VC partial (unstable/NSTEMI) or full (STEMI) occlusion c. End result is ischemia switch to inefficient anaerobic metabolism, if >20m cell death
- Signs/Sx a. Prolonged (>30m) severe crushing chest pain at rest, radiation to jaw/neck/arms, cool/clammy skin, SOB i. atypical sx like fatigue, NVD, MSΔs, esp in women/elderly b. NSTEMI tends to have “stuttering” CP as reperfusion through partial occlusion comes and goes
- Physical Findings (depend heavily on location of ischemia) a. Rales – as EF declines, pulmonary congestion will occur b. S4 – impaired relaxation (ATP-dependent) stiff LV c. Mitral regurg – papillary m becomes ischemic (posterior medial papillary m is perfused only by PDA) d. High JVD – indicative of R infarct, especially if no pulm congestion
- Lab values a. Troponin: found only in myocytes, thus presence indicates cell lysis, virtually dx of MI b. CK-MB: creatine kinase specific for myocytes, again, indicates cell lysis
- EKG changes (ST segment elevation, T wave inversion, new Q waves are characteristic) a. STEMI: EKG is abnormal and generally dx of MI i. ANT infarction (LAD): V1-V4 changes ii. INF infarction (RCA): II/III/aVF changes iii. LAT infarction (LCF): V5-V6, I, aVL changes iv. POST infarcts (RCA): consistent chest pain, ST elevation w/ mirror v. If V1 is involved (1) it’s a proximal occlusion (2) both LV/RV probably involved b. NSTEMI i. EKG usually normal, dx by elevated serum troponin levels c. Unstable angina i. EKG is normal, (and since no evidence of troponin/CK-MB), dx is one of exclusion
- Tx a. Acutely: ASA, clopidogrel, heparin, NTG + restart perfusion ( 90m or less = dramatic benefit) i. If door to needle <90m, PCI (if stenting, ASA/clopidogrel/IIbIIIa(-) for surgery, continue ASA/clopidgrel post-op) ii. If door to needle >90m, thrombolytics (t-PA) b. Post-MI: = ASA, clopidogrel, statin, ACE(-), b-blocker (last 3 decrease mortality) 7. Vessel involved predicts where the infarct will occur a. Anterior LV wall – LAD b. Lateral LV wall – LCF c. Inferior/posterior – RCA d. Posterior septum – usually RCA (since 90% of people are R heart dominant) e. Extent of collateral blood vessels, duration, and metabolic demand of tissue near the lesion affects extent of infarct
- Pathological Classification a. Subendocardial infarction (by definition, does not extend into epicardium) i. Partially occlusive thrombus from diffuse plaques w/ patchy areas of necrosis, smaller in size ii. EKG normal b. Transmural infarction (worse Px) i. Completely occlusive thrombus from single artery w/ solid area of necrosis, large in size ii. EKG shows Q waves, ST elevation iii. Commonly pericarditis ~3d postMI
- Dressler’s syndrome = pericarditis due to auto-Ab, 2-10w postMI iv. If posterior infarct, more likely to cause conduction disturbances, as nodes are predominantly supplied by RCA c. “Wavefront phenomenon” i. Necrosis begins at level of subendocardium (due to less perfusion, higher workload) and expands out toward epicardium ii. Want to intervene before wavefront expands so that a greater portion of heart can be spared
- Pathological Findings a. Contraction band necrosis i. Hyper-eosinophilic contraction bands indicate reperfusion before death (cells dying in presence of O2) b. Pallor or hyperemia (if reperfusion) w/in 12-24h c. Dating of MIs (after the event) i. 12 hrs – earliest histologic changes (wavy fiber change) ii. 24 hrs – earliest gross changes (coag necrosis) iii. 1-5 days – neutrophilic infiltrate predominantes iv. 7-10 days – macrophages predominate, beginning granulation tissue v. Weeks – fibrosis
- Complications of MI
ii. Bilateral RAS: renal hypoperfusion AND low GFR/expanded intravascular volume iii. Both lead to renal HTN, which is refractory to antiHTN tx (much worse in bilateral, tho diuretics help w/ vol overload)
- ACE(-) are contraindicated b/c they exponentially increase sCr irreversible injury
- HTN and CNS complications a. HTN right shift of whole curve, thus upper and lower limits of autoregulation are set at a higher overall BP i. BP below lower limit max VD but still unable to maintain flow ischemia/ stroke ii. BP above upper limit max VC but still unable to slow flow increased hydrostaticP edema/ HTN encephalopathy b. BP reflexively rises during acute ischemia (stroke) huge increase in SBP and paradoxical cerebral edema i. “Watershed” around ischemic area is unresponsive to autoregulation and thus depends entirely on SBP for perfusion ii. Instinct is to give antiHTN meds to prevent edema, but that would worsen ischemia and cause greater infarct iii. DO NOT give antiHTN drugs unless SBP >
- 2° hypertension a. Hyperaldosteronism – increased aldosterone due to increased renin (usually tumor increase Na reabsorption high BP b. Pheocytochrotoma - neuroendocrine tumor of the adrenal glands or other catecholamine secreting tissues i. Measure by serum metanephrine levels c. Pregnancy - normally falls during 1st/2nd^ trimester but rises back to normal during 3rd^ trimester i. Pre-eclampsia – onset of high BP after 20th^ week of pregnancy, emergency
ENDOCARDITIS
- Infectious endocarditis: deposition of adherent/thrombotic debris (vegetation) on the valves or mural endocardium a. Acute i. More virulent orgs ( Staph aureus ) assoc w/ IV drug use ii. Can infect normal valves iii. Most commonly tricuspid valve (injection via IV use brings orgs to R heart first) iv. Can rupture, valve ring abscess, septic infarct, chronic regurg b. Subacute i. Less virulent orgs ( Strep viridans ) assoc w/ dental procedures ii. Only infects damaged valves iii. Most commonly mitral/aortic valves iv. Less destruction/less complications/less likely to cause septic infarction than acute infections v. Common finding is granulation tissue at the base of the vegetation c. Predispositions = congenital heart defects, prosthetic valves (think Staph epidermidis ), IV drug use, catheters
- Non-bacterial thrombotic endocarditis (NBTE) a. Sterile vegetation of fibrin/plts which do not directly cause valve damage (underlying tissue is normal) b. Form nodules along the line of valve closure (similar to RF), valve does not have to be damaged for this to occur c. Most commonly aortic/mitral valves d. Predispositions = hypercoagulable states (think malignancy), chronic diseases (think SLE, RA)
- Prosthetic valves a. Bioprosthetic (from pig) eventual deterioration of tissue b. Mechanical (man-made) thrombi, hemolysis (metal parts cause sheer stress)
- Clinical manifestations of endocarditis a. Most common presentation: i. Fever of 1-2w ii. Murmurs (can be new, or a change in current)
- Always regurgitation due to perforation/malcoaptation of valve
- Ring abscesses, chordal rupture, shunts contribute iii. Acute onset CHF due to regurg iv. Bacteremia v. Embolization of veg (esp if >1cm) septal infarct vi. Constitutional sx like weight loss, night sweats, athralgias vii. Various immune effects : petechaie, splinter hemorrages, Osler nodes (painful), Janeway lesions (non-tender), Roth spots (retinal hemmorage white center) viii. Pericarditis b. ECHO is gold standard to ID vegetation, a negative ECHO essentially rules out IE c. Dx requires combination of major/minor criteria to make definitive diagnosis i. MAJOR: 2 positive blood culture , positive ECHO, new regurgitation ii. MINOR: fever, predisposing cardiac condition, IV drug use, vascular sx, immunologic sx*
- Definitive IE = 2 major OR 1 major/3 minor OR 5 minor + histologic evidence from vegetation/emboli
- Possible IE = 1 major/1 minor OR 3 minor
- Negative IE = no histological evidence, resolved sx <4d w/ antibiotics, better explanation d. Tx aims to sterilize vegetation through high [] of Abx i. Low virulence = 2w IV Abx ; high virulence = 4+w IV Abx 1. Amoxicillin or Clindamycin (if allergic to penicillin) ii. May need surgery if fungal endocarditis (Abx barely effective), abscess (no access), uncontrolled infxn iii. Prophylaxis for various procedures (e.g. dental work) if have predisposing factors (congenital, prosthetic, prior IE) 1. MVP w/ MR is NOT an indication for prophylaxis
PERICARDITIS
- Definition a. Inflammation of the pericardial surfaces, assoc with inflammatory infiltrate and fibrin exudate b. If pericardial pressure rises, the cardiac chambers may become compressed impaired ventricular filling decreased CO c. Small amounts of fluid accumulated rapidly is usually worse than large amounts accumulated over time b/c tamponade
- Acute Pericarditis (pericardium is actively inflamed) a. Primarily secondary to bacteria, viruses, TB, autoimmune (lupus, RA, Dressler’s), uremia/renal failure (accumulate slowly so can see HUGE effusions), malignancy ( breast, lung, lymphoma most common), radiation, drug induced i. Fibrinous pericarditis (most common), causes = acute MI, Dresslers, uremia/renal failure, lupus, RA, radiation ii. Serous pericarditis, causes = noninfectious, thus scant inflamm cells seen in exudate iii. Suppurative pericarditis, causes = bacteria, thus tons inflamm cells seen in exudates + pus
- Organization commonly constrictive pericarditis*
iv. Hemorrhagic pericarditis, causes = malignancy, TB, bleeding disorder v. Caseous pericarditis, causes = TB (usually only in AIDS pts) b. Clinical signs/sx i. Chest pain (palliative on leaning forward), fever, tachycardia ii. Loud friction rub
1. 3 component scratchy sound: mid-systolic (vent contraction), mid-diastolic (rapid vent filling), late diastolic (atrial contraction) iii. EKG changes = ST elevation in all leads except aVR c. Tx w/ NSAIDS, steroids, colchicine
- Constrictive pericarditis (chronic pericarditis) a. Chronic inflammation + fibrosis thickening/adherence to mycocardium calcification limited diastolic filling b. Most common etiology is post-cardiac surgery c. Present with signs of right heart failure (JVD, hepatomegaly, peripheral edema) i. Kussmaul’s Sign – inspiration increase in JVP ii. Pericardial Knock
- Cardiac tamponade a. rise in pericardial pressure and compression of cardiac chambers in diastole impaired diastolic filling decreased CO b. Clinical signs/sx i. Hypotension, reflex tachy, shock ii. Pulsus paradoxicus – accentuated RA filling during inspiration substantial decrease in LA volume (bulging through IV septum) exaggerated lowering of systolic blood pressure (>10mm) iii. JVD due to augmented venous return with compression of right heart c. Tx = pericardiocentesis
- Pericardial effusions a. Usually serous effusion that slowly fills the pericardium (slow enough not to impair diastolic filling) b. Common in renal or heart failure c. Clinical signs/sx i. ECHO positive for fluid in pericardium ii. Muffled heart sounds iii. Ewarts sign (dullness, decreased breath sounds, and egophony over left posterior lung due to compression by the enlarged pericardial sac) iv. EKG changes = alternating hi/lo QRS complexes due to heart “swinging” back and forth in fluid
CONGENITAL HEART DISEASE
- Caused by defective heart development in 1st^ trimester
- VSD is most common congenital defect, also common in chromosomal d/o (ex: 40% of trisomy 21)
- Fetal Circulation a. Fetal circulation usually prevents sx until after birth b. Placenta is the oxygenating organ and umbilical vein is most highly oxygenated c. Fetal shunts – prevent blood from entering highly constricted pulmonary vascular bed i. Ductus venosus – allows 50% of blood in umbilical v to bypasses the liver and enter IVC instead ii. Foramen ovale – allows blood in RA to bypass the lungs and enter LALVaorta instead (goes to heart/brain) iii. Ductus arteriosus – allows small amt of blood in pulm a to bypass the lungs and enter aorta (goes to splanchnic/limbs) d. Transitional circulation i. First breath expands lungs and its vasculature – b/c lower resistance, blood flows into lungs and shunts close
- Clinical Consequences a. Congestive heart failure (L R shunts) i. CO cannot meet needs of the body ii. Mostly due to abnormal distribution of CO (b/c of shunt) iii. Sx: feeding intolerance , failure to grow , respiratory infections
iv. Signs of CHD heart failure:
1. Tachypnea (indicates pulmonary edema) 2. Tachycardia (indicates sympNS trying to increase CO) 3. Hepatomegaly (indicates RAS* fluid retention, trying to increase SV) b. Cyanosis (R L shunts) i. Easier to detect cyanosis at higher Hb levels ii. Signs of CHD cyanosis: 1. clubbing (hypoxia stimulates VEGF more capillaries) 2. cerebral absesses / stroke (R L shunt bypass filtering ability of lung) 3. polycythemia (increased RBC in attempt to increase O2) c. Pulmonary vascular disease (L R shunts) i. Inc pressure and flow intimal hyperplasia/vessel narrowing by 12-24 month ii. Eventually damage is irreversible increase PVR, once it exceeds SVR, switches to R L shunt ( Eisenmenger’s ) iii. Signs of CHD-induced pulm vascular disease: exercise intolerance, strokes, pulmonary hemorrhage
- Classification a. Left to Right Shunts (PDA, ASD, VSD) i. Pulmonary flow exceeds systemic flow 1. increased volume in lungs/LA/LV pulm congestion + chamber dilation a. pulm vasculature remodeling (remember: pulmonary vascular dz) 2. some oxygenated blood lost abnormally distributed CO that is perceived as “low” CO compensation a. RAS activation fluid retention systemic congestion (remember: tachypnea/cardia, h-megaly) ii. VSD = most common 1. severity is due to size of defect and degree of pulmonary vascular resistance 2. signs/sx: a. Poor feeding, growth impairment, triad b. Loud S2 due to pulm HTN c. Holosystolic murmur (due to VSD) + diastolic murmur (due to increased flow across mitral valve)
ii. Some of CO circulates through low resistance AVf thus reducing CO to other organs = circulatory failure c. Dysrhythmias: chronic, inappropriate elevation of heart rate (atrial fib, flutter) d. Pericardial Disease: normally pliable, but in tamponade/constrictive pericarditis it stiffens restricted pumping/filling e. Valvular Dysfunction: either regurgitation/stenosis circulatory failure f.
- Hemodynamic a. In CHF, problem is inadequate CO +/- pulm congestion various stages of warm/cool, dry/wet, etc. b. Frank-Starling curve shows CHF heart w/ lower contractility, lower EF
- Neurohumoral: overall, NOT helpful a. Sympathetic increased HR/contractility (b1) + VC (a1) i. Elevated levels long-term increase mortality, but catechols are necessary evils – the increased HR/contractility helps maintain CO/BP but also increased O2 demand, the VC helps maintain BP but also increases afterload to a failing heart b. RAS angioII VC + Na retention + SNS activation (aldosterone contributes to these effects) i. Same as above, it works to maintain BP but over time will only worsen the failure due to increased afterload ii. Renin released due to decreased CO/renal perfusion, decreased Na @ macula densa, a1 symp stimulation c. BNP VD + Na excretion i. Works to decrease afterload, but VD decreases resistance/BP which forces failing heart to pump harder to maintain CO ii. Normally effects are outweighed by RAS
- Clinical presentation a. Low CO fatigue, DOE, cool skin, increased BUN:Cr (due to low renal blood flow) b. Pulmonary edema SOB, orthopnea, PND, cardiac asthma, rales, S c. LV dilation laterally displaced PMI, cardiomegaly on CXR, holosystolic murmur (MR) d. RV failure JVD, hepatomegaly, pitting edema, (+) hepatojugular reflex, elevated LFTs (due to hepatic congestion) e. Other Labs: hypoNa/hypoK (normally induced by therapy, ex: diuretics), high BNP
- Tx: See pharm chart below, also bedrest (reduces workload), low Na diet (reduces Na retention)
PHARMACOLOGY
1. HTN
a. Normal <120/<80, PreHTN: 120-140/80-90, Stage 1 HTN: 140-160/90-100 , Stage 2 HTN: >160/> b. Goals: HTN alone <140/90, diabetes/renal dz <130/85, LV dysfxn <120/ c. Commonly 1st^ line: thiazides, beta blockers, ACE (-), Ca channel blocker (if A-fib)
DIURETICS
MOA Place in Therapy Clinical Pearls Thiazides HCTZ Chlorthalidone
Blocks Na reabsorption in DCT DOC in isolated mild hypertension Preferred in AA pts Less effective in RF
SE: hypoK , hypoTN, ARF*, DM , gout decrease stroke/MI too *decreased perfusion due to hypovolemia
Loop Diuretics Furosemide Torsemide
Blocks Na/Cl reabsorption in LOH excessive vol loss
Uncommon for HTN Used in RF (Cr<20)
SE: hypoK , hypoTN, ARF, hypoMg, ototox
Potassium Sparing Triamterene Amiloride
Blocks Na reabsorption in CT less K lost in urine
Adjunctive therapy SE: hyperK caution w/ chronic renal insufficiency, or any situation w/ high K (supplements, salt substitutes)
ANTI-ADRENERGICS
MOA Place in Therapy Clinical Pearls Beta-Blockers Metoprolol Atenolol Carvedilol
Block cardiac beta 1 R decr HR decr CO decr BP
Use if concurrent heart dz DOC for hypertrophic CM
SE: bradycardia (caution w/ EF <40%), hypoTN contraindicated in asthma may mask hypoglycemia in DM decreases mortality
Alpha-Blockers Terazosin Prazosin Doxazosin
Block vascular alpha R VD decr resistance decr BP
Uncommon due to hypoTN Used if uncontrolled despite other meds
SE: hypoTN, O-hypoTN, syncope never use as monotherapy
RAS INHIBITORS
Drug MOA Place in Therapy Clinical Pearls ACE (-) Lisinopril Captopril Ramipril
Blocks Ang I Ang II, thus blocks VC (decr afterload) + blocks Na retention (decr preload)
1 st^ line tx due to many compelling indications (heart failure, DM, CAD) DOC for heart failure
SE: ARF, cough* , angioedema, hypoTN, hyperK monitor creatinine & K decreases mortality after MI prevents remodeling
*decreased GFR due to dilation of efferent arteriole
ANG II R Blockers Valsartan Losartan
Blocks Ang II receptor same effects as above
Used if ACE (-) can’t be SE: similar to ACE (-) but no cough
Aldosterone Antag Spironolactone Eplerenone
Comp antag of aldosterone R prevention of Na retention
Limited role SE: hyperK (K-sparing)
Renin (-) Self-explanatory Newer drug, unknown SE: hyperK
Aliskiren
VASODILATORS
Drug MOA Place in Therapy Clinical Pearls Ca Channel Blockers Amlodipine (di) Nifedipine (di) Diltiazem (non) Verapamil (non)
Block L-type decrease Ca influx into vascular smooth m cells VD
DHP: lower BP non-DHP: lower BP AND heart rate non-DHP often DOC in A-fib
SE: bradycardia (non), periph edema/hypoTN (di) constipation (verapamil)
Clonidine Alpha-2 agonist 3 rd^ line rebound HTN with abrupt discontinuation (taper) Hydralazine Direct vasodilator 3 rd^ line Requires 3x/day dosing Can induce drug-induced SLE-like rash Minoxidil 3 rd^ line orthostasis
2. CAD – goals of therapy a. inhibit platelet aggregation = aspirin, clopidogrel b. reduce myocardial O 2 demand = β-blockers, Ca channel blockers c. increase myocardial O 2 supply = nitrates, Ca channel blockers d. prevent plaque formation/reduce lipid levels = Statins e. lower overall CV risk = ACE (-), ARBs, Eplerenone
INHIBIT PLATELET AGGREGATION
Drug MOA Place in Therapy Clinical Pearls Aspirin Irreversible (-) of COX less TXA2 less plt activation
Secondary prevention for all pts with CAD and DM
SE: bleeding, GI decreases mortality in post-MI
Clopidogrel Block ADP R irreversible (-) Used in pt w/ ASA allergy Used in combo w/ ASA
SE: bleeding
DECREASE MYOCARDIAL O 2 DEMAND
Drug MOA Place in Therapy Clinical Pearls Beta-blockers Block cardiac b1 R decrease HR/contractility decrease 02 demand
DOC stable angina ALL post-MI
SE: bradycardia (caution w/ EF <40%), hypoTN contraindicated in asthma may mask hypoglycemia in DM decreases mortality
Ca Channel Blockers NON-DHP ONLY!
Block L-type decr Ca influx decreased HR/contractility decreased O 2 demand
Use if contra to beta-blocker Adjunct to beta-blocker
SE: bradycardia, constipation (verapamil)
INCREASE MYOCARDIAL O 2 SUPPLY
Drug MOA Place in Therapy Clinical Pearls Nitrates NTG Iso mononitride
Exogenous source of NO VD ALL stable angina pt should have SL NTG for rescue
SE: headache, hypoTN
Ca Channel Blockers BOTH DI/NON!
Block L-type decr Ca influx VD increased blood flow increased O 2 supply
Use if contra to beta-blocker Adjunct to beta-blocker
SE: above + peripheral edema, hypoTN
REDUCE LIPID LEVELS
Drug MOA Place in Therapy Clinical Pearls Statins Simvastatin Atorvastatin Rosuvastatin Pravastatin Lovastatin
Inhibits HMG-CoA reductase thus preventing synthesis of cholesterol lowers LDL
Tx to goal LDL in “30s” Hi risk CAD < CAD/DM < No CAD/DM+2RF < No CAD/DM+1RF <
SE: rhabdomyolysis/myopathy CYP3A4 system many DDI decreases mortality in ACS
LOWER OVERALL CV RISK
Drug MOA Place in Therapy Clinical Pearls ACE (-) See above decreases mortality in post-MI/CAD AngiotensinRBlock Self-explanatory Use if s/e to ACE (-) Eplerenone decreases mortality in post-MI Ranolazine indirectly prevents Ca overload less ischemia
Still undefined Used in refractory stable angina
Case 48y African American F, no PMH BP = 150/90 (Stg 1), SCr = 1.5, K= No compelling indications + AA + cheap/easy = HCTZ
Dobutamine Beta R agonist (b1 increases cardiac contractility, b decreases blood pressure)
Emergency IV ionotropes improve sx and are only temporary (e.g. use while waiting for transplant)
Milrinone PDE(-) no breakdown cAMP increased muscle contract
Emergency As above
Nitroglycerine VD HTN emergency Nitroprusside Nitrite bound to cyanide VD HTN emergency Cyanide or thiocyanate toxicity Nesiritide BNP analog Rarely used Trial found increased mortality
PRESSORS (SBP<90 w/o hypovolemia, i.e. cardiogenic/septic shock, SHORT TERM ONLY!!! ) Drugs MOA Effects Dopamine Low – dopamine R Med – dopamine/beta R High – dopamine/beta/alpha R
Low VD Med b1 stimulation (increased HR/contractility) High a1 stimulation (increased SVR/BP/afterload) Epinephrine b1, b2 stimulation Increased CO/SVR NE alpha stimulation Increased SVR
OTHER
Drugs MOA Place in Therapy Clinical Pearls Amiodarone Dofetilide
Antiarrhythmials CHF + atrial fibrillation
Amlodipine AntiHTN/antianginal CHF + HTN/stable angina Warfarin Anticoagulant CHF + CAD/afib/etc Efficacy not proven
HIGH YIELD
Adriamycin Can cause drug-induced dilated cardiomyopathy Anterior infarction LAD, leads V1-V Aschoff bodies Dx nodules of rheumatic fever Atrial fibrillation NO S4!!!! Can’t hear sound that reflects atrial contraction if there IS NO atrial contraction Buerger dz Small/medium vasculitis of young male smokers C-ANCA Wegener’s granulomatosis Caravello’s sign holosystolic murmur that increases w/ inspiration, seen in tricuspid regurgitation Chagas dz Infxn Trypanosoma that can lead to myocarditis Cheyne-Stokes respirations Cyclic pattern of respirations w/ increasing breaths followed by apnea, seen in CHF Commissural fusion Dx of rheumatic heart disease Concentric hypertrophy Increased thickness:vol, due to pressure overload Coxsackie B Myocarditis Cystic medial degeneration Seen in Marfans pts w/ dissecting aneurysm Delta wave Shortened PR segment seen in Wolfe-White-Parkinson Diastolic murmur, blowing decres Aortic regurgitation Diastolic murmur, rumbling Mitral stenosis Dressler syndrome 2-10w postMI fibrinous pericarditis, due to autoAb Eccentric hypertrophy Normal thickness:vol (both dilation & hypertrophy), due to volume overload Ejection click Aortic stenosis Eisenmengers RL shunt that results from untreated LR shunt, see cyanosis Ewarts sign decreased breath sounds in L post lung due to compression by enlarged pericardial sac Friction rub Fibrinous pericarditis Globoid heart Dilated cardiomyopathy Hypercyanotic spells Seen in Tetralogy of Fallot, sudden increase in RL shunting causes cyanosis/syncope Inferior infarction RCA, leads LII, LIII, AVF James bundle Accessory pathway in LGL = no PR interval w/ P-QRS-T right in a row Janeway lesions Non-tender nodules in palms/soles, suggestive of infectious endocarditis Kaposi sarcoma Vascular sarcoma seen in AIDS pts Kussmaul’s sign JVP increases w/ inspiration, seen in constrictive pericarditis and hypertrophic CM Lateral infarction LCF, leads LI, AVL Lewis index Height of LI R wave + depth of LIII S wave >25mm, + for LVH Mid-systolic click Mitral valve prolapse
Opening snap Mitral stenosis Osler nodes Tender nodules in palms/soles, suggestive of infectious endocarditis P-ANCA Microvascular polyangitis Pulsus paradoxus Exaggerated decrease of SBP during inspiration (>10mm), seen in pericarditis/tamponade Pulsus parvus et tardus Pulse is weak and later than normal, seen in aortic stenosis PVC a premature beat, hidden P wave + huge QRS + pause, due to ischemia R on T PVC falls on middle of T wave, bad b/c ventricle is vulnerable to developing VT Roth spots Retinal hemorrhages w/ central white spot, suggestive of infectious endocarditis S3 Rapid ventricular filling, heard in CHF/mitral regurg S4 Atrial contraction into stiff LV, heard in AS/HTN/hypertrophic cardiomyopathy Septic emboli/infarct Acute bacterial endocarditis Sick Sinus Syndrome SA node dysfxn + failure of all supraventricular automaticity foci bradycardia Sokolow index Height of V5 R wave + depth of V1 S wave >35mm, + for LVH Systolic murmur, harsh cres/decres Aortic stenosis Systolic murmur, holosystolic Mitral regurgitation Transition Zone +/- deflection of R wave is equal, usually at V3/V
After 938575 hours of trying to figure out the murmurs w/ Chris, this is what we boiled it down to. I know it doesn’t actually make any sense, but I really don’t care anymore.
Aortic Stenosis Pure AS concentric LV hypertrophy Mitral Stenosis Pure MS eccentric LA hypertrophy, LV is unchanged
Dr. V’s 5 basic principles of regurg state:
- “ Regurg causes a volume overload of the chambers proximal and distal to the leaking valve.”
- “The atria/ventricles must pump the normal amount of blood plus the regurgitant blood increased preload.”
- “The response to an increase in preload is eccentric hypertrophy – both dilation and hypertrophy.”
THUS…
Aortic Regurgitation Pure AR eccentric LV hypertrophy + systemic VD (i.e. the distal dilation) Mitral Regurgitation Pure MR eccentric LA AND LV hypertrophy
