Professional Documents
Culture Documents
RV 25 5
Pulm a 25 10
LA ------- 10
LV 120 10
a. LA (aka PCWP or pulmonary capillary wedge pressure where balloon floated to block RV outflow tract, effectively determining
the pressure on the other side of the pulmonary circulation, the PVP (pulmonary venous pressure) which is equal to LA
pressure which in turn determines the magnitude of the EDV in the LV)
b. During diastole, pressures in the atria/ventricles should be equal, since the AV valves are open
c. O2 sat should be about 75% in RA/RV/pulm a and 100% in PCWP/pulm v/LA/LV (important when determining shunts)
5. Resistance = mean pressure gradient / mean flow in dynes·sec·cm-5 or Woods units
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 40-90
6. Shunts
a. If LR, see increase in O2 in right heart; if RL, 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. Eisenmenger’s Syndrome
i. LR shunt causes pulm congestion/↑PVR which causes right-sided hypertrophy until eventually the pressure is
greater in the R heart than the L heart and the direction of the shunt switches to a RL shunt
7. Hypertrophy
a. An increase in myocyte volume (more sarcomeres/mito) in response to chronic abnormalities of wall stress
b. Reactive hypertrophy is non-pathological and usually affects all chambers (myocardial work NOT increased)
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 to 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)
iv. Cardiac work maintained at elevated level
e. Clinical consequences of hypertrophy
i. Increase in collagen decrease in compliance
ii. Hypertrophy faster than capillary growth perfusion deficit/reduced coronary reserve
iii. Decreased myosin ATPase activity impaired contractility
8. Remodeling – refers to LV volume ↑ and shape change in Pts w/ acute MI due to slippage of myocytes in days following MI
9. Failure
a. Circulatory failure – insufficient oxygen delivery to tissues (may be independent of heart function)
b. Heart failure – insufficient pump function (may be myocardial failure, valve rupture, etc)
c. Myocardial failure – insufficient myocardial contractile function
i. Not every Pt in myocardial failure is in heart/circulatory-failure (which always have systemic adaptations) b/c of
compensation, usually via 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 (flat Frank-Starling curve) so ↓EF + poor response to ↑ afterload
10. Aging
a. Normal changes: lipofuscin, protein x-linking w/ glucose, oxidative damage, decrease VO2 max (O2 consumption)/max
HR/A-V 02 diff, decrease SV (thus an increase preload to maintain CO), impaired β-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. High glucose x-links proteins (caramelization) → reduced elasticity
iv. Earlier return of reflected pressure wave adds resistance (i.e. increases afterload) to LV → hypertrophy and
stiffening
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1. As LV contracts, young compliant aorta stretches/stores potential energy and remaining energy generates
the pulse wave velocity that pushes blood thru the systemic circulation. In old person where aorta
stretches less and less LV contraction energy stored in stretched wall as potential energy, more energy
converted to pulse wave velocity so blood moving faster/reflected back faster at aortic valve.
2. More common for reflected wave to reach aortic valve while it’s still open in women b/c aorta shorter
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 LV EDP > increase LA size > a-fib, (2) increase in 02 demands > ischemia, (3) impaired diastolic fxn > CHF
CORONARY PHYSIOLOGY
1. Blood supply of the heart
a. RCA: supplies inferior/right heart, courses in right AV groove, can give rise to conus artery
b. LCA: branches into…
i. Left anterior descending (LAD) – supplies anterior/apical heart, courses in anterior IV groove
1. Gives rise to diagonal branches 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
1. Gives rise to marginal branches 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 meaning that RCA gives rise to PDA
iii. 10% are left dominant where LCF continues to crux and gives rise to PDA
d. Anterior papillary m = LAD/LCF, posterior papillary m = LCF/RCA (poorer supply than anterior)
i. postero-medial papillary m of mitral valve only supplied by PDA so MI involving PDA can cause mitral regurg
e. Venous return from coronary blood flow
i. Thebesian veins drain blood feeding RV into RV (small w/ little flow)
ii. Anterior cardiac veins drain RV into RA (intermediate size)
iii. Coronary sinus drains 85-90% of blood feeding LV to RA; in left AV groove
2. 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 (wall stress), contractility will increase demand
c. Increased coronary perfusion pressure/decreased resistance will increase supply (remember: Q = P/R)
3. Factors which regulate coronary blood flow:
a. Anatomic:
i. Perfusion pressure drop when epicardial coronaries branch/pierce myocardium to feed subendocardium ↓ in flow
ii. Collateral vessels can provide additional routes for flow in atherosclerosis if occlusion is gradual
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 + ↑ O2 demand VD of sub-endo vessels
iii. VD in sub-endo allows for homogenous blood flow but decreases VD reserve = ↑ risk of ischemia
c. Autoregulation: can refer to maintenance of flow/perfusion across myocardium despite changes in resistance throughout
thickness or to maintenance of flow over wide range of perfusion pressures
i. Vessels decrease resistance via VD using “vasodilatory reserve”
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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 (also acidosis, CO2, prostaglandins)
i. Metabolic vasodilation is predominant mechanism controlling coronary blood flow in normal heart and is driven by
O2 consumption demands of myocardium
ii. However, when atherosclerosis results in obstruction of coronary flow, hydraulic/anatomic/neural/humoral factors
assume much greater importance
e. Neural: net effect sympathetic tone is VD (β2 outweighs α )
i. β2 cause vasodilation (isoproterenol) while α 1/2 cause vasoconstriction (clonidine, methoxamine)
f. Humoral: intact endothelium helps regulate vascular tone and coagulant state
i. NO will VD normal vascular SM via guanylate cyclase activation, nitroglycerine will work even if endothelial cells
damaged b/c is metabolized to NO in SM cells
1. NO and platelet-derived prostacyclins inhibit platelets and VD
2. Both HTN and atherosclerosis impair NO release by endothelium
ii. Endothelin-1 causes VC and is stimulated by thrombin/angiotensin II/epi
iii. ACh will VD normal endothelium by ↑NO but VC if it’s damaged (i.e. in HTN/atherosclerosis) by causing
direct VC or vascular SM
4. Ischemia = inadequate perfusion/flow occlusion low tissue O2 (hypoxia) and inadequate waste removal angina
i. Atherosclerosis pressure gradient across the lesion (lower P distally) decreased flow compensatory VD of
distal vessels increases flow at the expense of VD reserves
ii. Eventually vessels are max VD, so in periods of high O2 demand, perfusion pressure is insufficient ischemia
iii. Fixed stenotic lesion >70% = ischemia w/ exercise, if >90% = ischemia at rest
b. Metabolic consequences: decreased HEP (high energy phosphate → ATP and creatine PO4 stores), activation of anaerobic
glycolysis w/ production of lactate (heart usually takes up lactate but here it produces it)
c. Fxn’al consequences:
i. ↓systolic contraction w/in seconds of ischemia onset (get hypokinesis (uniform shortening↓)/akinesis (no
shortening)/dyskinesis (paradoxical lengthening) effects on myocardial fiber shortening w/ ↑ing decrement in blood
flow) and ↓ diastolic relaxation (get ↓ compliance) result in lower coronary perfusion gradient
ii. Myocardial stunning: reversible loss of fxn/contractility due to acute ischemia → fxn returns days post-reperfusion
1. Often seen after thrombolytics given for an MI (flow re-established by function lags behind)
iii. Myocardial hibernation: reversible loss of fxn due to chronic ischemia where fxn returns immediately post-
reperfusion
iv. <15-20 min of ischemia is normally reversible (attack of angina)
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 (0.3-1 m/s) and Purkinje fibers (1-4 m/s)
ii. Slow response = SA/AV node (0.02-0.1 m/s)
1. SA node is intrinsic pacemaker (60-100) due to overdrive suppression of slower automaticity foci
a. In upper posterior wall of RA
2. AV node is sole structure capable to conduct depolarization to ventricles
f. Depolarization is a wave of positive charges contraction
g. Repolarization is a wave of negative charges relaxation (at rest, negative intracellular charge)
2. Logistics
a. Paper
i. Horizontal is time, small sq = 0.04s, large sq = 0.2s, 5 large sq = 1s
ii. Vertical is deflection, small sq = 1mm (amplitude) = 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) -+-++- clockwise from top L
1. LI: R arm negative, L arm positive (+0°)
2. LII: L foot positive, R arm negative (+60°)
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6. Heart rate
a. = # of QRS complexes per minute
i. Look for R wave peaking on line of big square
ii. Rate is approximated # of big squares to next R (300, 150, 100, 75, 60, 50)
iii. In cases of slow or irregular heart rates, count how many QRS complexes w/in 6 seconds (30 large sq), then x10
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b. Overdrive suppression is mechanism by which faster beating pacemakers take priority to alternative automaticity foci
i. SA node pacemaker gives a “sinus rhythm” of 60-100bpm
1. Sinus tachy/brady is when rate is fast/slow but the heart is still under control of the SA node
ii. Atrial automaticity foci rate = 60-80bpm
iii. Junctional automaticity foci rate = 40-60bpm
iv. Ventricular automaticity foci = 20-40bpm
7. Mean QRS axis
a. Determination
i. Look at QRS complexes in LI and AVF
ii. Look for most biphasic QRS complex of limb leads and move from that lead’s postion 90° in the direction of the
quadrant identified above to determine more exact mean QRS axis
b. Clinical relevance
i. Tall/thin individuals – vertical heart (not pathological), apex points at 90°
ii. Obese individuals – horizontal heart (not pathological), apex points at 0°
1. So, if see biphasic QRS complex in LI or AVF, consider it as + so as not to assume an axis deviation when
in fact you simply have one of the above 2 normal variants (must really be – to say it’s -)
iii. Hypertrophy – enlarged heart dominates = deviation of axis toward hypertrophied chamber
iv. Myocardial infarction – infracted area loses electrical activity = deviation of axis away from infarct
8. Hypertrophy
a. Atrial = split P wave in LII, uneven biphasic P wave in V1 (<2.5mm)
i. In atrial dilation, larger chamber will become predominant over the other atrium, thus a splitting of the P wave
1. Amplitude of one of the phases is predominant (first – R ; second – L) in V1
ii. Normally atria contract together and P wave is a continuous hump
1. If one is hypertrophied, P hump will have an added bump (first – R ; second – L) in LII
b. RV hypertrophy
i. Huge R wave in V1 (tends to be bigger than S wave)
ii. Right axis rotation (DIFFERENT than deviation) – R wave transition zone moves to V1/V2
c. LV hypertrophy
i. Precordial leads – see deep S in V1 and tall R in V5
1. Dx of LVH by Sokolow index = height of V5 R wave + depth of V1 S wave >35mm
ii. Limb leads – see deep S in LIII and tall R in LI
1. Dx by LVH by Lewis index = height of LI R wave + depth of LIII S wave >25mm
iii. Ventricular strain, often associated with LVH, characterized by ST depression/ inverted T wave in V5/V6
9. Infarction
a. Three Stages to STEMI (ST segment Elevation acute MI)
i. 1st stage – T wave peak/T wave inversion (first 10 min of MI)
ii. 2nd stage – ST segment elevation (first 15 min of MI) – most commonly seen in ER depts
iii. 3rd stage – appearance of Q waves, which never disappear, thus a sign of previous infarction
1. Q waves are longer (˃0.04s) and at least 1/3 amplitude of R wave of same complex
b. Localization
i. Anterior infarction – V1-V4
ii. Lateral infarction – LI, AVL
iii. Inferior infarction – LII, LIII, AVF
iv. Posterior infarction – No leads, thus invert and look at mirror image, then should see ST elevation in V1, V2
c. Pericarditis differs in that there are NO Q waves and diffuse ST elevation (multiple leads)
10. Ischemia resulting in angina
a. ST segment depression often associated with T wave inversion
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ARRYTHMIAS
1. Arise from impaired initiation (SA node dysfxn), anomalous initiation (ectopic foci), impaired propagation (AV/His dysfxn)
2. 3 main mechanisms:
a. Enhanced automaticity: β1 stimulation, hypokalemia, hypoxemia, ↑ stretch due to ↑preload or mitral valve prolapsed
make slope of slow diastolic depolarization steeper such that HR increases
b. Triggered automaticity: abnormal depol interrupts normal cardiac AP (EADs and DADs)
i. DADs due to intracellular Ca overload and ↑HR
ii. EADs due to marked prolongation of AP
c. Reentry (most common): can be anatomical (due to accessory pathway connecting atria and ventricles as in Wolff-
Parkinson-White or WPW) or fxn’al (due to slow conduction region such as infarct)
3. Sinus “arrhythmia” is slight variation in R-R interval due to inspiration, otherwise…
4. ALWAYS ALWAYS ALWAYS have a continuously varying R-R interval, this is the definition of an arrhythmia
a. Ablation is curative for many types of arrhythmias (surgical removal of tissue causing the problem)
5. Irregular rhythms (atrial ectopic foci)
a. Wandering pacemaker: pacemaker activity wanders from SA node to atrial foci
i. P’ waves (not from SA node) of different shapes, rate <100, irregular ventricular rhythm (continuously varying R-R)
b. Multifocal Atrial Tachycardia: same as WP
i. Same as WP but rate >100, assoc w/ COPD due to chronic hypoxia
c. Atrial Fibrillation: multiple atrial foci with very rapid rate
i. No complete atrial depol b/c of rapid rate, thus no P waves, only a segmented baseline
ii. AV node acts as a filter to allow only a few impulses to depol ventricles = protective (still irregular R-R)
6. Escape (SA node failure)
a. Escape rhythm is when SA node fails completely alternative automaticity focus escapes and paces at its inherent rate
b. Escape beat is when SA node fails transiently alternative focus produces single escape beat before restart of sinus rhythm
i. Atrial escape: pause + P’ waves with varying morphology + normal QRS; inherent rate 60-80
ii. Jxn escape: pause + no P wave + normal QRS; inherent rate 40-60
1. Jxn beat MAY produce retrograde atrial depol, seen as inverted P’ wave
iii. Ventricular escape: pause + no P wave + huge wide QRS; inherent rate 20-40
1. Due to complete failure of SA node + atrial/jxn foci OR 3rd degree AV block
2. QRS becomes wide when ventricle depolarization via regular myocytes rather than Purkinje fibers
3. May cause cerebral hypoperfusion (Morgagni-Adams-Stokes) and episodes of syncope
7. Premature beats (irritable foci) – atrial, junctional, and ventricular types
a. A beat is generated earlier than expected in the normal rhythm due to an irritable focus
b. PAB (premature atrial beats): 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 refractory 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 w/in QRS) + 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
1. PVCs caused by ischemia/hypokalemia/anti-arrhythmic drugs/mitral valve prolapse (MVP)
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 systole local ischemia activation of irritable foci)
1. More common in women
e. Any of the premature beats can occur in bigeminy/trigeminy/quadrigeminy (repetitive pattern w/ premature beats dispersed
after given # of regular sinus beats)
8. Tachyarrhythmias (sudden series of very fast beats)
a. Paroxysmal Tachycardia = rate 150-250
i. Paroxysmal Atrial Tachycardia: P’ wave followed by QRS-T
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ii. PAT w/ AV Block: two P’ waves followed by QRS-T, think digitalis toxicity esp. if hypokalemic
iii. Paroxysmal Jxn Tachy: no P wave (or inverted P’ if retrograde atrial depol) followed by QRS-T, may involve reentry
iv. PAT/PJT (aka supraventricular tachy or SVT) 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 (Lown-Ganong-Levine): James bundle is the accessory pathway no PR interval w/ P-QRS-T right in a row
vii. Paroxysmal Ventricular Tachy or simply VT: no P wave (hidden) + huge QRS (>0.14s), basically a run of PVCs
1. SA node continues to pace normally and occasionally, an atrial depol ventricular depol, seen as normal
QRS within all the crazy PVCs (capture beat) or normal QRS fused w/ PVC (fusion beat)
b. Flutter (single foci) = rate of 250-350
i. Atrial flutter: still get complete atrial depol→ seen as series of P’ waves (sawtooth), every 3rd one depol vent
ii. Ventricular flutter: still get complete vent depol→ seen as series of smooth sine waves
1. Despite depol, the rate is too high to eject blood decreased coronary perfusion ischemia multiple
irritable foci ventricular fibrillation (type of cardiac arrest requiring CPR and defibrillation)
c. Fibrillation (multiple foci) = rate of 350-450
i. Atrial fibrillation: no identifiable P waves, jagged baseline w/ a few QRS
ii. Ventricular fibrillation: totally erratic
9. Blocks
a. Sinus block: temporarily fails to fire dropped beat w/ pause (maybe escape beat)
i. Sick Sinus Syndrome (SSS): SA node dysfxn + failure of all supraventricular automaticity foci marked sinus
bradycardia (sometimes w/ intermittent episodes of SVT)
b. AV Block: slow/eliminate conduction from atria to ventricles
i. 1st degree block: prolonged PR interval >0.2s, usually benign
ii. 2nd degree block:
1. Wenckebach (AV node affected): progressively lengthening PR interval until P wave is not followed by a
QRS complex, then restarts (QRS complexes normal)
2. Mobitz (Purkinje fibers affected): some P waves just don’t make it to ventricles (normal PR w/ wide QRS)
a. conduction ratio - # of P attempts:# of conducted beats; ex: 3:1 means 2 blocked/ 1 conducted
b. pathological, must Tx w/ pacemaker (vs. Wenkebach, which is benign)
iii. 3rd degree block: complete block of SA impulse (P waves still regular!), QRS escape rhythm is 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
2. RBBB complexes (NOT pathological) seen in V1/V2
a. Brugada Syndrome – familial condition caused by dysfunctional Na channels
i. RBBB assoc w/ ST elevation in V1-V3 w/o coronary occlusion
ii. Causes ~50% sudden death in healthy people w/o structural heart dz
iii. Need implant device to detect VT/VF and deliver shock
3. LBBB complexes are seen in V5/V6 and indicate cardiac ischemia
11. Steps to EKG Interpretation
a. Rhythm
i. P waves present? Look at LII (max +) and V1 (biphasic)
ii. Is QRS wide or narrow/normal?
iii. Is the rhythm regular or irregular
iv. Is the relationship of P to QRS regular?
b. Rate
c. Mean QRS Axis
i. Look at LI and AVF for quadrant
ii. Find most biphasic limb lead and move 90° toward quadrant identified
d. Intervals (PR, QT, QRS)
e. AV Blocks (PR elongation or T drop)
f. BBBs
g. Hypertrophy
h. Ischemia
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HEART SOUND/MURMURS
S4 S1 S2 S3 S4 S1
S2 Aortic/pulmonic valve closure Diaphragm, over Physiologic splitting: pulmonic closes later due to ↑ RV ejection time
entire precordium b/c of ↑ venous return during inspiration (single during expiration)
Pathologic splitting: wide fixed = ASD, narrow fixed = pulm HTN*,
Normal splitting of reverse split = left BBB, aortic stenosis (closes so late its after P2)
P2 heard only over
pulm valve* *with pulm HTN, can hear elsewhere
S3 Sudden distention of Use bell, at apex Considered normal in young, healthy pt
ventricles during rapid filling Always abnormal if pt >50, assoc w/ heart failure, mitral regurg,
Early diastole VSD (high flow across open valve)
“Ken-tuc-ky”
BBB= bundle branch block
Clicks
Ejection Opening of stenotic or Over involved valve Assoc w/ bicuspid aortic valve or aortic stenosis
deformed semilunars Directly after S1
Opening snap Opening of stenotic Diaphragm, at apex Assoc w/ mitral stenosis
mitral valve Directly after S2
Mid-systolic Sudden tensing of At apex Assoc w/ mitral valve prolapse
deformed mitral @ start of murmur
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valve
Knocks Sudden tensing of the At apex Assoc w/ constrictive pericarditis or restrictive cardiomyopathy
pericardium during Early diastole (same
rapid filling as S3)
Bruits Turbulent flow due to Heard over affected Assoc w/ vascular stenosis
stenosis blood vessels
Rubs
Pericardial Inflamed serosal At apex Assoc w/ pericarditis
surfaces rubbing Described as “squeaky leather”
together
Thrills Flow obstruction Vibrations felt during systolic flow; assoc w/ aortic stenosis
MURMURS BY TIMING
Sound Causes Notes
Systolic Aortic/pulmonic stenosis Between S1S2
Mitral/tricuspid regurgitation
holocystolic Mitral regurgitation Blowing (w/ mid-systolic click if also MVP)
VSD 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 2nd 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 Between S2S1
Mitral/tricuspid stenosis
early Aortic regurgitation High-pitched decrescendo (sounds like someone breathing out hard)
Best heard w/ bell in 2nd 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 From uninterrupted flow of high P/R to low P/R w/o phasic
Arterio-venous connections (AV fistula) interruption
Extremely loud murmurs
MURMURS BY CAUSE
1. A primer on Rheumatic Heart Dz
a. Post-group A β-hemolytic strep sequela
b. Due to Abs to bacterial proteins (SLO and strep DNase B) that resemble proteins of the human heart
c. Acute rheumatic fever w/ Sx onset several wks after strep throat
i. Pancarditis
1. Aschoff bodies (foci of swollen degenerated collagen surrounded by lymphocytes/plasma cells/MØ
and caterpillar cells)
2. Fibrinous pericarditis (“bread and butter”)
3. MacCallum plaques (subendocardial thickenings) and small vegetations along valve closure lines/cusps
ii. Migratory polyarthritis of large joints
iii. Subcutaneous nodules
iv. Erythema marginatum
v. Sydenham chorea
d. Chronic RHD
i. See commissural fusion resulting in “fishmouth” or “buttonhole” valvular stenosis, esp. mitral valve
ii. See shortening of chordae tendinae
iii. See neovascularization and fibrotic valvular deformities
iv. See hypertrophy and/or dilatation of chambers pushing against stenotic valves
2. 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 maintained
d. Heart sound: ejection click (if aortic cusps mobile) followed by harsh crescendo-decrescendo systolic murmur + S4
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
1. no Sx = no limitations
2. pressure gradient >30 but no Sx = exercise limitations/avoid diuretics
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VASCULAR DISEASE
1. Arteriosclerosis has 3 varieties
a. Athero- and arteriolo- sclerosis (2 of 3) discussed separately
b. Calcific Medial Sclerosis (Monckeberg Dz)
i. Deposits of Ca w/in media of small/medium muscular arteries
ii. Usually incidental and w/o Sx
2. Arteritis or Vasculitis = inflammation of arteries due to direct infxn, immune response, or unknown causes, and are systemic
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a. Auto-immune responses due to ANCAs (anti-neutrophil cytoplasmic Abs) w/ immune complex deposition
i. P-ANCA = perinuclear ANCA = Ab against MPO (microscopic polyangitis)
ii. C-ANCA = cytoplasmic ANCA = Ab against proteinase-3 (Wegeners)
b. May also see auto-immune rxn to endothelial cells (Kawasaki)
c. Affecting elastic main arteries
i. Temporal Arteritis – segmental vasculitis of temporal/ophthalmic/carotid a. branches, F>50 w/ acute loss of vision;
biopsy shows giant cells/granulomatous inflamm disrupts int elastic lamina →fibrosis/luminal narrowing
1. steroid responsive
ii. Takayasu Arteritis (“pulseless dz”)– vasculitis of aortic arch and its major branches, F<40 w/ cold fingers, weak
upper extremity pulses, visual deficits, aortic regurg, etc; biopsy shows giant cells/ granulomatous inflamm
throughout thickness of vessel wall/aortic root dilation/narrowing of ostia/luminal narrowing
1. NOT steroid responsive unlike the other 2 granulomatous vasculitides
d. Affecting medium/small arteries
i. Wegeners Granulomatosis – necrotizing granulomas in vessels of resp tract/kidneys, 40-50y M w/ (+) C-ANCA,
1. steroid responsive
ii. Polyarteritis Nodosa – affects kidney/GI/heart (NOT lung), transmural focal/episodic vasculitis infarction/
thrombosis, biopsy shows fibrinoid necrosis (immune complexes deposited in artery so complement comes and
destroys the vessel wall making it leaky to fibrinogen); young adult w/ episodic fever/malaise/myalgia
1. steroid responsive
iii. Thromboangiitis Obliterans (Buerger dz) – recurrent vasculitis in radial/tibial art lead to obliterative thrombi and
inflammation affecting adjacent veins and nerves, 25y M smoker w/ severe pain at rest & gangrene
e. Affecting arterioles/capillaries/venules
i. Microscopic Polyangiitis – rxn to Ag (drugs, microbe) see leukocytoclasia (fragmented PMNs), vascular lesions of
same age, present w/ hemoptysis/hematuria/palpable purpura & (+) P-ANCA, responsive to removal of Ag
f. Affecting coronaries
i. Kawasakis Disease – young child w/ acute febrile illness cardiac complications due to anti-endothelial cell Abs,
present w/ 5 classic sx: fever, non-purulent conjunctivitis, palm/sole erythema, desquamation, peripheral edema
g. Affecting Veins
i. Varicose veins due to chronically high pressure and poor wall support (usually NO thromboembolism)
1. Commonly superficial veins of lower extremeties (cosmetic other than poor drainage of area)
2. Submucosal varicose veins can bleed fatally
ii. Thrombophlebitis and Phlebothrombosis of deep veins of legs due to stasis and hypercoagulability
1. Can lead to pulmonary thromboembolism in addition to leg edema and tenderness
h. Affecting Lymphatics
i. Lymphangitis and Lymphadenitis where bacterial infxn causes vessel/node inflammation
ii. Lymphedema where obstruction of vessels/nodes leads to proximal dilatation and edema of affected area
3. Aneurysms = abnormal focal dilatation of vessel, usually artery
a. True aneurysms are dilatation of intact vessel wall
i. Saccular subtype is focal/spherical/vascular outpouching and is usually more surgically-resectable b/c it involves
only part of the vessel wall, not entire circumference
ii. Fusiform subtype is linear dilatation involving entire circumference of vessel (most AAAs)
b. False aneurysms are collections of extravascular blood that is contained from rupture only by CT
c. Atherosclerotic – most common, fusiform type, M>40 w/ subrenal AAA (abd aortic aneur), rupture = death, Tx by graft
d. Syphilitic – fusiform type, ischemic destruction of elastic tissue of thoracic aorta (aka tree barking) due to obliterative
endarteritis of the vasa vasorum vessels (by lymphocytes and plasma cells) that feed large arteries
i. Unlike atherosclerosis, usually affects aorta at its root (dilatation of aortic arch) aortic regurg
ii. See ribbon-like effect on aortic intima w/ alternating bulges into lumen that can cause turbulence/↑thrombus risk
iii. Complications include aortic insufficiency due to dilatation of aortic valve ring, superimposed atherosclerosis leading
to narrowing of coronary art ostium/ischemic heart dz, and compression/erosion of adjacent structures
e. Dissection– transverse intimal tear in proximal aorta (usually near aortic valve) dissection of blood down laminar plane
b/w inner 2/3 and outer 1/3 of aortic wall death w/o surgery
i. Either 50yo M w/ HTN (not assoc w/ atherosclerosis) or Pt w/ CT abnormality (Marfans/Ehlers Danlos) w/ acute
onset excruciating chest pain
ii. Cystic medial degeneration more common if CT abnormality (replacement of elastic tissue w/ ECM)
iii. Classification
1. Type A (proximal) are most common and involve ascending aorta +/- descending aorta
2. Type B (distal) only involve descending aorta beyond branching of L subclavian art
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4. Vascular Tumors
a. Benign
i. Vascular ectasias (dilatations) present in skin/mucosa
1. Congenital = nevus flammeus
a. Flat reddish-purple rgns on head/neck that usually regress
b. Larger port wine stains, which often enlarge rather than regress
2. Acquired = spider telangiectasia assoc w/ ↑ E2
3.
ii. Hemangioma = blood filled cap
1. Capillary subtype are red/blue spongy lesions that often spontaneously regress
2. Cavernous subtype are reddish-blue spongy honeycomb mass
a. Dilated caps filled w/ blood or thrombi but endothelium normal
b. Generally do NOT regress
iii.Lymphangiomas (capillary and cavernous subtypes)
1. Capillary looks like blisters
2. Cavernous usually in neck (cystic hygroma) and will require surgery
b. Malignant
i. Kaposi’s sarcoma – classic/endemic/epidemic (in immunosuppressed) forms, see nodular reddish-purple lesions
1. Classic (chronic) is indolent dz affecting distal extremeties of old Mediterranean men
2. Endemic is aggressive and involves lymph nodes (Africa)
3. Immunosuppression-related (HIV) affects multiple organs
ii. Angiosarcoma – affects skin/soft tissue/liver (assoc w/ PVC/Thorotrast/arsenic exposure)/and breast
1. Assoc w/ chronic lymphedema and radiation
2. Poorly-circumscribed soft invasive mass
3. Very POOR Px
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f. Identifiable causes include sleep apnea, drugs, chronic kidney dz, primary aldosteronism, thyroid dz, cushing’s, coarc aorta,
etc
g. Classification:
i. Primary or essential HTN (majority)
1. Genetics/family hx and environmental factors contribute
ii. HTN secondary to another condition such as pregnancy/pheochromocytoma/coarctation of aorta/endocrine
dysfunction or, most often, renal dz w/ chronic activation of the renin-angiotensin-aldosterone system
1. Atherosclerosis +/- superimposed thrombus at origin of renal artery (common in old men) will cause
kidney to perceive hypovolemic state (I’m not getting enough blood!) and to activate renin-angiotensin
system
2. Fibromuscular dysplasia can occur anywhere along renal a (common in young women) w/ same result
3. Note that the kidney on the affected side suffers diffuse ischemic changes, but it’s the kidney on the
contralateral side, the one that has to compensate, that experiences more severe arteriolosclerosis/HTN
effects
h. Complications
i. Vascular pathology resulting in ischemic organ damage
1. Atherosclerosis of large arteries (already discussed)
2. Arteriolosclerosis of arterioles and small muscular arteries
a. Hyaline form is most common
i. Leakage of plasma proteins into vessel wall w/ ↑ deposition of basement membrane
material and luminal narrowing (see diffuse pink thickening of wall)
b. Hyperplastic w/ fibrinoid necrosis can be seen w/ severe malignant HTN where DBP ˃130
i. small vessel injury leads to leakage of plasma proteins (including fibrinogen) and
thrombosis w/ release of GFs that lead to intimal hyperplasia/luminal narrowing
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7. 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
8. 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)
9. 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
10. 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
1. 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 outward
ii. Want to intervene before wavefront expands so that a greater portion of heart can be spared
11. 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
12. Complications of MI
a. Pump failure CHF, cardiogenic shock (low CO despite high preload, lethal)
i. ↓myocardial contractility or ↑ resistance to ventricular filling or ejection can cause CHF
1. L heart failure
a. Usually see dilatiation of LV then LA
b. Assoc w/ dyspnea/orthopnea/Paroxysmal nocturnal dyspnea/cyanosis/↓exercise tolerance
c. Here rales on exam due to interstitial pulmonary edema
d. See micro-hemorrhages (if chronic will see hemosiderin-laden MØ)
2. R heart failure
a. Usually secondary to L heart failure where lung becomes congested and ↑ pressure R side of heart
must pump against or significant lung dz (cor pulmonale)
b. Causes backward failure where see systemic congestion/pitting edema
b. Arrhythmias
c. RV infarction (inferior/posterior MI) shows signs of RV failure (ex: high JVP), often assoc w/ LV dysfxn
d. Rupture
i. If free wall, 3-5d postMI tamponade, death
ii. If IV septum L to R shunt, shock
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BLOOD PRESSURE/HTN
1. Epidemiology
a. 65million American, extremely common in population, higher in obese and AA women
b. Hypertension >140/90 or with complications (diabetes/renal insufficiency) >130/80
c. CV risk starts below hypertensive state
d. People at highest risk have large pulse pressure (high SBP and low DBP), which occurs as arteries lose elasticity
2. Determinants of blood pressure
a. Physical – blood volume (balance b/w SV input + output to high capacitance venous system) and arterial compliance (dV/dP)
b. Physiologic – cardiac output and peripheral arterial resistance (mainly @ level of arterioles)
c. Nuances
i. Ausculatory gap – silent gap between SBP/DBP, true systolic can be missed if pump up cuff to a point in that gap
ii. Pulsus paradoxus – pathological fall in SBP (>10) during inspiration, common sign in cardiac tamponade
3. Influence of peripheral vasculature
a. If CO and peripheral run-off are equal, BP is constant
b. Elasticity of aorta
i. Highly elastic aorta can dampen degree of SBP elevation per stroke volume by storing elastic recoil energy
1. Result is continuous perfusion in vasculature and heart can increase CO yet minimize work
ii. Distensibility, i.e. compliance, decreases with age or with diabetes, which widens PP
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1. Increase in pressure wave reflection increase in systolic + increase in run-off decrease in diastolic
iii. Central Aortic BP is typically lower than brachial a BP and is pressure that brain vasculature is exposed to
c. Importance of endothelial integrity
i. NO (from L-arginine via eNOS or endothelial NO synthase) acts correctly on healthy endothelium
1. Generates smooth muscle relaxation
2. prevents platelet adhesion
3. antagonizes angiotensin II–mediated vasoconstriction
ii. “endothelium dysfunction” (often in obesity/diabetes) causes ↑destruction/↓production of NO oxidative stress
4. Diurnal variation – BP follows circadian rhythm & is lower at night
a. Non-dippers (night BP doesn’t fall at least 10%) and hyperdippers (falls >20mm) = higher risk for pressure-related CV injury
5. Autoregulation – sigmoidal curve, thus perfusion is maintained within a range of blood pressures
a. NOTE: when BP rises, brain & kidney don’t VD to decrease resistance, rather they VC to slow down the flow, this is
protective!
b. Cerebral Blood Flow
i. As above, important b/c prevents ischemia (if BP falls) and edema (if BP rises)
c. Renal Blood Flow – mechanisms act to maintain the GFR
i. Myogenic reflex: increased afferent pressure aff VC lower flow, decreased afferent pressure aff VD more
flow
ii. Tubuloglomerular feedback: increased Na at macula densa (i.e. flow is hi) aff VC, decreased Na aff VD
iii. Local RAS activation: low Na (i.e. flow is lo) renin release angiotensin II efferent VC more flow
6. Obesity-related HTN is characterized by:
a. Increased sympathetic activity – insulin resistant visceral adipocytes release NEFAs into blood, which (1) increase a1
vasomotor tone and (2) decrease NO levels
b. Activation of RAS – angiontensin II Na reabsorption + aldosterone release more Na reabsorption. Thus, less Na is
sensed by JG inappropriate dilation of aff arteriole and eventual destruction of nephrons due to high glomeruler
pressures
c. Increase ECF – all the Na reabsorption leads to water retention too
d. Hypovitaminosis D/secondary hyperparathyroidism – Vit D3 is sequestered by adipocytes reactive rise in PTH
e. Increased Na sensitivity (i.e. requires higher pressure to rid sodium) kidney rises BP to stimulate naturesis
f. Pregnancy issues - obese mothers often have low birth wt/premature babies low # glom which lack autoregulatory ability
7. HTN and CARDIO complications
a. Increased hemodynamic stress plaque rupture
b. Increased stretch of vasculature RAS activation arterial remodeling/hypertrophy vessel narrowing ischemia
c. Increased stretch of vasculature also aneurysms
d. Increased afterload LV hypertrophy heart failure
8. HTN and RENAL complications
a. HTN is 2nd leading cause of end stage renal dz or ESRD (DM is 1st) and is also linked to chronic kidney dz
b. Nephron loss due to transmission of high SBP into the glomerulus
i. HTN afferent remodels and is fxn’ally incapable of maximally dilating loss of autoregulation
1. Autoregulation normally via myogenic reflex (constriction of afferent arteriole when SBP↑ to protect glom)
and tubuloglomerular feedback based on NaCl at macula densa in distal tubule (constrict w/ ↑NaCl)
ii. Now, relationship btw SBP/GlomP is close to linear, nephrons cannot tolerate such high pressures and die
iii. As # of nephrons declines, kidney relies on fewer nephrons to maintain GFR at necessary rate & has to compensate
1. Dilate afferent arteriole via prostaglandins and NO
2. Constrict efferent arteriole via angiotensin II (RAS = renin-angiotensin system)
3. Both lead to higher GlomP which perpetuates cycle
iv. Tx is ACEIs (or ARBs) which will decrease the SBP and thus the GlomP, slowing the damage
1. ↓ GFR ↑ sCr, but don’t take pt off ACEI!! Short-term rise in serum Cr due to ↓GFR is lesser of two evils
c. Ischemic kidney due to atherosclerotic blockage of renal artery(ies)
i. Unilateral RAS: renal hypoperfusion but NO compromised GFR or expanded intravascular volume
1. Contralateral kidney is fine and maintains GFR
ii. Bilateral RAS: renal hypoperfusion AND low GFR/expanded intravascular volume
iii. Both cause renal HTN refractory to anti-HTN Tx (bilateral much worse, though diuretics help w/volume overload)
1. ACEIs are contraindicated b/c they exponentially increase sCr irreversible injury
i. Normally autoregulated over wide range of perfusion pressures (sigmoidal curve w/ plateau from 50-150)
b. HTN right shift of whole curve, thus upper and lower limits of autoregulation (plateau rgn) are set at a higher overall BP
i. BP below lower limit of autoregulation max VD but still unable to maintain flow ischemia/stroke (can extract
more O2 from blood for little while w/ ↓perfusion so some cushion, but can’t maintain very long)
ii. BP above upper limit max VC but still unable to slow flow ↑ hydrostaticP edema/HTN encephalopathy
c. 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 (this region is called the ischemic penumbra where cells damaged but still viable)
ii. Instinct is to give anti-HTN meds to prevent edema, but that would worsen ischemia and cause greater infarct
iii. DO NOT give anti-HTN drugs unless SBP >230 or DBP ˃130
10. 2° hypertension
a. Hyperaldosteronism – increased aldosterone due to increased renin (usually tumor) increase Na reabsorption high BP
b. Pheochromocytoma - 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
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ENDOCARDITIS
1. Valve histology:
a. Very few blood vessels
b. Fibrosa = dense collagenous layer facing outflow force
c. Spongiosa = central core of loose CT w/ proteoglycans
d. Elastin-rich layer facing chamber receiving inflow (called atrialis or ventricularis)
2. Endocarditis = deposition of adherent thrombotic debris (vegetation) on the valves or mural endocardium
3. Infective Endocarditis (most serious type b/c destroy valve leaftlets and can lead to sepsis = medical emergency)
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 cause 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 (coagulase neg Staph epidermidis), IV drug use, catheters
4. 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 rheumatic fever), valve doesn’t have to be damaged for this to occur
c. Most commonly aortic/mitral valves
d. Don’t usually bother the valves but can throw emboli that cause infarcts
e. Predispositions = hypercoagulable states (think cancer pts), chronic diseases (think SLE, RA)
i. Libman-Sacks Endocarditis is assoc w/ SLE
1. Vegetations on AV valves, chordae tendinae, or endocardial surface
2. Thrombi adherent to areas of subendocardial fibrinoid necrosis/inflammation
ii. Carcinoid Heart Dz
1. Pts have carcinoid syndrome w/ wheezing, flushing, diarrhea due to 5HT released from abnormal
neuroendocrine cells
2. Endocardium of R heart thickened by accumulation of MPS-rich matrix w/ SM cells
3. L heart protected b/c 5HT is metabolized in the lungs
5. Prosthetic valves
a. Bioprosthetic (from pig) eventual deterioration of tissue
b. Mechanical (man-made) thrombi, hemolysis (metal parts cause sheer stress)
6. Clinical manifestations of endocarditis
a. Most common presentation:
i. Fever (possibly low and intermittent; present in 90%)
1. Suspect IE if fever present ˃1wk
ii. Murmurs (can be new, or a change in current)
1. Always regurgitation due to perforation/malcoaptation of valve
2. Ring abscesses, chordal rupture, shunts contribute
iii. Acute onset CHF due to regurg
iv. Bacteremia
v. Embolization of veg (esp if >1cm) septic infarct
vi. Constitutional sx like weight loss, night sweats, arthralgias
vii. *Various immune effects: petechaie, splinter hemorrhages (nail beds), Osler nodes (painful) and Janeway lesions
(non-tender) on palms/soles, 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*
1. Definitive IE = 2 major OR 1 major/3 minor OR 5 minor + histologic evidence from vegetation/emboli
2. Possible IE = 1 major/1 minor OR 3 minor
3. 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 = 2wk IV Abx ; high virulence = 4+wk IV Abx
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1. Amoxicillin or Clindamycin
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
1. 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
2. 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. Serous pericarditis, causes = noninfectious, thus scant inflamm cells seen in exudates
1. Closest one to a transudate
ii. Fibrinous pericarditis (most common), causes = acute MI, Dresslers (occurs wk-mo post-MI), uremia/renal failure,
SLE/RA (AI attack on heart), radiation
1. There is enough vascular permeability that fibrinogen leaks out (“bread and butter”)
2. Moderate # acute inflammatory cells associated w/ eosinophilic fibrinous exudates
3. Gives characteristic friction rub
iii. Suppurative pericarditis, causes = bacteria, thus tons inflamm cells seen in exudates + pus
1. See creamy white/yellow fluid and granular hyperemic pericardial surfaces
2. Commonly leads to constrictive pericarditis (chronic)
iv. Hemorrhagic pericarditis, causes = metastatic malignancy w/ angiogenesis, TB, bleeding disorder
v. Caseous pericarditis, causes = TB (usually only in AIDS pts)
1. See foci of crumbly white material w/in pericardial surfaces (necrotizing granulomas)
b. Clinical signs/Sx
i. Chest pain (palliative to lean forward), fever, tachycardia, dyspnea
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
iv. Potential lab changes = ↑WBC count, ESR, CK-MB and troponin
c. Tx w/ NSAIDS, steroids, colchicine (anti-inflamm alkaloid)
3. Chronic pericarditis
a. Adhesive pericarditis (common following serous or fibrinous acute pericarditis)
i. Residual strands of CT b/w visceral/parietal pericardial surfaces
b. Soldier’s Plaques = focal firm collagenous thickening of pericardium that become calcified
c. Constrictive pericarditis (common following suppurative or caseous acute pericarditis)
i. Pericardial space replaced by shell of dense fibrous/fibrocalcific CT that impairs diastolic filling
ii. Chronic inflamm + fibrosis thickening/adherence to mycocardium calcification limited diastolic filling ↓CO
iii. Most common etiology is post-cardiac surgery
iv. Present with signs of right heart failure (JVD, hepatomegaly, peripheral edema)
1. Kussmaul’s Sign = inspiratory ↑ in JVP
2. Pericardial Knock (early in diastole)
3. Fatigue/hypotension/tachycardia
v. If calcified, may require pericardiectomy where peel calcified tissue off of heart (10% die during surgery)
d. Adhesive mediastinopericarditis, causes = radiation/surgery involving mediastinum or suppurative or caseous pericarditis
i. Adhesion of parietal pericardium to mediastinum/surroundings ↑ cardiac workload hypertrophy/dilatation
4. Cardiac tamponade
a. Dependent on both the rate and volume of fluid collection
b. Rise in pericardial pressure and compression of cardiac chambers in diastole impaired diastolic filling decreased CO
c. Clinical signs/sx
i. Hypotension, reflex tachy, shock
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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/hepatomegaly/ascites/edema due to augmented venous return with compression of right heart
d. Tx = pericardiocentesis
5. 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
6. Cardiac tumors
a. Primary tumors (usually benign)
i. Myxoma (most common cardiac tumor in adults)
1. Can be familial assoc w/ Carney syndrome which is autosomal dominant
2. Most commonly affects the LA (then RA), usually w/ a single polypoid gelatinous mass that can
obstruct/injure valves, embolize, and/or release cytokines
3. Tumor is minimally cellular w/ scattered small spindle cells and stellate cells w/in myxoid matrix
ii. Rhabdomyoma (most common cardiac tumor/hamartoma in kids)
1. Bulging intra-myocardial mass that can cause obstruction
2. Characteristic large polygonal cells w/ central nuclei, intracellular vacuoles, and radiating bands of
eosinophilic cytoplasm
iii. Papillary fibroelastoma
1. Myxoid fibrillary processes on “uptstream” surface of valve (looks like Alien face-sucker); can embolize
b. Secondary tumors (malignant)
i. Direct tumor spread leading to:
1. Metastasis
a. Pericardial/epicardial surfaces see hemorrhagic effusion and cardiac constriction
b. Myocardium metastases w/in muscle can disrupt electrical signals
2. Vascular obstruction
a. SVC syndrome where SVC obstruction leads to congestion/edema of head/neck/arms
b.IVC syndrome where IVC obstruction leads to ↓ venous return
c. Pulmonary emboli can lead to impaired RV output
ii. Tumor-derived mediators
1. NBTE can be due to mucinous adenocarcinoma
2. Carcinoid heart dz due to 5HT in circulation (R heart)
3. Amyloidosis due to excessive Ig production
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3. If have higher Hgb level (g/dL), that 3 g/dL is a lot smaller percentage of the total Hgb, and smaller
percentage changes in oxygen saturation are easier to detect than large percentage changes
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
5. Classification
a. Left to Right Shunts (PDA, ASD, VSD)
i. Pulmonary flow exceeds systemic flow
1. As PVR ↓ over 1st 6 wks of life, the difference b/w SVR and PVR ↑ and more blood crosses the L→R shunt
↑ volume to lungs ↑ volume to LA/LV LA/LV dilatation w/ ↑L heart DBP + pulm congestion/edema
a. pulm vasculature remodeling if pulm HTN allowed to persist
2. Loss of ox blood to R heart abnormally distributed CO that is perceived as “low” CO compensation via
RAS activation fluid retention systemic congestion (remember: tachy-pnea/cardia, hepatomegaly)
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 ↑ flow across mitral valve)
i. Loudness of murmur inversely related to defect size b/c small defects = more turbulence
3. surgery often required or will eventually lead to Eisenmenger’s if untreated
a. pulm HTN leads to remodeling of pulm vasculature ↑PVR until PVR exceeds SVR and direction
of shunt switches to R→L (usually by teenage yrs w/o Tx)
b. Note, however, that 1/3 of VSDs have spontaneous closure
b. Obstructive Lesions
i. Elevation of pressure proximal to the obstruction hypertrophy → hypertrophic ventricle will eventually fail
ii. Coarctation of the Aorta (CoA) = most common
1. obstructive thickening of aortic wall >50% (a problem once ductus closes & blood can only go down aorta)
2. usually near/distal to left subclavian a
3. signs/sx:
a. HTN proximal to coarctation (think: right arm HTN) + normal/↓ blood pressure in legs
b. Collaterals often develop to bypass obstruction systolic murmur hear over spine
iii. Infant CoA syndrome = severe obstruction leads to acute LV failure (thus no time for hypertrophy)
1. see gallop rhythm, pulm edema, weak pulses, mottled skin, possible cardiogenic shock w/ tachy-
pnea/cardia and hepatomegaly
c. Right to Left Shunts (ToF, tricuspid atresia, truncus arteriosus)
i. Systemic flow exceeds pulmonary flow
1. deox blood in systemic circulation cyanosis
2. bypassing of lungs and their filtering emboli to brain
ii. Tetralogy of Fallot = most common
1. severity is proportional to degree of RV outflow obstruction (deox blood will take path of least resistance)
2. signs/sx:
a. RV outflow obstruction
b. RVH
c. Large VSD
d. Overlying/overriding aorta
e. Holosystolic murmur (due to VSD) + systolic murmur (due to RV outflow obstruction)
f. Single S2 (VSD equalizes pressure so aortic/pulmonic valves close simultaneously)
g. Cyanosis does NOT respond to O2 therapy
3. Hypercyanotic spells (Tet spells)
a. ↑PVR or ↓SVR causes sudden ↑ in R L shunting
b. Causes significant cyanosis syncope
d. Transposition
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CARDIOMYOPATHY
1. Results from a primary abnormality in myocardium
2. Dilated Cardiomyopathy (DCM; most common):
a. Gradual degeneration of myocytes four chamber dilation w/ reactive hypertrophy (globoid heart) + systolic dysfxn
i. Extensive dilation stretches valve annulus mitral regurg, also predisposes to mural thrombi b/c of hypokinesis
ii. Very low contractility/EF
iii. Histologically see non-specific myocyte atrophy/hypertrophy + fibrosis
b. True DCM is idiopathic, but similar clinical pic from EtOH, genetic (AD, cytoskeletal proteins), drugs (adriamycin),
pregnancy, viral
i. Viral form is aka myocarditis
1. Inflamm (esp. lymphocytes) is primary cause of cell degeneration
a. See soft mottled myocardium w/ normal to dilated chambers and sometimes mural thrombi
2. 1˚ Coxsackie B, but can be due to other orgs (ex) diphtheria, in which exotoxin causes myocarditis
3. Tend to be acute/self-limiting/subclinical (assoc w/ persistent viral genome in myocytes), rarely fulminate
4. Other forms = sarcoidosis, drug hypersensitivity rxn (lots eosinophils), SLE
ii. Arrhythmogenic RV cardiomyopathy characterized by replacement of RV myocardium w/ fat/fibrous tissue leading to
R-sided heart failure and arrhythmias
3. Hypertrophic Cardiomyopathy:
a. Massive LV hypertrophy (“banana-shaped” LV cavity) small LV/impaired relaxation diastolic dysfxn
i. High contractility but low SV due to inadequate pumping (uncoordinated LV contraction)
ii. Histologically see myofiber disarray (poorly conduct, which predisposes to arrhythmias)
iii. See sub-aortic stenosis due to opaque white endocardial thickening in sub-aortic region (systolic ejection murmur)
b. Usually 1˚ familial (AD, sarcomere proteins), cause of death in young athletes
4. Restrictive Cardiomyopathy:
a. Subendocardial fibrosis/infiltration by substance firm myocardium w/ normal/↑ thickness of ventricle wall low LV
compliance diastolic dysfxn
i. Contractility is normal but low SV due to inadequate filling
ii. Characteristic is Kussmaul’s sign (loss of the normal variation in JVD due to inspiration)
iii. Histologically see amyloid, iron, glycogen vacuoles
b. Due to amyloidosis (Congo red), hemachromatosis, or glycogen storage dz whose accumulated substances stiffen heart
i. Senile cardiac amyloidosis (amyloid from transthyretin)
ii. Systemic amyloidosis (AL amyloid from Ig light chains and AA amyloid from serum amyloid-assoc prot)
iii. Isolated atrial amyloidosis (amyloid from atrial natriuretic peptide)
HEART FAILURE
1. CHF is dz of elderly, most common cause is ischemic heart dz due to coronary atherosclerosis, also most # of hospitalizations
2. Heart cannot pump enough blood to meet bodies demand circulatory failure, most commonly due to myocardial failure
a. Myocardial Dysfxn
i. Systolic failure (2/3 cases): impaired pumping due to loss of muscle mass (i.e. postMI) low EF
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1. Need greater preload (higher EDV) to increase SV and maintain CO (Frank-Starling) infarcted tissue
thins LV dilation stretches annulus mitral regurgitation
a. Positive inotropic agent (ie catecholamines)= results in upward shift of Frank-Starling curve such
that ↑CO achieved for given EDV (see downward shift of curve w/ CHF)
2. Increased EDV is transmitted back to LA, lungs (pulm edema), RV (RV failure mostly due to LV failure)
3. Other causes = EtOH (damages contractility), adriamycin, cocaine, hypothyroidism, myocarditis
ii. Diastolic failure (1/3 cases): abnormal relaxation due to stiff LV (i.e. hypertrophy), but EF preserved
1. Need greater pressure than normal to eject a given preload
2. Sx dramatically worsened due to:
a. Ischemia (low O2), since relaxation is an ATP-dependent process
b. Elevated heart rate since the duration of diastole (filling time)
3. Causes: severe HTN, hypertrophic cardiomyopathy, amyloidosis/hemochromatosis
a. Sx of HCM: DOE, syncope, a-fib, S4, systolic murmur that increases w/ Valsalva
iii. Cor pulmonale: increased pulm vascular resistance due to lung dz RV failure
1. ↑ R EDV is transmitted back to systemic venous circulation JVD, hepatomegaly, pitting edema
2. Left heart typically unaffected, unless compressed by large RV
3. Causes: fibrosis, silicosis, COPD, PE
4.Oxygen therapy to dilate pulm arterioles helps by easy strain on RV
b. High Output Failure
i. AV fistula (bypasses capillary bed) ↓ resistance, so in order to maintain BP/perfusion, CO increases dramatically
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) or uncoordinated contraction
d. Pericardial Disease: normally pliable, but in tamponade/constrictive pericarditis it stiffens restricted pumping/filling
e. Valvular Dysfunction: either regurgitation/stenosis circulatory failure
3. 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
4. Neurohumoral: overall, NOT helpful
a. Sympathetic increased HR/contractility (β1) + VC (α 1)
i. Elevated levels long-term increase mortality, but catechols are necessary evils – the increased HR/contractility helps
maintain CO/BP but also ↑O2 demand, the VC helps maintain BP but also increases afterload to a failing heart
b. RAS angioII VC + Na retention + SS 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, α 1 SS stimulation
iii. angioII is growth factor leading to cardiac myocyte hypertrophy
c. BNP (brain natriuretic peptide) VD + ↑ Na excretion + ↓renin secretion
i. Elevation is highly sensitive/specific test for heart failure
ii. Works to ↓ afterload, but VD decreases resistance/BP which forces failing heart to pump harder for sufficient CO
iii. Normally effects are outweighed by RAS
5. Clinical presentation
a. Low CO fatigue, DOE, cool skin, increased BUN:Cr ratio (due to low renal blood flow)
b. Pulmonary edema SOB, orthopnea, PND, cardiac asthma, rales, S3
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
6. Tx: See pharm chart below, also bed-rest (↓ workload/catechol release + leg elevation = spontaneous diuresis), low Na diet (reduces
Na and water retention)
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PHARMACOLOGY
1. HTN
a. Normal <120/<80, PreHTN: 120-140/80-90, Stage 1 HTN: 140-160/90-100, Stage 2 HTN: >160/>100
b. Goals: HTN alone <140/90, diabetes/renal dz <130/80, LV dysfxn <120/80
c. Commonly 1st line: thiazides, beta blockers, ACE (-), Ca channel blocker (if A-fib)
DIURETICS
MOA Place in Therapy Clinical Pearls
Thiazides Blocks Na reabsorption in DCT DOC in isolated mild SE: hypoK, hypoTN, acute renal failure-ARF*, DM, gout
HCTZ systolic HTN decrease stroke/MI
Chlorthalidone Preferred in AA pts
Less effective in RF *decreased perfusion due to hypovolemia
Loop Diuretics Blocks Na/Cl reabsorption in Uncommon for HTN SE: hypoK, hypoTN, ARF, hypoMg, ototox
Furosemide LOH excessive vol loss Used in RF (Cr<20)
Torsemide
ANTI-ADRENERGICS
MOA Place in Therapy Clinical Pearls
Beta-Blockers Block cardiac β1 R ↓ HR Use w/ concurrent heart dz SE: bradycardia (caution w/ EF <40%), hypoTN
Metoprolol ↓ CO ↓ BP DOC for hypertrophic CM contraindicated in asthma (metoprolol best)
Atenolol May not be as effective in AA may mask hypoglycemia in DM
Carvedilol decreases mortality
Alpha-Blockers Block vascular α R VD Uncommon due to hypoTN SE: hypoTN, orthostatic hypoTN, syncope
Terazosin ↓ resistance ↓ BP Used if uncontrolled never use as monotherapy
Prazosin despite other meds
Doxazosin
RAS INHIBITORS
Drug MOA Place in Therapy Clinical Pearls
ACE (-) Blocks Ang I Ang II, thus 1st line tx due to many SE: acute renal failure, cough, angioedema,
Lisinopril blocking VC (↓ afterload) and compelling indications hypoTN, hyperK (monitor creatinine & K)
Captopril Na retention (↓ preload) (heart failure, DM, CAD) decreases mortality
Ramipril DOC for heart failure after MI prevents remodeling
Renin (-) Inhibits renin to block Newer drug, unknown SE: hyperK
Aliskiren conversion of
angiotensinogen→ ang I
VASODILATORS
Drug MOA Place in Therapy Clinical Pearls
Ca Channel Block L-type Ca channels DHP: ↓ BP SE: bradycardia (non), periph edema/hypoTN (di)
Blockers decrease Ca influx into non-DHP: ↓ BP AND HR constipation (verapamil)
Amlodipine (di) vascular SM cells VD
Nifedipine (di) non-DHP often DOC in A-fib
Diltiazem (non)
Verapamil (non)
Clonidine α 2 agonist 3rd line Rebound HTN with abrupt discontinuation (taper)
Hydralazine Direct vasodilator 3rd line Requires 3x/day dosing
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Ca Channel Block L-type ↓ Ca influx VD Use if contra to β-blocker SE: above + peripheral edema, hypoTN
Blockers ↑ blood flow ↑ O2 supply Adjunct to β-blocker
BOTH DHP/NON!
Case1
48y African American F, no PMH
BP = 150/90 (Stg 1), SCr = 1.5, K=4
No compelling indications + AA + cheap/easy = HCTZ
Case 2
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ANTI-THROMBOTICS
Drug MOA Place in Therapy Clinical Pearls
UFH Enhances action of antiTHB3 NSTEMI, STEMI SE: HIT ( 50% decrease in plts)
inactivation of IIa/IXa/Xa Peak effect w/in minutes
Prevent new thrombi but NO lysis of existing thrombi
LMWH Same but more specific for Xa NSTEMI, STEMI SE: less chance of HIT
Eliminated renally
Fondaparinux Direct Xa inhibitor Prevent DVT No monitoring/dosed daily (predictable); low HIT risk
If get HIT w/ heparin Inactive against preformed IIa
Renal clearance
Bivalirudin Direct thrombin (-) If get HIT w/ heparin (-) both free and fibrin-bound thrombin
Thrombolytics Convert plasminogen STEMI (vessel totally Used mostly now for stroke (w/in 3h) and STEMI pt
tPA plasmin clot lysis occluded & need to where percutaneous intervention no readily available
streptokinase dissolve the clot)
Note: Blocking 1 molecule of Xa will block ~50 molecules of IIa
ANTI-PLATELETS
Drug MOA Place in Therapy Clinical Pearls
ASA Irr (-) COX no TXA2 no Pretty much all heart probs SE: GI sx, bleeding
plt activation Decreases risk of another MI by 20%
Clopidogrel Irr (-) ADP R no activation If allergic to ASA
GP IIb/IIIa antag Prevent plt aggregation by STEMI (abciximab) Both have t½ ~2.5h
Abciximab blocking fibrinogen x-linking NSTEMI (eptifibatide)
Eptifibatide
ANTI-COAGULANTS
Drug MOA Place in Therapy Clinical Pearls
Warfarin Prevents synth of vit K-dep a-fib + any high risk SE: bleeding (esp. intracranial), anaphylaxis (IV)
factors II/VII/IX/X factor* Use low dose IV AND oral Vit K to reverse
via VKOR inhibition/lack of DVT or PE Long t1/2, hard to dose, check INR frequently
oxVitK recycling Takes ~48h for peak effect (10+d to Css)
DDIs w/ cyp2C9/3A4 users
ASA As above a-fib but no risk factors
and <65yo
*note: risk of ischemic stroke is 2x greater in a-fib, CHADS2 Score gives stroke risk based on co-morbities (CHF, HTN, DM, TIA, age˃75)
----3+ of the 5 CHADS risk factors makes pt good candidate for warfarin due to high risk of stroke
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4. HEART FAILURE
(Refer to previous charts for more drug data)
a. Classes based on sx (go back one if sx improve) vs stages based on LV fxn (CHF is progressive, thus can only get worse)
i. Normal
ii. 1 – Asymptomatic w/ LV dysfunction = ACE(-), ARBs
iii. 2 – DOE w/ compensated CHF = diuretics, b-blockers
iv. 3 – Limited physical activity w/ decompensated CHF = increased diuretics, spirnolactone, digoxin
v. 4 – Bedridden w/ refractory CHF = inotropes, vasodilators, transplant
b. Drugs that may hurt CHF pts
vi. Diltiazem and Verapamil are only safe when treating diastolic failure
vii. Flecainide and Moricizine are antiarrhythmics that can kill CHF pts
viii. Prazosin just doesn’t have any benefit
PRESSORS (SBP<90 w/o hypovolemia, i.e. cardiogenic/septic shock, SHORT TERM ONLY!!!)
Drugs MOA Effects
Dopamine Low – dopamine receptor Low VD
Med – dopamine/β receptors Med β1 stimulation (↑ HR/contractility)
High – dopamine/β/α High α 1 stimulation (↑ SVR/BP/afterload)
receptor
Epinephrine β1, β2 stimulation ↑ CO/SVR
NE α stimulation ↑ SVR
Note: Long-term catecholamine tx (including dobutamine, dopamine, epi, NE) leads to desensitization and receptor downregulation
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OTHER
Drugs MOA Place in Therapy Clinical Pearls
Amiodarone Antiarrhythmic CHF + atrial fibrillation
Dofetilide Atrial fibrillation
Dronedarone Atrial fibrillation and flutter CI in heart failure
Amlodipine AntiHTN/antianginal CHF + HTN/stable angina
Warfarin Anticoagulant CHF + CAD/afib/etc Efficacy not proven
Tolvaptan Vasopressin antagonist Correct hypoNa in CHF pt No impact on mortality
HIGH YIELD
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.
THUS…
Aortic Regurgitation Pure AR eccentric LV hypertrophy + systemic VD (i.e. the distal dilation)
Mitral Regurgitation Pure MR eccentric LA AND LV hypertrophy