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Cardio Module

An overview of the cardio module.

David Mathews

on 6 April 2013

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Transcript of Cardio Module

30 60 90 <120 Left Atrium Left Ventricle Aortic Root AV MV close AV Open AV Close MV open S4 S1 S2 S3 Systole Diastole 2/3 of volume leaves LV/RV 2/3 of volume enters LV/RV 120/80 25/10 4 7 120/10 25/8 12 Chamber pressure/O2 Sat P wave= Atrial Polarization Q wave= Vent Depol. R wave= Vent. Depolarization S wave= Vent. Depolarization QRS= Vent Depol Accentuated Diminished 1. Shortened PR 2. Mild MS 3. CO/Tachycardia 1. Long PR
2. MR
3. Severe MS
3. Stiff LV 1. distance spearating leaflets
2. mobility of leaflets
3. rate of rise in Ventricular pressure Accentuated Diminished System HTN/Pulm HTN Severe Aortic/Pulm Stenosis Splitting Physiologic: On Inspiration A2 P2 Widened: HTN, Severe stenosis Fixed: ASD Paradoxical: LBBB, Aortic Stenosis A2 P2 A2 P2 P2 A2 Inspiration Ejection
Sound Aortic/Pulmonic Stenosis
Aortic/Pulmonic Root Dilation heard at base and Apex Only heard @ base
diminishes Opening Snap Best heard between Apex and Left Sternal border Due to Mitral (more common) or Tricuspid stenosis
MORE advanced= SHORTER interval, in mild disease there is less pressure difference between LA and LV, so it takes longer for LV pressure to drop below LA, ergo Opening Snap is farther away from A2. Ventricular filling ("vent. gallop") Associated with the tensing of the chordae tendinae
-Common in young
-Older= volume overload (CHF
OR transvalvular flow (MR/TR) 1. Dull low pitched sound
2. Associated with decreased Ventricular compliance, ie., MI or hypertrophy.
3. "atrial gallop" murmur: turbulent flow 1. flow over obstruction
2. increased flow
3. Ejection into dilated chamber
4. regurgitation
5. shunting Systolic= Grade 1-6 Intensity Diastolic= Grade 1-6 Intensity Ejection Type= crescendo/decrescendo: A/P stenosis holosystolic= MR, TR, VSD late systolic: ___(click)||||| : MVP Ejection decrescendo= AR (LSB, lean forward, high pitch)& PR Mid to Late= mild MS/TS
Prolonged Mid-Late=severe MS/TS Continuous: PDA To/Fro: Aortic Stenosis and Regurgitation, Pulmonic Stenosis/ Regurgiation Apex Base Mid-Late clicks MVP
TVP high pitched. Apex Dull. 139 159 pre 1 2 di=80-89 di=90-99 See you at Grady! di=>100 Ideal Ventricular pressure falls below Aortic Pressure CO PVR 90% Essential 10% Secondary BP Technique bare arms,
seated, straight back, feet on floor
correct cuff size- too small means it's falsely high
deflate 2-4 mmHg/s Rate Stroke Volume x Regulators Innervation Local Regulation Blood Viscosity Contractility Venous Return & PSNS decreases
SNS increases
Catecholamines Increase SNS increasesCatecholamines Increase SNS increases
Catecholamines Increase Renal Retention Blood volume Venous Tone Aldosterone increases
ADH Increases
SNS increases
NP decreases Catecholamines Increase Alpha 1 increases
Beta 2 decreases hematocrit Increases NO decreases
H+ decreases
Adenosine Decreases
Prostaglandins Decreases Endothelin Increases
Oxygen increases contribution to
HTN decreases with Age Contribution to HTN increases with age Primary Aldosteronism Chronic renal Disease Renovascular Pheochromocytoma Coarctation Cushing Syndrome Endothelins Angio II* CN IX, Carotid Sinus
CN X, Aortic Arch CN IX, Carotid Sinus
CN X, Aortic Arch Atrial Contraction A Atrial kick causes transient increase in JVP C Sligh upward deflection as Tricuspid closes X pressure decline following a wave. V Passive filling y Blood rapidly leaves upon Tricuspid opening CHA RV(v) RV(p) LV(v) LV(p) PH
stenosis Ostium secundum
Unclosed FO,
most common Pulm dilation, PH, A fib. Paradoxical embolus dx: fixed split s2, Incomplete RBBB, Echo L-R Shunt L-R Shunt L-R Shunt L-R Shunt L-R Shunt Cyanotic Lesions TOF Transposition BLUE baby, cyanosis depends
loud cystolic murmur (PS)
usually sporadic but can be genetic 22q11
Tx: pulm valve replacement, use "complete repair" surgical. Dylipidemia Fatty acid beta oxidation
glycolysis Acetyl-CoA HMG-CoA HMG-CoA
Reductase Mevalonate Cholesterol VLDL
Bile Acids "statins"= reversible competetive inhibitors
first line in pt's with elevated LDL (>100)
TG up to 500mg/dl =responsive bile acids cholesterol ester transfer protein Reverse cholesterol transport Bile acid sequestrants (Bile Acid Binding Resins) Decrease: Hepatic bile acids, intrahepatic cholestorl pool, LDL in Plasma
Increase: Bile Acid synthesis from cholesterol, increase LDL receptors, LDL Clearance Cholesterol Uptake inhibitor blocks Neiman-Pick C1 Like 1
(enterocyte C transporter) Ezetemibe (zetia) Niacin inhibits DGAT2,
Decreases TG synthesis Niacin also inhibits HDL
Receptor breakdown,
increases HDL & reverse Cholesterol transport microsomal
TG transfer
proteins facilitate
addition of lipids to
lipid binding domains Fibrates:
binds Peroxisome
activated receptor prototype: fenofibrate Omega 3 FA's (EPA, DHA) inhibit TG synth
reduce VLDL (secretion,prd)
binds PPARa Decreased C, increased LDL Receptors FH
ApoC2 or LPL Auto Dom.
high fasting TG
low LDL Tx: fat free diet long chain FA are esterified into TG (get in via lymphatics) xanthoma corneal arcus *early onset
*fam Hx
*extreme or unusual labs proteins affected fam hx=
more predictive than genetics Atherosclerosis Heart Failure preload. EDV (EDP) afterload. (TPR), Contractility. hemodynamic cardiorenal neurohormonal Cardiac energetics Sympathetic tone Aldosterone is good in the short term, but long term it increases myocardial hypertrophy, fibrosis and uptake of NE. Arginine vasopressin: Ang2 stimuates thirst, and increased aqua porins (water retention) Natriuretic peptides: released from ventricles in response to stretch (ANP & BNP). good for heart. (increase Na/water excretion, inhibit renin/aldosterone release, vasodilate) effects long term on kidney are blunted though Index events
Abrupt:MI, acute AI or MR (ie., infective endocarditis)
Gradual: HTN, chronic AI or MR, genetic Cardiomyopathy Models of HF Decreased CO, too much salt & fluid LVEDV-LVESV LVEDV EF LV(edv) LV(edv) preload. EDV (EDP) afterload. SVR (TPR), (systolic HF,
Reduced EF) (diastolic HF,
normal HF) high PVR "Forward failure" "backward Failure" increased venous pressure
*transudative process parasympathetic tone RAAS Time: good patches, bad fixes pressure overload increased Systolic stress volume overload increased diastolic wall stress increase: Dilation, sphericity, thinning, MR LV myocyte remodeling Proteins Fibroblasts Substrate utilization Ox Phos High energy Phos Metabolism HF HF HF Cells take up FFA, glucose, & other krebs metabolites. FFA utilization decrease, shifted to only Glucose metabolism doing regular Ox Phos in the mitos mitos are strxlly broken, atp synthetase is flawed ATP is readily transferred and utilized CK activity is reduced and ATP is impaired phospholambans are dephos'd, inhibit sarcolemma Decreased, destroyed
malformation LV hypertrophy HTN= decreased NO, increased Vasc. Perm, and increased Leukocyte adherence Smoking
Diabetes too all NO VCAM=vascular cell adhesion molecule monocyte colony
stimulating factor Ischemic heart Disease Unstable Angina Q-Wave Sudden Death Non-Q-Wave STEMI NSTEMI > 90% due to
atherosclerosis Clinical Manifestation Angina Pectoris MI Chronic Ischemic HD Death ACS Pinzmetal "subendocardial" transmural vasospasm
cocaine induced sometimes COMPLICATED: 1. disrupted/ulcerated- exposed lipid core= tissue thromboplastin.
2. superimposed occlusion, mural thrombus, or hemorrhage.
3. injury to media. loss of elasticity, development of aneurysm Vasculitis Inflammatory damage to blood vessels
vascular damage (hemorrhage, ischemia distal to lesion) ecg findings Ischemia
timeline 1hr 2hr 3hr 4hr 8hr CK-MB rises 12hr 18hr CK-MB peak 1d 2d 3d 4d 7d 10d ck normal troponin elevation trop
stays high *can be high because of pericarditis, HF, PE, sepsis, shock, renal failure, CV incident, extreme exertion dark mottling Macro Micro coag necrosis Macro mottling/yellow center Macro Micro neutrophils red border/ yellow center Macro Micro neutrophils & macroph. 14d red-gray Macro Micro granulation tissue >3m white/scar Macro scar Micro 12-24h CAD -exposure of platelet adhesion factors
-collagen, vWF, fibronectin
-vWf + glycoprotein 1b/IX/V complex
-platelet activation & granule release
-gpIIb, IIIa binding of vWF and fibrinogen
-platelet aggregation
-activation of coagulation cascade:
-thrombin converts fibrinogen to fibrin occlusive thrombus 90% CAD, Other causes normal Atp begin to deplete in seconds Loss of contractility (2 min) Atp 50% in 10 min ATP to 10%
in 40 min Irreversible cell injury
20-40 min microvascular injury >1hr Post MI 1. recurrent ischemia 2. arrhythmias 3. Myocardial dysfnxn CHF
Cardiogenic shock 1. V. Fib
2. Supraventricular arrhythmias
3. Conduction blocks *. RV Infarction 4. pericarditis 4. Mechanical Cx papillary muscle rupture (PM LV)
Ventricular free wall rupture (women & hypertensives)
Ventricular septal rupture (L-R shunt, subsequen RHF)
True Vent. Aneurysm (emboli, arrhythmias, HF- clue is persistent ST elevation) sharp pain, fever, pericardial friction rub.
Dressler Synd: fever, malaise, sharp pleuritic cehest pain, leukocytosis, 6. Thromboembolism stasis in areas of impaired LV contraction Chronic Ischemic HD elderly, progressive HF due to ischemic damage (CAD, MI)
LV enalrged,
hypertrophic 30-40% of MI 15-20% of MI 40-50% of MI Full thickness *preferred biomarker Large Vessel Giant Cell Takayasu females 3:1
pain/tenderness in head/temporal scalp Visual disturbance
*BLINDNESS* Polymyalgia rheumatica ESR, CRP hx/px Uh-OH >140/90
pulse pressure (SBP-DBP)
paradoxical pulse
arm difference
arm/leg difference >55-60 SV (eg AR)
Compliance (elderly)
DBP (eg fever) <20-25 LVOT (eg AS)
LV Volume (eg MS) STEMI or Non STEMI That is the question well, not really. Rate of rise Resting membrane potential is more + AP is shorter Repol is longer = "current of injury" "inferior injury" II, III, aVF usually due to RCA
occlusion Anterior Injury V1,V2 (septal)
V3,V4 (apical) ST depression, tall R waves, VI, V2 RCA, LCx I, avL, V5, V6 Posterior Acute Heart Failure Lateral Pregs? CO, HR, Flow, plasma & MCV,
Resistance, Preload, NO, PG, Ao Diameter SVR, afterload,
Resistance, lying supine
Decreases CO left lateral decub, alleviates compression of uterus on IVC Hypercoag. DVT
decrease protein S
increase clotting factors Post preg >3 mo, before decrease CO CO goes up during, after and right after RV Dilates MS<<AS poorly tolerated NYHA <2
LV dysf
Hx of CHF, Arrhyth, PPCM Counseling PDA TGA synth
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