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564 Cards in this Set
- Front
- Back
- 3rd side (hint)
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Stages of Atherosclerosis
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1: smooth lumen
2: fatty streaks, early immune response 3: cholesterol, calcium crystals, cellular debris. intima bulges into lumen 4: thrombus formation, embolus |
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diet/atherosclerosis
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decrease sodium, increase Mg, Ca, K, fiber, folate, vit K, antioxidants, fish oil
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Atherogenic
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LDL, lipoprotein, homocysteine, hypertension, diabetes mellitus, artery harden, vitamin K deficiency, male over 55, female over 65, FH(x) coronary heart disease, smoking
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thrombogenic
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low fish, low fruit, low veggie, high fat, obesity
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atherogenic LPs
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chylo remnants
LDL VLDL remnants |
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nonatherogenic LPs
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chylomicrons
HDL VLDL |
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chylomicrons
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intestine to other organs
carry TGs, cholesterol, Vit A, D, E, K |
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pancreatic lipase
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cleaves dietary fat in small intestine
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increase in TGs
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independent risk factor for CHD
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high fat diet
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saturates chylo remnant clearance, prolongs circulation
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VLDL
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TGs, cholesterol, Vit E from liver to other organs
half converted to LDL, half taken up in receptor mediated process |
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cholesterol raising
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myristic, (butter, milk, meat, coconut)
palmitic (shortening) trans fats (partially hydrogenated) |
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neutral fats
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stearic (beef, chocolate)
oleic (olive, canola, almond) palmitoleic (palm oil) |
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decrease cholesterol fats
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linoleic (seeds, veggies, walnuts)
alpha-linolenic (flaxseed, linseed) epa/dha (fatty fish) |
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left axis shift
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hypertrophy
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bold lines ekg pulse
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300-150-100-75-60-50-40
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p>5 blocks
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first degree heart block
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no P wave
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av impulse, no SA
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normal axis
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-30 to +120
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right axis deviation
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negative in lead I
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normal axis leads I, II, III
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upright
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RVH
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positive R wave in V1
right axis deviation pulmonary hypertension negative in I, II, AVF (rt axis shift) positive AVR (should be negative) |
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LVH
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left axis deviation
positive I negative II, III, AVF aortic stenosis, HTN huge R waves in V leads Flipped T waves (ischemia) |
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Determine LVH
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add amplitudes V1 and V5, >35 = LVH
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flipped T waves
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ischemia
tissue hypoxia |
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infarction
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paradoxical wall motion
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Inferior STEMI
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STE in II, III, AVF
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Wall Injury
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Q wave 1mm x 1mm or 1/3 height QRS
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Lateral STEMI
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I, AVL, V5, V6
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Anterior STEMI
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V3, V4
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Septal STEMI
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V1, V2
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RCA occlusion
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inferior stemi
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acute septal MI
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V1, V2
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irregularly irregular
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atrial FIB
hard time finding P waves |
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saw tooth pattern
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atrial flutter
atrial rate 300bpm ventricle 1/2 (150bpm) |
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Dig Toxicity
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salvador dali mustache, depression ST segment
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single chamber pacemaker
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huge spikes, looks like left axis shift
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dual chamber pacers
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double spikes
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hyperkalemia
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peak T
wide QRS renal failure give Calclium |
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hypokalemia
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U wave instead of T wave
repolarizing abnormality |
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biphasic P waves
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atrial enlargement (left, right, biatrial)
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LBBB
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biphasic R waves
QRS widened V5, V6 |
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pericarditis EKG
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STE everywhere because enflamed pericardium
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AV valves mumurs
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vegetation systolic
damage diastolic |
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left atrium dilated
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MS
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LVH
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AS
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functional regurgitation causes
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dilated ventricle causes papillary muscle to be pulled down and out
dilated aorta or PA pullls valve commisures apart, prevents closure |
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MCC valve disease
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acquire MS/AS
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Calcific AS
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MC valve abnormality
acquired calcific cusps hard to open LV pressure overload ischemia, angina, CHF |
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Rheumatic AS, Congenital AS
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commisural fusion
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AS prognosies
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ASx, good
Sx, bad high pitched systolic murmur |
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COngenital Bicuspid AV
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MC congenital cardiac malformation
calcific |
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mitral annular calcification
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calcium deposits cause stony nodules
doesnt usually affect Fx can cause Sx nodules can embolize, be nidus for infx, ringlike opacities CXR |
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myxomatous degeneration mitral valve
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MVP, young women, midsystolic click, chorda tendinae long, thin, depot mucoid material
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secondary changes to MVP
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fibrous leaflets, thickening endocardium from friction injury by leaflets, thrombi on atrial surface leaflets,focal calcifications
marfan |
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rheumatic fever
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follows group A strep pharyngitis
IgG cross react with tissue glycoproteins in heart, joints, etc (M proteins) takes 20 years to develop in western individuals, happens in children in 3rd world pancarditis MV Most commonly migratory polyarthritis erythema sydenham choria (involuntary rapid purposeless movements) jones criteria group A pharyngitis fever, athralgias, acute phase reacts |
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aschoff bodies
acute RF |
fibrinoid necrosis surrounded by mononucleocyte infiltrates
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anitschow cells
RF |
large histiocytes with vesicular nuclei, basophilic cytoplasm, owl eye ross section
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chronic RF
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irreversible valve deformity, increased vascularity, lymphocyte infiltrates, chordae fibrous and fused, valvular annular calcification
mv MC women more than men fish mouth deformity Left atrium dilation, mural thrombi, arrythmias, |
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carotid upstroke
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sound during-systole
sound before-diastole |
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S1
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closure MV, TV, hear at TV
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SPLIT S1
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RBBB
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INcreased S1
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MS, Increased CO, short PR
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Decreased S1
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long PR, decreased CO, MR
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S2
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closure PV/AV
splits on inspiration hear at PV |
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SPlit S2
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AS,LBBB, PUlmonary HTN, Trans Venous PAcers
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wide splitting
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volume overload, AR (diastolic murmur, Eccentric Hypertrophy (heart folds back in on itself)), PDA
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Systolic murmur aorta
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AS
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S4
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diastolic mumur
over ventricle with bell Left Lateral Decubitus separate S1 (inspirate) from S4 (hand grip) long term HTN and organ disease |
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S3
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diastole
increases with hand grip, ventricular overload |
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increase venous return
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squatting, inhalation
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decrease venous return,
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standing, expiration
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handgrip
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increase left sided murmurs
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inspirate
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increase right sided murmurs
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opening snap
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MS, calcification
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ASD murmur
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systolic murmur
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MS murmur
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diastolic rumble
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Normal S3
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up to 40 years of age
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S4 normal
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never
into non compliant ventricle need atrial contraction to augment CO |
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extra beats
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PAC hear it fear it
PVC, hear dont feel, could be benign |
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inspiration
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S2 moves from S1
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S3
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inspiration increases over sternum, handgrip increases left lateral decub, big heart
filling problem |
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S4
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handgrip with bell left lateral decbuoitus
small heart PV, TV, IHSS, MS |
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MR
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handgrip, apical
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AS
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bilateral carotid bruits, 2nd right intercostal, handgrip, angina, shortness breath,
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PS
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2nd left intercostal, doesnt radiate, shortness breath angina, increased volume acomodated,neck vein distension, longer with inspiration
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ASD
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neck vein distension, doesnt respond to maneuvers, incomplete RBBB,
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VSD
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hand grip exaggerate, 4th intercostal, left sternal border
Ddx-TR, inspiration increases this |
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PDA
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only holosystolic murmur, heard best over clavicle, machinegun murmur
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AR
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two and blow
handgrip 2nd left or 2nd right intercostal |
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MS
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diastolic murmur
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chronic aortic valvulitis
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males, mitral valvulitis, LVH, thick adherent cusps OR fibrosis and retraction
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calcific AS
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LVH, ASx, fibrosis with calcification
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Non Bacterial Thrombotic Endocarditis
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aka marantic endocarditis, in pts with sepsis or cancer, small nodules on valve, no inflammation no damage but embolize
happen in endocardial trauma valve free of inflammation and bacteria. associated with cancer,mucin producing carcinomas, resolve spontaneously AV most commonly involved |
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carcinoid heart disease
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endocardium, right sided valves
cardiac manifestation systemic syndrome tumors, malignant potential produce products called carcinoid cardiac, wheezing, rash, gi, diaphoresis plaquelike thickenings on cardiac chambers major right side blood vessels, valves acid/mucopolysaccaride rich matrix thicken from serotonin and histamine inactivated in pulmonary system, so the lesions stop in right side of heart |
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Endocarditis of SLE
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libman-sachs endocarditis
sterile, pink warty vegetations valve, chords, mural endocardium |
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artificial valves
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infx at tissue, prosthesis interface, hemoloysis, overgrowth of tissue
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infective endocarditis
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bulky friable vegetation, microbe, fibrin, bacterial, destruction common,
IVDA ricekttsiae, fungi aslo possible infx occurs during bacteremia IVDA, prosthetic valves, cardiac abnormalities |
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acute endocarditis
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highly virulent organisms
destructive infx in previously normal difficult to treat necrotizing, ulcerative, invasive lesions |
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subacute endocarditis
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lower virulence, previously abnormal valves, recovery with antibiotics
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IE previoulsy damaged valves
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strep viridans
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prosthetic valves IE
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staph epi
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IVDA IE
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staph aureus, TV (usually MV/AV in IE)
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IE difficult to treat
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avascular valves
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IE morphology
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ring abcesses, veg erodes into myocardium, fungal causes larger, systemic infarcts possible
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IE clinical
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fever, janeway lesions (purpura soles/palms),, osler nodes (tender pulp digits), roth spoths (retinal hemmorages), splinter hemmorages
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SLE IE
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undersurface of AV valves
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NBTE
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depot platelets, fibrin, hypercoagulable state, sterile, debilitated patients
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artificial valves complications
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up to ten years post op, hemolysis, exuberant, inappropriate healing, mech. valves need anticoagulation, bioprosthesis degrades
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paronychia
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inflammation around nail bed
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pupura
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purple-brown-red discoloration of skin greater than .5cm
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vegetation
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tissue/blood clot
fungating-spongy |
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MCC IE
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staph aureus
2nd-viridans |
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clinical indication IE
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febrile illness, no resolve and murmur
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staph bovis
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if isolated check colon
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IE e. feacalis
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GI surgeru
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MCC culture negative antibiotics
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early antibiotic dosage
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RHD IE
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young, group A strep pyogenes, beta hemolyric, genetically susceptible hosts or those in 3rd world, Ig to M protein,
licks the joints bites the heart |
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IE elderly
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no fever
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peripheral IE
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splinter hemmorage, janeway, oslers, roth spots, conjunctival petechiae, sudden blindness in one eye, clubbing fingers (scharoth's sign)
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HACEK organisms
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gm negative
Heamophilus actinobacillus Cardiobacterium hominus Eikenella Corrodens (human bites) Kingella (children arthritis) |
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prophylactic tx for IE
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prosthetic valve, previous IE< CHD, invasive dental procedure, resp tract incision, surg procedures with INFX tissue
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strep pyogenes
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developing countries
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MCC acquired heart disease kids developing world
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kawasakis
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pericarditis clinical
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uncomfortable laying down, prefer to sit upright
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PVC/VPC
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PQRST + abnormal wave
opposite widened axis |
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prolonged QT
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T wave is 1/2 distance between Rs
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P wave close to T wave
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atrial depolarizes when ventricle is sensitive-->vfib
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antihistamine and decongestant
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prolong QT, add coughing fit, VTACH/VFIB
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pulmonary emobolus
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S1Q3(enlarged 1/3 height complex)T3 (flipped)
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Right Atrial Enlargement
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bigger P wave
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RBBB
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R and R'
QRS bigger than 3 boxes |
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PR elevated
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primary av block
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PR 6,8,10,12,6,8,10,12
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wenkebachs
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T close to P
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prolonged QT
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Supraventricular Tach SVT
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suspect if HR greater than 150
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Rate dependent ST depression
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ischemia with tach
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VTACH
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ectopic electrical impulses, ventricle firing away, poor blood flow, doesnt repolarize, deep troughs, concordance (superimposable waves)
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Wolf Parkinson White Syndrome
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Q-R slope instead of spike
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normal intervals
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PR less than 5
QRS less than 3 QT less than 1/2 R to R |
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long PR
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first degree block
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STE II, III, AVF
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inferior MI
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STE I, AVL, V5, V6
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Lateral MI
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Peak Ts
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hyperkalemia
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U waves
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hypokalemia
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circumflex occlusion MI
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lateral
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LAD MI
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anterior (v3,v4)
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right coronary MI
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(posterior, st depression v1,v2)
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right/left cornoary MI
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inferior
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hypocalcemia
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prolonged PR
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hypercalcemia
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shortened PR
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VFIB
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pulseless, squiggly
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Torsades de Pointes
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VFib Up/down/up/down like party streamer (rhythm exists but difficult to visualize)
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cpr?
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asystoly
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Murmurs characteristics
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Timing, grade, location, duration, pitch, radiation, intensity, shape, maneuvers
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MCC rupture papillary muscle
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posteromedial papillary receiving blood supply from posterior descenidng branch of a dominant RCA associated with inferior MI
anterolateral papillary has dual blood supply and less common to ruptire |
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MCC valvular lesion
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AS 1, MR 2
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MCC mitral abnormalities
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myxomatous degeneration
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MCC MR third world
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rhd
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MR relations
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not diabetes, dyslipidemia.
female, lower bmi, old age, renal, prior mi, ms, mvp |
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acute MR
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sudden volume overload on left atrium and left ventricle
no hypertrophic compenation, SV decreases because TSV increased but FSV is same severely Sx normal LV because not hypertrophic |
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hyperdynamic systolic Fx of left ventricle on TTE in patient with acute CHF
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suspect acute severe MR
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acute MR tx
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nitroprusside
increase aortic flow, if normotensive if hypotensive nitroprsside and inotropic |
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chronic MR
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LA/LV, sufficient time to dilate and accomodate volume
tsv/fsv preserved by hypertrophy LV dilates, pulls MV leaflets, worsens MR |
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indications for MV surgery
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patients with poor heart function but no Sx
severe cardiac dysfx will not do well |
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AS
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obstructive murmur
syncope angina dyspnea radiates to carotid, consistent with gallalvardin effect prominent S4 (left atrium contracting into stiff ventricle) crescendo-decrescendo (mid to late peaking) increased squatting, reduced valsalva |
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MCC AS
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caclific
calcification of annulus can lead to heart blocks |
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pulsus parvus et tardus
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delayed carotid pulse
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gallavardin
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mimics MR, doesnt radiate to axilla
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MCC congenital AS
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bicuspid
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Rheumatic AS
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commisures fuse, fibrosis, aortic insufficiency from retracted leaflets, mitral and aortic valvular disease
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aortic sclerosis
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calcification not hemodyanamically significant
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mortality from onset of symptoms
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angina 5 years
syncope 3 years heart failur 2 years |
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AS heyde syndrome
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gi bleeds due to angiodysplasia or other vascular malformation b/c enhanced vWF-platelet interactions increases shear stress
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signs AR
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muller sign (pulsation uvula)
musset sign( bobbing head) water hammer pulse corrigan pulse (pulsating filling cap bed under fingernail) pulsus bisferiens( dual impulse in same cardiac cycle fatigue, angina, dyspnea, |
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TX valve stuff
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echo, cath, CXR.
acute-pressor/inotropic/vasodilator, avoid beta blockers to not disrupt compensatory mechs) |
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ischemia beyond 30 minus
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irreversible cell injury begins (down ATP, up lactate)
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activate PKCE before ischemia
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cardioprotective, upregulates Katp channels
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inhibit PKC after ischemie
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cardioprotective
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eNOS and BH4
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coupled, cardioprotective, produce NO
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eNOS and BH2
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uncoupled, produce SO anion, bad
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increases bh2
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atherosclerosis, HTN, DM
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LNAME
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not cardioprotective, blocks NO
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VIt E
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promote couples eNOS, Ig to adhesion molecules, cytokines, complement
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statins
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antiinflammatory, reduce plaques, augment enos
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BH4 and PKCE during reperfusion
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good
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BH2 and PKC inhibitor
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increase NO, cardiprotective
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decrease phase 4 slope
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Na, Ca, Beta blockers
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increase threshold potential
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Na Blockers
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increase maximum diastolic potential
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adenosine (hyperpolarize cell, open K+)
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increase action potential duration
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K+ blockers, longer ERP
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digoxin
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risk of arryhtmias, calcium buildup
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gen anesthesia
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arryhtmia isk
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80% MI patients
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at risk for later arryhtmia
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automaticity
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slope phase 4
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increases slope/automaticity
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SNS, ischemia
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decreases slope, automaticity
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PNS
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IA/IC agents
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increase APD
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IB agents
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increase ERP
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abnormal automaticity
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SA node up-tach
SA node down-brady digoxin triggers automaticity (eartly/delayed afterpolarizations) |
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conduction block
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ischemia
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SVT
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ectopic atrial foci
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PVC
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ectopic foci
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VTACH
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ectopic foci, torsades de pointes
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class I antiARR
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NA blockers
decrease phase 0 upstroke rate (increase threshold) |
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class II antiARR
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beta blockers
decrease phase 4 slope |
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class III antiARR
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k+ blockers
increase APD |
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class IV antiARR
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K+ blockers
increase APD |
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adenosine
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increase diastolic potential, open K+ channels
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IB agent
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lidocaine, up ERP
affinity for inactivated channels |
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IA/IC agents
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open channels, on upstroke, low affinity for resting or closed channels
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IA agents
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quinidine, procainamide, dispoyramide
also block K+ increase HR hyperkalemia toxicity increase QRS, QT |
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Quinidine
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PO
IA chronic control alpha blocking, cause hypotension ADRS cinchonism increased DIg toxicity |
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Procainamide
|
short T1/2,
PO/IV sides: SLE |
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Disopyramide
|
IA
2nd line drug inotropically negative ADR urinary retention, constipation |
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Lidocaine
|
IB
inactivated channels NOT K block IV only DUAL CNS effects adr mixilitine/tocainide -po lidocaine for vtach |
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IC agents
|
mortality
popafenone, morcizine, flecainide |
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beta blockers
|
propanolol, esmolol, metoprolol, acebutolol
prevent MI |
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esmolol
|
emergency IV tx
|
|
|
|
K blockers (class III)
|
increase plateau, APD
|
|
|
|
Sotalol
|
class III wit BB properties
increase RP ventricular arrthymias |
|
|
|
bretylium
|
class III
iv emergency, VFIB |
|
|
|
ibutilide
|
atrial fib/flutter
|
|
|
|
dofetilide
|
PO, atrial fib, inpt setting
|
|
|
|
amiodarone
|
class III with I,II,IV effects
thyroxine iodide analog for V/SV tach loading doses ADR skin, eye neuro deposits increase tox dig, warfarin |
|
|
|
Class IV calcium blockers
|
supraventricular tach
slows SA-AV conduction ADR Gi/CHF |
|
|
|
adenosine
|
av node tach
open k channels increase max diastolic potential short T1/2 decrease AV node conduction vasodilator, can cause bronchospasm |
|
|
|
magnesium sulfate
|
diuretics cause MG def. arrythmias
|
|
|
|
Adenosine
|
for acute aV tach
|
|
|
|
lidocaine
|
MI, VTACH
|
|
|
|
cause of ILLNESS
|
SNS
|
|
|
|
traube-herring-meyer wave
|
central-->interstitial-->veins/lymph
|
|
|
|
raynauds syndrome
|
peripheral reaction to cold, vasoconstrict, worse with previous hypersympathetic tone
|
|
|
|
scleroderma
|
fibrosis, slow with fascial release
|
|
|
|
largel lymphatic vessels
|
contrlled by SNS
|
|
|
|
T2-T7
|
upper extremity
|
|
|
|
T9-L3
|
lower extremity
|
|
|
|
unilateral issue
|
muscle trap
|
|
|
|
bilateral issue
|
lymph ducts
|
|
|
|
primary lymphadema uncommon, 2ndary common
|
mastectomy, radiation, infx, parasite, crush injury, cancer, surgery
|
|
|
|
AV/Lymph/CSF
|
primary, secundary, tertiary circulation systems
|
|
|
|
right lymph duct vs left lymph duct
|
right arm, right chest, right head/neck
left-everything else |
|
|
|
lymph flow
|
respiration plus heart pump plus muscle
|
|
|
|
false diaphragms
|
popliteal fossa etc
|
|
|
|
lymph anchoring filaments
|
keep vessel open/closed depending on pressure
|
|
|
|
cisterna chyli
|
congestion problems, false diaphragm
|
|
|
|
lymphatic ducts connect to thoracic ducts
|
multiple places in subclavian venous trunk
|
|
|
|
thoracic duct control
|
sympathetic
|
|
|
|
50% plasma proteins and salts
|
return via lymphatics
|
|
|
|
na blockers
|
faster heart rates
|
|
|
|
esmolol
|
iv emergency atrial flutter
|
|
|
|
bretylium
|
vfib
|
|
|
|
ibutilide
|
afib
|
|
|
|
dofetilide
|
afib
|
|
|
|
amiodarone
|
vtach, svt
|
|
|
|
ca blockers
|
svt, vt
|
|
|
|
PSVT, AV tach acute
|
adenosine
hyperpolarizes, prevents AV conduction |
|
|
|
increase PR interval
|
verapimil
|
|
|
|
VTACH
|
lidocaine
|
|
|
|
TV IE
|
IVDA
|
|
|
|
IE MC VALVE
|
AV,MV
|
|
|
|
IE gp a strep
|
uncommon
|
|
|
|
IE more common
|
immunocompromised
|
|
|
|
MCC IE in native valve
|
staph aureus
2nd viridans |
|
|
|
MCC in prosthetic valve
|
staph epidermidis
|
|
|
|
MCCIE in IVDA
|
s. aureus
ivda greatest risk factor patients under 40 |
|
|
|
HACEK
|
assoc w endocarditis
|
|
|
|
HIV infx IE
|
indpendent risk factor
|
|
|
|
3/4 IE patients have a structural abormality
|
yes
|
|
|
|
Major criteria IE
|
+ blood culture (3 every 12 hours)
echo evidence endocardial involvement |
|
|
|
minor criteria IE
|
predisposition, fever, vasc/immunologic phenomenon
microbio/echocardio evidence not meeting major glomerulonephritis rheumatic fever oslers nodes roth spots janeway lesions |
|
|
|
positive echo IE
|
oscillating mass on valve/structure or in path of regurgitant jets with absence of alternate explanation
abcess partial dehiscience of prosthetic valve (w/ or w/o veg) valve regurgitation (new) |
|
|
|
less common IE risk factors
|
pregnancy, central lines, shunts, av fistulas, ulcerative colon lesions
|
|
|
|
native valve IE in MVP
|
coagulase negative staph
subacute staph lugdanensis can attack heart valve with no previous abnormality |
|
|
|
group B strep IE
|
aortic valve
large friable veg VHD, DM, EtOH, Neoplasia, GUinfx, Abortion, cirrhosis, ivda pneumococcal IE -rare austrians triad-meningitis, pneumonia, IE assoc with EtOH |
|
|
|
gram negative bacillary IE
|
IVDA. Nosocomial
persistent baceteremia despirt antibiotic tx unlikely on prosthetic valve |
|
|
|
PHV IE
|
50% patients with nosocomial bacteremia/fungemia had PHV endocarditis
|
|
|
|
HACEK
|
hemophilus,actinobacillus, cardiobacterium, eikenella, kingella
large friable veg frequent emboli, frequent valve replacement sub acute clinical presentation |
|
|
|
IE clinical
|
fever, murmur, petechia, skin, conjunctiva, oral mucosa, anorexia, wt loss, malaise, night sweats, splenomegaly, splinter hemmorages, osler nodes, janeway lesions
goes to areas of previous trauma |
|
|
|
MCC culture negative endocarditis
|
previous antibiotic treatment
|
|
|
|
Hx most important part of diagnosing IE
|
yes.
|
|
|
|
TEE
|
better than TTE
|
|
|
|
indications for surgery
|
CHF, persistent/uncontrolled infx, recurrent emboli, fungal, highly resistant organism
if neuro, wait until sterile b/c heparin during bypass |
|
|
|
IE prophylaxis
|
invasive dental procedures, other situations only if high risk
previous IE prosthetic valve congenital cyanotic heart disease with prosthetic shunts first six months after repair repaired CHD with residual defects cardiac transplant with valvular disease |
|
|
|
acetazolamide
|
carbonic anhydrase inhibitor
pct glaucoma ADR metabolic acidosis |
|
|
|
mannitol
|
osmotic agent
PCT for cerebral edema worsen CHF |
|
|
|
furosemide
|
loop agents
thick ascending limb for acute chf |
|
|
|
HCTZ
|
thiazide
DCT mild pulmonary edema spares calcium |
|
|
|
carbonic anhydrase inhibitors
|
increases loss HCO3
PCT Sulfonamides Urine alkaline/blood acidic for glaucoma, to alkanalize urine |
|
|
|
mannitol
|
osmotic diuretic
IV increased urine volume with little NA loss PCTcause fluid overload CHF extracts intracellular water decreases ICP ADR hyponatremia, hypokalemia |
|
|
|
furosemide
|
loop diuretics
high ceiling diuretic excretes everything for severe chf, renal failure, hypercalcemia ADR Ototoxic contraindicated with aminoglycosides Increase LDl/TGs Sulfa Rxns |
|
|
|
Hs
|
hyponatremia
hypotension hypokalemia (arr) hypocalcemia (muscle excitabilityi) hypomagnesia(convulsions) hypochloremic alkalosis (excessive loss Cl) hyperuricemia hyperglycemia |
|
|
|
thiazides
|
DCT
lower ceiling calcium sparing ADR sulfa LDL.Tg for moderate CHF, hypocalcemia, diabetes inspidsus, decreasing URINE calcium to decrease kidney stones |
|
|
|
K+ sparking diruetics
|
spironoloactone, amiloride
|
|
|
|
spironolactone
|
aldosterone antagonist
collecting ducts aldosterone dependent diuretic for 2nd aldosteronism to CHF, cirrhosis, hypokalemia ADR hyperkalemia, impotence, gynecomastia |
|
|
|
amiloride
|
triamterene
not dependent on aldosterone K+ sapring combo with other diuretics sides hyperkalemia |
|
|
|
ADH antagonists
|
conivaptan/demeclocycline
collecting tubule |
|
|
|
conivaptan
|
PO
adrenal insuff, hypothyroid, too much ADH ADR hypokalemia |
|
|
|
demeclocycline
|
ADR Diabetes inspidus, renal failure, photosensitivity, no children under 12
|
|
|
|
acute CHF tx
|
furosemide
|
|
|
|
moderate chf tx
|
HCTZ
|
|
|
|
cause of hypercalcemia
|
HCTZ
|
|
|
|
decreases urine Ca
|
HCTZ
|
|
|
|
tx renal failure, hyper kalemia
|
HCTZ
|
|
|
|
need to void calcium?
|
furosemide
|
|
|
|
need to get Ca out of urine
|
HCTZ
|
|
|
|
have a metabolic acidosis? what did you take
|
acetazolamide
|
|
|
|
for acute CHF
|
furosemide
|
|
|
|
systolic dysfunction
|
younger, pump dysfunction, decrease CO
|
|
|
|
diastolic dysfunction
|
older, TPR, renal HTN, vascular
|
|
|
|
increase sodium in SMC
|
increase calcium, increase sensitivity to NE/EPI/ANGII with increase in calcium -->vasoconstriction
|
|
|
|
diuretics antihypertensives
|
decrease NA, CA, TPR
k sparers paired with loops interfere with compensatory reflexes, baroreceptors, RAA |
|
|
|
protect against osteoporosis
|
HCTZ
|
|
|
|
spironolocatone useful in chf 2nd aldosteronism
|
k+ sparing
|
|
|
|
beta blockers
|
NS propanolol, B1 Atenolol and metoprolol
decrease CO, Renin (B1) use with younger patients with increased SNS tone, hyperkinetic circulation decrease LVH ADR depression, fatigue, TG.Chol, IMportence |
|
|
|
labetalol/carvedolol
|
alpha 1 and non specific BB
decrease TPR and CO IV in HTN emergency, pheochromocytoma |
|
|
|
alpha 1 blockers
|
prazosin
decrease pre/afterload maintain RBF increase CO in CHF, decrease LVH ADR postural hypotension, impotence, tachycardia |
|
|
|
alpha 2 agonists
|
presynaptic in PNS/CNS exerts negative feedback, decrease NE release
postsynaptic in CNS inhibit SNS outflow from vasomotor/cardiac centers decrease vasomotor tone, BP, HR |
|
|
|
Clonidine
|
alpha 2 agonist
decrease BP HR CO, increase PNS, vagal PO, transdermal ADR cns depression, sedation abrupt cessation, rebound effect |
|
|
|
methyldopa
|
alpha 2 agonsit
decrease BP, less HR and RAA than clonidine useful with diuretic safe in preg but cause hemolytic anemia cns sedation, disturbances |
|
|
|
hydralazine
|
arteriolar vasodilator
decrease diastolic more than systolic, decrease TPR activates baroreceptor/RAA reflect diuretic and BB in severe HTN ADR excessive vasodilation, edema, flushing, SLE, arthalgia |
|
|
|
minoxidil
|
arteriolar dilator
open K+, decrease SMC contraction ADR relfex tach, edema, chf, tamponade, hair growth used for severe htn w diuretic |
|
|
|
HTN crisis
|
nitroprusside, diazoxide
|
|
|
|
nitroprusside
|
IV, increase HR, decrease BP,
adr flushing |
|
|
|
diazoxide
|
K+ channels
arteriolar dilator increase HR used with BB |
|
|
|
antiHTN Ca blocker verapimil diltaizem
|
arteriolar dilators, decrease CO
too much cause CHF ADR av block, constipation |
|
|
|
nifedipine, dihydropyradines
|
cal channel more potent but reflex tach,
adr excessive vasodilator, chf, edema |
|
|
|
minoxidil
|
increase hair and heart rate
|
|
|
|
dose dependent HR decrease
|
verapimil
|
|
|
|
ACEI
|
decrease angiotensin II, decrease TPR, decrease vasoconstriction
increase bradykinin (vasodilator) (decrease pre/afterload) increase CO in CHF, maintain renal Fx in diabetic neuropathy no metabolic, no impotency issues ADR hypotension, hypokalemia, cough contraindicated in preg |
|
|
|
captopril
|
aceI, fast, short t1/2
|
|
|
|
enalapril/lisinopril
|
prodrugs, long t1/2
|
|
|
|
losartan
|
ang II inhibitor
ATI blocker long t1/2 arterial SMC, kidney, adrenal effects does not increase bradykinin ADR cough, angioedma, fatigue, hypotension, liver enzymes, |
|
|
|
verapimil
|
constipation, no reflext tach
|
|
|
|
enalapril
|
decrease AngII
|
|
|
|
methyldopa
|
hemolytic anemia
|
|
|
|
postural hypotension
|
alpha receptor blockers
|
|
|
|
captopril
|
cough
|
|
|
|
propanolol
|
FHx HTN, MI, LVH
|
|
|
|
lidocaine
|
increase ERP/APD ration
|
|
|
|
procainamide
|
SLE
|
|
|
|
verapimil
|
av node tach
|
|
|
|
ibutilide
|
reduces k+ repolarizing current, increase APD duration
|
|
|
|
edema and metabolic acidosis
|
HCTZ
|
|
|
|
mannitol
|
cerebral edema
|
|
|
|
conivaptan
|
SIADH
|
|
|
|
myocardial preconditioning
|
activation KATP channels helps mediate
|
|
|
|
PKCE activator before transplant
|
cardiportecitve
|
|
|
|
BH2 and PKCEativator
|
increase H202 during reperfusion
|
|
|
|
coupled enos
|
limits reperfusion injury
|
|
|
|
mcc genetic congenital heart disease
|
down syndrome
|
|
|
|
lesion chromosome 22
parathyroid. thymus, heart |
digeorge syndrome
|
|
|
|
asd
|
Asx until adulthood
irreversible pulmonary HTN can develop l2r secundum 90% fossa deficieny or fenestrated primum adjacent to aortic valve, MV defect too sinus venosus near entrance to SVC-conection to right pulm veines cardiac cirrhosis, paradoxical embolization, cor pulmonale |
|
|
|
vsd
|
l2r
most involve membranous septum others liie beneath PV some close spontaneously large defects result in RVH, switches r2l, pulm htn, cyanosis, death |
|
|
|
tet of fallot
|
r2l shunt
vsd w/overriding aorta RVOTO RVH boot shaped heart transposition of great vessels need vsd to survive pulm stenosis protects lungs from RVH |
|
|
|
pda
|
r2l
no issues at birth machinery like murmur shunt left to right at birth then pbstructive pulm vascular disease and flow shifts r2l |
|
|
|
av septal defect
|
poor formation of av valves
partial, MR complete all four chambers communicate, four chamber hypertrophy assoc w down syndrome |
|
|
|
transposition of great vessels
|
PA/Aorta reversed
systems separated, must have shunt to live vsd=stable shunt PFA=unstable, needs surgery |
|
|
|
truncus arteriosus
|
fail;ure embryologic TA to separate into aorta and PA
single artery receive blood from both ventricles VSD irreversible pulm HTN cyanosis |
|
|
|
tricuspid atresia
|
TV occlusion
unequal division AV valves RV atrophy right to left shunt through PFA or ASD VSD allows for communication to RV/PA |
|
|
|
MCC congenital heart disorder
|
ASD
2:1 female to male subtle clinical findings |
|
|
|
MC ASD
|
ostium secundum
ostium primum sinus venosus |
|
|
|
eisenmenger system
|
chronic L2R shunt causes irreversible pulm HTN and a reversal into R2L shunt
|
|
|
|
ASD
|
dyspnea
fatigabnility palpitationms atrial arrythmias syncope stroke MI palpable pulsation of PA and ejection click S1 split S2 widely split, fixed acyanotic, no tx necessary spontaneous closure is frequent in children repair not recommended in insignificant shunt, severe PA HTN, Pulm Vascular Occlusion |
|
|
|
PDA
|
female to male 2:1
Thoracic aorta-> pulmonary artery congenital-rubella children born at high altitude or premature infants perinatal asphyxia, low birth wt, siblings of PDA Recurrant Laryngeal loops around DA L2R shunt PDA is repsonible for 60%of CO in fetal life patency promoted by PGE2 NSAIDS in mother can close absence of DA contraction--hypoxemia, aspphyxia, renal failure, resp disorders fetal alcohol congenital rubella amphetamine, phenytoin use DX echo, CXR, catheter to measure O2 sat in RV IV indomethacin, ibuprofen, coil embolization, ligation |
|
|
|
ortners syndrome
|
pulm htn, left atrial enlargement, impinge on recurrent laryngeal
|
|
|
|
MC VSD
|
perimembranous
|
|
|
|
VSD
|
L2R shunt
AR LVH, Dilation Eisenmengers complex -VSD. HTN. CYANOSIS CHF, cardiogenic shock murmur systolic, left upper sternal border radiate to back crescendo-decescendo ECHO, CATH, MRI diagnose surgical repair good prognosis |
|
|
|
coarctation of Aorta
|
constrictioed aortic segment
pre/post ductal can get post stenotic dilation M:F 2:1 young: CHF old:htn LVH acute right heart dilation if FO is not patent less severe coarctation will produce collateral circulation greater than 20mmHg difference in blood pressure between upper/lower extrmity absent lower extremity pulse cyanotic lower extremity R2L shunt murmur nonspecific infraclavicular under left scapula delay between femoral and brachial pulses cath with contrast to see aortic pinch rib notching from collateral circulation associationd VSD, Bicuspid AV, Abnormal retinal blood vessels tx baloon angioplasty poor prognosis uncorrected |
|
|
|
TET of fallot
|
cyanotic
RVOTO VSD overriding aorta Aorta Dextroposition RVH PV stenosis congenital rubella, poor prenatal nutrition, FAS, older mothers, mothers with PKU, DM down syndrom related to TET blue skin during crying tet spells squatting is compensatory mechanism surg repair necessary cyanosis, clubbbing, systolic thrill, PV closure not heard polycythemia, embolize, low O2 sat, boot shaped heart propanolo can correct RVOTO prognosis sudden death, PE, parradoxical emboli, |
|
|
|
MCC cyanotic congenital heart defect
|
TET
|
|
|
|
BP
|
=COxTPR(SVR)
CO=HRxSV |
|
|
|
SV low and WET
|
LVEDV increased
|
|
|
|
SV low and DRY
|
LVEDV decreased
|
|
|
|
RAA stimulated
|
when kidney is not perfused
|
|
|
|
NE
|
drives HR, increases TPR
|
|
|
|
systolic HF
|
EF <40%, cant pump
right side of starling curve |
|
|
|
diastolic HF
|
EF>40%, cant fill
left side of starling curver |
|
|
|
Systolic and Diastolic HF Sx
|
dyspnea, edema
age, htn, dm, overwt |
|
|
|
systolic Dysfx
|
enlarged apex, displace ventricle down and to left
S3 kyperkinesis |
|
|
|
diastolic Dysfx
|
S4 (atrial sound, heard best with bell over left ventricle)
|
|
|
|
volume overload
|
neck veins up, systolic dysfx
|
|
|
|
afterload reducer of choice for systolic dysfx
|
ACEI
|
|
|
|
reduce preload
|
furosemide
|
|
|
|
reduce afterload
|
beta blockers, block NE, indirect afterload reducer
|
|
|
|
Tx of choice to prolong life
|
ACEI BB Diuretic
|
|
|
|
use hydralazine/nitrates?
|
ACEI contrindicated, ACEIBBDIURETIC not effective
|
|
|
|
causes of systolic dysfx
|
htn, mi, IHD, cardiomyopathy, Valvular heart disease, congenital
|
|
|
|
Big heart
|
S3 cant pump
|
|
|
|
diuretic treatment of choice
|
CHF and uncontrolled HTN
|
|
|
|
digitalis
|
when dont respond to BB ACEI DIURETIC and in CHF
|
|
|
|
diastolic dysfx
|
left side starling curver underfilled
small cavitieis scarred, fibrotic ventricle cavity constricted from outside IHSS, AS, LVH, HTN |
|
|
|
LVH because HTN
|
beta blocker
no acei no diuretic |
|
|
|
cant give beta?
|
give ca blockers verapimil/diltiazem, block AV node
|
|
|
|
cardiomyopathy
|
chronic systolic dysfx
big hearts, poor pumps, S3, shortness breath |
|
|
|
TB
|
chronic/night sweats, cough, hiv
Dx with TAP fro adenosine deaminase thickened restrictive pericardium needs to be peeled off |
|
|
|
hypothyroidism
|
after radiation
pericardial effusion gold paint over time leads to bradycardia Tx treat hypo T4 |
|
|
|
CHF and bradycardia
|
either thyroid or conduction system block
|
|
|
|
acute pericardial effusion
|
X descent
|
|
|
|
chronic pericardial effusion
|
y descent
|
|
|
|
constricitve/restrictive disease Sx
|
dyspnea, neck vein, X/Y descent, small hearts, edema
gget an echo and doppler ultrasound |
|
|
|
restrictive problems
|
show peak and plateau
RV diastolic pressure <1/3 RV systolic pressure elevated pulmonary pressures virus, infx, metastatic breast cancer tanned skin? could be hemochromatosis and liver dysfunction |
|
|
|
constrictive problems
|
filling pressures elevated
RV/PA pressures not elevated |
|
|
|
doppler patterns
|
Normal. E=Violent, A=atrial contract
Early Diastolic dysfx cavity thick, e wave smaller, atrial contract harder very large E very small A =restrictive disease |
|
|
|
diastolic dysfunction
|
arrhythmia, atrial fibrilation
afib can be caused by hypothyroidism |
|
|
|
atrial fibrillation with rapid ventiricular respoinse 2nd to hyperthytoidism,
|
use b blocker because it blocks conversion t4 to t3 in periphery
|
|
|
|
good ventricle, bad atrial arryhtmia
|
can walk around for a long time
|
|
|
|
increased NE levels
|
chronic systolic dysfx,
|
|
|
|
HOCM
|
restriction due to obstructive disease of ventricle when septum is thicker than posterior wall and overall heart thickened
valsalva, murmur ets longer treat obstruction with BBLocker if not, ca vlockers get desperate>? use disopyramide (cant pee, cant poop, no good) |
|
|
|
causes heart failure
|
ischemic
non-ischemic-familial, infx, alcohol, thyroid, acromegaly, thiamine def, HTN in developing world? CHAGAS |
|
|
|
causes myocarditis
|
viral, fungal, bacterial, parasitic, toxins, anthracycline, cocain, chemo
|
|
|
|
amyloidosis
|
deposition of insoluble extracellular fibrillar deposits forming b-pleated cheets
senile-depot transthyretin-better prognosis firm rubbery dilated nodules on atrial endocardium stains congo red positve (green birfringeringences) rings around myocytes, capilarrioes compress lumen, capillaries-->ischemie |
|
|
|
iron overload
|
hemochromatosis or excess blood transfusions
heart dilated iron in ventricles systolic dysfx-ROS, mess up enzymes hemochromatosis-chromosome 6 rusty borwn color hemosiderin in perinuclearregon cell degeneration, fibrosis iron containing lysosomes |
|
|
|
long QT
|
dominant gene
antipsychotic, antiarrhythmic, allergy meds common genetic cause sudden death Sx during rigorous activity Dx with ekg females more likely to experience symptoms prolonged ventricle repolarization Torsades de Pointes/VFib autopsy normal, test for mutated genes |
|
|
|
Brugada syndrome
|
SE asia
inherited, sudden death middle aged males RBBB defectin sodium channel autosomal dominant |
|
|
|
catecholaminergic Polymorphic Vtach
|
associated with sudden death with exercise
finnsih/italian syncopal spells in childhood/adolescence with exercise/stress 50% mortality by 30, resting ekg normal |
|
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|
short QT syndrome
|
sudden death, premature atrial fib, adolescence
|
|
|
|
commotio cordis
|
sudden blunt impact to prcordial area
abnormal ventricle activity, cardiac arrest sudden death no structural injury low speed imapct VFib impact coincides with period ventricle repolarization |
|
|
|
myxomas
|
50% of primary heart tumors
sporadic-middle aged females, left atrium single familial-young males, not left atrium multple |
|
|
|
carneys syndrome
|
myxoma, fibroadenomas breast, sertoli cell tumors, adrenocrotical nodular dysplasia (cushings)
|
|
|
|
left sided myxomas
|
MS/MR
|
|
|
|
Right sided myxomas
|
dyspnea, syncope, neck vein, emboli, infarcys
|
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|
|
myxomas
|
soft, pale, lobulated, stalk attached to septum,
round stellate cells, loose stroma, mucopolysaccarides, no mitotic figures, arises from mulitpotent stem cells |
|
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|
rhabdomyoma
|
benign tummor skeletal muscle
early life, congenital adults-tuberous sclerosis or congenitalnheart disease regress in childhood well circumscribed nodiles, spider cells with radial cytoplasmic extensions |
|
|
|
cardiac fibroma
|
solitary, 2nd decade, sudden death, outflow tract obstruction
|
|
|
|
gorlins syndrom
|
basal cell carcinoma, cardiac fibroma, rhabdomyosarcoma
|
|
|
|
sottos syndrome
|
cerebral gigantism, cardiac fibroma
|
|
|
|
hamartoma of cardiac myocytes
|
extensive production
localize hypertrophic cardiomyopathy myocyte disarray focal scarring coronary thickenig of bridging arteries left ventricle |
|
|
|
calcified amorpous tumor of the heart
|
nodular depot calcium in background of degenerating blood cell elements, chronic inflammation
benign clinical course pathogenesis obscure |
|
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|
Cardiac MICE
|
mesothelial/monocyte incidental cardiac excrescences
incidental microscopic findings at time of surgery can attach to heart, floating in cavity,inside an aneurysm strips of mesothelial cells, tubular and micropappillary formations surrounded by smaller histiocytes bengin, non neoplastic, no clincal significance |
|
|
|
cystic tumors of av node
|
developmental abnormality of epithelial nature, endodermal origin
may be associated wit other congenital abnormalities cause complete heart block tumors rarely seen grossly micro ductal structures, cysts, nests of epidermal cells, desmosomes,microvillia sudden death |
|
|
|
papillary fibroelastomas
|
small papillary growth on valves, etc
incidental finding hyperplastic endocardial cells covering core of hyalinized hypocellular stroma end stage organization of thrombus seen more frequently after cardiac surgery |
|
|
|
paraganglioma
|
primary cardiac neoplasm
left atrium is most common location HTn, elevated, urine catecholamine |
|
|
|
sarcoma
|
very rare
highly pleomorphic, difficult to classify angiosarcoma is most common usually large mass in right atrium |
|
|
|
fibrosarcoma
|
chf, arrhytmhias, svc obstruction
malignant tumors more likely on right side of heart |
|
|
|
synovial sarcoma
|
biphasic pattern
carcinoma/sarcoma |
|
|
|
high grade sarcoma
|
pleomorphic, high n:c ration, spindle cells, mitotic figures
|
|
|
|
lymphoma
|
primary is rare, 2nd more common
associated with aids, large cell lymphomas |
|
|
|
metastatic timors
|
primary usually in thoracic area, mediastinal lymph nodes, hematogenous route (breast, kidney, melanoma, choriocarcinoma)
|
|
|
|
tamponade
|
compression of atria and ventricles restricting cardiax filling
|
|
|
|
pericarditis
|
almost always viral origin
chronic forms seen in TB, fungal but most is acute secondary thoracic/systemic issues, cardiac surg, metastasis |
|
|
|
serous pericarditis
|
acute
can be noninfx, RF, SLE, uremia, scleroderma, viral associatied straw colored fluid viral infx elsewhere, few leukocytes small volume (10-50 normal) rarely organizes rich protien content |
|
|
|
fibrinous pericarditis
|
acute, protein adherent pericardium to epicardium
most common serous with fibrinous exudate assoc with acute mi dressler sydrome0autoimmune etiology, weeks to months around acute MI) uremia, chest radiation, RF, SLE, trauma dry surface, fine granular roughening |
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serofibrinous pericarditis
|
combo of two
thicker fluid WBCs can become organized |
|
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|
purulent/suppurative pericarditis
|
infective organisms, pus
-extension from neighboring inflammation -seed blood- -lymphatic extension -direct induction during surgery acute inflammatory RXN -organization is likely (constrictive pericarditis) resolution infrequnct |
|
|
|
hemmoragic peridcarditis
|
blood w/ fibrinous or suppurative
malignant tumor of pericardial space inovolved bacterial infx, bleeding disorders, tb follows surgery, serious blood loss, tamponade |
|
|
|
caseous pericarditis
|
tb fungal
spread through nodes chronic, constrictive |
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|
chronic pericarditis
|
plaque like fibrous thickneing of serosal membrane called soldiers plaque
adhesions found at autopsy with no clinical significance in severe cases organization can obliterate pericardial sax, cause stringy adhesions bewtween visceral pareityal pericardiim called adhesive pericarditis |
|
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adhesive mediastinal pericarditis
|
follow suppurative, caseous pericarditis, cardiac surgery, mediastinal irritation
pericardial sac obliterated great strain on cardiac fx RVH mimic cardipmyopathy |
|
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|
constrictive pericarditis
|
dense, fibrous scar
decrease diastolic expansion, decrease CO hypertrophy, dilation can occur because dense fibrous scar pericardial space obliterated |
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right ventricle
|
preload pump, conduit, dictates volumes
|
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|
|
pulmonary venous resistance
|
right ventricle afterload
|
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|
|
MCC rt atrial failure
|
left ventricle failure
|
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|
neck vein, edema, cold distal digits
|
right heart
|
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|
|
starling curve
|
to the right, volume overload
to the left, dehydration |
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|
right side maneuvers
|
inspire, leg raise squat increases
expirate, valsalva decrease |
|
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|
left side maneuvers
|
hand grip squat.
|
|
|
|
left MV
|
htn dyspnea mid to late systolic murmur at apex
|
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|
|
AS
|
old person, syncope, DM, htn, cigarrettes, parvus et tardus, bilateral carotid bruits, systolic at base of hear
|
|
|
|
decrease venous return valsalva, stand up
|
4-6 beats later it decreases volume returning
less venous return, less blood pushing walls out, gradient up, longer murmur |
|
|
|
ihss
|
tx with beta blocker
septum wall thicker than posterior, obstructed at rest in diastole |
|
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|
tee
|
left side valve lesions
|
|
|
|
MC etiology of diastolic dysfx
|
HTN/LVH
|
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|
|
RV dysfx
|
begets lv dysfx
|
|
|
|
constrictive disease
|
pericardium, matted on epicardium, doesnt allow filling
|
|
|
|
restrictive disease
|
normal fx, normal size
|
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|
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rt side faiilure
|
heptaomegaly, fatigue, neck vein, edema
|
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visceral and somatic afferents
|
meet at dorsal horn
|
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|
|
sympathetic
|
red then skin blanch quickly
biochemical stays eed |
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|
|
t1-4
|
eent heart lungs
|
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|
|
t5-9
|
stomach, gallbladder, liver
|
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|
|
t10-11
|
kidney, intestine, gonads
|
t12-l2
|
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|
t2-8
|
upper extremities
|
|
|
|
t11-l2
|
lower extremities
|
|
|
|
direct stimuli
|
more nociception is easier facilitated set up
overload, fatigue, cold, trauma, gravity, nutrition, endocrine |
|
|
|
indirect stimuli
|
arthritic joint,visceral afferent, segmental somatic dysfx
|
|
|
|
type II
|
hyperextension to side of organ by rotators (sympathetics)
|
|
|
|
V-S clues
|
1st-celiac-tightness
segmetnal paraspinal tissues texture changes somatic dysfx enoough visceral nociception sets up facilitated segment more tissue texture change than restriction=V-S S-V more restriction |
|
|
|
S-V
|
type II more likely
postural crossovers apexes of curver right pec is a major trigger point |
|
|
|
neurologic autonomic
|
treat FS first
|
|
|
|
kerr/denslow
|
more facilitated,, less weight to fire segments
|
|
|
|
neurological lens
|
stressors
|
|
|
|
t5-9
|
upper gi to ligament of trietz (celiac ganglion)
|
|
|
|
t12-L2
|
descending colon, inferior mesenteric ganglion
|
|
|
|
t10-11
|
superior mesenterica ganglion
|
|
|
|
VS TYPE II
|
more likeley
|
|
|
|
V primary
|
more tissue texture recurrence post somatic treatment harder rubber hvla response
|
|
|
|
s primary
|
posturally challenged, biomechanically challenged
|
|
|
|
SNS dysfx
|
decrease blood flow, gland activity up, pain, sensitivitiy up, more anxiety
|
|
|
|
tissue drain dysfx
|
biochemical pH changes
lymph congestion, fibrosis, rediced angiogenesisi |
|
|
|
tumor
|
by the time it sets up FS is probably far along
|
|
|
|
posterior chapmans reflexes
|
NLV bundle piercing muscle btween spinous and transverse processes
|
|
|
|
VS
|
deep fascia against periosteum
small tapioca nodules palpation nonradiates sharp pain |
|
|
|
supra/infraclavicular
|
EENT
|
|
|
|
2,3,4 intercostal
|
heart, lungs
|
|
|
|
5,6 intercostal lefft
|
stomach pyloris
|
|
|
|
5,6 intercostal right
|
liver, gallbladder
|
|
|
|
umbilicus
|
bladder kidneys
|
|
|
|
symphysis
|
gonads,
|
|
|
|
anterior iliotibial
|
colon
|
|
|
|
posterior iliotibial
|
prostate, broad ligament
|
|
|
|
base of skull
|
sinuses, middle ear
|
|
|
|
anteriro chapmans points
|
more tener, spread out, dx beforeomt
|
|
|
|
posterior
|
therapeutic, closer, less tender less specific
|
|
|
|
visceral reflex pain
|
early-vague, deep, diffuse, poorly localized.
|
|
|
|
T1-6 paraspinal C2 base of skull
|
CV parasympathetics
|
|
|
|
T5-9 T10-L2 C@ base of skull
|
GI parasympathetics
|
|
|
|
IC2 left
|
heart, esophagus, bronchus
|
|
|
|
peritoneocitaneous reflext
|
direct irritation of parietal peritoneoum abdomincal wall, rebound tenderness, wall rigidity, surgical intervention
|
|
|
|
middle ear
|
supraclavicular
|
|
|
|
sinus
|
infraclavicular
|
|
|
|
pharynx tonsils
|
rib 1 rib 2
|
|
|
|
2nd ics
|
bronchus
|
|
|
|
3rd ics
|
upper lung
|
|
|
|
4th ics
|
lower lungs
|
|
|
|
base skull
|
heent
|
|
|
|
2/3 posterior interspaces
|
bronchus lungs
|
|
|
|
pancreas
|
right 5/65 ics
|
|
|
|
superior,inferior mesenteric
|
supra,umbilicus
1inch up and lateral, kidney 2 inch up and lateral adrenal bladder-flipped upside don |
|
|
|
small intestine
|
10-12 ribs
tip 12th rib on right appendix |
|
|
|
ascending bowl right quad to pelvis
|
descending bowel left quad to pelvis
|
|
|
|
ibs
|
posterior iliotibial band, low back pain
|
|
|
|
OA, OM suture, C2
|
parasympathetics for heart
|
|
|
|
right side to sa
|
left side to av
|
|
|
|
t1-3
|
ventricles
|
|
|
|
t4-6
|
atria
|
|
|
|
sns pathohysiology
|
vasoconstriction, increase tpr, bp, hr, constractility, decrease venous return, co
|
|
|
|
right heart
|
tachyarryhtmias
|
|
|
|
left heart
|
pvc, long qt, ectopic foci, vfib
|
|
|
|
left pex
|
major trp, possible cardiax, treat to reduce sns facilitated segmetns
counterstrain |
|
|
|
svt rt pec minor trp
|
convert to sinus when trp removed
|
|
|
|
2nd rib anterior and posterior alternating pressure
|
treat tach
do quickly on right side, speed heart up |
|
|
|
rt vagus
|
sa node bradycardia
|
|
|
|
lft vagus
|
av node block
|
|
|
|
anterior heart refers to thoracic
|
posterior radiate to skull
|
|
|
|
open thoracic duct
|
help chf
throacic duct valve under sns control |
|
|
|
total anomalous pulmonary venous connection
|
no pulmonary veins join left atrium
common pulmonary vein fails to join or becomes atretic primitive systemic from lungs remain patent drains into coronary sinus either patent foramen ovale or asd allows venous blood to enter atrium RVH, RAH with dilation hypoplastic LA, LV normal cyanosis |
|
|
|
aortic coarctation
|
2:1 male to female
common turners syndrome - 45X- rib notching collateral circulation through intercostals short low ears, barrel chest, cafe au lait spots infantile-tubular hypoplasia of aortica arch proximal to PDA adult-ridge like aortic infolding w/PDA infants die without intervention w/o pda asx until adults, htn upper extremities, weak low bp pulse lower extremiteies, collateral rib circulation lnotches, systolic murmurs |
|
|
|
pulmonary stenosis/atresia
|
RVH
if atretic, hypoplastic RV, ASD< blood enters lungs through PDA mild stenosis is ASx |
|
|
|
Aortic stenosis/atresia
|
valvular-cusps messed up, hypoplastic LV
PDA necessary highly infant fatal subaortic-thick ring of dense fibrous tissue below cusps supravalvulvar ascending wall thick, williams syndrome with developmental disorders and hypercalcemia mutation of elastic gene can cause can be well tolerated, sudden death possible |
|
|
|
CHF
|
heart cant eject blood delivered by venous system
left side failure-htn, AV/MV disease, IHD right side failure - LV failure, cor pulmonale, PV/TV disease dyspnea, orthopnea, paroxysmal nocturnal dyspnea, lung rales, edema |
|
|
|
left sided CHF
|
pulm congestion, edema, increased pulm venous pressure, heart failure cells, brown induration, lungs with hemosiderin and fibrosis
|
|
|
|
right sided failure
|
abdominal visceral congestion
soft tissue edema peritoneal, pericardial, pleural fluid chronic passive congestion cardiac cirrhosis |
|
|
|
cardiomyopathy
|
disease from abnormality to myocardium
often idiopathic some genetic abnormalities in cardiac energy metabolism MC: dilated |
|
|
|
DILATED CMP
|
progressive, 1/3 genetic, toxicities, myocarditis, pregnancy, nutrition def., immnologic
mural thrombi common, thromboembolism nonspecfic histo muscle cellshypertrophied, elongated, stretched, irregular interstitial fibrosis, small subendocardial scars due to healing previous mi 2-3x normal wt flabby thinning or thickening walls dilation all four chambers coronaries unremarkable heart hypocontractile myocyite cytoskeltal protiens or beta oxidation fatty acids mitochondrial defects cause DCMP in kids x linked-teens, dystrophin actin, desmin, lamin |
|
|
|
DCMP myocarditis
|
mcc viral in young
cocksackie b virus |
|
|
|
DCMP etoh
|
etoh and acetaldehyde have direct impact on myocardium
chronic etoh beri beri thiamine def |
|
|
|
dcmp preg
|
peripartum cmp
late preg, sev months post aprtum HTN, nutritonal def. increase levels prolactin |
|
|
|
arrhtymogenic RV dysplasia
|
in herited
rv failure, tach/fib sudden death in young rv wall thin, loose myocytes, fibrotic defective cell adhesion desmosomes |
|
|
|
DCMP
|
20-50 years, dyspnea, fatigue, death: arrhytmia or cardiac failure
|
|
|
|
hypertrophic cmp
|
abnormal diastolic filling
intermittent ventricular outflow obstruction thick, flabby, hypercontractile mimic amyloidosis, hypertensive heart disease massive hypertrophy without dilateion disproportional thickenign of ventricular septum (sub aortic) vent cavity loses round shape banana liek configuration bc septum bulging into lumen mutant sarcomere genes, troponin T myosin binding protien reduced chamber size, low compliance, impaired filling, VOTO focal mi afib, mural thrombi MC genetic cause sudden cardiac death MCC death young athletes |
|
|
|
restrictive cmp
|
decrease Ventricle complicane, filling
contractility normal can be idiopathic radiation, fibrous, amyloidosis, sarcoidosis, metaastasis, inborn erros metabolism normal size ventricles undilated cavities biatrial dilation patchy fibrosis |
|
|
|
RCMP endomyocardial fibrosis
|
young adults africa and tropics
fibrosis at apex and upwards tv. mvm fibrous tissue decrease volume decrease compliance mural thrombus |
|
|
|
loeffler endomyocarditis
|
fibrosis, mural thrombi, eosinophilic leukemia abnormal eosinophils, poor prognosis
|
|
|
|
RCMP endocardial fibroelastosis
|
rare, lv endocardium fibrous, first 2 years of life
congenital av obstruction rapid death |
|
|
|
cor pulmonale
|
right ventricle hypertrophy
|
|
|
|
left hhd
|
dilation chf death, LVH in absence of other path, Hx HTN
stiff wall LA enlarged increase transverse diameter of myocytes fibrosis in advanced stage |
|
|
|
RHHD
|
cor pulmonale
increase pressure rt atrium RVH, dilation emphysema, PE, etc acute or chronic compression lv (regurg tv) |
|
|
|
myocarditis
|
coxsackie A.B.
chagas neisseria candida sarcoid SLE radiation drugs dilated heart, soft focal hemmorage viral-mononuclear ccell infiltrate bacterial-neutrophil infiltrate myocyte necrosis |
|
|
|
giant cell myocarditis
|
young, middle aged
giant cells, eosinophils macs lymphocytes, plasma cells, necrosis rapid, lethal |
|
|
|
hypersensitivity myocarditis
|
older age
interstitial cell infiltrates eosin, mac, , perivascular lymphocytes drug hypersensitivity, methyl dopa |
|
|
|
cardiac sarcoidosis
|
ASx, conduction system lesions-->death
noncaseating granulomas with giant cells no necrosis, no eosinophils |
|
|
|
cardiac drugs
|
immuno/chemo, dilated CMP, lithium, phenothiazides, chloroquine, cocain.
remove drug may resolve problem |
|
|
|
catecholamines
|
intense ans stimulation, exogenous stimualtion by large doses vasopressors
necrosis, contraction bands, some monocell infiltrate pheochromocytoma, cocain, emoptional, physical stress calcium overload to myocytes, constrict coronary arteries increase HR |
|
