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35 Cards in this Set
- Front
- Back
Disorders Assoc w/ CV Defects1
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1. Downs - endocardial cushion defects (ASD, regurgitant valves)
2. DiGeorge- tet of Fallot - interrupted aortic arch 3. Friedrich's ataxia - hypertrophic cardiomyopathy 4. Marfan Syndrome - cystic medial necrosis of aorta 5. Tuberous sclerosis - valve obstruction from rhabdomyoma 6. Diabetic mother - transpos GV's |
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Carotid Sheath
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1. Internal jugular vein (lateral)
2. Common carotid artery (medial) 3. Vagus Nerve (posterior) V A N |
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Mediastinum
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Anterior-->Posterior
1. Adipose w/ thymus remnants 2. R/L brachiocephalic veins 3. SVC 4. Aorta & brachiocephalic trunk 5. L common carotid and L subclavian arteries 6. Trachea 7. Esophagus 8. Thoracic duct |
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Auscultation
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Aortic area:
- systolic murmur (AS) Pulmonic area: - sys ejection murmur (Pulm Sten, ASD) Tricuspid Area: - pansys murmur (tricus regurg, VSD) - diast murmur (tricus sten, ASD) Mitral area: - sys murmur (MR) - dias murmur (MS) Left sternal border: - sys murmur (hypertrophic cardiomyopathy) - diast murmur (AR, pulmonic regurg) |
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CV equations
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CO = SV x HR
MAP(afterload) = CO x TPR Pulse pressure ~ SV Force of contraction ~ initial length of muscle fiber (=preload) Ejec Fraction >55% (nl) |
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Resistance, Pressure, Flow
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Total resistance in series = R1 + R2 + R3
Total resistance in parallel = 1/R1 + 1/R2 + 1/R3 (*remember to invert your final answer!!) Arterioles = account for most of TPR (thus they regulate cap flow) Viscosity - mostly depends on Hct Inc in 1. Polycythemia, 2. Hyperproteinemia (MM), 3. Hered spherocytosis Resistance ~ Viscosity |
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Atrial Natriuretic Peptide (ANP)
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28AA peptide secreted by atrial myocytes in response to atrial stretch (=sys vol expansion)
Decreases BP via periph dilation, natriuresis, diuresis Binds to NPR-A on cell membranes and activates guanylate cyclase --> inc cGMP Organs: 1. Kidney - dilate afferent arterioles, inc GFR, urinary Na+/H20 excretion, limit Na+ reabsorption, inhib renin 2. Adrenal gland - restrict aldosterone secretion 3. BV's - relax smooth m, vasodilate, inc cap permeability --> fluid extravasation into interstitium to decrease circ BV |
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Abnormal Heart Sounds
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S3 = early diastole; rapid ventricular filling phase - common in dilated ventricles
- pt in lateral (left) decubital position or exhale completely to dec lung volume and bring heart closer to chest wall S4 = late diastole; atrial kick - high atrial pressure. Ventric hypertrophy (LA pushing against stiff LV) |
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JVP
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3 main peaks:
1. a wave - atrial contraction (ABSENT in Afib) 2. c wave - RV contraction (tricuspid valve bulging into atrium) 3. v wave - inc atrial P due to filling against closed tricuspid valve (max atrial filling) |
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S2 splitting
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Occurs bc aortic valve closes before pulmonic valve
1. Wide splitting = pulm stenosis 2. Fixed splitting = ASD 3. Paradoxical splitting = AS |
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Valsalva maneuver
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Bear down on closed glottis
Systolic murmurs in L heart Dec venous return to heart, dev LV vol and BP MVP & hypertrophic cardiomyopathy more audible AS less audible |
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MR
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holosystolic murmur
loudest at APEX, radiates toward AXILLA |
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AS
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cresc-decresc sys murmur
Ejection click Radiates to carotids/neck Pulsus parvus et tardus Syncope Age-related calcified aortic sten |
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VSD
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holosys harsh murmur
loudest at tricuspid area |
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MVP
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late sys murmur w/ midsys click
Loudest @ S2 |
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AR
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blowing diastolic murmur
Wide pulse pressure Head bobbing w/ carotid pulsations |
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MS
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After opening snap
late diastolic murmur heard at Apex LA dilation --> Ortner syndrome (impinge on L recurrent laryngeal n = hoarseness) |
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PDA
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continuous machine murmur (sys +dias)
Loudest at S2 Fetal period: R-L shunt (nl); should close after birth Neonatal: L-R shunt w/ RVH + failure (abnl) Patency: PGE2 synth |
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Which side is valvular defect on?
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If murmur loudest during inspiration:
Defect on R side b/c more blood flows into RA If murmur loudest during expiration: Defect on L side b/c more blood flows into LA |
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Cardiac myocyte v. Skeletal muscle
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Cardiac depends on EC Ca+ (Ca-induced Ca release!)
Skel depend on IC Ca+ (thus resist to CCBs) Cardiac muscle: 1. PLATEAU - Ca+ influx 2. Spontan depol = automaticity (If channels) 3. Gap jxns - electricle coupling |
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Ventric AP
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Phase 0 = rapid upstroke; Na+ channels open
Phase 1 = initial repol: inactiv Na+ channels, K+ channels begin to open Phase 2 = plateau - Ca2+ channels balance K+ efflux; Ca-induced Ca release from SR --> myocyte contraction Phase 3 = rapid repol = MASSIVE K+ efflux, close Ca+ channels Phase 4 = resting potential (high K perm) ** COMPARE TO PACEMAKER AP** |
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Pacemaker AP
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- no v-gated Na+ channels --> slow conduct vel
- no plateau - Phase 4 slope determines HR (If Na+) |
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Impaired SA node
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rate of SA node = 70-80 bpm
If impaired, AV cells take over = 45-55 bpm - no P waves (= atrial depol) - normal QRS (= ventric depol normally) AP velocity slowest in AV node, fastest in Purkinje system |
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Congenital QT Interval Prolongation
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1/5000 pts
predisp to syncope, ventric tachy (torsades) mut's in genes for cardiac cell K or Na channels Jervell & Lange-Nielsen syndrome (AR) - accomp by congen neurosensory deafness |
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ECG
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P wave = atrial depol
PR interval = conduc delay through AV QRS = ventric depol (atrial repol occurs here) QT interval = ventric contraction T wave = ventric repol ST segment = ventric depol U wave = hypokalemia/brady |
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Binge drinking
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Can cause Afib
- absent P waves (b/c uncoord atrial contractions) - irreg irreg QRS complexes |
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Wolff Parkinson White Syndrome
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Delta wave on ECG
Accessory pathway from Atria-->Ventric Bypasses AV Node May result in supraventric tachy |
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Baroreceptors
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Aortic Arch
- vagus nerve transmission to medulla - only responds to inc BP Carotid sinus - only via glossopharyngeal nerve to medulla - responds to dec and inc BP |
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Cushing triad
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HTN, brady, resp dep
- caused by central chemoreceptor which is responding to PCO2 and causing inc ICP, constricting arterioles and leading to cerebral ischemia --> HTN and reflex brady |
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Heart Circulation
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Increased oxygen demand met by increased coronary blood flow, not increased O2 extraction
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Capillary fluid exchange
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Starling forces - determine fluid movement through cap membranes
Pnet = [(Pc-Pi) - (pc-pi)] Kf = filt constant Net fluid flow = Pnet(Knet) |
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R-L shunts
Blue Babies |
1. Tet of Fallot
2. Transpos GV's 3. Truncus arteriosus 4. Tricuspid atresia 5. Total anomalous pulmonary venous return |
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L-R shunts
Blue Kids |
1. VSD - MCC
2. ASD - loud S1, wide S2 3. PDA - indomethacin closes * can all result in Eisenmenger's syndrome (shunt becomes R-L, clubbing, polycythemia) |
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Tet of Fallot
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Etiology: anterosuperior displacement of infundibular septum
1. Pulm stenosis - most important px factor 2. RVH 3. Overriding aorta 4. VSD Pt squats to improve sx's via femoral artery compression to dec R-L shunt and direct more blood into lungs |
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Coarctation of Aorta
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Infantile type:
Preductal aortic stenosis Adult type: Postductal aortic stenosis - rib notching (collateral circ) + HTN in UE's + hypoTN in LE's (check femoral pulses on P/E) Turner's association Can cause aortic regurg Usu bicuspid aortic valve |