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35 Cards in this Set

  • Front
  • Back
Disorders Assoc w/ CV Defects1
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
Carotid Sheath
1. Internal jugular vein (lateral)

2. Common carotid artery (medial)

3. Vagus Nerve (posterior)

V
A
N
Mediastinum
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
Auscultation
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)
CV equations
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)
Resistance, Pressure, Flow
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
Atrial Natriuretic Peptide (ANP)
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
Abnormal Heart Sounds
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)
JVP
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)
S2 splitting
Occurs bc aortic valve closes before pulmonic valve

1. Wide splitting = pulm stenosis

2. Fixed splitting = ASD

3. Paradoxical splitting = AS
Valsalva maneuver
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
MR
holosystolic murmur

loudest at APEX, radiates toward AXILLA
AS
cresc-decresc sys murmur

Ejection click

Radiates to carotids/neck

Pulsus parvus et tardus
Syncope

Age-related calcified aortic sten
VSD
holosys harsh murmur
loudest at tricuspid area
MVP
late sys murmur w/ midsys click

Loudest @ S2
AR
blowing diastolic murmur

Wide pulse pressure

Head bobbing w/ carotid pulsations
MS
After opening snap

late diastolic murmur

heard at Apex

LA dilation --> Ortner syndrome (impinge on L recurrent laryngeal n = hoarseness)
PDA
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
Which side is valvular defect on?
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
Cardiac myocyte v. Skeletal muscle
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
Ventric AP
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**
Pacemaker AP
- no v-gated Na+ channels --> slow conduct vel
- no plateau
- Phase 4 slope determines HR (If Na+)
Impaired SA node
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
Congenital QT Interval Prolongation
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
ECG
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
Binge drinking
Can cause Afib

- absent P waves (b/c uncoord atrial contractions)
- irreg irreg QRS complexes
Wolff Parkinson White Syndrome
Delta wave on ECG

Accessory pathway from Atria-->Ventric
Bypasses AV Node

May result in supraventric tachy
Baroreceptors
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
Cushing triad
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
Heart Circulation
Increased oxygen demand met by increased coronary blood flow, not increased O2 extraction
Capillary fluid exchange
Starling forces - determine fluid movement through cap membranes

Pnet = [(Pc-Pi) - (pc-pi)]
Kf = filt constant
Net fluid flow = Pnet(Knet)
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
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)
Tet of Fallot
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
Coarctation of Aorta
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