First Aid Errata

First Aid Errata

May 18 Lecture

Love

acquired heart disease is something that happens after 6 months of age


Kawasaki's disease - immune response to gram positive infection (toxic shock) - complication = coronary aneurysms.  no specific lab test. Treatment = IV immunoglobin (IgG)

survivors grow up with abnormal coronary arteries (no adenosine response)

Kawashocki   - >8yo girls; refractory to IVIG; high incidence of aneurysms

Rheumatic heart disease - comes from previous strep infection.  polyarthritis (painful and swollen) antibody protein complexes in myocardium (Aschoff bodies) - mitral valve disease.  St. Vitus' dance - inflammation of basal ganglia (Sydenham's Chorea). (St. Vitus is the patron saint of dancers, young people and dogs.)

Pericarditis - lower preload = low stroke volume (diastolic failure).  JVD and hepatomegaly. -70-80% of cases idiopathic (probably viral); also post surgery.  treat with steroids. pericardiocentesis.  preload exaggerated with respiratory cycle and pulsus paradoxus present.


Myocarditis - viral etiology most common = entero (Coxsackie B) or adenovirus
patchy involvement - Echo shows dyskinesis.  MRI useful for Dx.  Biopsy may not show anything if normal area of heart is sampled.  Tx ACE ARB Beta blockers, digoxin (but proarrythmic), milrinone (a PDE 3 inhibitor; positive inotropic, vasodilating, also facilitates ventricle relaxation (positive lusitrope) by enhancing Ca++ ATPase reuptake by sarcoplasmic reticulum.

May 17 Lecture

good acid base tutorial website
http://fitsweb.uchc.edu/student/selectives/TimurGraham/Welcome.html


good congenital disease website
http://pediatriccardiology.uchicago.edu/mp/CHD/pcmedpro-CHD.htm

Goens

ASD

Qp/Qs normally =  Sat ao - Sat svc /  Sat pv - Sat pa  = 1 in normal hearts (cardiac output is the same to lungs and body)

How do you get this equation?  recall the Fick Principle

volume overload of right heart ((left to right shunt)

stretch of atria leads to afib

pulmonary htn.  Eisenmenger syndrome (irreversible pulmonary htn)

ASD silent but overload causes pulmonic systolic murmur.

split S2 (late P2)

VSD (paramembranous or muscular or supracristal) 

Q = P/R   direction of Q depends on resistance.  If pulmonary resistance is high there will be small shunt; i.e., after birth.  As PVR comes down, the shunt increases.

volume load on left atrium and ventricle.  RV handles extra flow as conduit chamber but left heart receives extra volume.

Qp/Qs > 1.5 = moderate symptomatic shunt

pulmonary HTN may progress to Eisenmengers

loud P2 narrow splitting S2

harsh high frequency murmur

small shunt at high altitude due to hypoxic vasonconstriction -

PDA

flow during systole and diastole   (pressure gradient present in both systole and diastole)

most likely to cause Pulmonary HTN

continuous murmur infraclavicular

roughens endothelium producing area where bacteria can stick (endocarditits)

Aortic stenosis

bicuspid valve - most common

pressure load - symptoms depend on how quickly load develops. LV hypertrophy = increased O2 demand;  coronary origins distal to stenosis and ostium is narrow = decreased coronary supply.

early systolic ejection click (like split S1) as aortic valve snaps open 

Coarctation of aorta

HTN in head and arm, not lower extremeties. risk of cerebral aneurysms, stroke

 Increased  O2 demand but supply is not decreased.

systolic murmur that spills into diastole, best heard over upper back.

radial femoral delay and radial pulse stronger than femoral

if with PDA, will see lower O2 sat in lower extremities. 

Combination Lesions

tetralogy of Fallot

shunt depends on resistance.   always some R to L, aorta sits on top of VSD.  pulmonary resistance = conus (dynamic obstruction) and valve (fixed) and distal resistance

pulmonary outflow murmur (stenosis)

Pulmonary stenosis with ASD

in systole, no effect on direction of flow through ASD

in diastole, tricuspid valve is open, so flow will decrease L to R

Coarctation with VSD

increase L to R shunt from higher resistance in aorta

Coarctation with VSD and ASD

increases Qp but reduces pressure in LA pts have less tachypnea (less pulmonary edema) versus pts with no VSD but no ASD

Aortic stenosis  and LV failure

diminished pulses in all 4 extremeties

inotropic drugs (drips)

opening DA with prostaglandins will increase systemic perfusion although O2 sat would be lower. 

VSD with bronchiolitis and Sat of 89%

treatment with oxygen will increase O2 sat but will also increase Qp/Qs from relieving hypoxic vasoconstriction.

but will produce congestive heart failure from increased pulmonary flow.

sending newborn with VSD from Albuquerque to sea level for surgery worsens L to R shunt by relieving pulmonary hypoxic vasoconstriction lowering RV pressure.

Hypoplastic left heart syndrome (single ventricle)

no LV and ASD

systemic flow occurs via PDA

Qp/Qs may be 3:1

pulses weaker in arm than leg (leg distal to PDA)

saturations = in arm and leg

life depends on PDA and ASD

brain development abnormal due to hypoxemia.

Aortic Stenosis with exercise

LV pressure increases with exercise.  myocardial O2 demand increases; risk of sudden death.

Love

cyanosis is apparent with 4 g deoxy Hb

normal vaginal birth squeezes out lung water.  Caesarean births may have tachypnea due to residual lung water.

transitional circulation

• PDA shunt reverses to R to L
• PFO closes when umbilical cord is clamped and sytemic resistance increases

• delayed by lung disease, altitude,

symptoms of cyanosis at SaO2 = 70%

adult = SNS activity - tachypnea, diaphoresis, 

newborn = no distress (same oxygen as in fetal life).  stable at PaO2 > 35 mm Hg.  fetal life has been termed "Everest in Utero"

comfortable tachypnea in adults - maintain minute ventilation with higher frequency

but not comfortable in newborns with higher work of breathing.

meconium aspiration plugs segments of lung.  

distinguish lung disease from heart disease by ABG on 100% O2

PaO2 goes from 30 to 50 with shunt (shunted blood never sees 100% O2)

PaO2 goes > 120 by treating V/Q mismatch

closure of ductus creates cyanosis in ductal dependent cyanotic heart defects:

• transposition of great arteries - switch of PA and Aorta - circulation in parallel, not series
•  need PFO to be stable 
• need PDA to be stable
• pulmonary valve atresis (no pulmonic valve)
• need PDA
• Tricuspid atresia
• need PFO and PDA (unless there is a VSD)

prostaglandin PGE used to keep PDA open (side effect = apnea) (countered by O2 treatment)

Total Mixing Lesions

• Truncus arteriosus - PA originates from aorta - total mixing in aorta
• total anomolous pulmonary venous return.  pulmonary venous return to RA.  Need PFO
• tricusid atresia.  all systemic return goes via PFO to LA
• hypoplastic left heart.  no LV so all pulmonary vernous return to RA through PFO.  total mixing in RA.

Tetralogy of Fallot

could be pink at birth, no R L shunt

management

increase systemic vascular resistance (legs to chest; iv fluids)

bring heart rate down (increase diastole)

Coarctation of Aorta

detect with 4 extremities blood pressure

VSD

no RV hypertrophy because R and L ventricles contract together.  LV hypertrophy due to increased diastolic filling due to L R shunt.  RV hypertrophy means Eisenmengers.

ASD

fixed splitting of S2 because RA volume stays high and doesn't vary with respiration.  diastolic filling through ASD.

May 11 Lecture

Shah

High compliance of bladder important in preventing post renal renal failure (high pressure in Bowman's capsule).

Micturition:  ANS modulates reflexes involved in micturition.  PNS facilitate voiding.  SNS facilitate storage. Somatics contract sphincter and can stop voiding.  Pontine micturition center is mainly inhibitory.  spinal cord damage = overactivity & incontinence.

Incontinence:  

1. Urge (failure to store)
2. Stress (failure to store; intrinsic sphincter deficiency; relaxation of pelvic floor muscles)
3. Overflow (failure to empty; BPH-urethral obstruction) 

Treatment of voiding disorders

• behavioral - 
• pharmacological 
• muscarinic antagonists - slow the bladder treats urge incontinence
• alpha blockers - inhibit prostate smooth muscle. treat BPH
• surgical - improve pelvic support structures; artificial sphincter

Ureters have pacemaker, propagation of urine to bladder

Kidney stones - phases of obstruction

1. increased ureteral pressure - increased renal blood flow
2. increased ureteral pressure - decreased renal blood flow
3. decreased ureteral pressure - decreased renal blood flow  (ischemia; renal damage)

risk factors
dehydration
high salt intake - increases calcium secretion (hypercalciuria)
acid urine - precipitates uric acid stones


kinds of stones

1. calcium oxalate - most common
2. uric acid
3. Struvite (Mg and ammonium phosphate) in recurrent UTI with urease splitting bacteria
4. Cysteine - autosomal recessive stone disease

Treatment

• alkalinize urine - uric acid stones
• hydration
• alpha blockers (expel stones)
• surgery

May 6 Lecture

Kanagy

Tx for hypertension
Ca channel blockers (e.g., verapamil) and K channel activators (e.g., minoxadil) dilate vascular smooth muscle.

circulating norepinephrine versus circulating epinephrine

 epi = increased cardiac output and vasodilation in muscle and liver (beta 2) Pressure does not change since increase in Q is balanced by decrease in R  (P = QR)

circulating norepi causes increased cardiac output (beta 1) and increased vascular resistance from vasoconstriction in most arteries and veins (alpha 1 and 2).  transient increase in heart rate is reduced via baroreceptor reflex.

May 3 Lectures

Roldan

in slide 5, the trivial to mild regurgitation % refers to percent of the population who show this, not the % regurgitation.

for slides no. 15 and 24 (compensated AS and AR), the increased contractility is due to beta adrenergic stimulation.


use Firefox not Internet Explorer to open.
a great PowerPoint by a friend and colleague on this topic is available at:
http://www.boom-outahere.com/cvpulmrenalConcepts/CV/Cardiac Valve Dysfunction.ppsx