Cardiology Flashcards
Percentage of fetal CO received by placenta
45%
Percentage of fetal CO received by lungs
7-35%
Less earlier in gestation (7-15% in second trimester)
In third trimester there’s increases pulm vessel growth and PBF ~35%
DA remains patent in utero due to?
Prostaglandins E2
Prostacyclin I2
Thromboxane A2
PDA closure after birth - mechanism
Higher O2 concentration within ductal tissue
Lower E type prostaglandins because you lose placental production and the increased PBF (lungs metabolize PG)
Bradykinin from lungs at birth further constricts the DA
Cardiac out =
CO = HR x SV
CO = SBP/total peripheral vascular resistance
Factors affecting CO
- Preload (degree of stretch at end of diastole)
- Afterload (tension/stress in ventricular wall during ejection)
- Contractility (force and velocity of contraction)
- HR (regulated by parasympathetic and sympathetic NS as well as hormonal system)
Afterload does not impact CO as much as preload because it does not alter the CO until the BP reaches a critical level
Neonates more dependent on HR than SV
What increases preload
Increased blood volume
Increased venous tone
Increased ventricular compliance
Increased atrial contraction
Decreased intrathoracic pressure
Ventricular wall stress =
Ventricular wall stress = (ventricular pressure x ventricular radius) / wall thickness
And wall stress is afterload
So increased vascular resistance distally -> increased proximal pressure -> increased wall stress aka afterload
So ventricular dilation -> increased radius -> increased wall stress aka afterload
So hypertrophied wall -> increased wall thickness -> decreased wall stress aka afterload
Afterload corresponds directly with end systolic volume (increased afterload means more blood left after he thin and increased in end systolic volume)
Stroke work =
Stroke work = mean arterial pressure x SV
Frank starling principle
Increased LV diastolic filling -> cardiac muscle stretch -> greater force of contraction -> increased stroke volume
O2 consumption =
O2 consumption = delivered - returned
= (BF x O2 arterial content) - (BF x O2 venous content)
Qp/Qs =
Qp/Qs = (1 / [pulm vein O2 sat - pulm artery O2 sat]) / (1 / [aortic O2 sat - mixed venous O2 sat])
PVR =
Resistance of flow as it passes through the lungs
PVR = (mean PA pressure - mean LAP) / PBF
change is pressure across a circulation divided by flow through that circulation
SVR =
SVR = (mean aortic P - mean RAP) / SBF
Resistance of flow as it passes through the body
change is pressure across a circulation divided by flow through that circulation
Cyanosis
Absolute amount of unbound (reduced) Hb NOT O2 saturation
Anemia can decrease clinical detection of cyanosis
Observed clinically if >3-5g of reduced Hb per dL of capillary blood
O2 saturation =
O2 saturation = HbO2 / (HbO2 + Hb)
Hb is reduced or unbound
HbO2 is saturated with O2
So it’s the percentage of bound / total
Specific cardiac lesions:
Right radial paO2 (pre ductal) 100mmHg
Umbilical arterial paO2 (post ductal) 45mmHg
Critical preductal CoA with PDA and increased PVR
Specific cardiac lesions:
Right radial paO2 (pre ductal) 45mmHg
Umbilical arterial paO2 (post ductal) 80mmHg
DTGA with intact ventricular septum and PDA with 1 of the following:
- PH
- Interrupted aortic arch
- Preductal coarctation of the aorta
Specific cardiac lesions:
Right radial paO2 (pre ductal) 75mmHg
Umbilical arterial paO2 (post ductal) 50mmHg
Pulmonary hypertension with right to left shunting across PDA
Specific cardiac lesions:
Umbilical arterial paO2 (post ductal) 65mmHg
Umbilical venous pO2 (high line) 95mmHg
Infradiaphragmatic TAPVR (usually obstructive)
Localization of murmurs
URSB
LLSB
ULSB
Apex
URSB - AS
ULSB - PDA, PS, ASD
LLSB - VSD, TR
Apex - MR, IHSS
Medication for pulmonary hypertension
Nitric oxide
Sildenafil (phosphodiesterase 5 inhibitor)
Bosentan
Iloprost
Nitric oxide mechanism
Endothelium derived molecule that relaxes vascular tone
NO formed from L arginine by NOS in endothelial cells lining blood vessel walls
Diffused to vascular smooth muscle and activates guanylyl cyclase which increased cGMP (from GTP) which decreases vascular tone
INO selectively vasodilates the blood vessels that are ventilated - improving VQ matching
Risk of another child with CHD
2-5% if one child with CHD
5-10% if 2 children with CHD
Recurrence risk
If mom with CHD the child 2-18% risk
If father with CHD the child with 1-3% risk
Cyanosis heart disease
5 Ts DO and ESP
Truncus arteriosus
TGA
TA
TOF
TAPVR
DORV
Ebstein anomaly
Single ventricle
Pulmonary atresia
dTGA repair and common complications
Repair at 1 week of age
Fairly common to develop main or branch PA stenosis
Fairly common to develop aortic insufficiency
TOF repair timing and common complications
Repair of TOF at 3-6 months
Fairly common for stenosis of pulmonary valve or RV-PA conduit
Most patients have RBBB on EKG
Fairly common for pulmonary valve regurgitation
Tricuspid atresia repair
Shunt at 1 week
Glenn at 3-6 months
Fontan at 2-4 years
Pulmonary atresia repair timing
PA with VSD repair with shunt at 1 week or conduit at 1 week and vsd closure at 3-6 months
Truncus arteriosus a/c what syndrome
DiGeorge syndrome
Truncus arteriosus repair timing and common complications
Truncus repair at 1-2 weeks of age with RV to PA conduit and VSD patch
Fairly common complications: consist stenosis and pulmonary hypertension
TAPVR repair timing and complications
Obstructive TAPVR is emergent surgery
Nonobstructive TAPVR surgery less than 6 months
Can get pulmonary being obstruction, atrial arrhythmias and PH
DORV timing of repair
DORV repair at 3-6 months with VSD closure and if TGA then it’ll be a RV to PA conduit across the VSD
VSD repair timing
VSD repair 6-12 months although some small ones spontaneously close
ASD timing of repair
2-4 years of age for ASD repair with patch or device
Complete AV canal repair timing and complications
Complete AV canal repair 4-8 months
Fairly common complications include residual ASD and VSD, TVR (which may result in atrial arrhythmia), MVR, ventricular arrhythmia
PAPVR associations with other defects
Right PVs draining into SVC a/c sinus venous
Right PVs draining into IVC a/c scimitar syndrome
Or right PVs can drain directly into RA
PAPVR repair timing
PAPVR repaired 2-4 years of age
Syndrome a/c coarctation of Ao and other defects seen with CoA
30% of turner syndrome have CoA
>50% also with bicuspid AV and increased risk of VSD
Syndrome a/c supravalvar AS
Supravalvar AS a/c Williams syndrome
Neonatal and fetal heart
Decreased heart compliance
Less ability to augment cardiac output with stroke volume
Sensitive to afterload
Less contractile elements and immature sarcoplasmic reticulum
Sensitive to calcium as an ionotrope
Less fluid or preload responsive because of less compliance
Presentation and types cardiac tumors
Asymptomatic, hydrops, fetal arrhythmia
Rhabdomyoma (m/c) usually multiple - risk of TS, can regress, surgery required of obstruction of flow
Fibroma - single and fibrous, usually do not regress
Myxoma - majority are found in adulthood
Sarcoma - very rare
Teratoma - typically intrapericardial
EKG right atrial enlargement
Peaked P-wave > 3 mm ( > 3 tiny squares) in any lead
EKG left atrial enlargement
Increase P-wave duration (>0.2-0.23 sec) in any lead. May have biphasic P-wave.
EKG Q wave abnormalities
Small Q waves <5mm fine in II III avF V5 V6
Abnormal:
No Q in V5 V6 = L TGA, single ventricle, L BBB
Deep Q left leads = LVH, BiVH, myocarditis, RCM
Deep wide Q = infarction, HCM
Deep Q in I avL V4 V5 V6 = ALCAPA
Normal QRS axis
In neonate 100 to 150°
Normal P-wave axis
Normally upright in lead 1 and aVF normal P axis 0 to 90°
Normal T-wave axis
Normally upright in inferior and lateral leads
Fetal SVT characteristics management, in utero, and postnatal management
Accounts for 70 to 80% of tachyarrhythmias. Presents between 28 and 32 weeks gestational age. Hydrops is dependent on duration of tachycardia not degree of SVT.
First line treatment is digoxin. Second line treatment. If the fetus is not sick is flecainide, but the mortality is 10 to 15% sotalol can also be tried but mortality is 30% and not as effective.
Other second line agent, if the fetus is sick, is amiodarone, usually given after 1 to 2 doses of digoxin. There are maternal complications with this.
Postnatal management includes monitoring of complications from antiarrhythmics, such as hyper bilirubinemia, anemia from BM Suppression, and greater risk of NEC. Infants remain on antiarrhythmics for six months generally 
Fetal atrial flutter presentation and treatments
Atrial flutter Accounts for 20 to 30% of tachyarrhythmias.
Presents later in pregnancy then SVT in hydrops is less common 
Digoxin is first line.  sotalol, is safe and works in 80% of atrial flutter and the treatment of choice for refractory atrial flutter. Amiodarone is not effective. 
What is associated with premature atrial contraction?
Hypokalemia, hypoglycemia, hypercalcemia, drugs, hypoxemia Central line irritation of right atrium
Premature beats
Premature atrial contractions are typically benign and treat underlying cause
Premature junctional contraction generally do not require treatment
Premature ventricular contractions - if asymptomatic and isolated PVCs with normal cardiac anatomy - do not usually need treatment
Underlying causes of PVCs
Digoxin toxicity
Infection
Ca/K/Mag abnormalities
Hypoxemia
Acidosis
CHD
Excess aminophylline/caffeine
Myocarditis
Ddx for wide QRS
SVT with BBB
AV Re-entry tachycardia/antidromic
Vtach
QTc
Corrected QT = QT(seconds) / square root of previous RR interval (seconds)
Normal is <0.45 sec if <6 months
EKG findings with hypercalcemia
Shortened QT interval
EKG findings with hypocalcemia
Prolonged QT interval
EKG findings with hyperkalemia
> 6 tall peaked T wave, shortened QT interval, depressed ST segment
7.5 prolonged PR interval, widened QRS complex, flattened P wave
9 absent p wave, sinusoidal QRS wave, asystole and v fib can occur
EKG findings with hypokalemia
<2.5 slightly widened QRS complex, depressed ST segment, biphasic T wave attributable to visible U wave
~1.0 prominent u wave, flat T wave, if sustained may develop prolonged PR and sinoatrial block
Screen for what with Truncus arteriosus?
Screen for digeorge - look for thymus and check calcium’s
Alpha 1 receptors
Location: arterial and venous smooth muscle, Cardiac myocytes
Action: sm muscle contraction by increasing calcium entry; increase contractility; gluconeogenesis; decrease insulin release
Alpha 2 receptors
Location: sympathetic nerves, CNS
Action: blocks NE release, inhibits sympathetic output; vascular smooth muscle relaxation
Beta 1 receptors
Location: sinoatrial node, atrial and ventricular muscle, conduction cells
Action: increases HR, increased conduction velocity, increases contractility, increases renin secretion
Beta 2 receptors
Location: arterial and venous smooth muscle, bronchial smooth muscle
Action: smooth muscle relaxation, bronchial relaxation, increases HR and contractility, decreased intestinal motility and tone, induces glycogenolysis, increases insulin secretion
What can PGE1 make worse
Tapvr obstructive
Hlhs with intact or restrictive atrial septum
TGA with restrictive atrial septum
Mitral valve atresia with restricted pfo
Carpenter syndrome a/c
PDA, VSD, PS, ASD, TOF, TGA
Cat eye syndrome a/c
TAPVR, persistent left SVC
CHARGE syndrome a/c
TOF DORV VAD ASD PDA right sided aortic arch (50-70%)
Cornelia de Lange syndrome a/c
VSD most common
Cri du chat a/c
Variable
DiGeorge syndrome a/c
Aortic arch abnormalities (right sided aortic arch, interrupted aorta, Truncus arteriosus), TOF, PA
Ehlers Danlos syndrome a/c
Aortic root dilation, MVP
Ellis van creveld syndrome a/c
50%
Common atrium
Glycogen storage IIa (pompe) a/c
Hypertrophic cardiomyopathy
Goldenhar syndrome a/c
VSD > PDA > TOF > CoA
Holt Oram syndrome a/c
ASD most common
Homocystinuria a/c
Arterial and venous thrombosis, medial degeneration of the aorta and elastic arteries
Hurler syndrome a/c
Thickened valves (especially mitral), CAD, HCM
Klinefelter a/c
TOF, MVP
Klippel feil sequence a/c
VSD
Marfan syndrome a/c
Dilated aorta and aortic root, aortic aneurysm, MVP
Meckel gruber syndrome a/c
ASD, VSD, PDA, CoA, PS
Noonan syndrome a/c
Dysplastic or thickened pulmonary valve, LVH, ASD VSD PDA, branch stenosis of pulmonary arteries
Rubenstein Taybi syndrome a/c
PDA VSD ASD
TAR syndrome a/c
TOF ASD
Trisomy 13 a/c
80-90% with VSD or PDA
Trisomy 18 a/c
VSD PDA PS CoA TOF polyvalvular disease
Trisomy 21 a/c
Complete AVC > VSD > PDA, also ASD and TOF
Turner syndrome 44, X a/c
Bicuspid aortic valve (30%), CoA (10%), aortic stenosis, MVP, aortic dissection, hypertension later in life
VACTERL association a/c
VSD > TOF, CoA
Williams syndrome a/c
Supravalvar subaortic stenosis > peripheral pulmonary artery stenosis, PS
Rubella a/c
PDA, peripheral pulmonic stenosis, PS, AS, TOF, myocarditis
Maternal diabetes a/c risk of infant CHD
DTGA, VSD, CoA, ventricular hypertrophy
Greater risk if insulin dependent prior to pregnancy.
AS a/c which syndromes
Turner
Jacobsen
Loeys Dietz
Kabuki
Shones syndrome
Small L sided structures, supravalvar mitral ring, parachute MV, subaortic stenosis, coarct, not quite LV apex
Supravalvar PS a/c
Noonan, holt oram, leopard
PPHN due to
Failure of 1 of 3 mechanisms
1. Abnormal lung parenchyma (MAS, RDS, PNA)
2. Hypoplastic vasculature (like CDH)
3. Remodeled pulm vasculature (idiopathic)
Trisomy 13 CHD
ASD
PDA
VSD
Trisomy 18 CHD
ASD
ECD
PDA
TOF
VSD
Trisomy 21 CHD
ECD
VSD
ASD
CHARGE CHD
TOF
ECD
Ao arch anomalies
Deletion 22q11 CHD
IAA
TOF
VSD
Truncus
Holt Oram CHD
ASD
VSD
COA
Kartagener CHD
Dextocardia
Loeys Dietz CHD
Aortic dilation
MVP
Marfan CHD
Aortic dilation
MVP
TVP
pulm artery dilation
Neuorfibromatosis CHD
PS
Aortic dilation
MVP
HCM
Noonan CHD
PS
HCM
Smith Lemli Opitz CHD
TAPVR
AV Canal
TAR CHD
ASD
TOF
Turner CHD
AS (BAV)
COA
HLHS
Williams CHD
Supravalvar AS
PPS
Alagille CHD
TOF
hypoplastic or stenotic pulm arteries
Maternal DM CHD
VSD
TGA
TOF
DORV
HCM
BVH
