NCC Content Flashcards
When can the fetal heartbeat be heard?
At 6 weeks
describe the four stages of cardiac formation
- Elongates & twists to right - if it doesn’t twist correctly, result can be dextrocardia
- Separates the atria and ventricles
- Formation of valves: mitral and tricuspid
- Great vessel formation: aorta, pulmonary arteries and vein
What does S1 represent?
Closing of the tricuspid and mitral valves at the end of atrial systole (aka the start of systole)
Where is S1 best auscultated?
Fifth intercostal space at the left midclavicular line or LLSB
What does S2 represent?
Closure of the aortic and pulmonic valves at the end of ventricular systole (aka start of diastole)
should be split until PVR is significantly lower!!
Where is S2 best auscultated?
At the ULSB
What are the semilunar valves?
Aortic valve
Pulmonary valve
Which side of the heart is dominant in fetal circulation?
The right heart is dominant - pumps 2/3 of combined ventricular output
What is one important function of the foramen ovale?
Allows oxygenated blood to bypass right ventricle and go to left side of heart (atrium) to eventually be delivered to the brain
What factors contribute to the closing of the PDA?
Oxygen, prostaglandins
What is cardiac output?
The volume of blood ejected by the heart in one minute
CO= stroke volume x heart rate
When do the PDA and the PFO usually close?
PDA = 15-48 hrs of life PFO = functionally closes soon after birth, structurally not closed until about 1 month of age
What is stroke volume?
The difference between the ventricular end diastolic volume and the end systolic volume
It is affected by preload, contractility and afterload
What is preload?
Volume of blood entering the ventricles
What is afterload?
The resistance that the left ventricle must overcome to circulate blood
What is contractility (inotropy)?
The speed of ventricular contraction
What factors affect contractility?
Catecholamines cause an increase
Acidosis/hypoxia cause a decrease
What does blood pressure represent?
Systole = pressure on the walls of the vessels at the end of each heart contraction Diastole = pressure on the walls of the vessels immediately before each contraction
Explain a widened pulse pressure with a PDA
Blood runs off into the pulmonary artery during diastole
Explain a narrow pulse pressure
Can indicate pericardial tamponade, intravascular depletion, or an ecmo pt
What is the definition of shock?
A state of inadequate circulatory blood volume
-Results in decreased perfusion and oxygenation to tissues - lactic acidosis - heart failure
3 types of shock
Hypovolemic: loss of volume
Cardiogenic: heart failure d/t tamponade, tension pneumo, CHD, etc.
Distributive: sepsis, toxins
Compensated vs. Uncompensated shock
Compensated: BP still normal; want to treat during this stage if possible
Uncompensated: hypotensive; occurs cause is untreated, much harder to reverse at this point
Where is the PMI best palpated?
Along lower left sternal border in the 5th intercostal space
What does S3 represent?
Extra sound that may be normal in the newborn related to ventricular filling
What does the S4 represent?
Rare, myocardial disease
Characteristics of a benign murmur.
- FT infant may have murmur at 24-48 hrs d/t PDA closing
- systolic murmur
Characteristics of a pathologic murmur.
- continuous?
- diastolic
VSD murmur
Harsh pansystolic LLSB
PDA murmur
Continuous machinery
Truncus Arteriosus murmur
Harsh systolic with single S2
Valvular stenosis murmur
Loud ejection click
PPS murmur
Persistent pulmonic stenosis?
Radiates to axillae and back
EKG changes with hyperkalemia
Peaked T waves
Widened QRS
EKG changes with hypokalemia
Prominent U waves
EKG changes with hypercalcemia
Short QT interval
EKG changes with hypocalcemia
Prolonged QT interval
SVT is caused by….
Dual firing at the AV node
By definition, HR sustained > 220 bpm
SVT treatment
- Ice/Vagal maneuver
- Adenosine (digoxin or propranolol also options)
- Cardioversion
What is the biggest risk factor for CHD?
Family history of CHD
What % of infants with chromosomal abnormalities have CHD?
30%
When does the heart begin and finish developing?
Starts between 3rd and 7th week of gestation
Completed at 10 weeks
1st organ to function in utero
What is the most common CHD?
VSD (20-25%)
What are the acyanotic heart defects?
- ASD
- VSD
- PDA
- AV canal
Characteristics of acyanotic heart defects.
- L to R shunt
- cardiomegaly
- increased pulmonary vascular markings
- CHF when PVR drops (6-8 weeks of life)
Characteristics of symptomatic PDA
- hypotension d/t systemic steal
- oliguria
- respiratory distress
PDA management in preterm infant
Conservative: fluid restriction and diuretics
Hemodynamically-significant PDA: ibuprofen/indomethacin, surgical ligation
PDA management in term infant
Typically let it close on its own
If still open later, can having coiling procedure at 3 months
Characteristics of ASD
Oxygenated blood from left atrium to right atrium, back to right ventricle and into the lungs
- rarely get CHF or show symptoms
- systolic ejection murmur
- increased volume and work of RV leads to RV hypertrophy
Management of ASD
75% resolve within first year of life
-treat CHF if symptomatic
Intractable CHF: surgical repair is necessary
Characteristics of VSD
L-to-R shunting via ventricular septum causing increased pulmonary blood flow
- harsh pansystolic murmur
- left ventricle can become hypertrophied from overworking
Management of VSD
Small or perimembranous: usually resolves by itself
Large or muscular: causes CHF in 6 to 8 weeks, needs repair
Mild VSD: fluid restriction, diuretics, digoxin
Moderate to severe VSD: pulmonary banding, suturing or patching of defect
Characteristics of AV canal
-most common in Trisomy 21
Complete = 1 valve
Partial = mitral regurgitation?
Management of AV canal
Treat CHF
- PA banding
- ASD, VSD closure and reconstruction of valve
symptoms of CHF
(When the heart is no longer able to pump adequate amounts of blood to meet the needs of the body)
- tachycardia, tachypnea
- sudden weight gain or poor weight gain
- poor feeding
- hepatomegaly
- arrhythmias
- cardiomegaly
What is Eisenmenger syndrome?
Occurs typically when an undiagnosed CHD with a left to right shunt causes enough significant damage to the lung tissue and heart that the shunt reverses and becomes right to left thus making the patient cyanotic
Name the obstructive lesions.
- aortic stenosis
- pulmonary stenosis
- coarctation of the aorta
Characteristics of pulmonary stenosis.
- obstruction of blood flow to lungs
- may be valvular (90%), subvalvular or supravalvular
- usually associated with large VSD or ASD which facilitates mixing of blood
- need PDA to then get blood to the lungs
- harsh systolic ejection murmur
Pulmonary stenosis on x-Ray
Decreased pulmonary markings
Usually normal heart size
Characteristics of aortic stenosis
- obstruction of blood flow to the body
- valvular, supravalvular (associated with William’s syndrome) or subvalvular
- peripheral pulses are weak and threads
- narrow pulse pressure in severe AS
Is PS or AS more concerning?
AS - because there is limited blood getting to the body
Characteristics of COA
- narrowing in upper part of aortic arch (most commonly at the point where the ductus arteriosus joins the aorta)
- strong pulses in upper extremities compared to lower extremities
- Severe cases: LV pressure overload
- Loud S3 gallop usually present
- Mild=headaches; moderate=CHF; severe=shock
Management of COA
- treat CHF (digoxin and lasix)
- prostaglandins
- surgery: anastomosis, grafting, balloon angioplasty
What kind of shunt has to exist to cause cyanosis?
Right to left
Name the cyanotic heart lesions.
TGA TOF Truncus Tricuspid atresia TAPVR
Ebstein’s anomaly
Single ventricle
Pulmonary atresia
Characteristics of TGA
- survival dependent on some communication between two circuits (VSD, ASD, PDA)
- amount of blood flows into and out of the pulmonary circulation must be equal (important with all cyanotic mixing lesions)
- patient will have hypoxia and cyanosis
What is the most common cyanotic heart lesion in the newborn period?
TGA
TGA on x-Ray
Egg on string
TGA management
- prostaglandin dependent: PDA is needed for systemic perfusion
- balloon septostomy
What is the most common cyanotic heart disease in general?
TOF
Name the 4 abnormalities in TOF
- VSD
- Right ventricular hypertrophy
- Right ventricular outflow obstruction
- Overriding aorta (aortic override of the ventricular septum)
Is TOF ductal dependent?
Not usually - only if pulmonary stenosis is significant or if pulmonary atresia is present
Blue Tet characteristics
-amount of cyanosis depends on how much deoxygenated blood is shunting right to left through VSD (less blood to lungs = increased cyanosis) which is determined by degree of pulmonary stenosis
Pink Tet characteristics
- oxygenated blood shunts left to right through VSD which can result in excessive pulmonary blood flow
- pink tets have mild pulmonary stenosis
TOF on x-Ray
- boot shaped heart (represents concave main PA segment with upturned apex secondary to right ventricular hypertrophy
- variable pulmonary vascular markings r/t degree of pulmonary stenosis
Management of TOF
- treat CHF
- provide O2 to relax pulmonary bed
- if O2 sats remain
TOF sat goal
75-85%
TOF murmur
Systolic ejection murmur
TAPVR characteristics
-pulmonary veins drain oxygenated blood directly or indirectly into the right atrium instead of the left atrium
TAPVR on xray
snowman
What is the Blalock-Taussig shunt?
subclavian is connected to pulmonary artery
-fixes TOF
What shunt has to exist in TAPVR?
some shunt needs to exist to move blood from the R to the L to supply the body
-usually mixing at the ASD level
TAPVR treatment
- manage CHF
- surgical correction= pulmonary veins are connected to the left atrium and ASD is closed (done within first few weeks of life)
Truncus arteriosus characteristics
- only a single arterial trunk leaves the heart; it supplies pulmonary, systemic and coronary circulation
- degree of cyanosis depends on amount of blood going to the lungs
What is always present with truncus?
large VSD (almost serves as single ventricle)
What genetic disorder is associated with truncus?
DiGeorge syndrome
Truncus arteriosus management
-Rastelli operation= attempts to separate the common artery; conduit is placed from the right ventricle to the pulmonary artery, VSD is closed
Tricuspid atresia characteristics
- tricuspid valve is absent
- RV and PA are hypoplastic with decreased pulm blood flow due to underuse
What opening is necessary for survival in tricuspid atresia?
-ASD, VSD or PDA necessary to get blood to the lungs
Surgical correction for tricuspid atresia
- B-T shunt
- Glenn (connect SVC to pulmonary artery)
- Fontan (connect IVC to pulmonary artery)
- all blood that should be going to right side of heart is going to lung after these procedures
pulmonary atresia characteristics
no blood flow from right ventricle to pulmonary circulation
What shunt is required in pulmonary atresia to survive?
- communication at atrial level (PFO/ASD)
- PDA must be present to get blood to the lungs!!
Epstein’s Anomaly characteristics
- abnormal development of tricuspid valve; hypoplastic right ventricle d/t tricuspid valve placement, but RV is also overworked
- sits deep in right ventricle and is dysplastic, allowing blood to regurgitate back to right atrium
- results in decreased blood flow to the lungs and cyanosis
Epstein’s anomaly on xray
-extremely large heart (“wall to wall”); considered diagnostic for EA
Epstein’s anomaly management
- prostins to get blood to lungs
- treat CHF
- pulmonary artery banding
- surgery?
HLH characteristics
- *left side of the heart is basically nonfunctional**
- hypoplastic left ventricle
- aortic valve atresia or stenosis
- mitral valve atresia or stenosis
- aortic arch is hypoplastic
What shunts are necessary for survival with HLH?
- must have PFO/ASD to allow LA to receive oxygenated blood
- must have PDA to ensure systemic circulation
HLH presentation
- cyanosis
- signs/symptoms of CHF
- poor perfusion:pulmonary over-circulation
- severe metabolic acidosis
HLH medical management
- prostins
- must balance circuit of pulmonary and systemic circulation
- keeps sats 75-85%
- avoid excessive pulmonary vasodilation (because that means not enough blood is going systemically)
HLH surgical management
- norwood: rebuild tiny ascending aorta
- stage II: glenn
- stage III: fontan
- cardiac transplant
What are is the “Rule of 4’s” in cardiac patients?
- pH= should be 7.40 (acidosis=lactic acid build up=muscle fatigue=bad cardiac contractility and function)
- CO2= in the 40s
- HCT= at least 40
- K= level in the 4 range (Na/K pump regulates influx of electrical impulses to regulate heart muscle contraction)
Maternal Diabetes =
- hypertrophic cardiomyopathy
- TGA
- VSD
Maternal Lupus =
heart block
Maternal Alcohol Abuse =
TOF
Maternal Rubella =
- PDA
- PPS
Down syndrome =
-AV canal
-VSD
(40% have CHD)
Turner syndrome =
-coarctation of the aorta
