Congenital Heart Defects and Arryythmias

risk factors for CHD

• genetic/chromosomal abnormalities (30%)

• environmental (intrauterine exposure) 

  • infections (rubella), maternal illness/meds, maternal alcohol/drug use 

• many are idiopathic 

4 main types of CHD

• increased pulmonary flow

  • patent ductus arteriosus, atrial septal defect, ventricular septal defect

• decreased pulmonary blood flow

  • tetralogy of fallot

• obstructive defects/decreased cardiac output 

  • coarctation of aorta, pulmonic stenosis, hypoplastic left heart syndrome 

• mixed

  • transposition of the great arteries 

general S/S

• murmurs

• cyanosis

• poor feeding → failure to thrive

• diaphoretic/cyanosis w/ feeding, crying

• dyspnea, tachypnea, retractions 

• respiratory infections

• edema - abdomen or periorbital 

patent ductus arteriosus - defect/BF

ductus arteriosus, b/n pulm artery and aorta, doesn’t close

• blood flows from high pressure aorta to low pressure pulmonary artery - left to right shunt 

patent ductus arteriosus - S/S

• increased pulmonary pressure/congestion - pulm. artery getting blood from RV and aorta = lot more BF to lungs 

• increased workload of RV - working against increased pressure in the pulm. art.

• increased workload of LV - losing blood that’s supposed to go to body to pulm. art, needs to work harder to increase CO 

atrial septal defect - define/BF

opening in atrial septum allowing blood to flow between RA and LA

• blood flows from high pressure LA to low pressure RA - left to right shunt

atrial septal defect - S/S

• RV overload

• increased pulmonary blood flow = pulmonary congestion

may be asymptomatic 

ventricular septal defect - define/BF

opening in ventricular septum allowing blood to flow between LV and RV

• blood flows from high pressure LV to low pressure RV - left to right shunt

• if the defect is so severe, the pulmonary vascular resistance can be higher than the systemic vascular resistance reversing the shunt and causing cyanosis

ventricular septal defect - S/S

• increased pulmonary pressure - more blood to RV that goes into pulm. art

• increased pulmonary resistance - overtime pulm. arterioles constrict + walls thicken leading to increased pulm. vascular resistance

• increased RV workload - has to push out lots more blood 

• increased blood return to LV 

may not appear until few days/weeks, poor feeding/respiratory distress

tetralogy of fallot - defect/BF

• four defects 

  • VSD

  • overriding aorta - aorta sits over VSD instead of only over the LV so it receives blood from both ventricles 

  • pulmonic stenosis - valve stiff + hard to open 

  • RV hypertrophy - from the pulmonic stenosis 

• decreased blood flow to lungs 

• right to left shunt - defects change pressure dynamics so pressure is higher on right, due to pulm. stenosis causing backup of blood in RV, VSD blow flows from RV to LV 

tetralogy of fallot - S/S

• cyanosis

  • because mixed blood being pushed to body (body should not receive any deoxygenated blood) 

• “blue spells” w/ crying/feeding

coarctation of aorta - defect/BF

narrowing aorta distal to subclavian arteries 

• high BP in upper extremities/head - before constriction and blood backs up 

• low BP in lower extremities - reduced blood flow to legs 

coarctation of aorta - S/S

• decreased pulses/BP in legs

• cool lower extremities

• LV hypertrophy/failure - LV has to generate much higher pressure to force blood past the narrowing and maintain normal systemic BF 

pulmonary valve stenosis - defect/BF

narrowing of entrance to the pulmonary artery 

• decreased pulmonary flow, right ventricular hypertrophy 

  • RV is working really hard to get blood to the lungs 

pulmonary valve stenosis - S/S

• RV hypertrophy

• dyspnea on exertion - decreased pulmonary blood flow

• cyanosis 

transposition of the great arteries - defect/BF

aorta and pulmonary artery switched

• deoxygenated blood is flowing from RV to aorta to body

• oxygenated blood flows from LV to pulm. artery to lungs but never reaches the body 

**need to keep patent ductus arteriosus (b/n aorta and pulm. art) and formane ovale (b/n RA and LA) open so blood can mix b/n the two circuits 

transposition of the great arteries - S/S

• severe hypoxemia

• cyanosis

• heart failure

hypoplastic left heart syndrome - defect/BF

underdeveloped LV

• RV becomes responsible for pumping both pulmonary and systemic circulation 

  • need to keep ductus arteriosis and foramen ovale open so blood can mix

hypoplastic left heart syndrome - S/S

• hypoxemia

• shock

kawasaki disease - patho

inflammation of the blood vessels like the coronaries

• 15-25% result in coronary aneurysms

  • MI (bc clot can form from inflammation)/sudden death 

kawasaki disease - cause

an ACQUIRED heart disease

• not known why it happens but starts with an inflammatory response

kawasaki disease - S/S

acute 

• abrupt fever, rash, redness of hands and feet, conjunctivitis, lymph node enlargement, strawberry tongue

subacute

• desquamation of skin, need to monitor for sequela/other complications

what is happening during P wave

atrial depolarization → atrial contraction

what is happening during the QRS complex

ventricular depolarization → ventricular contraction

what is happening during the T wave

ventricular repolarization (relaxation)

normal sinus rhythm

• rate: 60-100

• regular R to R 

• one P for every QRS 

sinus tachycardia

rate is fast, otherwise normal

sinus bradycardia

rate is slow, otherwise normal

what is causing atrial dysrhythmias

other atrial cells start firing impulses, not the SA node

atrial fibrillation

irregular, rapid atrial rhythm caused by many chaotic electrical impulses firing all over the atria instead of one organized signal from the SA node 

• atrai quiver instead of pumping blood effectively 

atrial fibrillation complication

risk for embolic stroke due to blood stasis in ventricles that lead to a clot

premature ventricular contractions

early impulses from ectopic ventricular pacemaker (random signals in/from ventricles)

ventricular tachycardia

• medical emergency’

• rate often greater than 200 bpm 

• greatly reduced CO (not diastolically filling ventricles) 

• may be pulseless and require defibrillation 

ventricular fibrillation 

• medical emergency

• no pulse or cardiac output

• treatment: defibrillation 

• ventricles just shaking