C - congential heart defects Flashcards
wk5-6: Finals
What’s physical examination for circulation? (6)
CCPCCU
- Compensatory phase:
- an early sign of Circulatory Dysfunction or respiratory distress
- ensure that vitals are within normal range so that pt is not in compensatory phase - Color of skin
- temperature
- colour: pale, cyanotic - Peripheral pulses
- weak/strong
- infant/young children: brachial/femoral -> accessible & reliable
- older children: carotid -> easier to locate - Capillary refill
- knee, foot, toes, hands or forearms - Consciousness
- alertness
- responsiveness
- early signs of inadequate blood supply - Urine output
- renal perfusion
- normal: 1-2ml/kg/hr
- Decreased urine output signals a need for immediate intervention to restore circulation
What are the signs of early & late cardiovascular collapse?
Early signs:
1. tachycardia
- Altered perfusion:
- Skin: long capillary refill
- Brain: altered consciousness
- Kidneys: decreased urine output
- Pulse: weak
Late signs:
1. Cold & clammy skin
2. poor capillary refill
3. hypotension
4. bradypnea - slow breathing rate
5. acidosis of the blood
6. flaccid muscle tone
7. decreased response to pain
What are the names of cyanotic & acyanotic heart defects?
Cyanotic (5Ts)
1. tetralogy of fallot ToF
2. tricuspid atresia hydroplastic left heart syndrome
3. transposition of great arteries
4. truncus ateriosus
5. total anomalous pulmonary venous return (TAPVR)
Acyanotic
1. VSD
2. ASD
3. Patent ductus arteriosus (PDA)
4. Coarctation of aorta
What are the 4 heart abnormalities that are present in the tetralogy of fallot? What is the consequence of ToF?
- Pulmonary stenosis = passageway inside your body is narrower than it should be
- Narrowing of pulmonary valve - Right ventricular hypertrophy
- Enlargement of right ventricle - Ventricular septal defect
- whole in the wall that separates right & left ventricles - Overriding aorta
- Aorta is in the wrong position/above VSD -> blood without oxygen can enter the aorta
Result
- Oxygen rich blood and oxygen poor blood in the right and left ventricle mix due to VSD → then pumped out of overriding aorta
What is and what happens when one has tricuspid atresia ? (1)
What other heart defects are people with tricuspid atresia born with?
- tricuspid valve that normally prevents blood from returning to R atrium when R ventricle contracts is malformed / fails to develop entirely
Result:
- o2-poor blood returning to RA cannot enter into RV
Born with other heart defects:
- Atrial septal defect (ASD) mixes blood in R and L atrium -> pumped to rest of the body
- Ventricular septal defect (VSD): mixes blood in R and L ventricle -> some o2-poor blood can be transported to the lungs
What is and what happens during the transposition of great arteries? (1)
> Aorta and pulmonary artery swap positions
- Aorta: Normally carries blood from the heart to the body
- Pulmonary artery: Normally carries blood from the heart to the lungs
Result:
- aorta carries o2-poor blood to rest of body instead of pulmonary artery -> lungs to be exhaled
Define and state the result of having truncus ateriosus. (1+1)
Truncus arteriosus does not split properly during fetal development -> only 1 blood vessel exits the heart instead of the aorta + pulmonary artery
- always occurs along with a Ventricular Septal Defect - VSD: deoxygenated + oxygenated blood mixes & exits the heart through the 1 BV -> pumped to lungs & rest of body
WHY must there be a VSD???
- o2-poor blood from R ventricle would be trapped and not reach the single arterial trunk.
- o2-rich blood from L ventricle would circulate exclusively to the systemic circulation & cannot reach lungs for further oxygenation.
Cyanosis: Truncus arteriosus is considered a cyanotic congenital heart defect because the mixing of oxygenated and deoxygenated blood leads to reduced oxygen levels in the body’s tissues, causing visible cyanosis
What is a total anomalous pulmonary venous return (TAPVR) and the result of it?
What is the condition for patients with TAPVR to live?
- all four pulmonary veins form abnormal connections -> connect to RA /IVC/ SVC
- o2-rich blood from the lungs enters RA instead of LA & is pumped back to lungs
Condition: only compatible with life if there is ASD that allows some of the blood in RA to flow into LA -> pumped into systemic circulation
What is a clinical manifestation specific to tetralogy of Fallot (ToF)?
Can have acute and severe cyanotic episodes / “Tet spells”
- feeding, exercise, or crying, causes septum spasms & worsens the stenosis/narrowing of passageway -> increases the obstruction to pulmonary blood flow
= right ventricular outflow tract obstruction ⇒ results in increased right to left shunting, = blood flows from R side to the L side of heart, instead of going to the lungs -> decreased arterial o2 saturation - Lack of oxygen -> tachypnea or rapid abnormal breathing -> increases activity of the sympathetic nervous system -> increasing heart contractility and even more obstruction of the right ventricular outflow tract -> cyanosis
What do Tet spell patients do?
- Seen squatting / assuming foetal position
- position increases the peripheral vascular resistance by kinking the femoral artery, which improves the pulmonary blood flow and relieves the client
- During auscultation → large defects can be heard as murmurs (from blood moving through defect)
MUST KNOW!!!
Nursing Care for CYANOTIC heart defects? (5)
!!!! Priority goal: assist in maintaining oxygen
- Assess infant’s oxygenation: initiate pulse oximetry, assess vital signs, respiratory effort, skin colour
Report to physician
- Signs of respi distress: tachypnea, nasal flaring, retractions, grunting, decreased oxygen saturation, and cyanosis
- Provide supplementary oxygen
- Decrease risk of hypercyanotic episodes (tet spells)
- Maintain calm, therapeutic environment to prevent agitation
- If tet spell occurs → place the infant into a knee-chest position, which will increase systemic vascular resistance and promote systemic venous return to the right side of the heart and into the pulmonary circulation - Administer medications (morphine — for sedation;
β-blockers — relax outflow tract of RV and promote pulmonary blood flow) - If these interventions don’t resolve the cyanosis, administer the prescribed phenylephrine which will improve outflow from the right ventricle to the lungs
- When the infant is stable, assist with preparing them for complete repair of the heart defect.
main types of ACYANOTIC heart defects? (4)
- ventricular septal defect (VSD) — most common
- atrial septal defect (ASD)
- patent ductus arteriosus (PDA)
- pulmonary artery (which carries deoxygenated blood to the lungs) remains connected to the aorta (which carries oxygen-rich blood to the body)
- o2-rich blood from aorta flows into the pulmonary artery -> increased blood flow to the lungs -> pulmonary overcirculation -> high BP in lungs & heart failure.
- Why it’s acyanotic: The key point is that the oxygenated blood from the aorta is recirculated to the lungs, and no deoxygenated blood is entering the systemic circulation, so the body still receives oxygen-rich blood. - coarctation/narrowing of aorta
- heart has to work harder to pump blood through the narrowed region -> increased pressure in the L ventricle and upper body (head, arms).
- Lower body (legs) may receive less blood and oxygen due to the narrowing -> decreased pulses in lower extremities
MUST KNOW!!
Priority nursing goals of ACYANOTIC heart defects?
Maintain adequate cardiac output and provide nutritional support!!!!
- Assess cardiopulmonary status
- vital signs
- auscultate heart and lung sounds
- palpate peripheral pulses
- Immediately report signs of decreased cardiac output and pulmonary congestion
-> tachycardia, decreased peripheral pulses, tachypnea, pulmonary crackles, intercostal retractions, or nasal flaring - Administer prescribed medications (eg. digoxin) to support adequate cardiac function and diuretics to reduce pulmonary edema.
- Assess growth & development
- plot weight, length, & head circumference on a growth chart.
- Ask caregivers about their infant’s feedings to determine how often and how much their baby eats.
- Infants with VSD often tire easily with feedings but also have increased nutritional needs due to their increased cardiovascular demands.
⇒ Encourage continued breastfeeding + need to supplement the infant’s diet by administering the prescribed high-calorie formula, by orogastric or nasogastric tube.
NOT IMPT JS READ
Risk factors of CYANOTIC & ACYANOTIC heart defects? (4)
For cyanotic & cyanotic:
1. Chromosomal abnormalities of foetus
- Maternal infections
- affects development of fetal heart - Chronic illnesses
- eg: poorly controlled diabetes -> hyperglycemia -> affects development of fetal heart - Teratogens = cause birth defects or other abnormalities in a developing fetus or embryo
○ Isotretinoin
- med for severe acne
○ Alcohol
○ Cocaine
○ Tobacco smoke
○ Heavy metals (eg. mercury)
For acyanotic ONLY:
- Specific risk factors for patent ductus arteriosus:
○ Premature birth
○ Asphyxia during delivery
○ Rubella infection during pregnancy
NOT IMPT JS READ
Complications of CYANOTIC & ACYANOTIC defects? (4)
- blood pumped out of the heart does not contain enough oxygen to adequately supply body -> cyanosis
- Persistence of deoxygenated blood in systemic circulation → chronic hypoxia → body responds by producing more RBCs (polycythemia)
- Heart fails to pump more o2-rich blood to tissues -> compensates by pumping harder -> fatigue & cannot pump effectively -> heart failure
- if O2 supply gets too low → cerebrovascular accident (CVA) / stroke
Complications of CYANOTIC & ACYANOTIC heart defects:
- heart has to work harder -> electrical disturbances that trigger Arrhythmias
- blood clot forms & travels through the the bloodstream -> embolism
- prolonged use of catheters and devices in the heart -> infection of the heart’s inner lining (endocardium) = infective endocarditis
Complications of CYANOTIC heart defects:
- abnormal blood flow and increased risk of infections -> allow bacteria to travel to the brain -> Brain abscess formation = collections of pus caused by infections
- high blood pressure in the lungs (pulmonary hypertension) from increased blood flow or poor oxygenation -> damaged BVs in lungs = pulmonary vascular disease
- Death
