10 - Cardiology Flashcards
1
Q
What are some cyanotic and cyanotic congenital heart defects?
A
- Cyanotic when they have a R to L shunt. Think of the 4 T’s plus Jamie
- Always need shunt and a hole for cyanotic
2
Q
What investigations should you do if you suspect congenital heart disease?
A
3
Q
What is the most common congenital heart defect?
A
VSD
Shortly followed by ASD
4
Q
Where are the 3 shunts in the CVS in fetal life?
A
Done to bypass the pulmonary circulation
Ductus venosus: connects the umbilical vein to the inferior vena cava and allows blood to bypass the liver
Foramen ovale: connects the right atrium with the left atrium and allows blood to bypass the right ventricle and pulmonary circulation
Ductus arteriosus: connects the pulmonary artery with the aorta and allows blood to bypass the pulmonary circulation.
5
Q
How do the shunts in the CVS close after birth?
A
The first breaths expands the alveoli, decreasing pulmonary vascular resistance which causes a fall in pressure in the right atrium.
At this point the left atrial pressure is greater than the right atrial pressure, which squashes the atrial septum to cause functional closure of the foramen ovale. Becomes fossa ovalis after a few weeks
Increased blood oxygenation causes a drop in circulating prostaglandins. This causes closure of the ductus arteriosus, which becomes the ligamentum arteriosum.
Immediately after birth the ductus venosus stops functioning because the umbilical cord is clamped and there is no flow in the umbilical veins. The ductus venosus structurally closes a few days later and becomes the ligamentum venosum
6
Q
What are innocent murmurs in children?
A
Flow murmurs that occur during systole in children
- Soft
- Short
- Systolic
- Symptomless
- Situation dependent, particularly if the murmur gets quieter with standing or only appears when the child is unwell or feverish
7
Q
Where is Still’s murmur best heard?
A
8
Q
When is a murmur not innocent in a child and what investigations should you do for this?
A
- Murmur louder than 2/6
- Diastolic murmurs
- Louder on standing
- Other symptoms such as failure to thrive, feeding difficulty, cyanosis or shortness of breath
Send for ECG, CXR, Echocardiogrm
9
Q
How do you grade the loudness of a murmur?
A
10
Q
What are some causes of pan systolic murmurs in children?
A
- Mitral regurgitation : fifth intercostal space, mid-clavicular line
- Tricuspid regurgitation: (fifth intercostal space, left sternal border)
- Ventricular septal defect: left lower sternal border
- Coarctation of the aorta
11
Q
What are some causes of ejection systolic murmurs in children?
A
- Aortic stenosis: second intercostal space, right sternal border
- Pulmonary stenosis: second intercostal space, left sternal border
- Hypertrophic obstructive cardiomyopathy: fourth intercostal space on the left sternal border
- Tetralogy of Fallot
12
Q
What is a split heart sound, why does it occur and where is it best heard?
A
- Occurs during deep inspiration
- Negative intrathoracic pressure causes increased venous return to right side of heart so takes longer to empty in systole so pulmonary valve closes slightly after aortic valve
- Best heard in pulmonary area
13
Q
Where are the following murmurs best heard?
- ASD
- VSD
- PDA
A
14
Q
What type of murmur do the following CHD cause?
- ASD
- Tet of Fallot
- PDA
A
- ASD: mid-systolic, crescendo-decrescendo murmur loudest at the upper left sternal border, with a fixed split second heart sound
- Tet of Fallot: Ejection systolic due to pulmonary stenosis
- PDA: continuous murmur
15
Q
What acyanotic heart disease can turn cyanotic?
A
ASD, VSD and PDA if pulmonary pressure increases to greater than left side of heart
Eisenmenger Syndrome
16
Q
How can you accentuate and diminish certain heart murmurs?
A
Inspiration: Can hear PS and TR best
Expiration: Augments VSD, MR, AS
Standing: Decreases innocent murmurs
17
Q
What is a cause of PDA and how may it present? (what murmur)
A
- Idiopathic or Rubella infection
- Prematurity is risk factor
18
Q
Why may a PDA not present until adulthood?
A
May have no murmur
Presents as heart failure
19
Q
How is PDA diagnosed with investigations and managed?
A
Investigations
- Echocardiogram with doppler flow to view shunt
- Can also assess LV and RV hypertrophy with this
Management
- Monitor with echos until aged 1 as may close spontaneously
- Give NSAIDs
- If over 1 do trans-catheter or surgical closure
20
Q
what is the difference between an ASD and PFO, as they are both openings between the same chambers In the heart
A
PFO is considered a smaller, more common opening that usually doesn’t cause issues, while an ASD is a larger, structural defect that may require medical attention depending on its size and symptoms.
21
Q
What are some risk factors for atrial septal defects?
A
- Family history
- Maternal smoking in 1st trimester
- Maternal diabetes
- Maternal rubella
- Maternal drug use e.g. cocaine & alcohol
22
Q
What are the types of ASD from most to least common?
A
- Patent foramen ovale
- Ostium secundum defect
- Ostium primum defect
- Sinus venosus defect
- Coronary sinus defect
23
Q
What are some complications with ASD’s?
A
- Stroke in the context of DVT
- Arrhythmias
- Atrial fibrillation or atrial flutter
- Pulmonary hypertension and right sided heart failure
- Eisenmenger syndrome
24
Q
How may an ASD present?
A
Childhood
- On antenatal scan
- Asymptomatic
- Mid-systolic,crescendo-decrescendomurmur loudest at the upper left sternal border with afixed split second heart sound
- SOB
- Difficulty feeding
- Poor weight gain
- LRTI
Adulthood
- Stroke
- Heart failure
- Dyspnea
25
Why does ASD have a fixed split heat sound?
Blood is always flowing from left to right atrium so right ventricle always has more blood to pump out than left before pulmonary valve can close
Normal to have a split in inspiration but ASD have split in expiration and inspiration
26
How is ASD diagnosed?
**_Diagnosis_**
* **Transthoracic Echocardiogram:** gold standard
* **ECG:** normal in child but may have AF or atrial flutter in adults
* **Cardiac MRI**
* **CXR:** look for cardiomegaly
27
How is ASD managed?
**_Conservative_**
* **If ASD \< 5mm**, spontaneous closure should occur within 12 months of birth
* In adults, no signs of right heart failure and a small defect, then **monitor every 2 – 3 years with echocardiogram**
**_Definitive management_**
* **Refer to paediatric cardiologist**
* **Surgical closure if ASD \> 1 cm:** transcatheter via femoral vein or open chest
* If arrhythmia in adult give anticoagulation whilst awaiting surgery
28
What are some complications of percutaneous closure of ASD?
* Arrhythmias
* VTE
* AV block
29
When would you chose open surgical closure for ASD repair over percutaneous?
percutaneous repair of an atrial septal defect (ASD) is generally considered a less invasive procedure with a shorter hospital stay, lower complication rate, and is often the preferred method for closing most types of ASDs, especially "secundum" ASDs, as it involves inserting a device through a catheter in the groin rather than open-chest surgery; however, surgical repair may be necessary for complex ASD anatomies or certain types of ASDs like "primum" defects where a percutaneous approach is not feasible
* TIA / stroke
* Ostium primum defects
* Sinus venous defects
* Coronary sinus defects
30
What is the most common type of VSD?
**Perimembranous**
Small ones are found in muscle and often close by age 10
31
What are some risk factors for VSD?
* **Uncontrolled maternal Diabetes Mellitus**
* **Maternal Rubella infection**
* **Foetal alcohol syndrome**
* **Uncontrolled** **maternal phenylketonuria** (PKU)
* **A** **family history of VSD**
* **Down’s Syndrome** (trisomy 21)
* Trisomy 18 syndrome
* Trisomy 13 syndrome
* Holt-Oram Syndrome
32
How may a VSD present?
* Asymptomatic
* **Pan systolic murmur** at left lower sternal border
* Poor feeding
* Dyspnoea (sign of congestive heart failure)
* Tachypnoea
* Failure to thrive
* Cyanotic
* Sweating
* Clubbing of fingers
33
What is the first sign of left sided heart failure in children with a VSD?
Tachypnea
34
What are some differential diagnoses for a VSD?
* MR
* TR
* ASD
* PDA
35
What investigations should be done if VSD is suspected?
* **Transthoracic Echocardiogram:** gold standard
* **ECG:** may show LV hypetrophy
* **CXR:** may show cardiomegaly, pulmonary oedema, pleural effusion
* **Cardiac CT angiography with ECG-gating**
* **Genetic testing:** especially if dysmorphic
* **U+Es:** before starting diuretics and ACEi
36
How should a child with a VSD be managed?
* **Good oral hygiene** as risk of infective endocarditis
* **Monitor if small**
* **If CHF:** Furosemide diuretics, ACEi, increased calorific feeds
* **If large**: Surgery. In adults do if Qp/Qs (**p**ulmonary-to-systemic blood flow ratio) of 2.0 or more
37
What are the different surgical procedures used for closure of VSD?
* Transcatheter
* Open heart
38
What are some complications of VSDs?
Need monitoring for life even if had a repair
* Congestive heart failure
* Growth failure
* Aortic valve regurgitation due to prolapse of a valve leaflet through the defect
* Eisenmenger’s Syndrome
* Frequent chest infections
* [Infective Endocarditis](https://teachmepaediatrics.com/cardiology/infection/infective-endocarditis/)
* Arrhythmias
39
What are AVSDs, who are they common in and how are they treated?
* Down's syndrome
* Failure of endocardial cushions to fuse correctly
* Need corrective surgery at around 3-6 months of age to prevent pulmonary vascular obstructive disease
40
How long does Eisenmenger syndrome take to develop?
a condition that occurs when a congenital heart defect causes abnormal blood flow from the heart to the lungs. It's a type of pulmonary hypertension, which is high blood pressure in the lungs
Eisenmenger syndrome is life-threatening.
In ASD, VSD and PDA
1-2 years if large, until adulthood if small
Always monitor pregnant women with hole in the heart as can develop this!
41
What will you find on examination of someone with Eisenmenger syndrome and why?
**_Pulmonary hypertension:_**
* ***Right ventricular heave:*** RV contracts against increased pressure in lungs
* ***Loud P2***: loud second heart sound due to forceful shutting of the pulmonary valve
* ***Raised JVP***
* ***Peripheral oedema***
**_Underlying septal defect:_**
* **ASD**: mid-systolic, crescendo-decrescendo murmur loudest at the upper left sternal border
* **VSD**: pan-systolic murmur loudest at the left lower sternal border
* **PDA**: continuous crescendo-decrescendo “machinery” murmur
**_Right to left shunt and chronic hypoxia:_**
* ***Cyanosis***
* ***Clubbing***
* ***Dyspnoea***
* ***Plethoric complexion*** (a red complexion related to ***polycythaemia***)
42
What is the prognosis with Eisenmenger syndrome?
* Reduces life expectancy by 20 years
* Risks of infection
* Heart failure
* VTE
* Haemorraghe
43
How is Eisenmenger Syndrome managed?
Should catch defect and surgically correct it before this happens!!
**Definitive management:** Heart-Lung Transplant
44
What is coarctation of the aorta and how may it present?
Narrowing of the aortic arch at the ductus arteriosus associated with Turner's syndrome. Leads to high pressure proximal to the narrowing and low pressure distal to it
* High blood pressure in upper right limb
* Systolic murmur below left scapula and left clavicle
* Weak femoral pulses
* ***Tachypnoea*** and increased work of breathing
* Poor feeding
* Grey and floppy baby
Additional signs may develop over time:
* ***Left ventricular heave*** due to left ventricular hypertrophy
* Underdeveloped left arm
* Underdevelopment of the legs
45
How is coarctation of the aorta managed?
* May just monitor
* In cases of critical coarctation where there is a risk of heart failure and death shortly after birth ***Prostaglandin E*** is used keep the ***ductus arteriosus*** open while waiting for surgery. This allows some blood flow flow through the ductus arteriosus into the systemic circulation distal to the coarctation. Surgery is then performed to correct the ***coarctation*** and to ***ligate*** the ***ductus arteriosus***.
46
What is Tetralogy of Fallot?
* VSD
* Overriding aorta - aorta is in the wrong place. Instead of sitting over your heart’s left side, your aorta is above a ventricular septal defect or damaged wall between the left and right ventricles. so it takes in a mix of oxygenated and deoxygenated blood
* Pulmonary valve stenosis
* Right ventricular hypertrophy
RESULTS IN A RIGHT TO LEFT SHUNT SO CYANOTIC
47
What are some risk factors for Tetralogy of Fallot?
* ***Rubella*** infection
* Increased age of the mother (over 40 years)
* Alcohol consumption in pregnancy
* Diabetic mother
* Family history
* CHARGE syndrome
* DiGeorge syndrome
* VACTERL
48
What are the different severities of TOF?
Severity depends on how bad PS is
## Footnote
**_Mild (‘Pink’ TOF)_**
Usually asymptomatic but by ***age 1-3 years*** they will develop cyanosis
**_Moderate-Severe (Cyanotic TOF)_**
May present in the ***first few weeks of life*** with cyanosis and respiratory distress. These infants may be prone to develop recurrent chest infections or fail to thrive.
**Extreme**
**TOF with pulmonary atresia** (10% of TOF patients) or **absent pulmonary valves** (6%).
These are true **‘duct** **dependent lesions’** as the only way deoxygenated blood can flow into the lungs is through a patent ductus arteriosus (PDA). These infants are often detected on antenatal scans. However, if undetected in pregnancy they will present within the ***first few hours of life*** with marked respiratory distress and cyanosis.
49
What will you find on examination of a child with TOF?
* Central cyanosis
* Ejection systolic murmur due to pulmonary stenosis (VSD too loud to cause a murmur)
* Right heave or thrill
* Clubbing
50
What will you find on examination of a child with TOF?
* Central cyanosis
* Ejection systolic murmur due to pulmonary stenosis (VSD too loud to cause a murmur)
* Right heave or thrill
* Clubbing
* Poor feeding and weight gain
* * **Signs of congestive heart failure:** sweating, pallor, tachycardia, hepatosplenomegaly, generalised oedema, bilateral basal crackles
51
When does TOF tend to present?
* Antenatal scans
* Newborn baby checks
* Signs of heart failure in early infant life
52
What are some differentials for TOF?
**Other cyanotic CHD**:
* Critical PS
* Transposition of the Great Arteries (TGA)
* Totally anomalous pulmonary venous drainage (TAPVD)
* Hypoplastic left heart syndrome (HLHS)
**Isolated VSD:** commonest CHD (15-20%). Does not cause cyanosis as the shunt is left-to-right unless Eisemenger syndrome develops
**Sepsis**: should be suspected in any infant with respiratory distress and hypoxia.
53
What is a Tet spell?
Intermittent symptomatic periods where the right to left shunt becomes temporarily worsened, precipitating a ***cyanotic episode***
**Precipitated by** waking, physical exertion or crying
**Symptoms**: irritable, cyanotic, short of breath, reduced consciousness, seizures and potentially death.
54
What is the pathophysiology of a Tet spell?
* Increased pulmonary resistance
* Decreased systemic resistance (e.g exercise, more CO2 so vasodilation)
Blood will take path of least resistance so more blood shunted from right ventricle to aorta so bypasses the lungs
55
How can Tet spells be managed?
CAN BE LIFE THREATENING!
* **Knee to chest position** or Squat to increase systemic resistance
* **Oxygen**
* **Beta blockers** to relax right ventricle and improve flow to the pulmonary vessels
* **IV fluids** can increase pre-load
* **Morphine** can decrease respiratory drive, resulting in more effective breathing
* **Sodium bicarbonate** can buffer any metabolic acidosis that occurs
* **Phenylephrine infusion** can increase SVR by vasoconstriction
56
What investigations should be done if Tetralogy of Fallot is suspected and what will they show?
* **ECHO:** gold standard
* **ECG**: may show signs of right axis deviation and RVH
* **Microarray:** if genetic syndromes suspected (e.g. dysmorphic features)
* **CXR**: may show ‘boot’ shaped heart (RVH) and reduced pulmonary vascular marking (decrease pulmonary blood flow)
57
How is Tet of Fallot managed?
**_Medical_**
* ***Manage Tet spells*** with positioning, fluids, propanolol, morphine
* ***Prostaglandin infusion*** at birth to keep DA open to allow flow from aorta to pulmonary arteries
**_Surgery_**
* Definitive repair can only be done from **3 months-4years**
* 5% mortality as open heart surgery
* Cardiopulmonary bypass via median sternotomy, this involves RVOT stenosis resection, RVOT/pulmonary artery augmentation and VSD patch closure
58
What surgery can be done for TOF to spare a child time until they are old enough to have definitive surgical repair?
* **Transcatheter RVOT stent insertion:** this is sometimes done in the neonatal period for infants with severe-extreme TOF to relieve RVOTO. This is done to buy time until the child is bigger whilst providing a patent passage for pulmonary blood flow
* **Modified Blalock-Taussig (BT) shunt:** This procedure aims to mimic a PDA and **increase pulmonary blood flow** before definitive repair. It can be done either by anastomosis of the subclavian artery to the pulmonary artery or by creating an artificial shunt using synthetic material (usually GoreTex). The latter is called a modified BT shunt.
59
What are the complications of TOF?
**_Untreated_**
* Polycythaemian- blood disorder that occurs when there are too many red blood cells in the body. This causes the blood to thicken, making it harder for it to flow through the body. body tries to increase red blood cells due to the low oxygenated blood flowing around the body -> stroke
* Cerebral abscess
* Stroke
* Infective endocarditis
* Congestive cardiac failure
* Death (up to 25% in the 1st year of life
**_Treated_**
* **Pulmonary regurgitation**
* Arrhythmias
* Reduced exercise tolerance
* Sudden death
60
How do patients with TOF need to be followed up?
**Lifelong follow up is essential**
**Regular ECG**, **echocardiography** and in cases of exercise intolerance,**cardiopulmonary exercise testing (CPET)**.
More than **85% children** with surgically repaired TOF now survive to adulthood
61
What is Transposition of the Great Arteries and the pathophysiology of this?
**Aorta arises from the right ventricle** and **Pulmonary Artery arises from left ventricle**, leading to two separate systems
Survival depends on shunt (PDA, ASD, VSD)
Due to no rotation of aortopulmonary septum
62
What are some risk factors for TGA?
Most common cause of cyanosis in the new born!
63
How may TGA present?
* Often picked up on **antenatal scan**
* **Cyanosis at birth** or within a few hours
* PDA/ASD/VSD can support for a few weeks but after this will lead to respiratory distress, tachycardia, poor feeding, poor weight gain and sweating
64
What investigations can be done to diagnose TGA and what will they show?
* **Echocardiogram:** shows abnormal position of vessels, gold standard
* **CXR:** ‘egg on a string’ due to cardiomegaly and narrowed upper mediastinum
65
How is TGA managed?
**_Initial management:_**
* **Emergency prostaglandin E1 infusion (alprostadil)** to keep the DA patent as a temporary solution that allows mixing of blood
* **Emergency** **atrial balloon septostomy** to allow for mixing
**_Definitive and Long‐term management:_**
* **Arterial switch operation** [ASO] via open heart surgery with bypass performed before the age of 4 weeks
* Long term follow up and counselling in the future if female patients wish to get pregnant
66
What are some complications with TGA?
* Neopulmonary **stenosis** - when the pulmonary valve is more narrow than normal and doesn't open the right way. This makes it harder to pump blood to the lungs.
* Neoaortic **regurgitation** - a condition where the neoaortic valve leaks. It's a common complication after the arterial switch operation (ASO) for transposition of the great arteries (TGA).
* Neoaortic root **dilatation**
* **Coronary artery disease**
* **Obstructed coronary arteries**
* **Sudden cardiac death**
* **MI**
* **Neurodevelopmental** **abnormalities**
67
What are some predictors of poor outcomes with TGA?
* **Low gestational age**
* **High pre-operative lactate**
Likely to have neurodevelopmental issues
68
What is Ebstein's anomaly?
Low set tricuspid valve so smaller right ventricle so poor flow into pulmonary vessels
Often right to left shunt
**_Presentation_**
* Evidence of heart failure (e.g. oedema)
* Gallop rhythm heard on auscultation characterised by the addition of the third and fourth heart sounds
* Cyanosis
* Shortness of breath and tachypnoea
* Poor feeding
* Collapse or cardiac arrest
69
What is hypoplastic left heart syndrome?
LV is so underdeveloped that it cannot be the source of systemic circulation
Survival depends on a PDA and ASD
70
What is the cause of congenital aortic stenosis?
* Bicuspid valve
* Turner's syndrome
* Rheumatic fever
71
What two cardiac defects is Turner's syndrome associated with?
* Aortic stenosis
* Coarctation of aorta
72
How may aortic stenosis in a child present?
* Asymptomatic
* **Ejection systolic murmur** that radiates to carotids
* **Fatigue**
* **Dizziness and SOB** that is worse on exertion
* ***Ejection click*** just before the murmur
* ***Palpable thrill*** during systole
* ***Slow rising pulse (pulse is not only low in volume but also slow in rising to a peak due to the delay in ejecting blood through the narrowed valve.)
**narrow pulse pressure (when the difference between your systolic and diastolic blood pressure is less than 25% of your systolic pressure.) ***
73
How is aortic stenosis diagnosed and managed in children?
**Definitive test:** Echocardiogram
**Other Ix:** ECG, exercise testing
**Management:** see image
74
What are some complications of aortic stenosis in children?
* ***Left ventricular outflow tract obstruction***
* Heart failure
* Ventricular arrhythmia
* ***Bacterial endocarditis***
* Sudden death, often on exertion
75
What conditions is congenital pulmonary stenosis associated with?
* Tetralogy of Fallot
* William syndrome
* Noonan syndrome
* Congenital rubella syndrome
76
How may pulmonary stenosis present in a child?
* Often asymptomatic and found incidentally by murmur
* If severe may have fatigue on exertion, shortness of breath, dizziness and fainting
77
How is pulmonary stenosis diagnosed and managed in children?
**Diagnosis:** Echocardiogram
**Mx:** If mild just watchful waiting under paediatric cardiologist. If severe can do ***balloon valvuloplasty*** through femoral vein to IVC with x-ray guidance. If still fails then open heart surgery
78
How is paediatric heart failure managed?
* Sit up- right
* Oxygen
* Calories via NG feed - because the condition can lead to a state of "hypercatabolism," where the body rapidly breaks down muscle tissue, requiring more calories to maintain muscle mass and prevent malnutrition, which can worsen symptoms and overall health outcomes
* Diuretics (furosemide 1mg/kg/24hr infusion ± spironolactone)
* Duct dependent cyanotic conditions will need alprostadil (PgE1) to maintain patency
* Transfer to neonatal cardiac centre
* beta blockers are not routinely prescribed in children
79
Babies cannot describe symptoms so how can we tell they may have paediatric heart failure?
* SOB
* Exercise intolerance
* Growth failure
* Poor feeding
* Tachycardia
* Sweating
* sacral odema > peripheral odeama because they are laying on their back
80
What is important about the volume of a murmur?
**VSD:** Larger the defect, quieter the noise
**Outflow obstruction e.g AS:** Worse defect, louder the noise
81
What rhythm suggests congestive cardiac failure?
Gallop rhythm
82
What are some signs that congenital heart disease has/is decompensating to heart failure?
* **Poor feeding**
* **Dyspnoea**
* **Failure to thrive**
* **Tachycardia** (bradycardia or inappropriately normal rate suggests imminent arrest)
* **Hepatomegaly**
* **Cool peripheries**
* **Acidosis on ABG**
* **Cyanosis** (TGA, tetralogy of Fallot, tricuspid or pulmonary atresia)
83
How is heart failure due to congenital heart disease investigated?
* FBC
* CXR
* *P*aO2 (air and 100% FiO2)
* ECG
* Echo, ± cardiac catheter/advanced imaging techniques
84
How is congenital heart failure managed?
* **Sit upright**
* **Oxygen**
* **Calories via NG feed**
* **Diuretics** (furosemide ± spironolactone)
* **Fluid restrict** to 130ml/kg/day
* Duct dependent cyanotic conditions will need **alprostadil (PgE1)**
* **Transfer to neonatal cardiac centre**
85
examination quick rundown
- femoral
- work of breathing
- liver edge
- murmur
86
18 day old baby
not feeding well
cool peripheries
appeared mottled
breathless
femoral are poor
what are we thinking
- sepsis
- coarctation - can present later due to the duct closing (prostaglandin)
- metabolic (enzyme deficiency)
87
6 week old term
not feeding well
not gaining weight
breathless
murmur
hepatomegaly
what are we thinking
- VSD
- congestive heart failure
- dilated cardiomyopathy
- not gaining weight as they are using high amounts of energy trying to breathe
- murmur due to VSD
- offer diuretics - furosemide and spironolactone
- resp support
- calories increased
- try to lower bP so less blood flows between the left and right shunt
88
18 day old baby
term
not feeding well
blue episodes when crying
stats 86%
loud murmur
TOF - tet spells
- keep baby calm
- give 02
- knees to chest - increase systemic vascular resistance and beings blood back to heart
- morphine - relax muscle either via IV or IM
- fluid bolus
- adrenaline - phenylephrine
post cell
- baby hydrated
- beta blockers
- parental advice
- surgical repair / RVOT stent
89
18 month baby
multiple viral infections
- growing well
- blue episodes when crying and getting out baths
- no murmur
- acrocyanosis
self resolving
90
15 y/o
previous heart surgery for TOF Pulmonary valve replacement
recent tooth extraction
unwell for 10 days
fever
infective endocarditis
DUKE criteria
91
emergency c section from pathological CTG
tachycardiac
haemadynamically stable
SVT
- vasovagal
- IV adenosine via a large wide bore cannula left (impending doom) stops AV node
- synchronous DC
