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My Phase 3a Revision > PAEDS - CARDIOVASCULAR > Flashcards

PAEDS - CARDIOVASCULAR Flashcards

1
Q

FOETAL CIRCULATION
What 3 foetal shunts are there?

A
  • Ductus venosus = connects umbilical vein + IVC so blood bypasses liver
  • Foramen ovale = connects RA+LA so bypass RV + pulmonary circulation
  • Ductus arteriosus = connects pulm. artery + aorta so blood can bypass pulm. circulation
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2
Q

FOETAL CIRCULATION
What are the foetal shunts called when they are closed?

A
  • Ductus venosus -> ligamentum venosus
  • Foramen ovale -> fossa ovalis
  • Ductus arteriosus -> ligamentum arteriosus
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3
Q

FOETAL CIRCULATION
What is the flow of foetal blood?

A
  • Oxygenated + nutrients at placenta for rest of body (umbilical vein) + disposes waste like CO2 + lactate (umbilical artery)
  • Umbilical vein > ductus venosus > RA > foramen ovale > LA > LV > rest of body > umbilical artery
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4
Q

FOETAL CIRCULATION
What are the pressures like within the foetal heart?

A
  • LA pressure low as relatively little blood returns from lungs
  • RA>LA pressure as RA receives all systemic venous return + blood from placenta
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5
Q

FOETAL CIRCULATION
What happens in the first few breaths in the foetus?

A
  • Resistance to pulmonary blood flow falls as alveoli expand + volume of blood flowing through lungs massively increases so increased LA pressure.
  • Volume of blood returning to RA falls as placenta removed
  • LA > RAp = foramen ovale closes
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6
Q

FOETAL CIRCULATION

What happens over the next few hours/days?

A
  • Ductus arteriosus will close (issue if duct-dependent CHD)
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7
Q

FOETAL CIRCULATION
What are physiological (innocent flow) murmurs?

A

4S’s –
- Soft blowing murmur
- Symptomless
- left Sternal edge
- Systolic murmur only

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8
Q

FOETAL CIRCULATION
When are physiological (innocent flow) murmurs seen?

A

Common during febrile illness or anaemia as CO increases

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9
Q

FOETAL CIRCULATION
What other features of innocent murmurs are there?

A
  • Normal heart sounds (none added),
  • no parasternal thrill or radiation,
  • may vary with posture
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10
Q

FOETAL CIRCULATION
When would you investigate an innocent murmur?

A

Louder than 2/6, diastolic,
louder on standing

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11
Q

FOETAL CIRCULATION
What are the 5 main types of congenital heart lesions?

A
  • L>R shunt (breathless) = ASD, VSD, PDA
  • R>L shunt (cyanotic) = ToF, TGA
  • Common mixing (breathless + blue) = complete AVSD, complex CHD (tricuspid atresia)
  • Outflow obstruction in well child = AS, PS
  • Outflow obstruction in sick neonate = coarctation, HLHS
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12
Q

FOETAL CIRCULATION
What is Eisenmenger’s syndrome?

A
  • L>R shunt as systemic pressure is higher than pulmonary pressure
  • Over time, pulmonary pressure may increase beyond the systemic pressure
  • This is due to pulmonary HTN > increasing RH pressures + so RVH leading to shunt reversal (R>L) + so cyanosis
  • May have plethoric complexion due to compensatory polycythaemia
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13
Q

FOETAL CIRCULATION
What are the main cyanotic heart diseases?

A

4Ts –
- ToF
- TGA
- Tricuspid atresia
- Truncus arteriosus
(Complete AVSD too)

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14
Q

FOETAL CIRCULATION
How can you determine if cyanosis is cardiac or respiratory?

A
  • Hyperoxic test, better = respiratory, still cyanosed = cardiac
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15
Q

FOETAL CIRCULATION
What is a complication of SLE?

A

Complete heart block

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16
Q

ATRIAL SEPTAL DEFECT
What is atrial septal defect (ASD)?

A
  • Hole in septum connecting atria as failure of septal tissue to form
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17
Q

ATRIAL SEPTAL DEFECT
What is the pathophysiology?

A

L>R shunt as LAp>RAp so increased flow into R heart + lungs
- Trisomy 21, foetal

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18
Q

ATRIAL SEPTAL DEFECT
What is it common in?

A

Trisomy 21,
foetal alcohol syndrome

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19
Q

ATRIAL SEPTAL DEFECT
What are the 3 main types of ASD?

A
  • Ostium primum (group with AVSD)
  • Ostium secundum (80%)
  • Partial AVSD
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20
Q

ATRIAL SEPTAL DEFECT
What is a partial AVSD?

A
  • Inter-atrial communication between bottom end of atrial septum + AV valves
  • Abnormal AV valves with a left AV valve which has 3 leaflets + tends to leak
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21
Q

ATRIAL SEPTAL DEFECT
What is the clinical presentation of ASD?

A
  • Dyspnoea, difficulty feeding, failure to thrive, recurrent chest infections
  • Arrhythmia in adulthood (may need VTE prophylaxis)
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22
Q

ATRIAL SEPTAL DEFECT
What signs would you find on clinical examination in ASD?

A
  • Fixed + widely split S2 (split does not change with inspiration/expiration)
  • ES murmur at upper L sternal edge (pulmonary) as increased flow across pulmonary valve by L>R shunt
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23
Q

ATRIAL SEPTAL DEFECT
What are some investigations for ASD?

A
  • Often antenatal Dx
  • CXR = cardiomegaly, enlarged pulmonary arteries + increased pulmonary vascular markings
  • Primum ECG = RBBB + LAD
  • Secundum ASD = RBBB + RAD
  • ECHO is diagnostic
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24
Q

ATRIAL SEPTAL DEFECT
What are the complications of ASD?

A
  • Eisenmenger syndrome = shunt switch = cyanotic

- Stroke risk in context of VTE (can be from AF or atrial flutter)

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25
Q

ATRIAL SEPTAL DEFECT
What is the management of ASD?

A
  • Small + asymptomatic = watchful waiting

- Large = transvenous catheter closure via femoral vein or open heart surgery

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26
Q

VSD
What is a ventricular septal defect (VSD)?

A
  • Hole in the septum between the 2 ventricles, most common heart defect
  • L>R shunt as LVp>RVp so increased flow to R heart + lungs
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27
Q

VSD
What are some conditions associated to VSD?

A
  • Trisomy 13, 18 + 21
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28
Q

VSD
What is the clinical presentation of VSD?

A
  • Small = ?asymptomatic
  • Large = heart failure with dyspnoea, failure to thrive, recurrent infections
  • Harsh pansystolic murmur
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29
Q

VSD
What are the features of the pansystolic murmur in VSD?

A
  • Left lower sternal edge
  • Loud murmur = smaller VSD (larger = quieter)
  • May have systolic thrill on palpation
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30
Q

VSD
What are the investigations in VSD?

A
  • Often antenatal Dx or murmur on NIPE
  • CXR + ECG often normal in small VSDs
  • CXR in large = cardiomegaly, increased pulmonary vascular markings ± pulmonary oedema
  • ECHO is diagnostic
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31
Q

VSD
What are some complications of VSD?

A
  • Increased risk of infective endocarditis > Abx prophylaxis during surgery
  • AR, Eisenmenger’s syndrome + right heart failure
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32
Q

VSD
What is the management of VSD?

A
  • Small VSDs with no signs of pulmonary HTN or heart failure may watch + wait as may close spontaneously
  • Transvenous catheter closure via femoral vein or open-heart surgery
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33
Q

HEART FAILURE
What are the causes of heart failure in neonates?

A

Obstructed or duct-dependent systemic circulation (HLHS, severe coarctation)

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34
Q

HEART FAILURE
What are the causes of heart failure in infants?

A

High pulmonary blood flow (VSD, AVSD, large PDA)

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35
Q

HEART FAILURE
What are the causes of heart failure in older children?

A

Eisenmenger’s syndrome (RHF),
rheumatic disease,
cardiomyopathy

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36
Q

HEART FAILURE
What is the clinical presentation of left heart failure?

A
  • SOB (esp. on feeding or exertion), sweating, recurrent chest infections
  • Poor weight gain, gallop rhythm
  • Cardiomegaly, cool peripheries
  • As a rule = increased HR, RR + creps
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37
Q

HEART FAILURE
What is the clinical presentation of right heart failure?
What are the causes?

A
  • Peripheral oedema
  • Hepatomegaly
  • TR, PS, large VSD (anything making fluid overload backwards > IVC)
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38
Q

HEART FAILURE
What is the management of heart failure?

A
  • Furosemide (loop diuretic)
  • Captopril (ACEi)
  • Increased calories
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39
Q

COMPLETE AVSD
What is a complete atrioventricular septal defect (AVSD)?

A
  • Defect in middle of heart with single 5-leaflet valve between atria + ventricles which stretches across entire AV junction + tends to leak
  • Large defect means pulmonary HTN too
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40
Q

COMPLETE AVSD
What condition is complete AVSD commonly seen in?
How does it present?

A
  • Down’s syndrome (need routine ECHO)
  • Cyanosis at birth with heart failure 2–3w of life, no murmur
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41
Q

COMPLETE AVSD
What is the management of complete AVSD?

A
  • May have antenatal Dx or on routine ECHO in Down’s baby
  • Medical Tx for heart failure + surgical repair at 3-6m
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42
Q

PDA
What is a patent ductus arteriosus (PDA)?

A
  • DA normally stops functioning within 1–3d
  • If patent, pressure in aorta higher than in pulmonary vessels so blood flows L>R
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43
Q

PDA
What is a consequence?

A
  • If patent, pressure in aorta higher than in pulmonary vessels so blood flows L>R
  • Can lead to Eisenmenger’s syndrome
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44
Q

PDA
What can happen due to increased blood flowing through pulmonary vessels?

A
  • More blood returning to left side of heart so can lead to LVH
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45
Q

PDA
What are some risk factors of PDA?

A

Prematurity is key + association with maternal rubella

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46
Q

PDA
What are the symptoms of PDA?

A
  • Small may be asymptomatic or present in adulthood with heart failure
  • May present with SOB, difficulty feeding, failure to thrive + LRTIs
47
Q

PDA
What are the signs of PDA?

A
  • Collapsing or bounding pulse as increased pulse pressure
  • Continuous ‘machinery’ murmur heard loudest beneath the L clavicle
48
Q

PDA
What are some investigations for PDA?

A
  • ECHO to confirm Dx
  • Doppler flow studies during ECHO can assess size + characteristics
  • Can also assess effects of PDA on heart (LVH/RVH)
49
Q

PDA
What is the management of PDA?

A
  • Monitor until 1y with ECHOs (treat early if Sx or heart failure)
  • NSAIDs (indomethacin) facilitates closure of PDA as inhibits prostaglandins
  • After 1y unlikely to resolve so trans-catheter or surgical closure to reduce IE risk
50
Q

TOF
What abnormalities are described in tetralogy of fallot (TOF)?

A
  • Large VSD
  • Pulmonary stenosis (RV outflow obstruction)
  • RVH
  • Overriding aorta
    (If ASD present too = pentad of Fallot)
51
Q

TOF
What is the pathophysiology of TOF?

A
  • Pulmonary stenosis leads to RVp>LVp so R>L shunt and cyanosis
  • Cyanosis presents later than in TGA, about 1–2m
52
Q

TOF
What is TOF associated with?

A
  • Trisomy 21 + 22q deletions
53
Q

TOF
What are some risk factors?

A
  • Rubella,
  • maternal age >40,
  • alcohol in pregnancy,
  • maternal DM
54
Q

TOF
What is the clinical presentation of TOF?

A
  • Severe cyanosis with exertional hyper-cyanotic ‘tet’ spells
  • Loud harsh ES murmur at left sternal edge (from PS)
  • Digital clubbing
  • Squatting on exercise = increased peripheral vascular resistance + decreased degree of R>L shunt so improved Sx
55
Q

TOF
What happens during a hyper-cyanotic tet spell?

A
  • Rapid increase in cyanosis, irritability + dyspnoea
  • If severe can lead to reduced GCS, seizures + potential death
56
Q

TOF
What are the investigations for TOF?

A
  • May be Dx antenatally or murmur on NIPE
  • CXR = ‘boot shaped’ heart due to RVH
  • ECHO ± cardiac catheterisation to show anatomy + degree of stenosis
57
Q

TOF
What is the management of a hyper-cyanotic tet spell in TOF?

A
  • Morphine for sedation + pain relief
  • IV propranolol as peripheral vasoconstrictor
  • IV fluids, sodium bicarbonate if acidotic
58
Q

TOF
What is the management of TOF?

A
  • Neonates = prostaglandin infusion to maintain ductus arteriosus to allow blood to flow from aorta > pulmonary arteries
  • Early surgical repair with closure of VSD + correction of pulmonary stenosis at 6m
59
Q

TGA
What is transposition of the great vessels (TGA)?

A
  • Aorta is connected to the RV, pulmonary artery is connected to LV meaning deoxygenated blood is pumped around body = cyanosis
60
Q

TGA
What is it associated with?

A

Duct dependent lesion, associated with PDA, ASD + VSD

61
Q

TGA
What is the clinical presentation of TGA?

A
  • Cyanosis at birth/day 1–2 as duct closes > life-threatening
  • Less severe if PDA, ASD or VSD to allow mixing
  • No murmur but S2 usually loud + singular
  • Prominent RV impulse on palpation
62
Q

TGA
What are the investigations for TGA?

A
  • May be Dx antenatally, pre (R arm) + post duct (foot) sats
  • CXR may show narrow mediastinum with ‘egg on its side’ appearance
  • ECHO confirms Dx
63
Q

TGA
What is the management of TGA?

A
  • Neonates = prostaglandin E1 infusion to maintain ductus arteriosus
  • Balloon atrial septostomy to create hole between 2 atria for mixing
  • Arterial switch procedure = open heart surgery, definitive Mx
64
Q

TRICUSPID ATRESIA
What is tricuspid atresia?

A
  • Only LV is effective, RV is small, non-functional + complete absence of tricuspid valve
65
Q

TRICUSPID ATRESIA
How does tricuspid atresia present?

A
  • ‘Common mixing’ of systemic + pulmonary venous return in LA = cyanosis + dyspnoea
66
Q

TRICUSPID ATRESIA
How is it managed?

A

Shunt between subclavian + pulmonary artery with surgery later

67
Q

COARCTATION OF AORTA
What is coarctation of the aorta?

A
  • Arterial duct tissue encircling the aorta at the level of the ductus arteriosus which causes constriction + narrowing when the duct closes
68
Q

COARCTATION OF AORTA
What is a consequence of coarctation of aorta?

A
  • Collateral circulation forms to increase flow to the lower part of the body leading to the intercostal arteries becoming dilated + tortuous
69
Q

COARCTATION OF AORTA
What is it associated with?

A

Turner’s syndrome

70
Q

COARCTATION OF AORTA
What is the clinical presentation of coarctation of aorta?
How may it present if severe?

A
  • Weak femoral pulses + radiofemoral delay
  • Systolic murmur between scapulas or below L clavicle
  • Heart failure, tachypnoea, poor feeding, floppy
  • LV heave (LVH)
  • Acute circulatory collapse at 2d as duct closes (duct dependent)
71
Q

COARCTATION OF AORTA
What are the investigations for coarctation of the aorta?

A
  • 4 limb BP (R arm > L arm), pre + post-duct sats
  • CXR may show cardiomegaly + rib notching (often teens + adults)
72
Q

COARCTATION OF AORTA
What is the management of coarctation of aorta?

A
  • ABCDE if collapse
  • Prostaglandin E1 infusion if critical
  • Stent insertion or surgical repair
73
Q

HYPOPLASTIC LEFT HEART
What is hypoplastic left heart syndrome (HLHS)?

A
  • Under development of entire left side of heart
  • Mitral valve is small or atretic, LV is diminutive + usually aortic valve atresia
  • Ascending aorta very small + almost invariably coarctation of aorta
74
Q

HYPOPLASTIC LEFT HEART
What is the clinical presentation of HLHS?

A
  • Sickest neonates with duct-dependent circulation
  • No L side flow so ductal constriction > profound acidosis + rapid CV collapse
  • Weakness or absence of all peripheral pulses
75
Q

HYPOPLASTIC LEFT HEART
What is the management of HLHS?

A
  • ABCDE
  • Prostaglandin E1 infusion to prevent duct closure
  • Surgical management
76
Q

EBSTEIN’S ANOMALY
What is Ebstein’s anomaly?

A
  • Low insertion of tricuspid valve on right leading to larger atrium + smaller ventricle
  • Leads to poor RA>RV flow + so poor flow to pulmonary vessels
  • Associated with R>L shunt via ASD + so blood can bypass lungs > cyanosis
77
Q

EBSTEIN’S ANOMALY
What is Ebstein’s anomaly associated with?

A
  • Wolff-Parkinson-White syndrome + lithium in pregnancy
78
Q

EBSTEIN’S ANOMALY
What is the clinical presentation of Ebstein’s anomaly?

A
  • Evidence of heart failure
  • SOB, tachypnoea, poor feeding, collapse or cardiac arrest
  • Gallop rhythm with S3 + S4
  • Cyanosis few days after birth if ASD when ductus arteriosus closes
79
Q

EBSTEIN’S ANOMALY
What are the investigations for Ebstein’s anomaly?

A
  • ECG = arrhythmias, RA enlargement (P pulmonale), LAD + RBBB
  • CXR = cardiomegaly + RA enlargement
  • ECHO diagnostic
80
Q

EBSTEIN’S ANOMALY
What is the management of Ebstein’s anomaly?

A
  • Prophylactic Abx to prevent infective endocarditis
  • Definitive Mx = surgical correction
81
Q

AORTIC STENOSIS
What is aortic stenosis?

A
  • Aortic valve leaflets partly fused together giving restrictive exit from LV
82
Q

AORTIC STENOSIS
What is aortic stenosis associated with?

A
  • Bicuspid aortic valve + William’s syndrome (supravalvular)
  • Also may be mitral stenosis + coarctation of aorta too
83
Q

AORTIC STENOSIS
What is the normal clinical presentation of aortic stenosis?

A
  • Most asymptomatic with ejection-systolic murmur at upper right sternal edge (aortic area) radiating to neck (carotid thrill)
  • Ejection click before murmur
  • Palpable systolic thrill
  • Slow rising pulses + narrow pulse pressure
84
Q

AORTIC STENOSIS
How does more severe aortic stenosis present?

A
  • Severe = syncope, chest pain + dyspnoea on exertion
  • Critical = severe heart failure + shock
85
Q

AORTIC STENOSIS
What are the investigations for aortic stenosis?

A
  • CXR (prominent LV),
  • regular ECHO to assess need for interventions
86
Q

AORTIC STENOSIS
What are some complications?

A

LV outflow tract obstruction,
heart failure
ventricular arrhythmias

87
Q

AORTIC STENOSIS
What is the management of aortic stenosis?

A
  • Balloon valvotomy/dilatation if symptomatic
  • May need surgical aortic valve replacement
88
Q

PULMONARY STENOSIS
What is pulmonary stenosis?
What is it associated with?

A
  • Pulmonary valve leaflets are partly fused together giving a restrictive exit from RV
  • ToF, Noonan syndrome + congenital rubella syndrome
89
Q

PULMONARY STENOSIS
What is the clinical presentation of pulmonary stenosis?

A
  • Ejection systolic murmur at upper left sternal edge with ejection click
  • ?RV heave due to RVH
  • Critical PS = duct-dependent pulmonary circulation so cyanosis in first few days of life
90
Q

PULMONARY STENOSIS
What are the investigations for pulmonary stenosis?

A
  • CXR normal or post-stenotic dilatation of the pulmonary artery
  • ECG may show RVH (upright T wave in V1)
  • ECHO Dx
91
Q

PULMONARY STENOSIS
What is the management of pulmonary stenosis?

A
  • Most asymptomatic so wait until pressure gradient across pulmonary valve increases > trans-catheter balloon dilatation
92
Q

INFECTIVE ENDOCARDITIS
Who are at risk of infective endocarditis?

A
  • All children with CHD (except secundum ASD)
  • Highest risk where turbulent blood flow = VSD, coarctation of aorta + PDA
93
Q

INFECTIVE ENDOCARDITIS
What is the pathophysiology of infective endocarditis?

A
  • Infection of heart valves, septal defects or endocardial lined structures consisting of vegetations which are masses of fibrin, platelets + infectious organisms
94
Q

INFECTIVE ENDOCARDITIS
What are some risk factors for infective endocarditis?

A
  • IVDU,
  • prosthetics,
  • structural heart defects
95
Q

INFECTIVE ENDOCARDITIS
What is the most common causative pathogen for infective endocarditis?

A

Staph aureus (previous Strep Viridians)

96
Q

INFECTIVE ENDOCARDITIS
What are the septic and systemic signs of infective endocarditis?

A
  • Fever, malaise, night sweats, arthralgia/myalgia
  • Systemic emboli from L sided vegetations may result in brain abscess + stroke
97
Q

INFECTIVE ENDOCARDITIS
What are the clinical signs of infective endocarditis?

A
  • Splinter haemorrhage under nail beds
  • Retinal infarcts (Roth’s spots)
  • Tender nodules on fingers + toes (Osler’s nodes)
  • Painless erythematous palms + soles (Janeway lesions)
  • Microscopic haematuria
98
Q

INFECTIVE ENDOCARDITIS
What are the investigations for infective endocarditis?

A
  • FBC (WCC raised), CRP/ESR raised
  • Blood cultures before Abx started
  • Echo to look for valve vegetations
99
Q

INFECTIVE ENDOCARDITIS
What is the management?

A

High dose IV Abx (penicillin with aminoglycoside like vancomycin) for 6w

100
Q

RHEUMATIC FEVER
What is the pathophysiology of rheumatic fever?

A
  • Multi-system disorder due to autoimmune response producing antibodies against group A beta-haemolytic strep pyogenes (after tonsillitis) that targets other tissues
  • T2 hypersensitivity reaction as immune system attacks cells throughout body
101
Q

RHEUMATIC FEVER
How is rheumatic fever diagnosed?

A

Jones criteria –
- Evidence of recent strep infection plus 2 major or 1 major + 2 minor criteria

102
Q

RHEUMATIC FEVER
What are the major criteria in rheumatic fever?

A

JONES –

  • Joint arthritis (migratory as affects different joints at different times)
  • Organ inflammation (pancarditis > pericardial friction rub)
  • Nodules (subcut over extensor surfaces)
  • Erythema marginatum rash (pink rings of varying sizes on torso + proximal limbs)
  • Sydenham chorea
103
Q

RHEUMATIC FEVER
What are the minor criteria in rheumatic fever?

A

FEAR –

  • Fever
  • ECG changes (prolonged PR interval) without carditis
  • Arthralgia without arthritis
  • Raised CRP/ESR
104
Q

RHEUMATIC FEVER
What are the investigations for rheumatic fever

A
  • Throat swab for MC&S
  • Anti-streptococcal antibodies (ASO) titres = anti-DNase B +ve indicates strep infection (repeat after 2w to check if negative)
  • Echo, ECG + CXR to check cardiac involvement
105
Q

RHEUMATIC FEVER
What are some complications of rheumatic fever?

A
  • Recurrence
  • Valvular heart disease (mitral stenosis especially)
  • Chronic heart failure
  • Recurrent acute RF > scarring + fibrosis of heart valves > chronic RF
106
Q

RHEUMATIC FEVER
What is the management of rheumatic fever?

A
  • Prevention by treating strep infections with 10d phenoxymethylpenicillin
  • Specialist Mx (NSAIDs for joint pain, aspirin + steroids for carditis)
  • Prophylactic 1/12 IM benzathine penicillin most effective to prevent recurrence (if not daily PO penicillin)
107
Q

DILATED CARDIOMYOPATHY
What is it?

A

Large, poorly contracting heart can be inherited or secondary to metabolic disease or direct viral infection of myocardium (myocarditis)

108
Q

DILATED CARDIOMYOPATHY
When would you suspect dilated cardiomyopathy?

A
  • Any child with enlarged heart + heart failure who was previously well
109
Q

DILATED CARDIOMYOPATHY
What is the management of dilated cardiomyopathy?

A
  • Dx by ECHO
  • Sx treatment with diuretics, ACEi + carvedilol (beta blocker)
110
Q

DILATED CARDIOMYOPATHY
What is the management of myocarditis?

A

Myocarditis usually improves spontaneously but some may need heart transplant

111
Q

SUPRAVENTRICLAR TACHYCARDIA
What is a supraventricular tachycardia?
Give a type

A
  • Re-entry tachycardia as circuit of conduction is set up with premature activation + excitation of the atrium via an accessory pathway
  • Wolff-Parkinson-White syndrome accessory pathway is Bundle of Kent
112
Q

SUPRAVENTRICLAR TACHYCARDIA
How does a supraventricular tachycardia present?

A
  • Sx of heart failure in young child,
    palpitations,
    dyspnoea
113
Q

SUPRAVENTRICLAR TACHYCARDIA
What is the ECG like?

A
  • Narrow complex tachycardia (250-300bpm)
  • WPW = delta wave (slurred upstroke to QRS) with a short PR interval
114
Q

SUPRAVENTRICLAR TACHYCARDIA
What is the management of a supraventricular tachycardia?

A
  • 1st line = Vagal stimulation (carotid sinus massage, cold ice pack to face)
  • 2nd line = IV adenosine
  • 3rd line = Electrical cardioversion
  • Long term = ablation of pathway or flecainide

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