Cardiology: PICU Handbook

Premature atrial contractions

• Usually idiopathic and benign
• May be due to catecholamine excess, electrolyte abnormalities, lines, hypoxia, or acid base disturbances
• Generally no treatment is needed
• Should correct lytes if abnormal and evaluate lineplacement
• Typically resolve w/ time

Premature ventricular contractions

• More worrisome than PACs
• Seen w/ electrolyte abnormalities, hypoxia, hypocalcemia, catecholamine excess
• Monitor how frequent, number in a row, unifocal or multifocal
• Treatment depends on frequency, rate, associated conditions, and if a structural or functional change
• Always correct lytes and evaluate line placement

Bradycardia

• If asymptomatic, usually no treatment
• Acute treatment: Atropine, isoproterenol, or temporary pacing
• Chronic treatment: Pacing

Heart block

• 1° heart block in absence of heart disease usually does not progress
• Watch 2° heart block closely as may develop into worsening heart block
• Avoid meds which slow AV conduction (β blockers Ca Channel blockers, Dig)
• Tx as above for bradycardia

Supraventricular tachycardia

• Follow PALS guidelines!
• If adequate perfusion
  • Vagal maneuvers (ice to face, knees to chest) 
  • Adenosine
    • Give 0.1 mg/kg IV/IO (max first dose 6mg) May double and repeat second dose (max 12 mg)
    • Give as rapid bolus followed by flush Try to use central line or IV closest to heart
     
  • Consult cardiology
    • Consider antiarrhythmic meds
    • esmolol, amiodarone or procainamide
    • Consider overdrive pacing
     
  • Cardioversion
    • Use 0.5 to 1 J/kg, may increase to 2 J/kg if initial dose is ineffective
    • Use sedation if possible (Etomidate 0.1mg/kg is a good choice, may repeat dose as needed)
     
   
• If inadequate perfusion
  • 1) IMMEDIATE Cardioversion
    • Use 0.5-1 J/kg, may increase to 2 J/kg if needed
    • Do not delay cardioversion for sedation
     
   

Junctional ectopic tachycardia (post-operative)

• Correct acidosis and electrolyte abnormalities (Mg, K, Ca)
• Mild hypothermia (35 degrees Celsius)
• Reduce inotropic agents (NE, Epi) as able
• Make sure adequate pain control (sedation)
• Consult cardiology
• Slower rates may not need treatment (<170 bpm)
• For higher rates, consider atrial overdrive pacing (higher rates may gain AV synchrony thus causing improved filling)
• Consider antiarrhythmic medications (amiodarone, procainamide)
• Chronic treatment: Pacing

 Premature atrial contraction

• QRS appears early
• P wave different morphology
• Incomplete compensatory pause

Premature ventricular contraction

• Differing morphology QRS w/o proceeding P wave
• Full compensatory pause
• Typically large T wave w/ opposite polarity of QRS

Supraventricular tachycardia

• Sudden start and stop
• Narrow complex
• Usually do not see P wave (may be retrograde P wave in T wave)
• No HR variability

1° AV block

• PR prolongation >0.2 sec

2° AV block

• Mobitz Type I (Wenckebach)
  • Increasing PR intervals prior to dropped QRS
   
• Mobitz Type II
  • Intermittently non-conducted P waves not preceded by PR prolongation 

3° AV block

• No apparent relationship between P waves and QRS complexes

 *Atrial activity is marked by blue and ventricular activity is marked by red. Note that some P waves follow the QRS = dissociation!

Junctional ectopic tachycardia

• Narrow complex tachycardia
• P waves not discernible, are dissociated from the QRS, or show retrograde conduction
• Typically "ramps up and ramps down"
• No HR variability

Terminology

Ability of pacemaker to cause depolarization of heart chamber

Sensitivity

Ability of pacemaker to detect intrinsic cardiac activity

The lower the number on the dial = the more sensitive the pacemaker

Important

If pt is being paced, always be sure to check for appropriate capture (pacer spikes followed by an electrical response).

The pacer mode should always be on the monitors if pt is paced.

If you suspect pacer has lost capture, notify fellow immediately and contact cardiology if  needed.

PATIENT

Atrial wires = White
Ventricular wires = Blue

Information to obtain

1. Details of repair… Ex: size of shunt, where incision was made, valve-sparing procedure, etc
2. Complications during repair (arrhythmias, bleeding, etc)
3. Post-operative TEE findings… Ex: gradients, residual VSD leak, valve regurg
4. Cardiopulmonary bypass time and aorta cross clamp times…longer times tend to have more complicated post-op courses
5. Specific post-operative parameters or goals… Ex: SBP <70 to prevent any tension on sutures or leak at anastomosis
6. Specific lines and tubes… Ex: IJ, art lines, MTs or CTs
7. Trends during case… Ex: what CVP did pt tolerate, BP trends, heart rate ranges
8. Blood product administration… Ex: FFP, plts, etc
9. Any worrisome labs… Ex: coags, lactate
10. Airway management… Ex: easy intubation, reasons why they did not extubate
11. Rhythm problems intra/postoperatively. Pacing yes/no

Helpful hints w/ post-op orders

• Tina Davenport usually takes care of all orders… go assess pt!
• For big cases on bypass, IVF are written for 1/2 maintenance b/c we try to account for
  1. Cardiac gtts
  2. Fluid boluses or blood product administration
  3. SIRS & capillary leak
  that can cause some edema
• IVF often are D5W so pay attention to pt's Na. Will need to adjust once Na is in the normal range.
• Hourly labs need to be drawn initially, adjust lab frequency as needed as pt stabilizes
• Please check over orders. Make sure the morphine dose, tylenol dose, etc are appropriate.
• Goal K > 4, iCa > 4, Mg > 2, replace as needed.

Important trends to follow

• SVO2 — good indicator of oxygen extraction,changes in trends may indicate change in pt status>
  1. High SVO2 — inadequate extraction
  2. Low SVO2 — inadequate oxygen delivery
   
• Cerebral & renal somenetics — also indicator of oxygen extraction
• Lactate — <2 is normal, watch trends!
• Hct — Many repairs require higher HCT to maintain good oxygen delivery
• CVP — marker of volume status, important b/c some repairs require higher CVP but may also indicate concern for issues like tamponade
• Vital Signs — Changes in HR may be a subtle sign of an arrhythmia
• UOP and I/O balance
• Chest, mediastinal, and peritoneal drainage

Important exam findings

• Murmurs — any changes in quality, new murmurs
• Edema/ wts — are they volume overloaded or dry
• Hepatomegaly — worsening CHF?
• Perfusion — warm, cool, clamped down
• Drainage from tubes — chylous, increased output, bloody

The fellow and staff are there to help

Please don't hesitate to ask questions

Diagram

• Inadequate tissue perfusion → anaerobic metabolism → accumulation of lactic acid → metabolic acidosis
• If acidosis is unrecognized → cell death, organ dysfunction, multi-organ system failure, and DEATH

• Goal is to improve tissue oxygenation by increasing oxygen delivery and decreasing oxygen demand
• Treat underlying process

• EARLY RECOGNITION IS KEY!!!
• Requires high index of suspicion
• Tachycardia and tachypnea often 1st sign
• Hypotension is a late finding in pediatrics

Etiology of shock

• Hypovolemic - characterized by inadequate circulating intravascular volume, ex: hemorrhage, fluid loss
• Cardiogenic - characterized by myocardial dysfunction, ex: arrhythmias, cong heart disease, myocarditis, cardiomyopathy
• Obstructive - characterized by inability to produce adequate cardiac output despite normal intravascular volume, ex: tamponade, pneumothorax, outflow obstructions
• Distributive - characterized by inadequate distribution of fluid volume, ex: anaphylaxis, spinal cord disruption, severe sepsis

General treatment principals

• ABCs - Consider intubation to decrease O2 demand
• Invasive lines often needed
• Fluid Resuscitation - If unresponsive, widen DDx!
• Vasoactive Infusions - Will provide CV support
• Sedation/Paralysis - Will decrease O2 demand
• Temperature Control
• Antibiotics

1. Pulmonary Stenosis
2. RV Hypertrophy
3. Overriding aorta
4. VSD

“Tet Spells”

• Agitation/irritability, hyperpnea, profound cyanosis, syncope
• Dynamic obstruction to pulm blood flow
• Tx: Oxygen, volume, sedation, positioning (knee-chest/squat) 
• Other options if above fail: Bicarb, phenylephrine

Pre-operative pathophysiology

• Physiology dependent on pulmonary blood flow
• Minimum obstruction : L → R shunt through VSD
  • Symptoms: Pulm overcirculation, CHF
• Severe obstruction:  R→ L shunt
  • Symptoms: Hypoxic, sat 70-80% 
• Balanced obstruction: Enough PS to prevent over-circulation, sats ~90%    

Key Questions to ask surgeon

1. How was the RVOT repaired? (transannular vs. valve sparing)
2. What did the RV and PAs look like? Any abnormal anatomy?
3. Post operative TEE findings?

Post-operative issues

• Residual VSD – May have hemodynamic instability, high atrial pressures
• RV Outflow tract obstruction –   Usually causes more long term issues, ventricular arrhythmias, and possible need for repeat repair
• RV Dysfunction – Consider if incision was made in RV or pulm regurg
• Arrhythmias – JET, ventricular ectopy, complete heart block

Supracardiac (A)

R & L Pulmonary veins (PV) join in a confluence posterior to LA & are connected via ascending vertical vein to innominate vein which drains into SVC (MOST COMMON)

Infracardiac (B)

Confluence of PV drains via descending vertical vein to portal venous system to IVC

Cardiac (C)

R & L PV drain into a dilated coronary sinus or directly into RA

Mixed pattern

4 PV drain into more than one venous structure (ie. R PV to RA while L PV into vertical vein)

Pathophysiology

Obstructed Veins: Pulmonary venous hypertension is seen w/ resultant pulmonary edema.  Reflex pulm arteriolar vasoconstriction and pulm HTN are seen w/ resultant right heart failure.

Unobstructed Veins: Pulm venous return is to systemic venous circulation and blood from both venous systems is mixed. Systemic cardiac output is maintained by R à L shunt at atrial level.

Post-op complications

Low cardiac output

Previously dilated R sided structures influenced LA and LV, which made LV less compliant. LV may need high filling pressure post-operatively.

Respiratory insufficiency

Fulminant pulmonary edema prior to surgery + cardiopulmonary bypass may lead to severe respiratory compromise.

Pulmonary hypertension

Due to medial hypertrophy of pulm arterioles, pulm HTN occurs in ~50% of pts. Significant risk factor for death in immediate post-op period.

Need to rule out residual pulm venous obstruction by echo if problems post-operatively.

Arrhythmias

Usually supraventricular, occur in ~20%.

***Import to know that lowering of PA pressures and increased pulmonary blood flow post-operatively can lead to increased preload to L side of the heart leading to a bad cycle of increased LA pressure, increased PA pressure, decreased LV compliance, and increased LA pressure which all exacerbate pulm HTN!

D-TGA is when aorta arises from RV and RA arises from LV. Most common form of transposition.

Important associated defects for surgical planning are malalignment septal defects.

Anterior (rightward) defects are associated w/ varying degrees of overriding of pulmonary annulus onto RV.

Posterior (leftward) malalignment defects are associated w/ varying degrees of subpulmonary stenosis, annular hypoplasia, or pulmonary valvar atresia.

Important pre-op physiology

Dominant problems are poor oxygen delivery and excessive R and L ventricular workload.

MUST HAVE AN INTRACARDIAC (PFO, ASD, VSD) or EXTRACARDIAC (PDA) shunt to survive – may need emergent balloon atrial septectomy if pt not responding to prostaglandins!

Poor mixing  is often seen by low pO2, elevated pCO2 (despite good chest movement/ ventilation) and a metabolic acidosis!  Important because pt has severely decreased effective pulmonary and systemic flows. Need to ensure mixing and maximize oxygen delivery!

Surgical repairs

Arterial Switch – Great vessels are transected, coronaries inspected and translocated to new aorta, septal defects are repaired.

Rastelli – Used mostly for TGA w/ large VSD and extensive LVOTO.

LV output directed to aorta by intra-ventricular patch tunnel technique and RV is connected to PA by extracardiac valved conduit.

Post-operative issues

1) Arrhythmias – especially b/c of transfer of coronary arteries

2) LV dysfunction – may be due to coronary insufficiency or “unprepared” LV. LV may be poorly compliant following Switch. Need to give volume slowly as acute change in preload may increase LA pressure, cause pulm edema, and decrease cardiac output.

3) Rule-out any residual stenosis or ASD/VSDs (if initially present). Rule out conduit obstruction or branch PA distortion if Rastelli was performed.