Torsades & Prolonged QT

= a type of ventricular tachycardia
-usually paroxysmal with runs lasting <90s

Unstable
-defibrillate if pulseless (indistinguishable from vfib)
-cardiovert or defibrillate* if unstable with pulse
*cardioversion may not work as the machine may not be able to synchronize with a polymorphic rhythm –> may need to defibrillate even if not pulseless

-do NOT give amio or procainamide – these worsen QT prolongation

Stable**
(1) give 2g magnesium sulfate over 2m
(2) increase HR in order to decrease QT interval
—-overdrive pacing (transvenous preferred) with rate for capture usually 110 or higher
—-chemical overdrive pacing via isoproterenol drip (beta1 & beta2 agonist) at 5 mcg/min (ONLY if acquired, NOT congenital)
(3) consider lidocaine (suppresses early after-depols and thus PVCs)
**May try cardioversion even if stable

Prolonged QT
(1) give 2g magnesium sulfate over 2m to prevent (or treat) torsades
(2) correct hypomagnesemia, hypokalemia, & hypocalcemia
-note: if pt found to have torsades, baseline QT prolongation is not always apparent

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Non-Torsades Polymorphic VT

-usually due to ischemia and accompanied by chest pain and ischemic EKG findings
-as opposed to torsades, amio and beta blockers (ex: esmolol) are indicated

 

PE

Steps for eval:
1. To test or not to test? Use PERC criteria (only low risk pts). If score zero, don’t test.
2. If testing: is pt is low-risk or not? Use Wells criteria. If low-risk, send D dimer. If not, CTA.
3. If by clinical gestalt determine high suspicion, forget criteria and CTA.

-a-massive PE (large central clot burden causing RV failure) is equivalent to submassive PE (RV dysfunction) in pt with poor cardiopulmonary reserve

-primary indication for surgical/catheter embolectomy is failure of hemodynamic improvement after fibrinolysis, however can consider it early in pts for whom you are considering giving fibrinolytic

-Geneva criteria for PE risk assessment – does not have vague criteria of “PE most likely diagnosis”

-Note: TWI in inferior and anteroseptal leads are highly suspect for PE

Stats
-MOPPET trial: low dose tPA reduces pulmonary HTN in pts with moderate PE (in terms of size and location) immediately after and the effect is present months afterwards but does not affect mortality or recurrent PE as
early heparin in PE pts reduces in-hospital and 30 day mortality (2010 Chest)

-a normal A-a gradient does NOT rule out PE
-hypoxemic has NPV of 70% (30% of pts with PE will NOT be hypoxemic)
-chart in the ICU book for PPV and NPVs of findings
-ICU book: p130 chart central line insertion depth
-new pleural effusion after central line placement – suspect SVC perforation! Must tap and sent analysis
-the MAP is more accurate estimate of aortic pressure (SBP increases closer to periphery)
-septic shock = defect in mitochondrial use of O2 -> elevated lactate (>2 is abnl). Also the respiratory burst adds to O2 demand.
-P/F ratio (PaO2:FiO2) = estimate of shunting. <200 = >20% shunting of deoxygenated blood through lungs
-PaO2 measures gas exchange in the lungs (NOT arterial O2 content bc doesn’t account for Hb). Pulse ox measures arterial O2 content.
-pulse ox not as accurate for black or brown nail polish – put oximeter on sides of finger
-*supplemental O2 can be safely withheld if SpO2 92% or greater on room air**
—which kind of pts are exceptions??? (given O2 dissociation curve)
-clinical studies: SpO2 accurately shows hypoventilation (low PaO2) if pt is on room air, but NOT if on supplemental O2
-pulse ox and ETCO2 can replace ABGs
-in cardiac arrest, the lack of color change from purple to yellow on a capnometer can occur even if ETT is in the trachea – representing low CO
-continuous ETCO2 almost identical to PaCO2 unless in cases of impaired gas exchange such as increased dead space (hypoventilation, obstructive lung disease) or low CO (PE, lung overinflation)
–changing the vent settings will change how well ETCO2 and PaCO2 correlate, so should repeat ABG to determine the difference each time the vent settings are changed
–can also use continuous ETCO2 to determine change in CO as a result of giving a fluid challenge or aggressively diuresing
-low flow O2 systems provide a variable FiO2 (depends on multiple factors, incl pt’s inspiratory flow rate), whereas high flow provide constant

Pulmonary HTN

Vicious Cycle
-hemodynamics worsen with excess preload –> increased RV volume leads to RV bowing into LV and prevention of LV from adequately filling –> decreased CO and coronary perfusion –> RV ischemia further limits LV filling and output  pulm HTN cycle.png
-red flags: hypoxemia, hypotension, hypercarbia, acidosis (signs of and triggers for further decompensation)

Management
-FIRST make sure pt has functioning epoprostanol iv infusion if came in with PICC line (half life minutes)
if in shock, may try 250mL boluses but what pt truly needs is inotropes: Norepi or dobutamine
—do NOT give push-dose phenylephrine – the afterload will kill pt
—terbutaline improves inotropy but can worsen ischemia
-allow for permissive hypercapnea with acidosis 7.15 – 7.2 tolerable

Ancillary management
-treat afib via aggressive rhythm control (cardioversion and amio) rather than rate control as these patients’ CO is heavily dependent on atrial kick
-if intubation necessary, consider propofol for bronchodilatory effect

Pediatric Shock

Definitions
-SIRS = tachycardia or bradycardia for age, tachypnea for age (acidosis), fever or hypothermia, elevated wbc or 10% bands
-sepsis = SIRS + source of infection
-severe sepsis = sepsis + end organ dysfunction
-septic shock = sepsis + hypotension (rare in peds) or poor perfusion

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Pediatric septic shock
-unlike adults, present as cold shock*:
—cool, mottled, cyanotic extremities
—narrow pulse pressure (high SVR)
—thready pulses
—delayed cap refill (check central skin in neonates)
—oliguria (place Foley, note I&Os)
—CNS dysfunction: irritable, lethargic, jittery, poor feeding

*exception: septic peds chemo pts tend to present in warm/vasodilatory shock (warm extremities, low SVR, bounding pulses, widened pulse pressure)
—bc tend to get Gram negative sepsis (endotoxin)
**note that the problem in peds septic shock (cold) is O2 delivery, whereas in adult septic shock (warm) is O2 extraction. It’s difficult to determine in neonates as their circulatory physiology is complex.

Screen Shot 2017-07-31 at 9.35.54 PM(lactate less useful in peds pts)

Management: early, aggressive intervention
60 mL/kg bolus, given rapid push
broad spectrum abx
early intubation: 30-40% of pediatric CO goes to WOB!

Fluid-refractory septic shock
-if malperfusion is NOT responsive to 60 mL/kg bolus, begin peripheral pressors immediately (within the golden hour, ideally within 15m of arrival)
-young kids cannot increase their cardiac contractility; their cardiac output is entirely dependent on increases in HR
—the younger the pt, the higher the baseline HR, the less likely pt is able to maintain adequate perfusion by increasing HR    =>    the younger the pt, the faster they crash

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*just go with Norepi as first-line and Epi as second pressor

-http://pedemmorsels.com/capillary-refill-shock/
-Hector’s peds sepsis PPT

 

ACLS

-q 2m pulse and rhythm check

Maintain perfusion:
-continuous chest compressions
-epi q 4m

Correct electrical problems:
-defibrillate, use max J (200), if shockable rhythm at each rhythm check
-give amio 300 mg if VT/VF

Correct other reversible causes (Hs and Ts):
-Hypoxia – improvement with airway control
-Hypovolemia – exam, history
-Hyper/Hypokalemia – blood gas, dialysis access, on diuretics
-Hypothermia – rectal T
-H+ (acidosis) – blood gas
-Hypoglycemia – BGM

-TPTX – lung sliding
-Tamponade – echo
-Thrombosis (coronary, PE) – risk factors/PMH, echo
-Torsades
-Tox – med list, h/o substance abuse or depression
-Trauma – eFAST

Status Asthmaticus

Medical management:
-O2, fluids*
-bronchodilators, magnesium
-heliox if NOT hypoxemic (using heliox means proportionally less FiO2)
-epi IM 0.01 mg/kg OR dirty epi drip
-BiPAP: 10 IPAP / 3-5 PEEP (EPAP) (aka “ZEEP”. When pts begin tiring out, inspiratory pressure support helps move air in and out)

*Note:
-hypoxemia is a LATE finding in asthma – give O2 EARLY to promote pulmonary vasodilation
-“normal” pCO2 on blood gas = pt tiring out (compensating pts will have low pCO2 as they hyperventilate to blow off lactic acid)
-these pts are severely volume-depleted due to insensible losses – need fluids! (30cc/kg)
-lung ultrasound has primarily A lines (no interstitial fluid)
-these pts can tolerate hypercapnea and acidosis

Absolute indications for intubation:
-deteriorating consciousness
-respiratory muscle fatigue nonresponsive to BiPAP
-cardiac/respiratory arrest

Avoid intubation as it does nothing to fix the underlying problem of bronchoconstriction and increases risk of hyperinflation.

Intubation:
-use DSI with ketamine 1-2 mg/kg*. Choose roc for longer paralysis to prevent vent asynchrony
-hyperinflation (due to breath-stacking) is your enemy — increased airway pressures = risk for tension PTX, decreased venous return and thus cardiac output
-strategy = permissive hypercapnea – to allow for full exhalation:
—-RR 6-8 breaths/min, TV 6cc/kg, <5 PEEP, inspir flow rate 100-120 L/min

Subdissociative dose ketamine 0.5-1 mg/kg

The Deteriorating/Coding Intubated Asthmatic:
-disconnect from vent, allow exhalation (may push on chest), and slowly bag at 6 breaths/min
-if no improvement and see breath-stacking on vent, needle decompression / finger thoracostomy
-DOPES: Displaced tube (use VL or bronchoscope to confirm), Obstruction (pass suction catheter, look for kinking of tubing), T-PTX, Equipment problem, Stacked breaths
-VV ECMO