tachycardia, DKA, sepsis Flashcards
As a general rule, narrow-QRS complex tachycardias arise from ? while wide-QRS complex ones may be ? in origin
narrow: above the ventricles (SVT)
wide (0.12+): supraventricular or ventricular
regular rhythms with narrow QRS
Sinus tachycardia Atrial tachycardia AV nodal reentrant tachycardia (AVNRT) AV reentrant tachycardia (AVRT) Junctional tachycardia Atrial flutter
regular rhythms with wide QRS
V tach
Antidromic AVRT
Narrow complex tachycardia with aberrancy
irregular rhythms with narrow QRS
Atrial flutter with variable block
Afib
Multifocal atrial tachycardia
irregular rhythms with wide QRS
Polymorphic Vtach
Narrow complex tachycardia with aberrancy
If the tachycardic patient is unstable (as evidenced by ?), ? should be performed immediately
hypotension, pulmonary edema, AMS, or ischemic chest pain
synchronized cardioversion
In stable tachycardic patients, what should be done?
12-lead ECG should be obtained, and medical therapy can be initiated
important hx to get in tachy pts
time/circumstances surrounding symptom onset, duration of symptoms
PMHx: history of CAD, CHF, dysrhythmia, valvular disease, thyroid disease
current meds (including herbal or homeopathic regimens, OTC meds, and illicit drugs)
Fam hx: sudden cardiac death, dysrhythmia, other types of heart disease
physical exam in tachy pt may reveal underlying cause i.e.
pale mucous membranes with anemia; thyromegaly or goiter with thyrotoxicosis, barrel chest or nail clubbing with chronic lung disease
Vtach may be difficult to distinguish from ?
SVT with aberrant conduction
Certain factors favor VT, including ?
age 50+, history of CAD or CHF, history of VT, AV dissociation, fusion beats, QRS 0.14+ second, extreme left axis deviation, and precordial concordance (QRS complexes either all positive or all negative)
certain factors suggest SVT with aberrancy
age less than 35, history of SVT, preceding ectopic P waves with QRS complexes, QRS less than 0.14 second, normal or almost normal axis, and slowing or cessation of the arrhythmia with vagal maneuvers
If cannot distinguish between VT and SVT with aberrancy with certainty, how should you treat the pt?
as if VT is present
other tests to get in tachycardia
CXR: chamber enlargement, cardiomegaly, pulmonary congestion or edema
BMP: r/o electrolyte abnormalities that predispose to tachyarrhythmias (eg, hypokalemia, hypocalcemia, hypomagnesemia)
possibly:
thyroid function studies (for hyperthyroidism) drug levels (eg, digoxin) or UDS (for cocaine, methamphetamines, other stimulants)
Potential interventions for regular narrow-complex tachyarrhythmias
vagal maneuvers (such as carotid massage and Valsalva)- will not terminate tachyarrhythmias that do not involve the AV node, but may slow the rate enough to unmask the underlying rhythm abnormality adenosine, B-blockers, and CCBs
Stable patients with regular wide-complex tachycardias may benefit from ?
Second-line therapy for stable patients with monomorphic VT is ?
amiodarone, procainamide, or sotalol
(don’t need if non- sustained VT)
lidocaine
AV nodal blocking maneuvers
Valsalva, diving reflex, and carotid massage
they act through the parasympathetic nervous system
typical labs in moderate DKA
glucose: 500-700
Na+: 130 K+: 4-6
HCO3-: 6-10
BUN: 20-30 pH: 7.1 PCO2: 15-20 (compensating)
typical labs in severe DKA
glucose: 900+ Na+: 125 K+: 5-7 HCO3-: less than 5 BUN 30+ pH: 6.9 PCO2: less than 20 (resp. failure)
DKA dx based on triad of
hyperglycemia, ketosis, and metabolic acidosis
what other states present with elevated serum ketones?
how to ddx from DKA
starvation, pregnancy, alcoholic ketoacidosis, and various toxic ingestions (isopropyl alcohol ingestion)
glucose is normal/low
DKA triggers
most common?
infection is most common! (UTI)
pancreatitis, MI, stroke, and many drugs including corticosteroids, thiazides, sympathomimetics including cocaine, and some antipsychotic drugs
voluntary cessation of insulin (in kids/y. adults)
massive fluid deficits in DKA, how to tx?
often up to 5-10L
adults: 2L bolus of NS
kids: 20 mL/kg of NS
- reverse shock with NS, and then continue an infusion of 1/2 NS at 2-3x maintenance
how to give insulin in DKA
regular insulin by continuous IV infusion (0.1 U/kg/hr - about 5-10 U/h in adult)
(IV boluses work ok in adults, not for kids)
-will lower glucose faster than clearing ketones BUT continue insulin until anion gap has narrowed
when to add dextrose in DKA?
when glucose falls to 200-300 mg/dL
HCO3- in DKA?
complications?
when is it important to give
studies have failed to show improvements with treatment
complications: hypernatremia, hypokalemia, paradoxical CSF acidoses, systemic alkalosis
* lifesaving in hyperkalemia
leading cause of morbidity and mortality in pediatric DKA
cerebral edema
- due to development of cryptogenic osmoles in the CNS to counter dehydration, which then draw water intracellularly during treatment (unproven)
- associated with overhydration and vigorous insulin therapy
- only reliable predictor of cerebral edema is the severity of metabolic derangements at presentation
- still important to reverse shock
most common causes of severe sepsis
urosepsis and pneumonia
Older, younger, or immunocompromised individuals with sepsis may present with subtle signs such as ?
lethargy, decreased appetite, or hypothermia
Early goal-directed therapy for sepsis includes ?
careful monitoring of multiple markers of organ perfusion, with aggressive measures to restore any imbalance between oxygen supply and demand
4 goals of sepsis treatment
fluids
discover source
then tx with abx
pressors: NE, dopamine
SIRS criteria
Temperature 38°C+ or less than 36°C
HR 90+ bpm
Tachypnea or hyperventilation (RR 20+ or Paco2 less than32 mm Hg)
WBC 12,000+ cells/mL or less than 4000 cells/mL, or more than 10% bands
Severe sepsis
sepsis + at least one sign of organ failure or hypoperfusion, such as lactic acidosis (lactate 4+ mmol/L), oliguria (urine output less than 0.5 mL/kg for 1 hour), abrupt change in mental status, mottled skin or delayed capillary refill, thrombocytopenia (platelets less than 100,000 cells/mL) or DIC, or acute lung injury/ARDS
Septic shock
Severe sepsis with hypotension (or requirement of vasoactive agents, eg, dopamine or NE) despite adequate fluid resuscitation in the form of a 20- to 40-cc/kg bolus
sepsis suspects if unknown source
Escherichia coli Staphylococcus aureus Streptococcus pneumoniae Enterococcus spp Klebsiella spp Pseudomonas aeruginosa
how to tx sepsis with unknown source
vanc and zosyn OR
antipseudomonal cephalosporin (eg, ceftazadine, cefepime) + FQ (levofloxacin, ciprofloxacin) OR
aminoglycoside (eg, gentamicin, amikacin)
pneumonia suspects
Streptococcus pneumoniae Mycoplasma pneumoniae Haemophilus influenza, Chlamydophila pneumoniae Legionella
how to tx pneumonia
Antipseudomonal cephalosporin (eg, ceftazadine, cefepime) + macrolide (eg, azithromycin)
Or
FQ (eg, levofloxacin, moxifloxacin)
UTI suspects
Escherichia coli
Klebsiella spp
Enterococcus spp
how to tx UTI
FQ (eg, levofloxacin)
Or
third-generation cephalosporin (eg, ceftriaxone)
meningitis suspects
Streptococcus pneumoniae
Neisseria meningitides
Listeria monocytogenes (primarily in adults over 50-60 or immunocompromised patients)
meningitis tx
Vanc +
ceftriaxone + Ampicillin if listeria is suspected
how to tx abdominal infections
Ampicillin +
aminoglycoside (eg, gentamicin, amikacin) +
metronidazole
devastating effects in sepsis caused by
(1) generalization of the immune response to sites remote from that of the infection (vasodilation and coagulation—>hypotension, hypoperfusion, coagulopathy, and resultant organ failure)
(2) derangement of the balance between proinflammatory and anti-inflammatory cellular regulators
(3) dissemination of the infecting organism
what correlates strongly with prognosis in sepsis?
higher presenting lactate levels and slow decline of lactate during resuscitation are associated with significantly higher mortality
initial sepsis management
supplemental O2 to keep above 93%
Two large-bore IVs
Lactic acid
Initial fluid bolus of 20-40 mL/kg or 2-4 L in adults
CBC
CMP
Blood cultures from two sites (ideally before abx)
Urinalysis with culture
Pregnancy test in women of childbearing age
CXR
Empiric antibiotics (goal is less than 1 h from initial presentation)
reassess septic pt after first fluid bolus
if continues to be hypotensive or has a lactate level greater than 4 mmol/dL or has other signs of continued hypoperfusion, then early goal-directed therapy (EGDT) should be initiated
Goal 1 of EGDT
CVP 8-12 mm Hg or 12+ if mechanically vented
500 cc of normal saline can be bolused every 15 to 30 minutes until the CVP goal is met
(may be 6-10 L over 1st hours)
Goal 2 of EGDT
MAP +65 mm Hg
if remains below despite adequate resuscitation, add NE (levophed) or dopamine, low dose vasopressin as 2nd/3rd line
Goal 3 of EGDT
central venous oxygen saturation (ScvO2) 70%+
if not met, optimize O2 delivery by:
-transfuse PRBCs 30%+
-if HCT up to 30%+, and other 2 goals met and SVC dobutamine
-then: intubate to maximize oxygenation and sedate to reduce O2 demand
Additional goal of EGDT
lactate clearance 10%+
recheck 2 hrs after initiating fluid resuscitation; if 10% not cleared, optimize O2 as in goal 3
lactate can be used in lieu of ScvO2 monitoring
how to monitor severely septic/septic shock pt
in ICU; measure BP, CVP, O2 sat, central venous sat, UOP, lactate
Ultrasound in sepsis
can be used to monitor CVP that does not require placement of a central venous catheter
-compression US of the forearm or measurement of the internal jugular vein to approximate CVP
steroids in sepsis?
- do not improve mortality
- not recommended that they be used in sepsis without shock unless there is a recent history of prolonged steroid use or history suggesting adrenal suppression
- may be considered in septic shock unresponsive to fluid resuscitation and vasopressors
activated protein C in sepsis?
an enzyme produced in the liver that inhibits thrombosis and promotes fibrinolysis. A patient’s native ability to activate protein C appears to be impaired in sepsis
- it should only be given to patients with sepsis-induced organ dysfunction that are deemed to be at a high risk of death
- never in kids of if CIs to anticoags
glucose goal in sepsis
between 140 and 180 mg/dL
used to be 80 to 120 mg/dL but this cause more cases of hypoglycemia
IVIG in sepsis?
improved mortality in neonates/children, recently inconclusive
mechanism: augmented clearance of pathogenic organisms and feedback inhibition of inflammatory cytokines
ECMO in sepsis?
Extracorporeal membrane oxygenation (ECMO), a form of mechanical heart-lung bypass
-inconclusive; may be tried in pt with cardiorespiratory failure that is refractory to traditional means of support
statins in sepsis?
being on a statin lowers human patients’ likelihood of death from sepsis
sepsis complications
ALI/ARDS DIC cardiac failure hepatic failure renal failure multi organ dysfunction syndrome
ALI/ARDS can be seen in sepsis due to
Buildup of inflammatory fluid in the alveoli impairs gas exchange favors lung collapse, and decreases compliance, with the end result of respiratory distress and hypoxemia
- bilateral pulmonary opacities consistent with pulmonary edema, may develop after fluid resuscitation
- may require mechanical ventilation; use low tidal volumes and limit PEEP
DIC in sepsis due to
coagulation cascade activated as well as fibrinolytic system- new clots always being formed, then broken down, clotting factors and plts being consumed, at risk for complications from both thrombosis and hemorrhage
give platelets if count is less than 5000 cells/mm3 without signs of bleeding, or less than 30,000 cells/mm3 with active bleeding (+FFP if bleeding)
cardiac failure in sepsis due to
direct action of inflammatory molecules, monitor preload (hydration and CVP monitoring), after load (pressers), and contractility (dobutamine)
-take caution when giving pressors/inotropes to elderly as may induce tachycardia–>increased workload–>acute coronary syndrom
hepatic failure in sepsis manifests as
cholestatic jaundice, with increases in bilirubin, aminotransferases, and alkaline phosphatase, synthetic function usually not affected
main cause of renal failure in sepsis?
manifests how?
how to tx, and if refractory?
Hypoperfusion
oliguria, azotemia, and inflammatory cells on urinalysis
adequately support perfusion with hydration and vasopressors
if still not perfusing, renal replacement therapy (eg, hemodialysis or continuous veno-venous hemofiltration) is indicated
multiorgan dysfunction syndrome
Dysfunction of two or more organ systems such that intervention is required to maintain homeostasis
primary: i.e. heart/lung failure in pneumonia (direct injury)
secondary: i.e. ALI/ARDS in urosepsis (generalized inflammatory response)
