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tachycardia, DKA, sepsis Flashcards

1
Q

As a general rule, narrow-QRS complex tachycardias arise from ? while wide-QRS complex ones may be ? in origin

A

narrow: above the ventricles (SVT)

wide (0.12+): supraventricular or ventricular

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2
Q

regular rhythms with narrow QRS

A 
Sinus tachycardia
Atrial tachycardia
AV nodal reentrant tachycardia (AVNRT)
AV reentrant tachycardia (AVRT)
Junctional tachycardia
Atrial flutter
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3
Q

regular rhythms with wide QRS

A

V tach
Antidromic AVRT
Narrow complex tachycardia with aberrancy

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4
Q

irregular rhythms with narrow QRS

A

Atrial flutter with variable block
Afib
Multifocal atrial tachycardia

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5
Q

irregular rhythms with wide QRS

A

Polymorphic Vtach

Narrow complex tachycardia with aberrancy

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6
Q

If the tachycardic patient is unstable (as evidenced by ?), ? should be performed immediately

A

hypotension, pulmonary edema, AMS, or ischemic chest pain

synchronized cardioversion

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7
Q

In stable tachycardic patients, what should be done?

A

12-lead ECG should be obtained, and medical therapy can be initiated

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8
Q

important hx to get in tachy pts

A

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

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9
Q

physical exam in tachy pt may reveal underlying cause i.e.

A

pale mucous membranes with anemia; thyromegaly or goiter with thyrotoxicosis, barrel chest or nail clubbing with chronic lung disease

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10
Q

Vtach may be difficult to distinguish from ?

A

SVT with aberrant conduction

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11
Q

Certain factors favor VT, including ?

A

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)

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12
Q

certain factors suggest SVT with aberrancy

A

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

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13
Q

If cannot distinguish between VT and SVT with aberrancy with certainty, how should you treat the pt?

A

as if VT is present

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14
Q

other tests to get in tachycardia

A

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)

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15
Q

Potential interventions for regular narrow-complex tachyarrhythmias

A

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

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16
Q

Stable patients with regular wide-complex tachycardias may benefit from ?
Second-line therapy for stable patients with monomorphic VT is ?

A

amiodarone, procainamide, or sotalol
(don’t need if non- sustained VT)

lidocaine

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17
Q

AV nodal blocking maneuvers

A

Valsalva, diving reflex, and carotid massage

they act through the parasympathetic nervous system

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18
Q

typical labs in moderate DKA

A

glucose: 500-700
Na+: 130 K+: 4-6
HCO3-: 6-10
BUN: 20-30 pH: 7.1 PCO2: 15-20 (compensating)

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19
Q

typical labs in severe DKA

A 
glucose: 900+
Na+: 125   K+: 5-7
HCO3-: less than 5
BUN 30+  pH: 6.9
PCO2: less than 20 (resp. failure)
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20
Q

DKA dx based on triad of

A

hyperglycemia, ketosis, and metabolic acidosis

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21
Q

what other states present with elevated serum ketones?

how to ddx from DKA

A

starvation, pregnancy, alcoholic ketoacidosis, and various toxic ingestions (isopropyl alcohol ingestion)
glucose is normal/low

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22
Q

DKA triggers

most common?

A

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)

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23
Q

massive fluid deficits in DKA, how to tx?

A

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

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24
Q

how to give insulin in DKA

A

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

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25
when to add dextrose in DKA?
when glucose falls to 200-300 mg/dL
26
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
27
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
28
most common causes of severe sepsis
urosepsis and pneumonia
29
Older, younger, or immunocompromised individuals with sepsis may present with subtle signs such as ?
lethargy, decreased appetite, or hypothermia
30
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
31
4 goals of sepsis treatment
fluids discover source then tx with abx pressors: NE, dopamine
32
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
33
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
34
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
35
sepsis suspects if unknown source
``` Escherichia coli Staphylococcus aureus Streptococcus pneumoniae Enterococcus spp Klebsiella spp Pseudomonas aeruginosa ```
36
how to tx sepsis with unknown source
vanc and zosyn OR antipseudomonal cephalosporin (eg, ceftazadine, cefepime) + FQ (levofloxacin, ciprofloxacin) OR aminoglycoside (eg, gentamicin, amikacin)
37
pneumonia suspects
``` Streptococcus pneumoniae Mycoplasma pneumoniae Haemophilus influenza, Chlamydophila pneumoniae Legionella ```
38
how to tx pneumonia
Antipseudomonal cephalosporin (eg, ceftazadine, cefepime) + macrolide (eg, azithromycin) Or FQ (eg, levofloxacin, moxifloxacin)
39
UTI suspects
Escherichia coli Klebsiella spp Enterococcus spp
40
how to tx UTI
FQ (eg, levofloxacin) Or third-generation cephalosporin (eg, ceftriaxone)
41
meningitis suspects
Streptococcus pneumoniae Neisseria meningitides Listeria monocytogenes (primarily in adults over 50-60 or immunocompromised patients)
42
meningitis tx
Vanc + | ceftriaxone + Ampicillin if listeria is suspected
43
how to tx abdominal infections
Ampicillin + aminoglycoside (eg, gentamicin, amikacin) + metronidazole
44
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
45
what correlates strongly with prognosis in sepsis?
higher presenting lactate levels and slow decline of lactate during resuscitation are associated with significantly higher mortality
46
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)
47
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
48
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)
49
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
50
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
51
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
52
how to monitor severely septic/septic shock pt
in ICU; measure BP, CVP, O2 sat, central venous sat, UOP, lactate
53
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
54
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
55
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
56
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
57
IVIG in sepsis?
improved mortality in neonates/children, recently inconclusive mechanism: augmented clearance of pathogenic organisms and feedback inhibition of inflammatory cytokines
58
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
59
statins in sepsis?
being on a statin lowers human patients' likelihood of death from sepsis
60
sepsis complications
``` ALI/ARDS DIC cardiac failure hepatic failure renal failure multi organ dysfunction syndrome ```
61
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
62
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)
63
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
64
hepatic failure in sepsis manifests as
cholestatic jaundice, with increases in bilirubin, aminotransferases, and alkaline phosphatase, synthetic function usually not affected
65
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
66
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)

EM case files (7 decks)

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