equal! But ADH and amio are both only 1 time, epi can be 1 mg q3-5 min (every other shock)
when consider antiarrythmics, and how (vfib/pulseless vtac)
amio if shock-refractory, 300 mg IV, inc survival to hosp admission but NOT d/c. SE: hypotension and brady
treatment for asthma
1. duo nebs x3 2. steroids - IV solumedrol or oral prednisolone 3. mag if severe 4. epi (0.3 - 0.5 mg SQ q20 min x3 or terbutaline 0.25 mg SQ q20 min if severe 5. supplemental O2 as needed 6. d/c home on steroid burst (pred 40 - 60 x 4-5 days)
treatment for COPD
similar to asthma - duonebs, steroids, d/c on steroid burst. Also consider BiPaP (but be careful b/c resp drive driven by hypoxia - need to titrate O2 carefully), short course of ABs like azithro if smoker, febrile, purulent sputum, WBC, worsening dyspnea
causes of CHF exacerbation
1. medication noncompliance 2. salt noncompliance 3. MI/ cardiac damage 4. dilated cardiomyop 2/2 cocaine or alcohol 5. arrythmia (often afib --> dec output) 6. thyrotoxicosis
physical exam findings in CHF
vol overload, HTN/tachy also possible
1. dec preload (rapid nitro SL or gtt) 2. O2 as need 3. BiPap to force fluid out of lungs 4. ASA 5. Morphine 6. Lasix (AFTER nitro. Start low - 10-20 if na´ve, or 2x dose if already on) 7. if bp low, consider dobutamine/dopamine 8. address underlying cause!
classic PNA pathogens
1. strep pneumo (rust colored sputum) 2. klebsiella - alcoholics and immunocomp 3. legionella (infiltrate and diarrhea- check urinary Ag) 4. mycoplasma 5. staph 6. TB - RUL infiltrate 7. h.flu 8. Gm-s/oral - aspiration 9. PCP --> HIV/AIDS,check LDH and PaO2 (if LDH up and PaO2 <70, steroids!!)
1. ABs within 4 hrs of arrival (CAP - ceftriaxone + azithro, levoflox). HAP - pseud +/- staph a. (vanc + cefepime) 2. blood cxs 3. if sepsis - goal directed therapy (maximize O2, aggressive fluids, monitor CVP, consider tx if Hct<30) 4. home if PORT score is low - age, sex, PMH, labs vitals
etiologies of 2ndary PTX
1. barotraumax (as from vent) 2. bleb rupture in emphysema / asthma 3. acute/chronic infec (TB)x - other causes: iatrogenic (central line, thoracentesis), catamenial (endometriosis of pleura), trauma
1. small - O2 helps resorb air, repeat CXR 4-6 hrs. Inc partial P O2 to drive air back in (inc nitrogen gradient) 2. mod - pigtail or small caliber CT 3. large/tension - large CT 4. consider pleurodesis if recurrent (scar together both pleura to eliminate pleural space)
pathologic q wave
>1 mm wide or > 1/3 QRS deep
when should you measure ST elevations?
1 small block (40 ms) after J-point
what additional concerns should you have with inf MI?
papillary m. rupture (2/2 dec supply via RCA), RHF (hypotension and JVD with clear lungs - beware of nitrates!)
Mobitz Type II indicates what kind of ischemia? What's the tx?
at or below bundle of his; can temporarily pace - transcutaneous or transvenous - if unstable)
1. rate control 2. cardiovert if unstable 3. consider anticoag if going on for unknown amt of time, inc CHADS2, worried abt clots
difference in treating Aflutter vs Afib
still rate control, but no need for anticoags (not worried about throwing embolus). Also give adenosine to slow down rhythm
cause and tx of aflutter w/ SLOW ventric rate
often from dig or other AV nodal blocker, pace if brady and unstable
define and treat stable vtac
rapid rate, wide QRS, regular. Stable if lethargy but stable VS, pulse. Tx with anti-arrythmics: amiodorone, lidocaine. Procainamide and sotalol first line for stable monomorphic Vtac with normal EF.
Torsades de point
polymorphic VT 2/2 electrolyte derangement or drug tox. Often responds to mag. Cardiovert. Can also do: overdrive pacing, lidocaine, phenytoin, isoproternol.
what does Afib/RVR w/ WPW look like? How tx?
irreg irreg, variable QRS morphology. If in sinus, would have delta waves. NO AV nodal blockers
what causes electrical alterans in pericardial effusion?
heart swinging in pericardial sac
EKG findings of hypothermia
J waves - broad positive deflection after QRS, delayed repolarization. Can mimic MI! tx = rewarm
criteria for ventric hypertrophy unreliable in bbb - T/F?
excess water compared to Na, sxs = lethargy, HA, seizures (at <120 mEq/L)
ddx hypovolemic hyponatremia
vol down (V, diarrhea, diuretics, adrenal insufficiency, sweat, burns)
ddx hypervolemic hyponatremia
body doesn't see vol but it's 3rd spaced - CHF, renal failure, nephrotic syndrome, cirrhosis
ddx euvolemic hyponatremia
SIADH, primary polydipsia, hypothyroidism
how know if hyponatremia is 2/2 kidney failure or not?
Una >20 means kidneys bad. <10 = good job.
management of dif volume-types of hyponatremia
0.5 - 1 mEq/L/hr to prev central pontine myelinolysis. If severe (Na<120 with CNS abnormalities), rate of 1 is fine w/ 3% hypertonic saline. - hypovolemic: normal saline at 100-150 cc/hr. - euvolemic: SIADH - water restrict + Lasix if Na<120 - hypervolemic: Lasix if vol up, with salt and water restrict. Fast correct of hypervol = IV NS and loop diuretics)
measuring Na+ deficit in hyponatremia
(0.6xTBW)x(140-actual serum sodium)
hypernatremia usually due to
poor access to water (elderly, infants, neurologically impaired thirst)
hypo vs hypervolemic hypernatremia
excessive volume depletion vs excess salt/poor kidneys
salt restrict + restore plasma vol (usually) w/ NS or D5 - 0.5 mEq/hr to avoid cerebral edema.
calculating free water deficit
(0.6xTBW)x(serum sodium/140 -1)
why repair wounds?
hemostasis, dec infection risk, cosmetic benefits
3 mechanisms of wound injury
shear (deep to n, vessels), tension/traction/tearing (assymetric borders), crush (devitalized tissue, underlying injury)
comfort, light, assess fxn distal to inj (n. vessel, tendon fxn), liberal use of x-rays to help assess for FB, fx
face/neck injury: look for - swelling (hematoma/edema for airway compression), bleed (nasopharyngeal - aspiration risk), crepitus (direct laryngeal/tracheal injury). High C-spine fx can impair resp drive. Burns - thermal injury (and inhalation --> hypoxia)
pulmonary life threats
tension pneumo, open pneumo, flail chest, massive hemothorax
what do you use for a needle decompression?
14-16g angiocath in 2nd intercostal space - insert to hub AND OPEN TO ROOM AIR - whoosh! Converts tension --> simple pneumo (one with an exit). Pleural pressure to atm pressure, still not neg until chest tube placed. Decompression NOT indicated for simple PTX!
tension vs simple pneumo - difs in presentation, tx
simple may have normal breath sounds, shock - tachy but no hypotension, no temporizing measures needed (as with needle decompression), and tx with O2, pleural drain, chest tube
what is unique about tension pneumo vs hemothorax in presentation?
hypoxia with resp distress! Massive hemothorax may cause shock but not hypoxia. PTX won't cause hypoxia till both lungs compromised (contralateral lung damaged in TPTX)
wound diam what size to cause hypoxia?
60% diameter of trachea. Tx = 3 sided flap!
flail chest cause and tx
ineffective vent + undelrying pulmonary contusion --> hypoxia. Supportive tx till surgical fixation of chest wall (if >1 L initial output, or 150-200 cc/hr output for 2-4 hrs)
circulatory life threats
hemorrhagic shock, tension pneumo, card tamponade
vital signs correlate well with hemorrhagic shock - t/f
True! Especially early
trneds in hemorrhagic shock
as blood loss goes up: inc tachycardia, dec BP, Inc resp, dec UOP to negligible, worsening mental status (lethargy eventually)
what is permissive hypotension?
adequate, though not nl BP - vol resus inc hydrostatic pressure, which may dislodge clots and cause further bleed, so find pt at which perfusion is optimized and minimize further bleed risk
what color are large-bore Ivs?
orange, grey, or green
what kind of fluid to vol resusc with?
isotonic crystalloid - same osmolality as blood NS or LR. Give 2L and reassess after every 500 cc for real-time improvement
what are the 3 dif kinds of blood you can order and what do they mean?
1. "trauma blood" - O+ for women >50 and men, O- for younger women 2. "type and screen" - just screens for ABO and Rh 3. "type and cross" - gets actual units of blood - specify #! Takes at least an hr, not used for life threatening hemorrhage
should you give epi in hypovolemic shock if not responding?
NO! body is already maxed out, and you may cause arrythmia/ischemia/arrest! Just give vol / eval for non-hemorrhagic causes of trauma (TPTX, tamponade)
what does FAST tell us? What doesn't it?
hemoperitoneum/hemopericardium/hemothorax? Not source, quantity, or ongoing nature of bleeding
indications for intubation (2 broad categories and then w/I it)
probs with vent: COPD, asthma, CHF; probs with oxygenation: CHF, PNA, hemm shock
purpose of rapid sequence intubation
provide rapid orotracheal intubation for patients with full stomachs to minimize risk of aspiration. C/I: difficulty to bag or severe laryngeal edema
patient has no gag reflex (otherwise can use nasal airway)
BVM challenging if:
BMI >30, beard (KY gel), Mallampati 3 or 4, poor jaw protrusion, snoring, face disfigured (edentulous, facial fx)
describe Mallampati score
Class I: Soft palate, uvula, fauces, pillars visible. Class II: Soft palate, uvula, fauces visible. Class III: Soft palate, base of uvula visible. Class IV: Only hard palate visible
difficult airway if:
Mallampati 3/4, thyromental distance <3 finger breads (<6 cm) in adult - i.e short neck
rapid orotracheal intubation for pts w/ full stomach, to minimize aspiration (paralyze and go)
RSI contraindicated in
difficult to bag or severe laryngeal edema
SOAP: suction, O2, airway equipment (laryngoscope - Mac or Miller,ETT - adult fem 7.5-8 cuffed, male 8 - 8.5 cuffed, child - (16+age)/4 or diameter of child's 5th finger - use Breslow tape and consider uncuffed in <8 yrs old); pharmaceuticals (induction agent, paralytic)
i. Preoxygenate (100% FiO2 via nonrebreather. Avoid BVM --> gas to stom). ii. pre-induction meds (atropine 0.02 mg/kg to dec brady a/w laryngoscopy, use in kids <10 yo. Also lido 1.5 mg/kg to suppress cough/laryngospasm/blunt ICP response). iii. Sedate - (Etomidate - rapid on/off and cardio neutral, but careful if septic shock or adrenocort insuffic. Also Ketamine - bronchodilat, good for asthmatics, careful b/c inc BP, HR, ICP and can p/w emergence syndrome - dissociate anesthetic. Also fentanyl, midazolam, thiopental). iv. Paralyze (nonparalyzing - vecuronium - 2-4 min on with 20-50 min duration, Pancuronium w/ 3-6 min on and 80-120 min long, too long. Depol - succs - most often used - rapid on and off, pseudocholinesterase metabolism, prolonged axn w/ deficient enz like coke users. bad b/c inc intraoc pressure, inc K+ 2/2 m. breakdown, malig hyperthermia). v. Intubate - (good view, cricoid pressure - sellick maneuver to prev aspiration and align, direct laryngoscopy, confirm via listen - L side first, look for chest rise + EtCo2 detector for color change, image - CXR to confirm 2 cm above carina) vi. Backup (glideoscope for trauma, bougie, combitube - blind insertion into esoph, LMA, cric - vertical!)
things in primary survey for RSI
ABCD, consider naloxone if resp dep and pinpoint pupils, thiamine if alcoholic
A(nasal trumpet), B (100% NRB), C (monitor), D. Ativan 2-4 mg x2, fospheny - 20 mg/kg takes 15-45 min, phenobarb 20 mg/kg (causes hypoTN nand apnea! prep to intub and call neuro/anaesthesia), GETA (midazolam, prop --> reqs ICU, intub, cont EEG monitoring. Lose neuro exam)
when to treat in sz
if hypoglycemic, or >5 min or mult sz or not tol (refractory hypoxia)
when to intubate in sz
hypoxia is what kills! clinical decision
how to intubate in status
barbituates (thiopental) - good ICP, anticonvulsant. Need to paralyze but short acting so don't mask sz (sux = 5 min, rocuronium if sux c/i, lasts 15 min)
workup after sz
CBC, CMP, coags, EtoH, UA, tox. Consider lactate, ABG, NH3, drug/tox levels. Lactate/prolactin can help distinguish from pseudo sz. Stat head CT for bleed (white --> gray, mass effect). CT if new focal deficits, first sz, persistent AMS, recent trauma, coagulopathy, HIV/immunosuppresion, meningismus, alcoholism, new sz pattern
paired vertebral a., basilar a., cereballar probs, CN palsies, BL limb wkness, common - crossed neuro deficits (ipsilateral CN, contralateral motor), PCA - contralateral homonymous hemianopsia, ocular probs. Basilar - brainstem deficits (coma, hemi/quadriplegia, constricted but reactive pupils, CN VI palsy, vert nystagmus, locked in), Wallenberg's (PICA) - impaired pain/temp in ipsilateral face and contralat limbs, ataxia, Horner's
ischemic stroke by anatomy: hemispheric stroke sxs
MCA - L: aphasia, R hemiparesis/sensory loss/poor conj gaze/dysarthria/difficulty reading/writing/calculating. R - poor L conj gaze, extinction of L sided stim, L vis neglect, L hemiparesis, L vis fielddeficit, dysarthria, spatial disorientation
tx of stroke
tPA w/i 3 hrs of last seen well. NIH stroke scale to quantify. C/I: prev stroke/head injury 185/110 (either number) prior to tx, anticoag use, active bleed
types of primary headaches
benign and recurrent w/ no underlying cause: migraine (unilat and pulsing), tension (diffuse pressure/tightness), cluster
inc risk SAH in first degree fam members, Grave's, PCOS, ADPKD, Marfan's, other aneurysm. Also consider CO expo if other fam members experiencing
Workup for HA
vitals, PE, CBC, chem. Possible CT/LP for SAH (CT 90% sens w/i 12 hrs, <80% sens after 24 hrs). Xanthochromia hg breakdown doesn't begin until 2-4 hrs after RBCs in CSF. Up to 5 RBC considered normal
1. reverse anticoag until aneuysm can be repaired via surgery or coiling. 2. Monitor ICP/CPP, don't use vasodilators b/c they inc cerebral blood vol and ICP 3. Nimodipine to "prevent vasospasm" - increases survival 4. consider sz prophylaxis (spasm causes inc ICP)
HTN, brady, irregular breathing (or wide pulse P) - suggests ICP, TX UNDERLYING CAUSE! brady w/o hypoTN does NOT have to be treated emergently
how to treat elevated ICP
1. raise head of bed 2. keep brain calm (dec pain, sz, fever) avoid ICP elevation (vomit, cough, posturing) 3. stop bleeding if present (PLTs, FFP, prothrombin + recomb VII for immed effect) 4. control BP (SBP cerebral vasoconstric, but causes cerebral ischemia and only good for impending herniation. Monitor EtCO2 to max dec of 30!) temp only - lasts 2-4 hrs 7. prep for neurosurg! dry CT. sub/epi dural --> burr hole. SAH --> clip aneurysm. intraparenchymal - monitor and supportive. Need to image to know which one!
Asystole - shock or no?
NO! still stun myocardium and cause parasymp outflow to dec likelihood of spon return
Ddx for asystole
true asystole, leads on wrong/patients clothes, confirm in mult leads!
reversible causes of asystole
airway/resp problems! DOPE: displacement of ETT, obstruction of ETT, PTX, equip failure. asystole also end result of all cardiac arrest rhythms, including VT/VF/PEA
management of asystole
1. start CPR 2. epi 1 mg q3-5 min 3. atropine up to 0.04 mg/kg max (no more than 3 mg total). admin 1 mg q3-5 min till reach max (theoretic benefit in dec parasymp to heart but no direct evi) 4. transcut pacing - must be done early to be successful! good if witnessed bradyasystolic arrest, post-defib asystole, drug ODs. Cont CPR till get pulse and keep giving drugs independent of pacing. periodically tun off pacer to re-evaluate rhythm)
when to stop in ACLS for asystole?
adequate CPR was provided, VF/VT was successfully treated, ETT properly placed and good O2/vent, IV access established, rhythm-approp drugs given, >10 min elapsed
definition of PEA
electrical activity w/o mechanical contraction or critically impaired cardiac filling.
1. dec preload (poor fill) - hypovolemia, tension PTX, tamponate, trauma, PE) 2. dec contractility (poor pump) - hypoglycemia, acidosis, hypoxia (contraction lost before conduction), OD, massive MI
treatment of PEA
1. ABCD 2. consider underlying cause 3. epi 1 mg q3-5 min, atropine 1 mg IV q3-5 min for max of 3 mg or 0.4 mg/kg, ONLY IF PEA RATE IS SLOW!!!
randomly fluctuating electrical activity with no identifiable QRS complexes, always pulseless!!
fast rate (>100,usu >150) w/ wide bizare QRS, can be stable, unstable, or pulseless
Tx of vfib and unstable vtac
defibrillate. 200J biphasic, 360J monophasic, lower dose if peds. One shock only, then 2ndary survey: airway, breathing, circ (get IVs,DDx - history, labs). Resume CPR
drugs for Vfib/pulseless Vtac
vasoconstrictors (enhance cardiac perfusion via peripheral constriction, via epi or vasopressin). Epi raises bp, improves blood flow, but can cause cardiac ischemia and tachyarrythmia. Can give x3 dose via ETT. ADH, on othe rhand, doesn't have same SE but can only be given 40 U IV once instead of 1st epi dose. ONLY FOR VF/VT, NOT PEA OR ASYSTOLE)
tx of vfib/vtac after shock and epi
if still VF/VT after 5 cycles CPR, shock, and epi, consider antiarrhythmics like amiodarone (helps survival to hospital admission, but no benefit in survival to discharge. 300 mg IV q2 min CPR in "shock-refractory vf/vt). Then, keep giving epi 1 mg q3-5 min (every other shock). ADH and amio are 1-time only.
what to do once regain rhythm from vtac/vfib?
CHECK PULSE! if not, cont CPR. if yes, secure airway, vent, check pressure, consider antiarrythmics, check 12 lead EKG, ABG labs, info
indications for rescue breathing
children, unwitness/prolonged arrest, non-cardiac arrest (drowning, asphyxia, apnea from drug OD, pulm disease)
advantage of intubation over BVM for hospital CPR
no air in stomach, but BVM ok for short term
best SBP that can be achieved with best CPR
defib is more important than A, B, and C - T/F?
True! precordial thump, however, unlikely to terminate Vfib/Vtac
abnl ABG only in 25% (inc A-a) and hypoxemia refractory to supp O2, sometimes Hampton's hump or "watermark sign" - decreased vascularity CXR, Q1S3T3 on EKG, trops mildly elevated with BNP 2/2 RH strain
immobility, PE more likely than alt dx, DVTs, prior hx PE/DVT, hemoptysis, tachycardia, malignancy - add up and tells you pretest prob
if meet all 8 criteria, 94% on RA, no exog estrogen, no hx DVT/PE, no recent surgery, no hemoptysis, no clinical sxs DVT)
steps to working up PE
1.) high pre-test prob: admit and anticoagulate regardless 2. pre-test prob low - safely exclude with d-dimer, get CT if pos 3. spiral CT/VQ - 53-100% sens, 80-95% spec, better if central/segmental rather than peripheral. VQ good if dye allergy but hard to interp, esp in context of underlying lung D+
Tx algorithm low risk PE
pos d-dimer --> pos CTA --> main/lobular pulm a = treat, if segmental/subsegmental, repeat a scan. Either repeat CTA, or US or MRI venography, pulm scintigraphy, serial U/S, digital subtraction angiography
Tx algorithm medium risk PE
pos d-dimer --> pos CTA --> tx. If these were neg, no tx.
Tx algorithm high risk PE
straight to CTA - if pos, treat, if neg, repeat the tests you used on low-prob to r/o, this time to rule in
indications for tpa
hemodynamically unstable, saddle embolus, +troponin, EKG abnormalities (i.e sig strain on heart). OR PEA arrest and high PE suspicion
causes of acute MI
ACS, hypertrophic cardiomyopathy, aortic stenosis, arrythmia with demand ischemia
atypical presentations of MI
weakness, dyspnea, AMS, abd pain (angina equivalents)
if sxs c/w AMI, 1 mm ST elev in 2 contig leads, >1 in V1 or V2, New LBB. Emergent CABG another definitive option
is CE rise criterion for lytics in acute MI?
CE ELEVATION IS NOT A CRITERION! doesn't rise till 4-6 hrs after start
Beck's triad is what, and seen in what?
low art bp, distended neck veins, distant heart sounds - signs of pericardial tamponade!
management of AAA dissection
immediately to ICU. Morphine. Reduce SBP to 100-120 or lowest tolerated. Use IV BB to reduce HR to 100 post BB (don't wnat to induce reflex inotropy by just vasodilating, need to control HR first). Type B (descending) - medical tx. Type A(scending) - surg! leads to Ao regurg, tamponade, MI. Treat all with life-long oral BB to reduce SBP and rate of SBP rise.
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