6113 final all Flashcards
significant levels of troponin
I - 0.35T - 0.2
cardiac tamponade
muffled heart sounds↑ CVPparadoxical pulse (gt 10mm)- abnormally large decrease in SBP during inspiration
CURB-65
PNEUMONIA! ConfusionBUN gt 7Respiratory rate g/e 30BP - SBP gt/eq 90 or DBP lt/eq 60)65Scoring:0-1: outpatient treatment2: hospital admission3-5: ICU consideration
SIRS Criteria
2+ of…HR gt 90RR lt 20 - 32 gtT lt 36 - 38 gt- 96.8 - 100.4FWBC lt 4k - 12k gt- immature neuts gt 10
sepsis
SIRS likely s/t infection; positive cultures add to validity but not requiredPROBABLE OR CONFIRMED INFECTION!!!clinical s/s: tachycardic, tachypnic, hypotensive, hypoxic, confused/lethargic/agitated, hyperthermic → Hypothermic
severe sepsis
sepsis + at least 1 sign of hypoperfusion or organ dysfunction (new, not explained by other etiology)
septic shock
severe sepsis associated with - refractory hypotension (BP lt 90/60) despite adequate fluid resus - and/or serum lactate gt 4.0occurs with evidence of perfusion abnormalities: lactic acidosis, oliguria, AMS- not perfusing brain, kidneys, lungs can’t compensate, other organ dysfunctions
shock: management & hemodynamics goals
supportive therapy while finding/managing/tx shock source- MAP gt 60- CVP 8-12- CI gt 2.1- UOP gt 0.5 mg/kg/hr- SaO2 gt 92%- SVO2 gt 70remember: septic has its own criteria
ARDS: definition
acute lung injury manifested by non-cardiogenic pulmonary edemaresult of inflammatory lung injury
2 things present in all shock
- inadequate tissue perfusion- cellular hypoxia (leads to dysfunction
s/s hypovolemic shock apparent when
gt 15% volume lost
vasopressors + hypovolemic shock
CAUTION. fill before you squeeze!
main causes of obstructive shock x3
THINK FILLING & EMPTYINGdecreased ventricular fill:- cardiac tamponade- tension pneumothoraxdecreased ventricular emptying- main PA or saddle PE
volume/vasopressor + obstructive shock
gentle - it’s temporizing
shock + vasopressin
adjunct if not getting a good response from patient
1 cause of cardiogenic shock
MI
neurogenic shock classic triad
bradycardiamassive vasodilationhypothermiad/t parasympathetic overstimulation
neurogenic shock: avoid what drug and why?
phenylephrine - unopposed A1 activity could potentially worsen the shockbradycardia d/t reflex vagus nerve - it’s a CNS effect esp at high doses
anaphylactic shock meds list
EPINEPHRINE !!! - CV collapse without- vasopressor & mast cell stabilizer (prevent histamine release)IM 1:1,000 → Dose 0.1-0.5mg q10-15 minIV 1: 10,000 → Dose 0.1 – 0.25mg q 5-15min H1 blocker: Benadryl (only block receptor)H2 blocker: Famotidine (Pepcid)Respiratory: AlbuterolCorticosteroid: methylprednisolone
epinephrine + anaphylactic shock
- CV collapse without- vasopressor & mast cell stabilizer (prevent histamine release)IM 1:1,000 → Dose 0.1-0.5mg q10-15 minIV 1: 10,000 → Dose 0.1 – 0.25mg q 5-15min
late phase anaphylactic reactions
- 6-12 hrs after initial rxn- typically follow favorable response to treatment- treated the same wayimplications: - airway mgmt: keep pts intubated 14-16 hours- line maintenance: leave big IVs in- ICU care: code cart & epi nearby
anaphylactic shock + airway management important implication
keep intubated 14-16 hours after event - concern for late anaphylactic reaction
sepsis: hemodynamic goals
within 6 hours of presentation/symptomsCVP g/e 8-12mmHg MAP g/e 65mmHgUOP g/e 0.5ml/kg/hrSVO2 g/e 70%Lactate lt 2mmol
surviving sepsis: goal directed treatment within 3 hours
Within 3 hours presentation of SIRS + strong indication organ failing- Measure lactate level- Obtain cultures before abx:– 2 blood cultures– +/- Urine culture- broad spectrum antibiotics - 30ml/kg crystalloid “fluid challenge” for: –hypotension OR– lactate g/e 4mmol/L
surviving sepsis: goal directed treatment within 6 hours
Within 6 hours presentation of SIRS + strong indication organ failing- vasopressors (for hypotension that doesn’t respond to initial fluid resuscitation) – GOAL: MAP g/e 65mmHg– NE first, then dopamine, then vasopressin - if persistent hypotension after initial fluid administration (MAP lt 65mmHg) ORinitial lactate was g/e 4mmol/L, re-assess volume status + tissue perfusion-re-measure lactate if initial elevated
septic shock treatment considerations
- Fluids (crystalloids; albumin if needed)- Vasopressors (NE, epi, vasopressin) -Inotropes if cardiac dysfxn (Dobutamine, esp. w/ HF)- Corticosteroids (only if unable to meet hemodynamic goal)- Blood product administration (Goal Hgb 7-9g/dL)- Sedation if intubated (Propofol, not benzos: ICU delirium risk)- BG monitoring q2h/insulin use (goal BG 110-180 mg/dL)- Renal replacement therapy in ARF- Early but slow enteral feeding (GI perf/peritonitis – be cautious) - DVT/GI prophylaxis (Lovenox, heparin, PPI/H2 antagonist)
septic shock
- Fluids (crystalloids; albumin if needed)
septic shock - Vasopressors
NE, epi, vasopressin
septic shock inotropes
- if cardiac dysfxn (Dobutamine, esp. w/ HF)
septic shock - corticosteroids
only if unable to meet hemodynamic goal
septic shock - goal hgb
Goal Hgb 7-9g/dLwith blood product admin
septic shock - Sedation if intubated
Propofol, not benzos: ICU delirium risk
septic shock - BG monitoring
q2h/insulin use (goal BG 110-180 mg/dL)
septic shock + ARF?
renal replacement therapy
septic shock - early but slow enteral feeding
GI perf/peritonitis – be cautious
septic shock - DVT/GI prophylaxis
Lovenox, heparin, PPI/H2
documentation/evaluation of volume resuscitation in septic shock x2
EITHER repeat focused exam (after initial fluid resuscitation) – VS, CV, cap refill, pulse, skin findingsOR 2+ → CVPScvO2 Bedside CV USdynamic assessment of fluid responsiveness with passive leg raise or fluid challenge
how do we know a shock patient is better?
- stable VS with ↓ pharm/non-pharm support: HR 60-90, MAP gt 65, CVP 8-12- adequate UOP: 0.5 - 1.0 ml/kg/hr- evidence of adequate O2 delivery/utilization: SVO2 65 - 75- lactate levels normalized- improvements in PE
SIRS: hypotension refractory to fluid replacement consideration
(a) hang 1000mL NS/LR, 200mL stays in vascular bed– LR requires functional liver to create buffer(b) hang 1000mL D5W bag, 800mL stays in vascular bed guidelines: LR or NS
ARDS: first major change
Inability to oxygenateFurther destruction of alveoli- shunting (blood passing by non-vent alveoli & bypassing ventilated)refractory to O2 increase: junk in alveoli = UP THE PEEP
ARDS: second major change
Narrowing of small airways Damage to lung microvasculature- V/Q imbalance d/t alveolar dead space (alveoli full of junk) = no gas exchange
ARDS: third major change
Elevated pulmonary artery pressure (vasoconstriction d/t hypoxia)Increased PVRNot an increase in wedge!
ARDS: first phasedefinition + s/s
exudative - first 72 hours- angry neuts increase lung injury & cap permeability– increased alveolar edema– macrophages + mediators = pulmonary bed vasoconstriction = V/Q mismatch (blood bypass ventilated alveoli) = pulm htnclinical s/s: may only see tachypnea & dyspnea• Coarse crackles• Cyanosis• Tachycardia• Lungs less compliant• Dec ventilation of alveoli• Hypercapnia
ARDS: second phasedefinition + s/s
proliferative - 4 to 21 days- resolution of pulmonary edema- type II pneumocytes hyperplasia- proliferation fibroblasts- hemorrhagic exudate → granulation tissue (hyaline membrane)s/s: PROGRESSIVE HYPOXEMIA
ARDS: third phasedefinition + s/s
remodeling & fibrosis - 14 to 21 days- alveoli + bronchioles obliterated- decreased FRC- more V/Q mismatch/shuntingclinical s/sinitial: restlessness, respiratory alkalosis s/t hyperventilation (↑ pH, ↓ paCO2, HCO2 normal) + non-specific complaintsrapid progression to: respiratory distress, non-compliant lungs (more P to get same TV), crackles everywhere, elevated pulmonary airway pressure (PIIP), REFRACTORY HYPOXEMIAP/F lt 200
P/F definition for ARDS
lt 200
normal PF
gt 286lt 200 represents significant shunt gt 20% - ARDS
a/A + PaO2/PAO2
a/A - what’s available in blood vs what’s available in alveoliP/P - % O2 diffusing across alveoli into bloodnormal: gt 45% or 0.75
diagnostic criteria for ARDS
• Bilateral pulmonary infiltrates (whiting out on CXR)• PCWP lt 18mmHg (no LVHF - normal 5-12)• Severe hypoxemia• PaO2/FiO2 lt 200
Berlin Criteria Definition of ARDS
mild: P/F 201-300moderate: P/F 101 - 200severe: P/F lt 100
ARDS management goals
maximize pulmonary gas exchangeoptimize O2 delivery to tissuesprevent further organ injury
septic shock: evidence of perfusion abnormalities
occurs with evidence of perfusion abnormalities (lactic acidosis, oliguria, mental status changes, other organ dysfunctions)
EF + sepsis
low d/t myocardial depressant factor
sepsis causes
bacteria 85% of time- gram neg (like e coli) release endotoxins - inflammatory cascade- gram pos
surviving sepsis: fluid resuscitation
crystalloids - begin in ED- 1st 30 min bolus 500-1000cc (cryst)- 30 ml/kg/hr for hypotension or lactate gt 4GOAL: CVP g/e 8 or CVP on vent g/e 12 goals not met? consider PBRC (goal hct g/e 30%)
surviving sepsis: blood products considerations
consider PRBC if hgb lt 7- goal hct g/e 30%platelets - plt lt 5000- plt 5-30k + high risk for bleeding
surviving sepsis: mechanical ventilation considertions
- target TV 6ml/kg (low)- PEEP (beware tension pneumo)- permissive hypercapnia- sedation: intermittent bolus OR continuous with daily interruption/lighting to produce awakening
MODS
begins with SIRS = subtle changes = dysfunction/ progressive failure 2+ organ systems d/t circulating mediators + clinical conditions
SIRS to MODS transition
a) Failure to control source of inflammation/infectionb) Persistent perfusion deficitc) Flow-dependent O2 consumption (abnormal DO2 & VO2)d) Necrotic tissue
SIRS/MODS patho summary
a) Maldistribution of vol → vasodilated + third spacing b) Imbalance O2 supply/ demand (abnormal DO2 and VO2)c) Hypermetabolicif A + C can’t be fixed MODS OCCURSthe problem: inflammatory/immune response is over-activated, the body can’t clear the mediators and toxic metabolites fast enough and a self-perpetuating cycle exists
when does MODS occur?
after SIRS when vasodilation, third spacing, and hypermetabolic state can’t be fixed
MODS: hyperdynamic CV response
INITIAL RESPONSE↑ CO, HR, DO2, VO2↓ PAWP, CVP, SVR
MODS: hypodynamic CV response
many mediators = myocardial depressants; their continued influence = ↓ myocardial contractility/function ↓ CO, DO2, VO2↑ CVPTachycardia, dysrhythmias, weak pulses
why does MODS hypodynamic CV response happen?
many mediators = myocardial depressants; their continued influence = ↓ myocardial contractility/function
cranial nerve III vs IV, VI
CN III is PERRLACN III, IV, VI is EOM intact - each is responsible for 2 movements
stage 1 hypertension + drugs
140-159/90-99Thiazide OR consider ACEi, ARB, CCB, BB (no comorbs)
stage 2 hypertension + drugs
≥ 160/100 2 drugs - Thiazide + ACEi, ARB, CCB, BB (no comorbs)
Target Organ Damage (MI, HF, CVA, DM, CKD) + htn drugs
- combo diuretic, ACEi, ARB, CCB, BB, Aldactone- lifestyle modification & pharm- if BP > 20/10 above goal → thiazide + other.
use diaphragm
Diaphragm: medium-high sounds,S1, S2
use bell
Bell: low pitched sounds mitral stenosis, diastolic murmurs, S3, S4
S3
indicates difficulty w/ passive filling LA to LV (mitral valve is open & blood is flowing in) VENTRICULAR gallop – “Kentucky”PASSIVE FILLING into noncompliant LVearly diastolic, bell, mitral area Left lateral position may increase the soundAssociate with HF (chronic or AMI)
S4
“atrial kick” - difficulty with active filling, LA actively contracting (typically, compensate↑ CO by ~25% but if bad contraction—heart will lose atrial kick = s4) - ventricle can no longer take any more ATRIAL gallop – “Tennessee”Blood entering noncompliant ventricle during ATRIAL CONTRACTIONlate diastolic, bell, mitral areaLeft lateral position may increase the soundAssociated with CHF, MI, AoS, HTN, and CAD A-fib will NOT have an S4 (no atrial kick)
you will not hear this heart sound with afib
S4 because a fib has no atrial kick
summation gallop
S3 and S4 Implies significant HF
S1
Best heard with the diaphragm Loudest at the apex Mitral and tricuspid valves close
S2
Best heard with the diaphragm Loudest at the base Aortic and pulmonic valves close
heart failure - decrease in CO leads to?
RAAS activation:sodium retention secondary to ALDOSTERONEfluid retention ADHvasoconstriction increases afterload - ANGIOTENSIN II
neurohormonal model
accounts for the effects of- prolonged sympathetic stimulation (first)- prolonged angiotensin release (kidneys need more volume)- prolonged aldosterone releaseserves as the basis for the treatment of heart failure
systolic heart failure: loop diuretics
do not impact neurohormonal model!
heart failure: beta blockers positive benefits
reduce sympathetic nervous system response by decreasing circulating catecholaminesreduce overstimulation of renin angiotensin system
most common reason for diastolic heart failure
chronic hypertension
acetaminophen consideration
Interferes with warfarin to prolong PT/INR Steven Johnson Syndrome
Tetraology of Fallot
Pulmonary stenosis, VSD, and R to L Shunt (cyanotic)
alpha nerve fibers release
NE - eye dilation, clammy, hypo bowelPERIPHERAL vasoconstriction, ↓ UOP, cool skin, gas exchange, bowel sounds
beta nerve fibers release
Epi - ↑ BG, heart & lung vasodilation, blood flow=O2 deliveryNE - ↑ free fatty, tissue perfusion, myocardial O2 needs
prolonged stress response is what?
medulla secreting more catecholamines
BP goal for young, healthy (less than 60)
lt 140/90
BP goal for older adult (60+)
lt 150/90
Max. Target HR
220 – Age
ideal body weight
Women: 100 lb + 5 lb for every inch over 5 feet Men: 106 lb + 6 lb for every inch over 5 feet
caloric need
IBW x 10 = basal caloric needs • Basal caloric needs + [IBW x activity level]= total cals neededActivity level • 3= Sedentary • 5= Moderate • 10= Strenuous
