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Flashcards in Resus 2 Deck (68):

historical features on headache history that suggest SAH

maximal at onset - peaking in seconds to minutes
onset with exertion/sex


headaches which can result with history of trauma

subdural, epidural, traumatic SAH, intraparenchymal hemorrhage, skull fracture and closed head injuries such as concussion and diffuse axonal injury


etiology of headache when pt headache rapidly improve when removed from environment

carbon monoxide


headaches which can occur in pregnant women (or postpartum)

pre-eclampsia, idiopathic intracranial hypertension and reversible cerebrovascular syndrome
venous sinus thrombosis, pituitary apoplexy, cervical artery dissection and stroke


critical and emergent headache diagnoses

CNS: SAH, carotid dissection, venous sinus thrombosis
tox: CO poisoning
rheum: temporal arteritis
ID: bacterial meningitis, encephalitis

CNS: shunt failure, traction headaches, tour or mass, subdural hematoma, reversible cerebral vasoconstriciotn syndrome
tox/enviro: mountain sickness
eye: glaucoma
ID: brain abscess
pulm: anemia, anoxic h/a
CV: hypertensive crisis
unspecified: preeclampsia, IIH


nonemergent headache diagnoses

vascular headahce
trigeminal neuralgia
post-traumatic (concussion)
post LP headache

TMJ dz.

tension headache
cervical strain

cluster or histamine headaches
febrile headaches


effort-dependent or coital headachaes


possible diagnoses to consider with sudden onset of pain in headache, with any decreased mentation, any positive focal finding, meningismus or intractable pain

SAH, cervical artery dissection, CVT


possible diagnoses to consider with sudden onset of pain in headache, with recurrent thunder clap episodes, may be associated with stroke-like symptoms

reversible cerebral vasoconstriction syndrome


possible diagnoses with sudden onset of headache with pre syncope or syncope

SAH, cervical artery dissection, CVT


possible diagnoses of headache with periorbital or rtetroorbital pain, sudden onset with tearing

temporal arteritis, acute angle closure glaucoma


risk factors consistent with headache caused by ____

breathing in enclosed space with engine exhaust or ventilation of heating equipment
multiple household members with same syptoms
wintertime and working around machinery or equipment ie. furnaces

carbon monoxide poisoning


risk factors consistent with headache caused by ____

hx of sinus/ear infection or recent surgical procedure
acute febrile illness
extremes of age
impacted living conditions (eg. military or college dorms)
lack of primary immunization

meningitis, encephalitis, abscess


risk factors consistent with headache caused by ____
age > 50
females more than males (4:1)
hx of other collagen vascular diseases
previous chronic meningitis
previous chronic illness - tb, parasitic or fungal infection

temporal arteritis


risk factors consistent with headache caused by ___
history of previous glaucoma
age > 30
history of pain increasing in a dark environment

acute angle closure glaucoma


risk factors consistent with headache caused by ___

pregnancy, postpartum, hormone replacement therapy or oral contraceptive use
prothromotic conditions

cerebral venous sinus thrombosis


risk factors consistent with headache caused by ____

episodic sudden severe pain with or without focal neuro deficits or seizure
recurrent episodes over a period of several weeks
exposure to adrenergic or serotonergic drugs
postpartum state

reversible cerebral vasoconstriction syndrome


risk factors consistent with headache caused by ____

sudden and severe pain
post exertion or sex
hx of SAH or cerebral aneurysm
hx of polycystic kidney disease
famhx of SAH
hypertension -severe
previous vascular lesions in other areas of body
young and middle aged



risk factors consistent with headache caused by ____

hx of EtOH defence with or withou trauma
use of anticoagulants

subdural hematoma


risk factors consistent with headache caused by ____

traumatic injury
lucid interval followed by acute altered mentation or somnolence
anisocoria on exam

epidural hematoma


headache red flags indicating higher risk for serious cause of headache

sudden onset
altered mental status
unexplained fever
focal neuro deficit on exam
symptoms refractory to torment or worsening despite
onset of headache during exertion
hx of immunosuppression
pregnancy or peripartum state


patients with abdominal pain who are are higher risk for serious underlying disorders

age over 60
previous abdominal surgery
hx of IBD
recent instrumentation (eg. colonoscopy w. biopsy)
known abdominal/pelvic/retroperitoneal malignancy
active chemotherapy
immunocompromised, including low dose prednisone
fever, chills, systemic symptoms
women of childbearing age
recent immigrants
language or cognitive barrier


what is mortality for all cuase shock

> 20%


categories of schok

hypovolemic shock
distributive shock
cardiogenic shock
obstructive shock
dissociative shock


types of hypovolemic shock

hemorrhagic: trauma, GI bleed, body cavity
hypovolemia: GI losses, dehydration from insensible losses, third-space sequestration from inflammation


types of distributive shock

septic shokc
anaphylactic shock
central neurogenic shock
drug overdose


types of cardiogenic shock

arrhythmia: fib, VT, sVT
overdose of negative inotropic drug - BB, CCB
structural - ventriculoseptal rupture, papillary muscle rutpure


types of obstructive shock

tension pneumothorax
valvular dysfunction: critical AS, acute thrombosis of prosthetic valve
congenital heart defects


types of dissociative shock



lab changes that typically occur with traumatic hemorrhage

lactate > 4
PaCO2 < 35
mild hyperglycemia
mild hypokalemia (3.5-3.7)


empirical criteria for diagnosis of circulatory shock

ill appearance or altered mental status
HR > 100
RR > 20 or PaCO2 < 32
base deficit < -4mEq or lactate >4
urine output < 0.5ml/hr
arterial hypotension > 30 min duration, continous


approach to undifferentiated shock

1. hx of trauma? - search for hemorrhage, tension pneumothorax, cardiac tamponade or cardiac injury
2. evidence of GI bleed, vomitng, diarrhea --> volume resuscitation
3. fever or hypothermia ? - treat sepsis, search for source, consider thyroid function tests
4. ECG evidence of ischemia or CP with risk factors -- treat for cariogenic shock from MI, consider massive PE with RV strain
5. unexplained bradycardia or hypotension? - evaluate for ingestion of negative inotropic drug
6. unexplained hypoxemia ? -rule out PE
7. abdo or low back pain - volume resuscitation, emergency CT abdominal or surg consult to evaluation for peritoneal inflammation or vascular rupture
8. wheezing with hives or skin flushing - tx for anaphylaxis


what effect does prehospital hypotension have on in hospital mortality rate (shock patients)

fourfold higher in hospital mortality rate


variables indicating tissue hypoperfusion

low cardiac output
dusky or mottled skin
delayed cap refill
altered mental state
low urine output
low CVO2
elevated lactate


management of hemorrhagic shock

ensure adequate ventilaiton/ oxygenation
control of hemorrhage (ie. traction for long bones, direct pressure) and obtain urgent consult prn
IV crystalloid bolus 10-20cc/kg
with evidence of poor organ perfusion and 30 min anticipated delay to hemorrhage control, being PRBC infusion 5-10ml/kg
with suspected massive hemorrhage, immediate PRBC transfusion may be preferable
treat coincident dysrhythmias (eg. fib with sync cardioversion)


management of cardiogenic shock

ameliorate increased WOB, provide O2 and PEEP for pulmonary edema
begin vasopressor or inotropic support (NE, E, and dobutamine)
reverse insult (i.e. thrombolysis)
consider intraaortic balloon pump for refractory shock


management of septic shock

ensure adequate oxygenation, remove WOB
administered 20cc/kg crystalloid and titrate infusion based on dynamics indices, volume responsiveness and/or urine output
beging abx, attempt surg drainage or debridement
begin PRBCs if Hb < 70
if volume restoration fails to improve perfusion, starts vasopressors, NE at 0.5ug/min


what marker can be used instead of central venous oxygen saturation

lactate clearance

if lactate has not dropped by 10-20% 2 hours after resist began, additional steps taken to improve systemic perfusion


what to do if patients require more than 2 units of PRBCs

start giving 1:1:1 of PRBC, FFP, platelets - better hemostasis and lower death rate due to exsanguination at 24 hours


what is starting dose of norepinephrine in septic shock

0.05ug/kg/min and titrated at 3-5 min intervals until MAP > 65 or SBP > 90


what is the max dose of norepinephrine - beyond which no further effect seen



what is next step if max dose of norepinephrine does not control bp

add vasopressin at a rate of 0.03-0.04 units/min and don't titrate it


what percent of cardiac arrest patients have VF as initial presenting rhythm



what percent of cardiac arrest patients receive bystander CPR



what percent of cardiac arrests get bystander AED

8% in public settings, 1% home arrest


what is survival rate of OOHCA EMS-treated

11% , ranges from 3-17% based on region


what percentage of patients with ROSC survive to hospital DC and have good nerve function

survival 19-59% based on centre

78% of those has good neuro outcome


if patient is comatose post cardiac arrest, and meets inclusion for TTM what is the survival rate with good neuro outcome



with primary respiratory failure cause of cardiac arrest what are vitals typically like

tachycardia and hypertensive, followed by hypotension and bradycardia progressing to PEA, VF or asystole


what do primarily circulatory obstruction (eg. tension pneumothorax, pericardial tamponade) and hypovolemia vitals on presentation typically like

initial tachycardia and hypotension, progressing through bradycardia to PEA, but may also deteriorate to VF or asystole


what do primary cardiac causes of arrest typically present like

VF or pVT


causes of non traumatic cardiac arrest

cardiac: CAD, cardiomyopathies, structural abnormalities, valvular dysfunction
-hypoventilation: CNS, neuromuscular, tox/metabolic encephalopathies
-upper airway obstruction: CNS dysfunction, fb, infection, trauma, neoplasma
-pulmonary dysfunction: asthma, COPD, pulmonary edema, PE, pneumonia
-mechanical obstruction: tension pneumothorax, tamponade, PE
-hypovolemai: hemorrhage
-distributive: sepsis, neurogenic
metabolic: hypo/hyperkalemia, hypo/hypermagnesemia, hypocalcemia
-rx: antidysrhythmics, digoxin, CCB, BB, TCAs
-rec drugs: cocaine, heroin
-tox: CO, cyanide
environmental: lightning, electrocution, hypothermia or hyperthermia, drowning or near-drowning


which H & T to consider in drowning patient



important history to obtain from cardiac arrest patient

witnessed vs. not ?
time of arrest
what pt was doing (eating, exercising, trauma, etc).
possibility of drug ingestion
time of initial CPR
initial ECG rhythm
interventions by EMS

PMHX: baseline health, previous heart, lung, or renal disease, malignancy, hemorrhage and infection
risk factors for CAD and PE

medications & allergies


overall goals of physical examination in cardiac arrest patient

ensuring adequacy of airway maintenance and ventilation
confirm diagnosis of cardiac arrest
find evidence of cause
monitor for complications of therapeutic intervention


approach to physical exam in cardiac arrest patient (detailed list)

general: pallor (hemorrhage), cold (hypothermia)
airway: secretions, vomit or blood (aspiration, airway obstruction), resistance to PPV ( tension pneumothorax, airway obstruction, bronchospasm)
neck: JVD (tension pneumo, tamponade, PE), tracheal deviation (tension pneumo)
chest: median sternotomy scar (underlying cardiac dz)
lungs: unilateral breath sounds (tension pneumothorax, R mainstream intubation, aspiration), distant or no breath sound or no chest expansion (esophageal intubation, airway obstruction, severe bronchospasm), wheezing (aspiration, bronchospasm, pulmonary edema), rales (aspiration, pulmonary deem, pneumonia)
heart: diminished heart sounds: hypovolemia, tamponade, tension pneumothorax, PE
abdomen: distended and dull (ruptured AAA or ectopic), distended, tympanic (esophageal intubation), gastric insufflation
rectal: blood, melena (GIB)
extremities: asymmetric pulses (dissection), AV shunt or fistula (hyperkalemia)
skin: track marks or abscesses (IVDU), burns (smoke inhalation, electrocution)


define cardiopulmonary arrest

unconsciousness, apnea and pulselessness


indications of inadequate blood flow during CPR

carotid or femoral pulse -not palpable
CPP < 15mmHg
arterial relaxation (diastolic) pressure <20-25mmHg
PETCO2 <10mmHg
SCVO2- <40%


what is SCVO2 representative of

during cardiac arrest SVO2 (O2 sat remaining in PA after systemic extraction) correlates well with SCVO2 - because O2 consumption and SaO2 remains constant any change in SCVO2 represents change in cardiac output


what is normal range os SCVO2

during cardiac arrest- 25-35% (greater oxygen extraction of tissues)


difference between EMD and pseudo-EMD

electromechanical dissociation: primary disorder of electromechanical coupling in myocardial cells, usually brady/wide QRS, associated with global myocardial energy depletion, and acidosis resulting from ishcemia or hypoxia
pseudo-EMD: myocardial contractions occurring but inadequate, usually transient before true EMD and has same causes, in addition can be causes by papillary muscle rupture and myocardial wall rupture; primary SVT can cause; extra cardiac causes: hypovoelmua, tension pneumothorax, pericardial tamponade, and massive PE


what therapies are useful for pseudo-EMD

volume loading or continuous vasopressor infusion,


what to do if see asystole on monitor

confirm with second lead


when is ECMO most successful for use in cardiac arrest

timely access and initiation of ECPR within 60 mins of arrest


complications of ECMO

coagulopathy, hemorrhage, limb ischemia, vascular injury, renal replacement therapy, and stroke


relative contraindications to TTM

another obvious reason for coma (drug overdose, status epilepticus), known end stage terminal illness, preexstiing DNR


complications to TTM



when to consider PCI post arrest

any pt with STEMI on ECG should have immediate PCI post ROSC
when high clinical suspicion of ACS without STEMI, rapidly post ROSC because improved survival to hospital DC


relative contradincaitions to fibrinolytics post arrest if at centre without PCI

evidence of significant CPR trauma such as pneumothorax, flail chest or pulmonary contusion with hemorrhage