Resus 2 Flashcards
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
critical: CNS: SAH, carotid dissection, venous sinus thrombosis tox: CO poisoning rheum: temporal arteritis ID: bacterial meningitis, encephalitis
emergent: 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
migraine vascular headahce trigeminal neuralgia post-traumatic (concussion) post LP headache
sinusitis
dental
TMJ dz.
tension headache
cervical strain
cluster or histamine headaches
febrile headaches
stn
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
immunocompromised
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 ___
female
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
SAH
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 WHOML altered mental status meningismus 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
MI
cardiomyopathy
arrhythmia: fib, VT, sVT
overdose of negative inotropic drug - BB, CCB
structural - ventriculoseptal rupture, papillary muscle rutpure
types of obstructive shock
PE tamponade tension pneumothorax valvular dysfunction: critical AS, acute thrombosis of prosthetic valve congenital heart defects HOCM
types of dissociative shock
CO
methemoglobinemia
HS
CN
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
- hx of trauma? - search for hemorrhage, tension pneumothorax, cardiac tamponade or cardiac injury
- evidence of GI bleed, vomitng, diarrhea –> volume resuscitation
- fever or hypothermia ? - treat sepsis, search for source, consider thyroid function tests
- ECG evidence of ischemia or CP with risk factors – treat for cariogenic shock from MI, consider massive PE with RV strain
- unexplained bradycardia or hypotension? - evaluate for ingestion of negative inotropic drug
- unexplained hypoxemia ? -rule out PE
- abdo or low back pain - volume resuscitation, emergency CT abdominal or surg consult to evaluation for peritoneal inflammation or vascular rupture
- 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
hypotension tachycardia 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
30ug/min
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
20%
what percent of cardiac arrest patients receive bystander CPR
45%
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
50%
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
respiratory:
-hypoventilation: CNS, neuromuscular, tox/metabolic encephalopathies
-upper airway obstruction: CNS dysfunction, fb, infection, trauma, neoplasma
-pulmonary dysfunction: asthma, COPD, pulmonary edema, PE, pneumonia
circulatory:
-mechanical obstruction: tension pneumothorax, tamponade, PE
-hypovolemai: hemorrhage
-distributive: sepsis, neurogenic
metabolic: hypo/hyperkalemia, hypo/hypermagnesemia, hypocalcemia
toxic:
-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
HYPOTHERMIA
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
60-80%
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
coagulopathy
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
