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Rosen's Cardinal Presentations > Resus 2 > Flashcards

Resus 2 Flashcards

1
Q

historical features on headache history that suggest SAH

A

maximal at onset - peaking in seconds to minutes

onset with exertion/sex

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2
Q

headaches which can result with history of trauma

A

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

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3
Q

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

A

carbon monoxide

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4
Q

headaches which can occur in pregnant women (or postpartum)

A

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

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5
Q

critical and emergent headache diagnoses

A 
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
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6
Q

nonemergent headache diagnoses

A 
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

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7
Q

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

A

SAH, cervical artery dissection, CVT

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8
Q

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

A

reversible cerebral vasoconstriction syndrome

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9
Q

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

A

SAH, cervical artery dissection, CVT

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10
Q

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

A

temporal arteritis, acute angle closure glaucoma

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11
Q

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

A

carbon monoxide poisoning

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12
Q

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

A

meningitis, encephalitis, abscess

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13
Q

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

A

temporal arteritis

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14
Q

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

A

acute angle closure glaucoma

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15
Q

risk factors consistent with headache caused by ___

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

A

cerebral venous sinus thrombosis

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16
Q

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

A

reversible cerebral vasoconstriction syndrome

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17
Q

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
A

SAH

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18
Q

risk factors consistent with headache caused by ____

hx of EtOH defence with or withou trauma
use of anticoagulants

A

subdural hematoma

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19
Q

risk factors consistent with headache caused by ____

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

A

epidural hematoma

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20
Q

headache red flags indicating higher risk for serious cause of headache

A 
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
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21
Q

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

A

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

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22
Q

what is mortality for all cuase shock

A

> 20%

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23
Q

categories of schok

A 
hypovolemic shock
distributive shock
cardiogenic shock
obstructive shock
dissociative shock
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24
Q

types of hypovolemic shock

A

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

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25
Q

types of distributive shock

A

septic shokc
anaphylactic shock
central neurogenic shock
drug overdose

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26
Q

types of cardiogenic shock

A

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

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27
Q

types of obstructive shock

A 
PE
tamponade
tension pneumothorax
valvular dysfunction: critical AS, acute thrombosis of prosthetic valve
congenital heart defects
HOCM
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28
Q

types of dissociative shock

A

CO
methemoglobinemia
HS
CN

29
Q

lab changes that typically occur with traumatic hemorrhage

A

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

30
Q

empirical criteria for diagnosis of circulatory shock

A 
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
31
Q

approach to undifferentiated shock

A
  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
32
Q

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

A

fourfold higher in hospital mortality rate

33
Q

variables indicating tissue hypoperfusion

A 
hypotension
tachycardia
low cardiac output
dusky or mottled skin
delayed cap refill
altered mental state
low urine output
low CVO2
elevated lactate
34
Q

management of hemorrhagic shock

A

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)

35
Q

management of cardiogenic shock

A 
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
36
Q

management of septic shock

A

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

37
Q

what marker can be used instead of central venous oxygen saturation

A

lactate clearance

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

38
Q

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

A

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

39
Q

what is starting dose of norepinephrine in septic shock

A

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

40
Q

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

A

30ug/min

41
Q

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

A

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

42
Q

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

A

20%

43
Q

what percent of cardiac arrest patients receive bystander CPR

A

45%

44
Q

what percent of cardiac arrests get bystander AED

A

8% in public settings, 1% home arrest

45
Q

what is survival rate of OOHCA EMS-treated

A

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

46
Q

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

A

survival 19-59% based on centre

78% of those has good neuro outcome

47
Q

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

A

50%

48
Q

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

A

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

49
Q

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

A

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

50
Q

what do primary cardiac causes of arrest typically present like

A

VF or pVT

51
Q

causes of non traumatic cardiac arrest

A

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

52
Q

which H & T to consider in drowning patient

A

HYPOTHERMIA

53
Q

important history to obtain from cardiac arrest patient

A 
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

54
Q

overall goals of physical examination in cardiac arrest patient

A

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

55
Q

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

A

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)

56
Q

define cardiopulmonary arrest

A

unconsciousness, apnea and pulselessness

57
Q

indications of inadequate blood flow during CPR

A 
carotid or femoral pulse -not palpable
CPP < 15mmHg
arterial relaxation (diastolic) pressure <20-25mmHg
PETCO2 <10mmHg
SCVO2- <40%
58
Q

what is SCVO2 representative of

A

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

59
Q

what is normal range os SCVO2

A

60-80%

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

60
Q

difference between EMD and pseudo-EMD

A

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

61
Q

what therapies are useful for pseudo-EMD

A

volume loading or continuous vasopressor infusion,

62
Q

what to do if see asystole on monitor

A

confirm with second lead

63
Q

when is ECMO most successful for use in cardiac arrest

A

timely access and initiation of ECPR within 60 mins of arrest

64
Q

complications of ECMO

A

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

65
Q

relative contraindications to TTM

A

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

66
Q

complications to TTM

A

coagulopathy

67
Q

when to consider PCI post arrest

A

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

68
Q

relative contradincaitions to fibrinolytics post arrest if at centre without PCI

A

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

Rosen's Cardinal Presentations (2 decks)

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