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"Rico has something in his eye" test hints Flashcards

1
Q

define + explain meumonic “DIMS”

A

mnemonic for differentiating seizures/AMS

Drugs (intoxication or withdrawal)
Infection (CNS or systemic)
Metabolic and Endocrine (hyper/hypoglycemia, thyroid, HPA axis, etceteraaaaa)
Structural (CNS lesion/mass)

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2
Q

“D” in DIMS

A

DRUGS

  1. Overdose of prescription drugs
  2. illicit drug toxicity
  3. withdrawl from drugs or illicit substances
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3
Q

“I” in DIMS

A

INFECTIONS

  1. pneumonia
  2. urinary
  3. skin/soft tissue
  4. abdomen
  5. CNS infection
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4
Q

“M” in DIMS

A

METABOLIC/ENDOCRINE

  1. altered pH
  2. hypo/hyper Na+ Ca++
  3. acute liver or renal failure
  4. diabetic ketoacidosis
  5. Endocrinopathies (hypo-/hyper-cortisol, hypoglycemia thyrotoxicosis)
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5
Q

Shock states diagram thing for different hemodynamic values (CO, SVR, MAP, CVP, PCWP)

CARDIOGENIC

A
  1. MAP: decreased
  2. CO/SV: decreased
  3. CVP: increased (right sided failure)
  4. PCWP: increased (left sided failure backing up into lungs)
  5. SVR: increased (clamping down, peripheral compensation)
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6
Q

Shock states diagram thing for different hemodynamic values (CO, SVR, MAP, CVP, PCWP)

EARLY DISTRIBUTIVE

A
  1. MAP: decreased
  2. CO/SV: increased
  3. CVP: decreased
  4. PCWP: decreased
  5. SVR: decreased
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7
Q

Shock states diagram thing for different hemodynamic values (CO, SVR, MAP, CVP, PCWP)

HYPOVOLEMIC

A
  1. MAP: decreased
  2. CO/SV: increased
  3. CVP: decreased
  4. PCWP: decreased
  5. SVR: increased
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8
Q

Shock states diagram thing for different hemodynamic values (CO, SVR, MAP, CVP, PCWP)

LATE DISTRIBUTIVE

A
  1. MAP: decreased
  2. CO/SV: decreased
  3. CVP: decreased
  4. PCWP: increased
  5. SVR: decreased
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9
Q

Shock states diagram thing for different hemodynamic values (CO, SVR, MAP, CVP, PCWP)

OBSTRUCTIVE (PE)

A
  1. MAP: decreased
  2. CO/SV: decreased
  3. CVP: increased (↑ RV afterload)
  4. PCWP: decreased
  5. SVR: increased (compensatory peripheral clamping down)
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10
Q

Shock states diagram thing for different hemodynamic values (CO, SVR, MAP, CVP, PCWP)

OBSTRUCTIVE (tamponade)

A
  1. MAP: decreased
  2. CO/SV: decreased
  3. CVP: increased
  4. PCWP: increased
  5. SVR: increased
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11
Q

“2 salt and a sticky BUN”

A

This is the formula for obtaining a CALCULATED serum osmolarity

  1. Serum calculated osmolarity = “2 salt and a sticky BUN”
  2. calculated by the following equation: Calculated osmolality = (2 x Na) + Glucose + BUN + (1.25 x ETOH)

the last portion is a correction factor for alcohol

To obtain your Osmolar gap take your serum Osmolality (measured) – serum Osmolarity (calculated). normal range is -10 to +10

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12
Q

muscarinic effects of organophosphate poisoning

A
  1. Muscarinic receptors in heart, eye, lung, GI, skin and sweat glands
  2. Bradycardia
  3. Miosis
  4. Bronchorrhea / Bronchospasm
  5. Hyperperistalsis (SLUDGE)
  6. Sweating
  7. Vasodilation
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13
Q

nicotinic effects of organophosphate poisoning

A
  1. fasciculations, flaccid paralysis

2. Tachycardia, hypertension

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14
Q

discuss + explain the hypothalamic pituitary adrenal (HPA) axis

A

DISCUSS

  1. The HPA axis is our central stress response system
  2. The HPA axis is responsible for the neuroendocrine adaptation component of the stress response

EXPLAIN

  1. hypothalamus releases corticotropin-releasing hormone. CRF binds to CRF receptors on the anterior pituitary gland → adrenocorticotropic hormone (ACTH) release
  2. ACTH binds to receptors on the adrenal cortex → adrenal release of cortisol
  3. At a certain blood concentration of cortisol, the cortisol exerts negative feedback to the hypothalamic release of CRF → stoppage of pituitary release of ACTH (via negative feedback loop)
  4. systemic homeostasis returns
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15
Q

AEIOU Indications for Dialysis in Patients with Acute Kidney Injury

A
  1. A – Acidosis – metabolic acidosis with a pH <7.1
  2. E – Electrolytes – refractory hyperkalemia with a serum potassium >6.5 mEq/L or rapidly rising potassium levels
  3. I – Intoxications – use the mnemonic SLIME to remember the drugs and toxins that can be removed with dialysis: salicylates, lithium, isopropanol, methanol, ethylene glycol
  4. O – Overload – volume overload refractory to diuresis
  5. U – Uremia – elevated BUN with signs or symptoms of uremia, including pericarditis, neuropathy, uremic bleeding, or an otherwise unexplained decline in mental status (uremic encephalopathy)
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16
Q

CCP Interventions to correct abdominal compartment syndrome

A
  1. sedation & analgesia (Improve Abdominal Wall Compliance)
  2. head of bed elevation at 30 degrees (Improve Abdominal Wall Compliance)
  3. neuromuscular blockade (Improve Abdominal Wall Compliance)
  4. gastric decompression with OG tube (Evacuate Intra-Luminal Contents)
  5. avoid excessive fluid (Correct Positive Fluid Balance)
  6. diuretics (Correct Positive Fluid Balance)
  7. maintain a APP > 60mmHg with vasopressors (organ support)
  8. optimise ventilation strategies (organ support)
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17
Q

Intra-abdominal pressure (IAP) definition

A
  1. the steady state pressure concealed within the abdominal cavity
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18
Q

Intra-abdominal Hypertension (IAH) definition

A
  1. sustained intra-abdominal pressure (IAP) of > 12mmHg
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19
Q

Abdominal Compartment Syndrome (ACS) definition

A
  1. sustained IAP > 20mmHg with new organ failure
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20
Q

Intraperitoneal Structures

A

S - stomach
A - appendix
L - liver
T -transverse colon, sigmoid colon, upper third of the rectum
D - duodenum (the first 5cm)
S - small intestine (the jejunum, the ileum, the cecum)
P - pancreas (tail)
R - reproductive organs uterus, fallopian tubes, ovaries, gonadal blood vessels (female)
S - spleen
S

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21
Q

Retroperitoneal Structures

A 
S - suprarenal structure 
A - aorta
D - duodenum 
P - pancreas 
U - ureters 
C - colon (A + D)
K - kidneys 
E - esophagus 
R - rectum
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22
Q

biliary tree anatomical/physiological pathway

A
  1. biliary tree is a series of GI ducts allowing newly formed bile from the liver to be concentrated and stored in the gallbladder prior to release into the duodenum
  2. Bile is secreted from hepatocytes and drains from both lobes of the liver via intralobular ducts and collecting ducts into the left and right hepatic ducts
  3. left and right hepatic ducts join to form the common hepatic duct, which runs alongside the hepatic vein
  4. common hepatic duct descends and is joined by the cystic duct which regulates bile flow in and out of the gallbladder for storage and release
  5. the common hepatic duct and cystic duct combine to form the common bile duct
  6. common bile duct descends and passes posteriorly to the duodenum and head of pancreas
  7. common bile duct now joined by main pancreatic duct, forming the hepatopancreatic ampulla (ampulla of Vater) – which then empties into the duodenum via the major duodenal papilla
  8. major duodenal papilla is regulated by a muscular valve, the sphincter of Oddi
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23
Q

define Budd-Chiari syndrome

A
  1. congestive hepatopathy caused by blockage of hepatic veins
  2. Two of the hepatic veins must be blocked for clinically evident disease
  3. Liver congestion and hypoxic damage of hepatocytes eventually result in predominantly centrilobular fibrosis
  4. The obstruction may be thrombotic or non-thrombotic anywhere along the venous course from the hepatic venules to junction of the inferior vena cava (IVC) to the right atrium
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24
Q

If someone has an elevated INR from cirrhosis and is not on warfarin should they get PCC’s for reversal of coagulopathy?

A
  1. No
  2. Don’t be stupid
  3. It’s not gonna do anything
  4. You’ll just look like an idiot
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25
Q

markers of liver injury vs LFT’s

A

Liver Injury

  1. There are five main markers of liver injury
  2. ALT, AST, gamma-glutamyltransferase (GGT), alkaline phosphatase (ALP) and total bilirubin

Liver Function Tests

  1. Bilirubin
  2. Glucose
  3. Albumin
  4. INR
  5. PT
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26
Q

Octreotide describe/define + dosage

A
  1. a somatostatin analogue in variceal and non-variceal upper GI bleeding (UGIB)
  2. binds with endothelial cell somatostatin receptors, inducing strong, rapid and prolonged vaso-constriction
  3. Decreases Portal/Splanchnic Pressure –> Potential to Decrease Bleeding and Rebleeding
  4. Decrease Acid Secretion –> Prevent Clot Dissolution
  5. 50 mcg IV bolus (range 25-100mcg), followed by 25-50 mcg/hr drip
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27
Q

common modes of RRT

A

Modes of continuous RRT (CRRT)

  1. Slow Continuous Ultrafiltration (SCUF)
  2. Continuous Venovenous Hemodialysis (CVVHD)
  3. Hemofiltration (CVVHF)
  4. Hemodiafiltration (CVVHDF)
  5. Continuous Arterio-Venous Hemofiltration (CAVHF),
  6. Slow low-efficiency daily dialysis (SLEDD)

Other:

Peritoneal dialysis (PD)
Plasmapheresis or plasma exchange
Intermittent Hemodialysis (IHD)
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28
Q

IHD vs CRRT

A

IHD:

Name: Intermittent hemodialysis
Mechanism and molecules removed: Dialysis – mostly low Molecular Weight
Use: Ambulatory CRF, Hyperkalemia
Blood flow: 300 - 400 mL/min
Dialysate flow: 500 mL/min or 30 L/hr
Efficiency: High
Urea clearance: (mL/min) 150
Hemodynamic stability: Poor (hypotension common)
Duration: 3-4 h 3x/week
Access: Fistula or vascath (must be good!)
Anticoagulation: Not needed
Dialysis Dysequilibrium Syndrome (DDS): Insufficient time for equilibration between compartments can cause cerebral edema
Drugs and toxicology: Risk of rebound if high VD. Better for low VD (e.g. toxic alcohols)
Logistics: Need tap water supply, need hygienic effluent removal, Technically difficult

CRRT:

Name: Continuous renal replacement therapy
Mechanism and molecules removed: Small + middle molecules with CVVHDF
Use: Critically ill/Non-ambulatory
Blood flow: 150 - 200 mL/min
Dialysate flow: CVVHF: nil/CVVHDF: 1 L/h
Efficiency: Low (but increased clearance of high VD molecules over time)
Urea clearance: (mL/min) 30 (CVVHDF)
Hemodynamic stability: Good
Duration: Continuous (24h/filter)
Access: Vascath only
Anticoagulation: Important (if filter clots can lose ~150 mL blood)
Dialysis Dysequilibrium Syndrome (DDS): N/A
Drugs and toxicology: Slower removal
Logistics: High workload, clearance limited by interruptions, costly sterile dialysate bags, immobility

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29
Q

SIADH versus CSW

A

SIADH

  1. hyponatremia (decreased serum Na+, increased urine Na+) LOW SERUM SODIUM
  2. euvolemia/slight hypervolemia NORMAL VOLUME
  3. CVP normal-high NORMAL VOLUME
  4. decreased urine output (d/t ↑ urine osmolality)
  5. Replace salt (3% HTS)
  6. water retention d/t elevated ADH levels
  7. increased urine sodium

CSW

  1. hyponatremia (decreased serum Na+, increased urine Na+)
  2. hypovolemia/dehydrated (patient is DRY)
  3. CVP low DECREASED VOLUME
  4. increased urine output
  5. Replace fluids (0.9% NS)
  6. excess secretion of sodium + water
  7. increased urine sodium
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30
Q

AKIN Classification for Acute Kidney Injury

A

Classifies severity of acute kidney injury, similar to RIFLE Criteria

To be diagnosed with acute kidney injury by the AKIN definition, patient must have at least one of the following within the past 48 hours

  1. Absolute increase in serum creatinine ≥26.4 μmol/L
  2. Increase in serum creatinine ≥1.5x above baseline
  3. Oliguria (urine output <0.5 mL/kg per hour) for >6 hours
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31
Q

RIFLE Criteria for Acute Kidney Injury (AKI)

A
  1. Classifies severity of acute kidney injury, similar to AKIN Classification
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32
Q

optimal blood product transfusion ratio in trauma

A
  1. Haemostatic resuscitation involves resuscitation with blood components resembling whole blood
  2. aims to avoid or ameliorate acute coagulopathy of trauma and the complications of aggressive crystalloid fluid resuscitation while maintaining circulating volume
  3. Involves blood component ratios of 1 unit PRBCs : 1 unit FFP : 1 unit platelets
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33
Q

how does ARDS relate to trauma (how does trauma lead to ARDS)

A
  1. Severe trauma predisposes to ALI and ARDS
  2. development of ARDS may be related to mechanism of injury (eg, lung contusion, long bone fracture leading to fat embolism) or resuscitation (eg, transfusion)
  3. In a study that included 1762 patients with major traumatic injury, ARDS occurred in 24%
  4. Predictors of ARDS after trauma included increasing subject age; increasing APACHE II score; increasing injury severity score; and the presence of blunt injury, pulmonary contusion, massive transfusion, or flail chest.
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34
Q

ACS treatment pathway

A
  1. Dual antiplatelet therapy (Aspirin + P2Y12 inhibitor)
  2. Anticoagulant (UFH/enoxaparin/fondaparinux)
  3. Oxygen (sats >90%)
  4. Rate control (Metoprolol)
  5. Analgesia (NTG, opioids)
  6. Statin therapy
  7. Reperfusion (TnK or PCI)
  8. Angiotensin-converting enzyme inhibitors or ARB’s
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35
Q

discuss “thrombolytic facilitated PCI”

A
  1. thrombolytic facilitated PCI is using thrombolysis as a mechanism to facilitate a “better” PCI. (Ie giving a dose of lytics’ before PCI even when the person would be within the window timeframe for primary PCI)
  2. Don’t do it
  3. Facilitated PCI is bullshit
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36
Q

mechanisms of preload assessment

A
  1. Passive leg raise
  2. Decrease in HR when you give a fluid bolus
  3. Use ultrasound to assess IVC collapsibility (patient must be sedated/paralyzed/on VCV
  4. CVP assessment
  5. JVP height measurement
  6. Arterial waveform pulse pressure variation (SBP delta P variation of 16%)
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37
Q

mechanisms of perfusion assessment

A
  1. Extremities colour, temperature, cap refill, mottling
  2. If cold skin, mottling, or delayed cap refill grab your ultrasound, look at the heart, consider dobutamine to improve forward flow
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38
Q

Discuss the appropriate times to contact PTCC during a scene response and IFT

A
  1. Upon receiving the initial call
  2. Upon takeoff/leaving for the call
  3. Prior to takeoff departing the sending heading for the receiving
  4. If there are any logistical changes that need to be clarified/made/communicated
  5. When you are clear of the call
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39
Q

Cranial nerves 1-12

A
  1. Olfactory
  2. Optic
  3. Oculomotor
  4. Troclear
  5. Trigeminal
  6. Abducens
  7. Facial
  8. Vestibulocochlear
  9. Glossopharyngeal
  10. Vagus
  11. Accessory
  12. Hypoglossal
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40
Q

Assessment for CN I (olfactory)

A

“Can you smell this” or “do you have any problems with your smell”

Official test is to hold up a jar of coffee or some such item

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41
Q

Assessment for CN II (optic)

A

“Can you see this”

Visual acuity, peripheral vision (Snellen Chart)

pure sensory

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42
Q

Assessment for CN III (oculomotor)

A

Open eyelids. Eye movement up and in (Perform H test)

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43
Q

Assessment for CN IV (trochlear)

A

Eye movement down. (Perform the H test)

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44
Q

Assessment for CN V (trigeminal)

A

Facial sensation x 3 “TRIgeminal”. Sensation at top, middle, bottom of face . compare right vs left

MIXED motor/sensory

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45
Q

Assessment for CN VI (abducens)

A

Eye movement lateral (Perform the H test)

motor

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46
Q

Assessment for CN VII (facial)

A

“smile, show me your teeth. Raise your eyebrows” looking for facial symmetry

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47
Q

Assessment for CN VIII (vestibulocochlear)

A

“Can you hear this”

Hearing bilaterally, balance (assessing for vertigo)

pure sensory

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48
Q

Assessment for CN IX (glossopharyngeal)

A

taste on the tongue (sensory), swallowing (motor)

mixed motor/sensory

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49
Q

Assessment for CN X (vagus nerve)

A

swallowing reflex (motor)/parasympathetic response (sensory)

mixed motor/sensory

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50
Q

Assessment for CN XI (accessory nerve)

A

have the patient shrug their shoulders up and down

pure motor

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51
Q

Assessment for CN XII (hypoglossal nerve)

A

stick out your tongue, move your tongue around (motor)

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52
Q

Cough reflex (unconscious/sedated patient)

CN’s and how to assess

A

CN X [Vagus]

can be stimulated by a suction catheter down and endotracheal tube

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53
Q

Gag reflex (unconscious/sedated patient)

CN’s and how to assess

A

CN IX [Glossopharyngeal] and X [Vagus]

Some sources recommend shaking the endotracheal tube, whereas others recommend inserting a tongue depressor or suction catheter into the posterior pharynx.

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54
Q

corneal reflex (unconscious/sedated patient)

CN’s and how to assess

A

CN V [Trigeminal] and CN VII [Facial]

the provider lightly touches a wisp of cotton on the patient’s cornea. This foreign body sensation should cause the patient to reflexively blink.

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55
Q

anions vs cations

A
  1. cations are positively charged

2. anions are negatively charged

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56
Q

Define the KULT acronym for metabolic acidosis

A
  1. KETOACIDOSIS
  2. UREMIA
  3. LACTIC ACIDOSIS
  4. TOXINS (includes medications)
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57
Q

What are the causes of a low AG?

A
  1. Decreased albumin
  2. GI ingestion (tums)
  3. Lab error
  4. Math error

most commonly it’s gonna be a math error or a lab error

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58
Q

what is the 5 step CCP process to ABG interpretation

A
  1. State the ‘emia’. Is it acidemia or alkalemia?
  2. State the ‘osis’. What is the driver? Metabolic vs Respiratory
  3. Calculate the AG. Na - (HCO3- + Cl) = x (corrected for albumin)
  4. Expected compensation? Does the patient have appropriate compensation?
  5. Is there a superimposition present?
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59
Q

Causes of NAGMA

A
  1. RTA (failure of kidneys to Reabsorb all of the filtered bicarbonate and/or failure of kidneys to Synthesize new bicarbonate to
    replace bicarbonate lost to metabolism
  2. GI losses (puking/shitting out all your bicarb)
  3. Hyperchloremia (too much NS)
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60
Q

MUDPILES CAT

A 
M - Methanol, metformin (increases lactate)
U - Uraemia
D - Diabetic ketoacidosis
P - paracetamol, paraldehyde, Phenformin, pyroglutamic acid, propylene glycol
I - Iron, isoniazid
L - Lactate (numerous causes)
E - Ethanol, ethylene glycol
S - Salicylates

C - Cyanide, carbon monoxide
A - Alcoholic ketoacidosis
T - Toluene

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61
Q

Expected compensation ratio (pCO2:HCO3-) for metabolic acidosis

A

1:1

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62
Q

Expected compensation ratio (HCO3- : pCO2) for metabolic alkalosis

A

1:0.7

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63
Q

Expected compensation ratio (pCO2:HCO3-) for respiratory alkalosis

A

1:0.5

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64
Q

Expected compensation ratio (pCO2:HCO3-) for respiratory acidosis

A

1:0.3

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65
Q

Liver function tests

A
  1. Bilirubin
  2. Glucose
  3. Albumin
  4. INR
  5. PT
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66
Q

Liver enzymes

A
  1. AST
  2. ALT
  3. GGT
  4. Alkaline phosphatase (ALP)
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67
Q

Which coagulation factors are dependent upon vitamin K for synthesis?

A

X, IX, VII, II (prothrombin group)

10-9-7-2

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68
Q

Normal range for platelets

A

130–380 × 10⁹/L

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69
Q

Normal range for INR (non anti-coagulated blood)

A

0.9–1.2

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70
Q

Normal range for Prothrombin time (PT)

A

10–14 seconds

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71
Q

Normal range for aPTT (non anti-coagulated blood)

A

22-30 seconds

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72
Q

Normal range for fibrinogen

A

2.0 to 4.0 g/L

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73
Q

Normal range for hemoglobin

A

Male 125–170 g/L

Female 115–155 g/L

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74
Q

Hemostatic goals in trauma

A
  1. Hgb > 70
  2. Platelets > 100
  3. INR < 1.8
  4. Temp > 36
  5. Fibrinogen > 1.5
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75
Q

4 A’s of anesthesia

A
  1. amnesia
  2. analgesia
  3. areflexia
  4. autonomic stability
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76
Q

Big syringe (“three syringes principle”)

A
  1. induction agent. “amnesia”.

2. typically a “big syringe” because push dose propofol is done in a 20cc syringe

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77
Q

Little syringe (“three syringes principle”)

A
  1. analgesic agent and/or paralytic agent. “analgesia” + “areflexia”.
  2. usually a 10cc syringe “little” because it’s smaller than the 20cc propofol syringe
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78
Q

Chaser syringe (“three syringes principle”)

A
  1. hemodynamic support agent.
  2. examples include push dose epinephrine, phenylephrine, atropine
  3. “chases” your induction to maintain autonomic stability. 4. depending on how unstable the patient is, you may lead with your chaser syringe
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79
Q

depolarizing NMBA and mechanism

A
  1. succinylcholine

2. binds to and activates the ACh receptor, at first causing muscle contraction, then paralysis

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80
Q

non-depolarizing NMBA and mechanism

A
  1. rocuronium

2. competitively blocks the binding of ACh to its receptors

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81
Q

causes of increased airway resistance

A
  1. bronchospasm
  2. ETT problems (too small/kinked/bitten/flexed/obstructed)
  3. mucus plugging/secretions
  4. water in HME
  5. blocked exhalation valve
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82
Q

causes of decreased lung compliance

A
  1. ARDS
  2. atelectasis
  3. abdominal distention (abdominal HTN)
  4. CHF
  5. consolidation
  6. fibrosis (pulmonary fibrosis)
  7. hyperinflation
  8. pneumothorax
  9. pleural effusion
83
Q

Oxygen delivery equation (DO2)

A
  1. DO2 = CO x CaO2 (mL/min/m2)

2. CaO2 = (1.34 X Hgb X SaO2) + (0.003 X PaO2)

84
Q

4 types of hypoxia

A
  1. hypoxic
  2. hypemic
  3. stagnant
  4. histotoxic
85
Q

5 causes of hypoxemia

A
  1. V/Q mismatch
  2. Diffusion impairment
  3. Shunt (think right to left shunt)
  4. Hypoventilation
  5. Decreased partial pressure of inspired oxygen (think high altitude)
86
Q

Virchow’s triad

A
  1. Hypercoagulability
  2. Vascular stasis
  3. Endothelial injury/dysfunction
87
Q

adverse effects of oxygen d/t hyperoxia and oxygen toxicity

A

Cellular injury due to increased ROS (reactive oxygen species)

  1. Increased ROS eg superoxide anion, hydroxyl radical, hydrogen peroxide
  2. ROS lead to inflammation and secondary tissue injury / apoptosis
  3. deplete cellular antioxidant defences
  4. react / impair function of intracellular macromolecules
    cell death

Respiratory

  1. pulmonary vasodilation resulting in V/Q mismatch and CO2 retention in COPD
  2. Haldane effect leads to decreased affinity of Hb for CO2 and contributes to CO2 retention in COPD
  3. increased mortality in CO2 retainers from high flow O2 compared with titrated O2 in a prehospital RCT
  4. increased respiratory rate
  5. Denitrogenation of the lungs causing resorption atelectasis
  6. Bronchopulmonary dysplasia: neonates
  7. > 60% O2 causes tracheal irritation, sore throat, substernal pain, pulmonary congestion, decreased VC
  8. Dry nose and mouth, increased susceptibility to mucous plugging
  9. Increased R to L shunt fraction
  10. Accelerated lung injury from bleomycin toxicity and paraquat poisoning
  11. Delay recognition of hypoventilation by SpO2 monitoring during sedation (irrelevant if using ETCO2 monitoring)

Immune

  1. Increased risk of secondary lung infection due to: impaired mucociliary clearance
  2. decreased bactericidal capacity of immune cells

Cardiovascular

  1. Increased mortality post-cardiac arrest with hyperoxia (PaO2>300 mmHg)
  2. Systemic vasoconstriction leading to increased SVR, increased BP, decreased heart rate and decreased cardiac output
  3. Normobaric hyperoxia reduces coronary blood flow by 8 to 29% in normal subjects and in patients with coronary artery disease or chronic heart failure
  4. Increased myocardial infarct size (AVOID study, 2015)
  5. No reduction in myocardial ischemia in the presence of coronary artery disease unless SpO2 <85-90%
  6. Impairs endothelium-mediated vasodilation

Neurological

  1. Acute toxicity with hyperbaric 100% O2 causing altered mood, vertigo, LOC, convulsions
  2. Retinopathy of prematurity
  3. Hyperoxia decreases cerebral blood flow by 11 to 33% in healthy adults
  4. Hyperoxia associated with increased mortality in stroke and TBI

Haematological

  1. Prolonged exposure to 100% O2 impairs erythropoiesis
88
Q

benefits of NIPPV

A
  1. increased oxygenation
  2. increased end organ perfusion of oxygen
  3. increased ventilation
  4. decreased work of breathing
  5. potentially avoids intubation
89
Q

Contraindications to NIPPV

A
  1. Cardiac arrest
  2. Respiratory arrest
  3. Unable to protect airway
  4. Upper airway obstruction with foreign bodies
  5. Untreated or loculated pneumothorax found on imaging
  6. SHOCK
  7. Post GI surgery (caution)
  8. Maxillofacial injury
  9. Intractable vomiting
90
Q

CCP approach to establishing Mech Vent

A
  1. Am I adequately oxygenating (PaO2)
  2. Am I ventilating appropriately (PaCO2)
  3. Am I on safe ground
  4. What is my current acid-base status
91
Q

Goals of NIPPV

A
  1. Decrease WOB (unload respiratory muscles)
  2. Increase FRC
  3. Improve atelectatic recruitment
  4. Improve lung compliance
  5. Improve oxygenation
  6. Decrease LV preload, decrease LV afterload, improve cardiac output, improve forward flow
  7. PEEP matching for autoPEEP
92
Q

Adverse effects of NIPPV

A
  1. Local skin damage around bridge of nose
  2. Mask leak
  3. Eye and mouth irritation from mask leak air flow
  4. Sinus pain and sinus congestion
  5. Claustrophobia
  6. Mild gastric distention
93
Q

target UO in sepsis

A
  1. > 0.5mL/kg/hr
94
Q

PULMONARY EDEMA + LOW BP (“wet and cold” Cardiogenic Shock) treatment algorithm

A
  1. IV/O2/Monitor
  2. Differentiating the shock (pump failure vs mechanical complications)
  3. fix the lungs
  4. optimize the MAP
  5. optimize volume status
  6. consider inotrope for HFrEF
  7. treat underlying etiology
  8. mechanical circulatory support
95
Q

treatment for patients who are “cold and wet”

A
  1. Systemic hypoperfusion due to low cardiac output (cold)
  2. Filling pressures are elevated (wet)
  3. Giving volume will worsen their pulmonary congestion (making them wetter)
  4. Removing volume will worsen their systemic hypoperfusion (making them colder)
  5. Management of cold and wet cardiogenic shock usually requires interventions to improve cardiac function (e.g., inotropic medications, revascularization, or a mechanical support device)
96
Q

discuss “fixing the lungs” in acute HF

A
  1. NIPPV will reduces cardiac preload and afterload, and improve VQ matching. The most important parameter is the expiratory pressure (CPAP), which should be ramped up rapidly if possible
  2. Intubation is Often needed for frank cardiogenic shock (especially patients with delirium due to brain hypoperfusion). Intubation Provides full support for the work of breathing, which may allow shunting of blood away from the diaphragm and towards vital organs
  3. If the patient has large pleural effusion and this is causing significant respiratory distress or hypoxemia, then therapeutic drainage may be beneficial
97
Q

discuss “optimize the MAP” in acute HF

A
  1. the blood pressure needs to be high enough to perfuse the organs. However, if the pressure is too high, this will ↑ the workload on the heart (excessive afterload) → increased MVO2
  2. Often an ideal BP will be in the low-normal range (e.g. MAP 60-65 mmHg)
  3. hypertension should be managed with afterload reduction. Afterload reduction may ↑ CO, ↓ pulmonary edema, and ↓ MVO2.
  4. In the acute phase, high-dose NTG infusion is the preferred vasodilator
  5. hypotension may be managed with an inopressor (e.g., epinephrine or norepinephrine). Norepinephrine is recommended as a front-line agent for cardiogenic shock. Epinephrine may be a reasonable choice for a patient with ↓ EF, hypotension, bradycardia. and poor CO
98
Q

discuss “optimize the volume status” in acute HF

A

Consider giving a fluid challenge if the following conditions are met:

  1. There is insufficient end-organ perfusion (e.g. acute kidney injury).
  2. No evidence of pulmonary congestion (e.g. no B-lines on lung ultrasonography).
  3. Overall assessment suggests true hypovolemia (e.g. no systemic congestion).

Consider diuresis if the following conditions are met:

  1. There is significant pulmonary and/or systemic congestion.
  2. Overall assessment suggests total body fluid overload.
99
Q

CCP approach to CXR interpretation

A
  1. Patient Information
  2. Previous Imaging
  3. Technique
  4. Adequacy
  5. Heart
  6. Mediastinum
  7. Lungs and Lung Borders
  8. Soft Tissues
  9. Bones
  10. Lines and Tubes
100
Q

NG versus OG tube on CXR

A

NG tube appears larger because it has two radiopaque line that create the illusion of a bigger structure

101
Q

3 zones of the neck

A

Zone 3 - Angle of mandible to base of skull
Zone 2 - Cricoid to angle of mandible
Zone 1 - Clavicle to cricoid cartilage

102
Q

Zone III (upper neck) structures

A 
Distal portion of the internal carotid arteries
Vertebral arteries
Jugular veins
Pharynx
Spinal cord
Cranial nerves IX, X, XI, XII
Sympathetic chain
Salivary and parotid glands
103
Q

Zone II (midneck) structures

A 
Common carotid arteries
Internal and external branches of carotid arteries
Vertebral arteries
Jugular veins
Trachea
Esophagus
Larynx
Pharynx
Spinal cord
Vagus and recurrent laryngeal nerves
104
Q

Zone I (low neck) structures

A 
Thoracic outlet vasculature (subclavian arteries and veins, internal jugular veins)
Proximal carotid arteries
Vertebral artery
Apices of the lungs
Trachea
Esophagus
Spinal cord
Thoracic duct
Thyroid gland
Jugular veins
Cranial nerve X (vagus nerve)
105
Q

peripheral vertigo

A 
1. describes vertigo caused by lesions affecting the
inner ear and cranial nerve VIII (vestibulocochlear nerve)
2. sudden onset
3. intermittent
4. more severe symptoms 
5. affected by head position/movement
6. motor function/gait typically intact
7. horizontal nystagmus

CAUSES:

benign paroxysmal positional vertigo (BPPV)
vestibular neuritis
Meniere's disease
acoustic neuroma
aminoglycoside toxicity
semicircular canal dehiscence syndrome
perilymphatic fistula
herpes zoster oticus (Ramsay Hunt syndrome)
106
Q

central vertigo

A 
1. vertigo caused by lesions affecting the
brainstem and cerebellum
2. gradual onset
3. constant  
4. more mild symptoms 
5. unaffected by head position/movement
6. motor function/gait unstable
7. vertical nystagmus

CAUSES:

vestibular migraine
brainstem stroke
multiple sclerosis
ischemic or hemorrhagic damage to the cerebellum
cerebral edema
high altitude cerebral edema
107
Q

differentiating central vs peripheral vertigo

A

PERIPHERAL: think SUDDEN ONSET, SEVERE, inner ear and cranial nerve VIII (vestibulocochlear nerve) involvement

CENTRAL: think CHRONIC, GRADUAL ONSET, MORE MILD, brainstem involvement

108
Q

Le Fort type I

A

Le Fort type I - horizontal maxillary fracture, separating the teeth from the upper face

Le Fort I is a floating palate (horizontal)

“moustache”

109
Q

Le Fort type 2

A

Le Fort type II - pyramidal fracture, with the teeth at the pyramid base, and nasofrontal suture at its apex

Le Fort II is a floating maxilla (pyramidal)

110
Q

Le Fort type 3

A

Le Fort type III - craniofacial dissociation

Le Fort III is a floating face (transverse)

111
Q

preload definition

A
  1. Myocardial sarcomere length just prior to contraction, for which the best approximation is end-diastolic volume
  2. Tension on the myocardial sarcomeres just prior to contraction, for which the best approximation is end-diastolic pressure
112
Q

preload equation (Laplace’s law)

A

Wall stress = (Ventricular pressure x Ventricular chamber radius) / 2x ventricular wall thickness (i.e. P⋅R/2h)

113
Q

afterload definition

A
  1. “load” that the heart must eject blood against
  2. a result of stress (or “tension”) that the cardiac wall (LV) experiences during systolic ejection
  3. the amount of pressure that the heart needs to exert to eject the blood out if it during the contraction
114
Q

cardiac afterload equation

A
  1. [(LV Pressure x LV Radius) / LV wall thickness] or [(P x r)/h]
  2. LV Wall Tension = [(SVR - Pleural Pressure) x LV Radius] / LV wall thickness

Afterload reduction can be achieved through:

  1. Decreasing SVR (arterial dilation)
  2. Increasing pleural pressure (PPV/PEEP)
115
Q

5 major densities seen on CXR

A
  1. Black (gas)
  2. Dark-grey (fat)
  3. Light-grey (soft tissue/fluid)
  4. Nearly-white (bone/calcification)
  5. White (metal)
116
Q

ONSD ultrasound depth target

A

3mm behind the optic disk

This ensures the area is undistorted by the optic disk

117
Q

coronal/frontal plane

A

plane dividing the body into dorsal and ventral parts.

118
Q

axial/transverse plane

A

plane that divides the body into superior and inferior parts

119
Q

saggital/longitudinal plane

A

anatomical plane which divides the body into right and left parts.

120
Q

Focal Airspace Disease

A

Increased Pulmonary Opacity

  1. Pneumonia, Atelectasis,
  2. Pulmonary embolism (i.e. infarct or hemorrhage)
  3. Neoplasm
121
Q

Diffuse or Multi-Focal Airspace Disease

A

Increased Pulmonary Opacity

  1. Pulmonary edema (CHF or non-cardiogenic) → Central opacification with peripheral clearing (bat-wing)
  2. Pneumonia
  3. Hemorrhage (i.e. trauma, immunologic)
  4. Neoplasm
122
Q

Fine Reticular Pattern

A

Increased Pulmonary Opacity

  1. Interstitial pulmonary edema
  2. Interstitial pneumonitis
123
Q

Radiographic Stages of CHF on CXR

A
  1. Cephalization (redistribution)
  2. Interstitial Pulmonary Edema (interstitial edema)
  3. Airspace Pulmonary Edema (alveolar edema)
124
Q

definition of “Cephalization” on CXR

A

Abnormal thickening of upper lung vascular markings

relative to lower lung vasculature

125
Q

Interstitial Pulmonary Edema findings on CXR

A
  1. Increased interstitial markings
  2. Pulmonary venous hypertension (upper zone hilar
    venous distension)
126
Q

Airspace Pulmonary Edema findings on CXR

A
  1. Air space filling, diffuse or patchy distribution
  2. “Bat-wing” central distribution is typical
  3. Perihilar haze is early sign
127
Q

ARDS definition (Berlin criteria)

A
  1. Respiratory symptoms within 1 week of known clinical insult
  2. Bilateral opacities on chest imaging not explained by other pulmonary pathology
  3. Respiratory failure not explained by heart failure or volume overload
  4. Decreased P/F Ratio
128
Q

Three plain film views required to r/o cervical spine on XR

A
  1. Lateral
  2. AP
  3. Open mouth (odontoid view)
129
Q

5 eye vital signs

A

1) Visual acuity
2) IOP
3) Pupils
4) Extraoccular movement
5) Visual Fields

130
Q

hyphema definition

A

Blood pooling in the anterior chamber of the eye

131
Q

iridocyclitis definition

A

Inflammation of the iris

132
Q

iridodialysis definition

A

Tearing the iris root from the ciliary body causing a double pupil

133
Q

what ophthalmic condition is characterized by a patient complaint of seeing “flashes and floaters”

A

Vitreous hemorrhage

134
Q

“Hard Signs” of neck trauma

A
  1. Airway compromise
  2. Air bubbling wound
  3. Expanding or pulsatile hematoma
  4. Active Bleeding
  5. Shock, compromised radial pulse
  6. Hematemesis
  7. Neuro Deficit/Paralysis/Cerebral ischemia
  8. Absent or unequal radial pulse
135
Q

“Soft Signs” of neck trauma

A
  1. Subcutaneous emphysema
  2. Dysphagia, dyspnea
  3. Non-pulsatile, non-expanding hematoma
  4. Venous oozing
  5. Chest tube air leak
  6. Minor hematemesis
  7. Paresthesias
136
Q

Ludwig’s angina definition

A

Bilateral infection of the submandibular space in the deep neck that begins as a cellulitis in the floor of the mouth

137
Q

TILE pelvic fracture staging

A
  1. The Tile classification of pelvic fractures is the precursor of the more contemporary Young and Burgess classification of pelvic ring fractures.
  2. TILE takes into account stability, force direction, and pathoanatomy.
  3. The integrity of the posterior arch determines the grade, with the posterior arch referring to all of the pelvis posterior to the acetabulum.
  4. Stability is defined as the ‘ability of the pelvis to withstand physiologic force without deformation’ by the original author
  5. Tile “A” = Stable (posterior arch intact)
  6. Tile “B” = Partially stable (incomplete disruption of the posterior arch)
  7. Tile “C” = Unstable (complete disruption of the posterior arch)
138
Q

Young and Burgess classification of pelvic ring fractures

A
  1. The Young and Burgess classification is a modification of the earlier Tile classification
  2. It is the recommended and most widely used classification system for pelvic ring fractures.
  3. It takes into account force type, severity, and direction, as well as injury instability.
  4. Three basic mechanistic descriptions are used, each with degrees of severity.

Anteroposterior compression

  1. APC I: stable
  2. APC II: rotationally unstable, vertically stable
  3. APC III: equates to a complete hemipelvis separation (but without vertical displacement); unstable

Lateral compression (Most common type)

  1. LC I: stable
  2. LC II: rotationally unstable, vertically stable​
  3. LC III: unstable
  4. Vertical shear (Most severe and unstable type with a high association of visceral injuries.)
139
Q

Transverse fracture

A

straight across bone

140
Q

Oblique fracture

A
  1. complete fractures that occur at a plane oblique to the long axis of the bone
  2. diagonal across bone
141
Q

Comminuted fracture

A
  1. shattered fragments of bone

2. break or splinter of the bone into more than two fragments

142
Q

Spiral fracture

A

broken by twisting
is known as torsion fracture
a complete fracture

a haiku for you 🌸

143
Q

segmental fracture

A
  1. at least two fracture lines that together isolate a segment of bone
  2. floating section of broken bone
144
Q

signs of impending airway failure in epiglottitis

A
  1. Drooling
  2. Muffled voice
  3. Stridor
  4. Hypoxia
  5. Sniffing position (sitting upright with neck extended)
145
Q

characteristic XR finding in epiglottitis

A
  1. Thumbprint sign of epiglottitis lateral neck XR

2. Presence of a “thumb-like” epiglottis on lateral soft tissue neck radiograph is concerning for epiglottitis

146
Q

pathophysiology of epiglottitis

A
  1. Inflammation of the epiglottis can lead to airway obstruction
  2. Epiglottitis was previously seen primarily in children as a result of Haemophilus influenzae type b infection
  3. Since the widespread adoption of vaccination against Haemophilus influenzae type B, the incidence of epiglottitis infections has decreased, and the mean age of patients with epiglottitis is now 45 years
  4. In the era following Haemophilus influenzae type B vaccination, Streptococcus and Staphylococcus are now the leading causes of epiglottitis
147
Q

Soft tissue risk factors for wound infection (risk factors for infection with soft tissue injuries)

A
  1. Immunocompromised (diabetic, chemotherapy, steroids, renal failure)
  2. Location of wound (less vascular areas are more prone to infection. shitty blood flow to bring in WBC’s to fight infection)
  3. Mechanism (blunt/crush are more susceptible for infections vs “clean” wounds like GSW or stab)
  4. inappropriate wound closure (not properly irrigated prior to closure)
148
Q

what soft tissue wounds should receive prophylactic ABX

A
  1. cat bites
  2. grossly contaminated wounds
  3. through and through oral wounds
  4. human fight bites
  5. burns
  6. foot wounds/wounds in a less vascular area
  7. open fractures
  8. tendons and joints
149
Q

Inclusion criteria for tPA in stroke

A
  1. Clinical diagnosis of ischemic stroke causing neurologic deficit
  2. Onset of symptoms less than 4 ½ hours before beginning treatment
  3. Age over 18 years
150
Q

Contraindications for tPA in stroke

A
  1. Intracranial hemorrhage on CT
  2. Clinical presentation suggests subarachnoid hemorrhage
  3. Neurosurgery, head trauma, or stroke in past 3 months
  4. Uncontrolled hypertension (>185 mmHg SBP or >110 mmHg DBP)
  5. History of intracranial hemorrhage
  6. Known intracranial arteriovenous malformation, neoplasm, or aneurysm
  7. Active internal bleeding
  8. Suspected/confirmed endocarditis
  9. Known bleeding diathesis
  10. Abnormal blood glucose (<2.7 or >22.2 mmol/L)
151
Q

“classic case” CT findings in SAH

A
  1. hyperdense material is seen filling the subarachnoid space
  2. Most commonly apparent around the circle of Willis
152
Q

“classic case” CT findings in IVH

A
  1. commonly occurs in the setting of intracerebral hemorrhage or subarachnoid hemorrhage
  2. Blood in the ventricles appears as hyperdense material
  3. blood is heavier than CSF, and thus tends to pool dependently
153
Q

“classic case” CT findings in cerebral contusion

A
  1. hyperdense foci in the frontal lobes
154
Q

“classic case” CT findings in DAI

A
  1. multiple focal lesions with a characteristic distribution
  2. typically located at the grey-white matter junction, in the corpus callosum
  3. in more severe cases present in the brainstem
155
Q

classic case CT findings in acute SDH

A
  1. 85% of SDH are unilateral
  2. extra-axial blood that spreads diffusely over the affected hemisphere
  3. crescent-shaped
  4. hyper-dense
156
Q

epidural hematoma CT findings

A
  1. appears as a “lens” on CT scan. bi-convex, hyperdense, sharply demarcated.
  2. follows the curvature of the skull and protrudes into brain tissue as a convex mass
157
Q

classic CT findings in elevated ICP

A
  1. Cisternal effacement
  2. sulcal effacement
  3. ventricular compression
  4. cerebral herniation
158
Q

Stanford type “A” aortic dissection

A
  1. Affects ascending aorta
  2. Accounts for 60% of aortic dissections
  3. Initially managed surgically
159
Q

Stanford type “B” aortic dissection

A
  1. Affects descending aorta
  2. “B begins beyond brachiocephalic vessels”
  3. Accounts for 40% of aortic dissections
  4. Initially managed medically
160
Q

DeBakey Classification

A

The DeBakey classification, is used to separate aortic dissections into those that need surgical repair, and those that usually require only medical management

  1. type I: involves ascending and descending aorta (Stanford A)
  2. type II: involves ascending aorta only (Stanford A)
  3. type III: involves descending aorta only, commencing after the origin of the left subclavian artery (Stanford B)
161
Q

typical value for right atrial pressure (RAP) in an adult

A

RA 5 mmHg

“nickel”

162
Q

typical value for right ventricular pressure (RVP) in an adult

A

RV 25/5 mmHg (systolic/diastolic)

“quarter”

163
Q

typical value for left atrial pressure (LAP) in an adult

A

LA 10 mmHg

“dime”

164
Q

typical value for left ventricular pressure (LVP) in an adult

A

LV 100/10 mmHg (systolic/diastolic)

“dollar”

165
Q

typical value for pulmonary artery pressure (PAP) in an adult

A

PA 25/10 (systolic/diastolic)

166
Q

typical value for aortic pressure in an adult

A

125/75 (systolic/diastolic)

167
Q

Heparin vs LMWHs vs Fondaparinux What’s the Difference?

A
  1. Heparin – Binds to and potentiates the actions of antithrombin (AT) to inactivate factor Xa and prevent the conversion of prothrombin to thrombin, as well as prevent the conversion of fibrinogen to fibrin.
  2. LMWHs – Also bind and accelerate the activity of AT, but with a preferential, and longer lasting effect on factor Xa. When compared to heparin, LMWHs are less able to inhibit the production of thrombin and bind to plasma proteins and endothelial cells less due to their decreased sized. This accounts for an 85-99% bioavailability when administered SC, more predictable anticoagulant response, less inter-patient variability, and longer duration of action than heparin
  3. Fondaparinux - Binds and enhances the anti-Xa activity of AT by 300-fold. AT specificity does not allow binding to other plasma proteins. It has no direct effect on thrombin, has excellent bioavailability after SC administration and a long half-life
168
Q

pathophysiology of RV failure in the setting of pulmonary hypertension

A
  1. The pulmonary vascular bed is normally a high-flow, low-pressure system. When there is an increase in the PVR, the RV cannot adapt as well as the LV, → RV dilation
  2. When faced with an acute increase in PVR, the RV can only generate systolic pressures up to 40-50 mm Hg
  3. With gradual, chronic changes, the RV systolic pressure can become equal to systemic pressures, up to 80-110 mmHg
  4. Volume overload, pressure overload, and dilation eventually lead to tricuspid regurgitation
  5. Normally, the RV is perfused in both systole and diastole, given the low RV pressures. Upon increased pressures within the RV, the wall tension leads to decreased RCA perfusion and eventual RV ischemia
  6. RV failure can develop with PH progression or an acute or chronic insult, particularly one that decreases RV perfusion or further increases PVR. This is why hypotension, decreasing RCA perfusion, or hypoxemia, hypercapnia, or positive-pressure ventilation can be so detrimental.
  7. The relationship between the RV and LV cavities is known as interventricular dependence. When the RV bulges with volume and pressure overload into the LV, the LV has decreased filling
  8. The RV is a conical structure and contracts in systole against the interventricular septum. Distortion of the RV not only decreases LV filling but also further decreases effective RV contractility
169
Q

CCPstaged approach to refractoryhypoxemia

A

1) Optimize FiO2 - Start 1.0 and work down after safe ground
2) Optimize PEEP - Consider PEEP scale, monitor Pplat and hemydynamics
3) Consider switching VCV → PCV (more area under the curve which is where oxygenation occurs)
4) Recruitment maneuver (repeat x ? - evaluated pH and effects when considering repeat)
5) ↑ RR (more area under curve) - (beware ↑ risk of dynamic hyperinflation)
6) Prone positioning
7) Inverse ratio ventilation (more area under curve)
8) ECMO

170
Q

Asthma treatment pathway

A
  1. Oxygen (target SpO2 >90%)
  2. inhaled β-agonist and anticholinergic (salbutamol + ipratropium)
  3. Systemic corticosteroids (methylprednisolone)
  4. MgSO4 infusion
  5. BiPAP (ketamine to facilitate if necessary)
  6. Epinephrine (first IM, then IV)
  7. Intubation
171
Q

ACA stroke clinical presentation

A
  1. primarily affect frontal lobe function
  2. Hemiparesis. Contralateral leg paresis more common than arm paresis
  3. bilateral leg weakness if both ACAs are involved
  4. Apraxia. disinhibition, diminished executive dysfunction
  5. Hemianesthesia
  6. Apathy
172
Q

MCA stroke clinical presentation

A
  1. MOTOR CORTEX - contralateral paralysis of upper arm + face
  2. SENSORY CORTEX - contralateral loss of sensation of upper arm + face
  3. SPEECH - aphasia if in dominant hemisphere (usually left)
  4. VISUAL - hemineglect if in non-dominant hemisphere (usually right)
173
Q

Internal capsule (lenticulo-striate artery) stroke clinical presentation

A
  1. MOTOR CORTEX - contralateral hemiparesis that affects the face, arm, and leg in equal parts

common site of lacunar infarcts

174
Q

PCA stroke clinical presentation

A
  1. VISUAL CORTEX - contralateral hemianopia (you knock out the 1/2 field of vision contralateral to the side of the infarct)
175
Q

Basilar artery stroke clinical presentation

A
  1. BRAINSTEM (pons/medulla/lower midbrain) - preserved consciousness but loss of voluntary facial/mouth/tongue movement. Loss of brainstem function with “locked in syndrome”

these guys are super tenuous. don’t sedate these guys. keep them on no sedation on pressure support ventilation. The reason why is that your brainstem exam (spontaneous respiratory effort) is your only component of the neuro exam you can trend because they are otherwise 100% flaccid

176
Q

clinical triad of symptoms in bacterial meningitis

A
  1. Fever
  2. Neuro symptoms (AMS/headache/photophobia/seizure)
  3. Nuchal rigidity
177
Q

BP goal for an unsecured aneurysmal SAH

A

SBP < 140 mmHg

178
Q

BP goals for acute ischemic CVA

A
  1. Pre lysis (r-TPA): SBP < 185 mmHg DBP <110 mmHg
  2. post lysis (r-TPA): SBP < 180 mmHg DBP <105 mmHg
  3. No lysis: SBP <220 mmHg DBP <120 mmHg
179
Q

BP goals for acute hemorrhagic CVA

A
  1. SBP < 140 mmHg

treat with labetalol, opioids for pain

180
Q

Differentiating SIADH from CSW

A

1 . Both conditions are characterized by hyponatremia with elevated urine Na+, concentrated urine, and no edema.
2. in CSW the patient is hypovolemic versus in SIADH the patient is euvolemic to hypervolemic.

181
Q

Aneurysmal Subarachnoid Hemorrhage treatment pathway

A
  1. IV/O2/Monitor
  2. Preliminary neuro exam
  3. secure the airway if req’d
  4. Art line/BP control (goal SBP <140 mm Hg, labetalol)
  5. reversal of anticoagulation (VitK/FFP/PCC/Plt/TXA)
  6. management of ICP (mannitol/HTS)
  7. prevent secondary brain injury (optimize venous drainage, treat pain/fever/electrolytes/glucose, Consider seizure prophylaxis, optimize BP/PaO2/pCO2)
182
Q

Mechanisms to reduce “blood” volume (Monroe-Kelly)

A
  1. Hyperventilation (decreased PaCO2 leads to cerebral vasoconstriction)
  2. Head in neutral alignment (cerebral venous drainage)
  3. HOB 30 degrees (cerebral venous drainage)
  4. Loosen C-Collar/ETT Ties (cerebral venous drainage)
  5. Decrease intra-abdominal pressure (cerebral venous drainage)
  6. PEEP <13cmH2O (cerebral venous drainage)
183
Q

Mechanisms to reduce “CSF” volume (Monroe-Kelly)

A
  1. EVD (direct CSF drainage)
184
Q

Mechanisms to reduce “parenchyma” volume (Monroe-Kelly)

A
  1. Osmotic therapy (mannitol/HTS)
  2. Sedation (decreased metabolic demand, decreased cerebral blood flow via flow-metabolic coupling)
  3. Temperature control (decreased metabolic demand, decreased cerebral blood flow via flow-metabolic coupling)
  4. Seizure control (decreased metabolic demand, decreased cerebral blood flow via flow-metabolic coupling)
185
Q

neuro insults where the target MAP should be 80-90

A
  1. Undifferentiated TBI (SBP >110 <160)
  2. Subdural bleed
  3. Traumatic subarachnoid bleed
  4. DAI
  5. SCI
  6. IVH
186
Q

goal BP/MAP in multi system trauma with comorbid TBI

A
  1. MAP >80mmHg

2. SBP >110 <160

187
Q

goal BP/MAP for ICH/intraparenchymal bleeds (deep brain parenchyma)

A
  1. ICH bleeds are normally venous = low pressure

2. Target SBP <160, follow normal TBI care plan (MAP >80, optimize venous drainage etc.)

188
Q

Central cord syndrome

A
  1. Hyperextension of the c-spine → buckling of the ligamentum flavum, which → localized injury within the center of the spinal cord → bilateral upper extremity motor weakness w/ relative sparing of the lower extremities
  2. Distal muscles (like hands) typically affected more than proximal
  3. occurs in ~10% of adult SCI. classically occurs during hyperextension injury
  4. May occur w/o fracture (SCIWORA), especially in older patients or those with spinal stenosis
189
Q

Brown-Sequard syndrome

A
  1. Lateral hemisection of the spinal cord
  2. typically from a penetrating injury
  3. Loss of ipsilateral motor function, light touch, proprioception.
  4. Loss of contralateral pain and temperature sensation.
190
Q

Anterior cord syndrome

A
  1. Characterized by damage to the anterior two-thirds of the spinal cord
  2. causes complete loss of motor function and sensation of pain and temperature below the injury
  3. Posterior column sensations of vibration, proprioception, and light touch are preserved
  4. typical mechanisms include flexion injuries, retropulsion of fracture fragments, or occlusion of the anterior spinal artery
191
Q

clinical significance of paralysis at or above level of the biceps in SCI

A
  1. biceps are supplied by nerves at the level of C6, meaning C5 and above are intact
  2. The phrenic nerve (diaphragmatic innervation) originates from cervical spinal roots C3, C4 and C5
  3. This means that patients have full diaphgramatic control and likely do not need to be intubated
192
Q

Dosing for HTS in elevated ICP

A
  1. Elevated ICP: 3mL/kg (3% HTS)

2. Brain Herniation: 5mL/kg (3% HTS)

193
Q

Dosing for mannitol in elevated ICP

A
  1. Elevated ICP: 0.25-0.5g/kg

2. Herniation: 1g/kg

194
Q

initial bundle of care for brain injury in trauma

A
  1. MAP > 80 mmHg, SBP < 110-160 mmHg
  2. Normal temp (avoid hyperthermia)
  3. PaCO2 35-40 mmHg (target normal)
  4. PaO2 80-120 mmHg (target normal)
  5. Hgb > 90 g/L
  6. HOB 30°, loosen collars/ties
  7. Optimize platelets/INR
  8. Propofol/ketamine to RASS -4
195
Q

indications for anticonvulsant therapy in TBI

A
  1. Hx of seizure associated with the TBI
  2. Temporal lobe pathology
  3. Depressed/open skull fracture
  4. Penetrating trauma to the cranium
196
Q

How much fluid must you replace when using mannitol for reduction in ICP?

A

Measure urinary output and replace fluid (normal saline) at a 1:1 ratio

197
Q

“Classic” clinical findings in uncal herniation

A
  1. ipsilateral dilated pupil that is unresponsive to light (CN III compression)
  2. altered mental status/coma
  3. contralateral hemiparesis
198
Q

Comprehensive neuro exam in an intubated patient

A
  1. Mode of ventilation
  2. Sedation level
  3. AVPU/Motor response/GCS
  4. Open eyes - is there movement? (CN III, midbrain)
  5. Pupil response to light (CN II, III, midbrain)
  6. Cough (CN X, medulla)
  7. Corneal reflex (CN V, VII, pons)
  8. Gag (CN IX, X, medulla)
  9. Evaluate intrinsic respiratory drive (respiratory center, medulla)
  10. Tone (flaccid, rigid, spastic)
  11. Reflexes (Biceps C5, C6; Triceps C6, C7, C8; Brachioradialis C5, C6, C7; Patellar L2, L3, L4; Achilles tendon S1, S2; Plantar/Babinski)
199
Q

Critical FVC for tubing GBS and MG

A

≤ 20mL/kg FVC

200
Q

cerebral perfusion pressure normal range

A

Normal CPP lies between 60 and 80 mm Hg

201
Q

lung volumes measured by spirometry

A

Spirometers can measure three of four lung volumes

  1. inspiratory reserve volume
  2. tidal volume
  3. expiratory reserve volume,

Spirometers cannot measure Residual volume

202
Q

pancreatic enzymes

A
  1. amylase

2. lipase (more sensitive and specific for pancreatic disease)

203
Q

acute pancreatitis treatment algorithm

A

“limit the severity of pancreatic inflammation and provide supportive care”

  1. IV fluid resuscitation (plasma-lyte or LR)
  2. correction of electrolyte and metabolic abnormalities
  3. Antiemetics
  4. Analgesia
  5. Vasopressor support for shock
  6. Nutritional support (enteral nutrition or NG feeds)
  7. Antibiotics (infected necrotizing pancreatitis or extrapancreatic infections)
  8. Management of complications (eg. EtOH withdrawal, infection, ARDS, shock)

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