EM Final exam Flashcards
(140 cards)
1
Q
What are complications of massive transfusion?
A
fluid overload, hypocalcemic, hypothermic, hyper coagulability
2
Q
What is the difference between T1 and T2 imaging?
A
T1 delineates different tissues and is considered the anatomy scan. T2 images reveal bright fluid with other tissues appearing grey and are considered the pathology scans.
3
Q
Advantages of MRI?
A
-No ionizing radiation
-can produce image slices of any orientation through body
-produces better contrast resolution and tissue discrimination than X-ray or US in many body areas.
(better than CT for osteomyelitis, AVN, brain, spinal cord, other soft tissue/nerve injuries)
4
Q
CI to MRI?
A
Pacemakers, aneursym clips, steel sliver in eye, cochlear implants
- not CI: stents (after 6 weeks), and prosthetic valves (most)
5
Q
What adverse reactions occur secondary to IV contrast?
A
1) Idiosyncratic anaphylactoid reaction (incr with prior run, asthma, dm, BB, metformin, renal or cardiac failure, extremes of age, hx of atopy
2) Allergic rxn
- can pre treat with steroids and benadryl
3) Contrast induced nephropathy- hydration may help reduce risk
6
Q
What is MRI best used for in ED?
A
Spinal cord
Occult femoral intertrochanteric and femoral neck fractures
Eval of posterior cranial fossa pathology
- Also has higher sens than CT for CVA
- Can also use for CVST, cardiac, PE,
7
Q
Indications for screening aortic US in ED?
A
age > 50 with unexplained back, flank, abdo, groin
Pt’s with hypotension, syncope, dizziness
8
Q
What thickness of GB on US is abnormal?
A
> 3 mm wall thickening - can be acute chile, also seen in ascites, and other hypo protein states
9
Q
Where do stones lodge in renal colic?
A
UVJ
UPJ
Pelvic brim
10
Q
What is difference between BLS/ALS crews?
A
BLS- only 02, AEDS, BMV, immobilization devices, and splinting equipment
ALS also has IV supplies, medications, advanced airways devices, cardiac monitors, and other specialized equipment
11
Q
What is the role of public safety agencies? (polics/fire departments)
A
Can provide medical support- CPR/AED
scense securty
public safey
12
Q
What are the key elements of EMS?
A
Manpower Training Communications Transportations Facilities Critical care untis Public safety agencies Consumer participation Access to care Pt transfer Coordinated pt record keeping Publin info and education Review and evaluation Disaster plan Mutual aid
13
Q
Criteria used in field to clear C spines?
A
No neck pain/tenderness/discomfort
Not in extremes of age ( 65 yrs)
No altered sensorium (no drugs/etoh/head injury)
No distracting injuries (long bone #, abdo/chest injury)
14
Q
What are issues r/t air transport?
A
Noise Vibration Temperature (cold higher up) Humidity (lack of causes dehydration) Altitude (decr p02, expansion of gases in closed space) Confined space Limited support Poor lighting
15
Q
Indications for helicopter transport?
A
Lengthy ground transport to tertiary centre
Ground vehicle transport time exceeds helicopter time
Entrapped trauma victim where extrication time expected to exceed 20 min
Many non trauma conditions: cardiac, critically ill, obstetric, neurologic, neonatal
Trauma scene indications:
1) Mech of injury
-unstable VS
-ped/cyclist struck
-ejeection from vehicle
-fall from ht
2) Neuro injuries (SC, skull #, GCS 20% BSA, inhalation, with trauma
16
Q
List factors unique to airline environment that affect medical care?
A
Lower partial pressure of 02 potential exposure to chemical irritants dry air virulent airborne particles venous stasis
17
Q
What are risk factors for developing hyponatremia in ultra distance athletes? (Na
A
Exercise time longer than 4 hrs
Female
Low BMI
18
Q
List the four components of negligence?
A
Duty
Breach of duty
Damages (loss or injury second to breach of duty)
Causation
(High risk areas include: failure to dx MI, abdo pain, wounds, fractures, paediatric fever/meningitis, airway obstruction, CNS bleed, AAA)
19
Q
What factors allow for determination of Capacity?
A
Presence of conditions impairing mental function
Presence of basic mental functioning
Pt has understanding of information r/t tx
Pt appreciates the significance of this info
Pt’s ability to reason about alternatives is intact
Complexity of decision
20
Q
What are the elements of informed consent?
A
A concise statement of pt’s medical condition or problem
An understandable statement of the nature and purpose of proposed test/tx/procedure
description of risks/benefits
statement regarding all alternatives
statement of prognosis if proposed test/tx/proced not given
21
Q
What are the five principles of medial ethics?
A
Veracity (telling the truth) Patient autonomy Beneficience Non Maleficence Justice
22
Q
What are the components of a disaster plan?
A
Hazard vulnerability analysis (which disasters are likely to hit where you are and what impact could they have)
Compliance with agency requirements
Hospital community coordination
Integration with national response assets
Training and disaster drills
23
Q
What comprises a hospital emergency operations plan?
A
Activation Establish emergency operations centre Assess hospital capacity Create surge capacity Establish communication systems Supplies Support areas Decontamination, triage, treatment
24
Q
Which field disaster triage techniques to reduce personnel use?
A
1) START- simple triage and rapid tx technique (quick assess of respirations, perfusion, and mental status)
2) Secondary assessment of victim endpoint- to determine use of field resusc resources (pt will die, pt will live, pt will benefit from austere field interventions)
25
Which triage system is used in ED for disasters/mass casualty?
Four colour coded categories:
Red- first priority, life threatening injuries, emergent
Yellow- second priority urgent (may decompensate but can wait 45-60 min)
Green- Third priority, non urgent
Black- Dead (sometimes victims with slim chance survival regardless of care are placed into this category)
26
What is normal muscle compartment pressure?
30 mmHg produces muscle ischemia, irreversible nerve and muscle damage occurs after 4-6 hrs
27
If a patient experiences prolonged entrapment and has a severe crush injury what medication should you consider?
Bicarb 1 amp
monitor K, Ca, pH
May need fasciotomy
28
What are the control zones of a chemical event?
Hot Zone- only rescue personnel in this zone
Warm zone- Immediate tx, decontamination
Cold zone
29
What are the levels of PPE?
A-Completley encapsulated protection
B- breathing appartus, supplied air, splash protection
C- gas mask, N95- air purifying respirator, skin splash protection
D-Disoposable gowns, gloves, booties
30
List the key elements of decontamination?
- Pt's exposed to solids, liquids, vapors or mists need to be decontaminated (not gases)
-Decontam one pt at a time outside hospital
-Don PPE level C
-Disrobe pt, brush off solid dusts/powders, then wash
-warm water is universal decontaminant
-
31
Which toxic gases interrupt oxygen transport?
CO and Methemoglobin forming agents
32
Which gases interfere with 02 utilization at the cellular level?
CN, Azide, sulfides (HS), CO (produce severe lactic acidosis)
33
Which gases displace 02 from air (simple asphyxiants)?
C02, H, N, hydrocarbons
34
Which irritant gases interrupt pulmonary diffusion?
ammonia, sulfur dioxide, hydrogen chloride
| Chlorine- is intermediate solubility- interacts with H20 to produce HCL and irritate upper airway
35
What toxicity do nerve gases cause?
Cholinergic
| * with cholinergic toxicity remember Sux onset of action is same but duration will be prolonged, up to several hours
36
List biotoxins and antidote?
Botulinum- antitoxin
| Ricin
37
List the radiation involved with common imaging modalities?
```
(Natural background rad 300mrem/y)
CXR 10 mrem
abdo xray 100mrem
l spine 70
CT head 200
CT chest 800
CT abdo pelvis 1000
Air travel london-new york 4 mrem each way
annual rad dose limit 100 mrem
lethal dose 450,000
```
38
What are the causes of sudden cardiac death?
• Structural heart disease (LVH)
• Conduction abnormalities
• Pre excitation ie WPW (if afib occurs can conduct into vnetrilces at rapid rate to initiate vfib)
• Brugada syndrome (syncope with or without sudden cardiac death caused by polymorphic vtach and ECG changes- downsloping ST seg elevation in v1-v3 often with ass RBB pattern. More in males, AD gene) More common in SE asia – tx implantable defib
• Long QT syndrome
Calculate QT with Bazett’s equation: QTc= QTm/R-R square root
• Acute triggers of SCD: electrolyte disturbance, heart failure, ischemia,
• Most SCD victims have cardiac abn on autopsy-most common CAD, cardiomegaly, LVH
39
What are the factors affecting survival for SCD?
```
witnessed,
prompt CPR early defib,
young age,
arrest away from home.
Vfib or vtach initial rhthms,
```
40
List the causes of Bradyasystolic arrest?
* Sick sinus syndrome
* Diffuse histologic degen of heart conduction system, worse with age, sometimes has tachy-brady component)
* MI (esp RCA as it supplies SA and AV nodes)
* Often in inferior MIs also have increased vagal tone hence inc n/v
* Hypoxia
* Hypercarbia
* Suffocation
* Near drowning
* Stroke
* Opiate od
* B blockers
* Ca ch blockers
* Digitalis glycosides
* Adenosine
* Massive hemorrhage
41
In what situations can you do open cardiac massage?
* Penetrating trauma to to the chest
* Perioperative period before or after cardiothoracic surgery
* Cardiact arrest secondary to hypothermia, PE, tamponade, abd hemorrhage,
* Chest deformity in which close chest cpr is inffective
* Penetrating abdo injury with deterioration and cardiac arrest
* Blunt trauma with cardiac arrest
42
List more common causes of ventricular arrhythmias?
```
MI
LVH
Preexcitation syndromes
Brugada syndrome
Long QT syndrome
```
43
What are the key points of newborn transition?
Transition includes: onset of resps, absorption of lung fluid, red of pulm resistance, closure of ductus arteriosus
44
What are key component of C for newborn CPR?
• IF after assisted ventilation for 30 sec and newborn still HR
45
List the key medications in neonatal resuscitation?
Epinephrine for asystole or HR 30 seconds). Dose 0.01-0.03 mg/kg (0.1-0.3ml/kg) IV push of 1:10000
• Follow epi with NS flush
• Can use same dose ET route and follow bu several positive pressure breaths.
• Sodium bicarb- once adequate ventilation given may give 1-2 meq/kg of 4.2% (0.5 mEq/ml) (equals 2-4 ml/kg)
• Naloxone- consider if persistent resp depression after resolution of bradycardia, maternal narcotic admin within 4 hours of delivery.
• Avoid if maternal narcotic addiction as may cause seizures
46
List the key features and tests associated with neonatal cyanosis?
Central vs peripheral differentiation is first step
⁃ Central indicates 4-5 g/dl of unsaturated hemoglobin. If lower newborn may present as pale.
⁃ Can obtain pre ductal (right radial) and post ductal (lower extremity or umbilical artery) ABGs to to dx persistent pulmonary htn of newborn
⁃ Also do upper and lower limb Bps to look for Coarct
⁃ Hyperoxia test: helps differentiate cardiac from non cardiac causes of cyanosis
⁃ 100% 02 hood for 5-10 minutes, those with cardiac cause (fixed shunt) cannot increase 02 where as those with pulm and other cause can
⁃ Tx: Treat with 02, and treat underlying cause
⁃ with o2, ET as needed, IV fluids 10% dextrose in water, monitor glucose levels, empirical antibiotics, obtain labs
⁃ If after initial testing and exam cannot rule out cyanotic heart lesion, treat with prostaglandin E1 continous infusion, 0.05-0.1 mcg/kg/min to maintain ductal patency (consult with peds cardio)
47
What are the components of the APGAR?
```
Color
HR
Irritability
Tone
Respiration
```
48
What are the key differences in the neonatal/infant airway?
Differences: smaller, higher and more anterior, relatively large tongue and epiglottis, prominent occiput causes flexion (therefore create mild extension for use of sniffng position), poorly formed cartlagenous rings, infants
49
What is the management of FB aspiration in paediatric pt?
-Conscious allow to cough
⁃ If child can't cough/breath/vocalize 5 back blows alternating with 5 chest thrusts
⁃ For child can do heimlich
⁃ Unconscious move to CPR
⁃ In ED for uncons can use DL with visualization and removal of FB with McGill forceps
- if unable to remove, intubate and push FB down right main stem
50
What are some differences in mechanical ventilation of paediatric patients?
Mechanical ventilation
| ⁃ Time flow or pressure preset ventilator should be use for children weighing
51
At what age do you move from 15:2 two person CPR to 30:2?
Age 8
| Newborn is 3:1
52
List common paediatric formulas for age/ET tube etc?
```
Wt predictation (kg): 8 + 2(age)
SBP: 70 + 2(age)
ET tube: Uncuffed age/4 + 4
ET tube insertion at lips: tube size x 3
Foley/NG: ETT size x 2
```
53
What is the indication for bicarb in paediatric arrest?
Prolonged resusc
54
What is the indication for calcium in paediatric arrest?
hyperkalemia, hypocalcemia, and CCB OD
55
List the management of paediatric dysrhythmias?
⁃ Agains mostly second to hypoxia so provide ventilation and oxygenation, correct hypoxia, acidosis, and fluid balance
⁃ Most common rhtyms are bradycardia
⁃ Unstable- = BP 2 yo)
⁃Sinus tacky in children and infants can be as high as 200-220, so a rate of > 220 in infancies or >180 in child should be considered likely for SVT
⁃ Tachydysrthymias can start at 0.5 J/kg
⁃ For bradycarda unresponsive to ventliation/etc can do transcutaneous pacing
⁃ adult patches can be used on children >15kg with negative electrode on anterior chest at V3 and + electrode on back between scapula at T4
⁃ For AED child > 8 yr or >25 kg can have adule AED pads applied, 1-8 years needs peds attenuator, uncertain benefit in infants
⁃ May use adult pads for 1-8 if no pecs around
56
What are the airway and ventilation issues associated with pregnancy?
Airway and vent issues
⁃ Decreased tolerance for hypoxia and apnea
⁃ Upper airway edema
⁃ Difficult mask ventilation (low FRC, elevated diaphragm, raise intra and pressures) - so avoid unless hyoxia present
⁃ Higher Malampatti class more common
⁃ Weight gain and obesity
⁃ increased risk aspiration (increased gastric emptying times, and diminished lower esophageal sphincter tone)
57
What is the pressor of choice for hypotension in pregnancy?
Pressor of choice for hypotension unresponsive to fluids is Ephedrine as epi and dopamine can cause uteroplacental vasoconstriction
58
List the steps of a peri morgen C section?
Peri mortem c section
⁃ Prognosis for intact survival of infant is best if delivery occurs within 5 minutes of maternal arrest
⁃ But still should do no matter how long after arrest
⁃ Ideally have obstetrician and paediatrician present at time of arrest
⁃ May put in catheter if able prior to, but do not delay to do this
⁃ Procedure
⁃ vertical imdline incision from 4-5 cm from xyphoid process to pubic symphysis through abdo wall
⁃ rectus muscles separated with blunt dissection and peritoneum separated vertically as well
⁃ apply retractors
⁃ Do small inferior incision until amniotic fluid is obtained and then extend with scissors by usin free hand to elevate uterus
⁃ Delivery fetus and placenta, and wipe clean uterus with sponge or towel
⁃ Close uterus with locked stitch and close abdo
59
List reasons for a low AG?
Low or negative AG due to
⁃ Increased unmeasured cations: High lithium, proteins such as in MM
⁃ Decreased unmeasured anions: hypo albumin, hypogammaglobumenia
⁃ Measurement confounders: Bromide, high tryglycerides
60
List reasons for elevated AG without acidosis?
High (Decreased unmeasured cations- hypo mg, k, or ca)
| Normal is 12 +-4
61
What is the relationship of HC03 to AG in AGMA?
Wide AG metabolic acidosis will have a delta of 1:1 (elevation in AG should exactly equal the drop in HC03
• This relationship can predict existence of other metabolic disturbances
• For example if HC03 is even lower than predicted by delay AG a concomitant hypercholremic (non AG) acidosis exists
• If HC03 is greater than expected a concomitant met alkalosis exists
• Acute resp conditions do not affect these but chronic ones do
• Triple acid- based disturbance of wide AG met acidosis, met alkalosis, and reap alkalosis occur with sepsis (lactic acidosis) and salicylate poisoning
62
List the normal values in acid/base balance?
pH 7.35
• Pc02 35
• AG 12
63
List the causes of AGMA?
MUDPILES
• M- Methanol (anion is formate)
• U- uraemia (due to protein metabolism and po4 s04 levels)
• DKA/ketoacidosis (diabetic due to B hydroxbutyrate, alcoholic due to ACetoacetate, and starvation- magnitude should be small)
• Probenecid
• Isoniazid
• Lactate- (can be increased due to many causes including CO poisoning and cyanide)
• Ethylene Glycol
• Salicylates
OR think in four broad categories
⁃ Renal failure (uraemia)
⁃ Lactic acidosis (sepsis, shock, liver disease, isoniazid, iron, CO, methemoglobin, metformin, and cyanide)
⁃ Ketoacidosis (DKA, Alcoholic, starvation)
⁃ Ingestions (methanol, ethylene glycol, salicylate)
64
What are the causes of NAGMA?
Causes of Non AG acidosis: (unchanged/hyperchloremic acidosis)
⁃ due to loss of HC03 or failure to excrete H+
```
Those with tendancy to hypo K:
⁃ RTA 1 and 11
⁃ Acetazolamide
⁃ acute diarrhea
⁃ Dilution acidosis
```
```
Those with tendancy to hyper k
⁃ Subsiding DKA
⁃ early uremic
⁃ RTA type iv
⁃ postassium sparing diuretics
```
65
What are the consequences of acidosis?
⁃ decreased cardiac function
⁃ decreased threshold for vfib with increased defib threshold
⁃ decreased hepatic and renal perfusion
⁃ decr BP
⁃ increased plum vacs resistance
⁃ vascular collapse due to decd in catecholamine effects in severe cases
⁃ Catabolic state with decr effects of insulin and inhibition of anaerobic glycolysis
66
What are the indications for bicarb?
⁃ Severe hypobicarbenemia 8 or clinical improvement in shock or dysrryhtmia
⁃ Allow time for effect to be achieved and monitor acid/base closely
67
List the causes of metabolic alkalosis?
Either Chloride sensitive (or insens) - due to gain of HC03 or loss of H
• Hc03 and Cl homeostasis is interconnected
• Chloride sensitive (situations that produce Cl loss reduce cl concentration and extracellular volume- this increases mineral corticoid activity which enhances Na resorption and K/H secretion in distal tubule which in turn enhance bicarb generation) (results in hypokalemic hypochloremic alkalosis that responds to NS- therefore is cl responsive) (urine cl usually 10 mEq/l)
⁃ due to incr mineral corticoid activity as well but it is not ass with hypovolemia
⁃ causes include gittleman and barter syndrome
⁃ Renal artery stenosis
⁃ Cushing syndrome
⁃ Exogenous mineral corticoids- licorice and fludrocortisone
68
List the causes of respiratory acidosis?
• Decreased ventilation leads to incr C02
⁃ head trauma
⁃ chest trauma
⁃ -lung disease
⁃ excess sedation
⁃ obesity (pickwickian syndrome)
• each 1 mm rise in Pc02 equals 1 mmol incr in H+ (or 0.01 decrease in pH)
• Treatment is to improve ventilation (i.e. bronchodilators, etc
69
List the causes of respiratory alkalosis?
```
• alveolar hypervntilation
⁃ CNS tumors
⁃ stroke
⁃ infections
⁃ pregnancy
⁃ hypoxia
⁃ and toxins
⁃ anxiety
⁃ pain
• Chronic resp alkalosis is unique among the acid base disorders in that it's compensation may be complete (reduction in H+ secretion and incr in HC03 secretion)
• Tx is tx underlying cause - Acetazolamide for mountain climbers
```
70
List the different concentrations of 02 for different delivery methods?
What is the expected pa02 based on the %02 inspired?
Each L/min of 02 flow increase the Fi02 by 4%
Therefore if RA is 21% 1l/min equals 25%, 2l/min equals 29%
02 nasal cannula up to 4l/min
simple mask 35-60% at 10-15l/mn
non rebreather 95% at 10-12l/min
Expected Pa02 is equal to 6 X percentage of 02 inspired
Thefore a person with 60% 02 should have pa02 of 360 mm HG
71
What are the key features of a V/Q mismatch?
V/Q mismatch
• Deadspace equal ventilation without perfusion (i.e. PE)
• Perfusion without ventilation equals right to left shunt (i.e. pneumonia)
• Normal A-a gradient is
72
What causes a right shift in the oxygen hemoglobin dissociation curve? (hgb easily let's go)
```
• Right shift (increase in these causes decrease in affinity for 02 by hgb and an increase in pp02): (%sat is on y axis, partial pressure 02 is on x axis)
⁃ increased Pc02
⁃ Acidosis (decr pH)
⁃ incr temp
⁃ increased 2,3 DPG
```
73
What causes a left shift in the 02 hgb dissociation curve? (hgb hangs on to 02 and pp02 decrease at given level)
Left shit (decd in these causes increased affinity with hgb for 02)
⁃ Increased pH
⁃ Decreased pC02
⁃ Decr temp
⁃ Decr 2,3 DPG
⁃ also: carboxyhemoglobin, methemoglobin, abnormal and fetal hemoglobins
74
What is the oxyhemoglobin dissociation curve?
Demonstrates the relationship of p02 in the plasma to the saturation of hemoblogin molecules with 02.
The P50 is the P02 at which hgb is 50% saturated and correlates with 27mHG normally
A pa02 of 60 mmHg normally results in approximately 90% saturation of hgb
75
List the causes of an elevated osmolar gap?
-any difference >10 (Measured - Calculated)
-Normal serum 275-295
• Lab analysis error
• Decreased serum h20 in setting of hyperlipidemia or hyperproteinemia
• Additional substances in serum
o Ethanol
o Methanol
o Isopropyl alcohol
o Ethylene glycol
o Acetone
o Ethyl ether
o Paraldehyde
o Lactate
o Mannitol
76
What are the clinical manifestations and ECG changes of hypokalemia? (K
* Manisfest clinically usually start around 2.5 meq/l
* sx: muscle weakness, paralysis, rhabdo, cardiac dysrrhythmia (PAC, PVC, sinus Brady, av block, vt/vf) Nephrogenic DI Invest: lytes, tTKg
* ECG change: ST depression, t wave flattening, u waves
77
List the tx for hypokalemia?
o Oral 20 mEq q 30-60 minutes until desired result achieved
o IV for severe hypokalemia: 10 meq q 30-60 minutes via well running peripheral IV
o 20 meQ raises serum k by 0.25 mEq/l
o Should not run more than 40 mEq/hr- cardiac monitoring is recommended for infusion rates >20 mEq/h
78
What are the clinical manifestations/ECG changes of hyperkalemia?
• Manisfestation due to disorderd membraine polarization
• ECG changes:
o 6.5-7.5: prlonged pr interval, tall peaked t waves, short QT interval
o 7.5-8.0 p wave flattening, QRS widening
o 10-12 QRS degradation with a sinusoidal pattern
79
List the tx for hyperkalemia?
o Tx:
```
immediate requires continous cardiac monitoring
• Three phases: 1 membrane stabilization
CaCl 5-10 ml (0.5-1 amp) (or Ca gluconate)
• Intracellular shift
-Insulin 10 units with 1 amp D50 IV
-NaHC03
-Salbutamol
• Removal/excretion
- Furosemide
- Resonium
-Hemodialysis
• Avoid Calcium gluconate in dig od as potentiates toxic cardiac effects
```
80
What are the effects of Acidosis/alkalosis on Calcium?
* Alkalosis cuases decrease in ionized calcium
| * Acidosis causes increase in ionized calcium
81
What are the causes/sx/ecg changes of hypocalcemia?
Hypocalcemia:
82
What is the treatment of hypocalcemia?
• Severe: IV tx (can cause vasoconstriction and possible ischemia
o 10 ml of CaCl or 10-30 ml Ca gluconate over 10-20 minutes followed by cont infucsion
o caution in pts taking digitalis because calcium can potentiate digitalis effect/toxicity
o During massive transfusion five Cacl q 4-6 units of blood
o Correct underlying decr Mg
83
What are the causes/sx/tx of hypercalcemia?
• Uncommon, usually sec to malignancy or hyperparathyroidism
• Affects every system
• Sx:
o Malaise, weakness, polyuria, polydipsia, confusion, hallucinations, h/a, arrythmias, htn, anorexia, n/v, constipation, pancreatitis, renal insuff
o ECG changes: QT shortening, depressed st segments, widening of T wave, digitalis sensitivity
84
What is the tx of hypercalcemia?
o Volume repletion
o Dcrease mobilization from bone (pamindronate, zoledronic acid) - bisphosphonate
o Correct underlying disorder
o Replace K if low as this often co exists , also low mg
o **the use of loop diuretics for malignance related hypercalcemia is no longer recommended
85
What are the causes/sx/tx of hypo magnesium?
• Most commonly in Alcoholism, malnutrition, cirrhosis, GI losses
• Sx: irritability – hyperreflexia, positive chvostek or trosseaus as well (see pic)
• ECG changes: prlonged pr and QT, widened QRS, dpression of ST segments, and inversion of T waves
• Tx: hypo k, ca, and p03 are often present with severe low mg so monitor pt carefully
o Mild: oral replacement 6 g/day
o Severe IV or IM up to 8-12 g in first day- first 1.5-2.0 given over 1-2 hours (approx ½ lost in urine)
86
What are the 3 mechanisms of tachyarrhytmias?
1) increased automaticity in a normal or ectopic site
2) reentry in a normal or accessory pathway
- Can occur around anatomically defined circuits result in regular rapid rhythm (AVRT
- Or can occur in disorganized chaotic fashion through myocardial tissue i.e.: afib or vfib
3) after depolarizations causing triggered rhythms
87
What is the tx of bradydysrhythmias?
• Tx only if HR
88
What are the indications and tx for tachydysrhytmias?
* Emergent tx with: shock, altered mental status, anginal chest pain, pulmonary edema
* Tx: Cardioversion or difib
89
What are the complications of defibrillation?
• Complications of defib include: myocardial damage, induce arrythmias, systemic embolization of a thrombus, and hypotension.
90
What is the definition and cause of sinus arrhythmia?
* 1:1 conduction with at least 0.12 s between shortest and longest p-p interval
* sinus node accelerations during inspiration and decelerates during expiration because of changes in vagal tone
* no tx
91
What are the features of a PAC?
• Ectopic p wave appears sooner than expected, has different shape and axis, and may or may not be conducted through the AV node
92
What are the ECG features of AVNRT?
P wave usually buried in QRS and not visible
1:1 conduction
normal QRS complex is normal
93
List the causes of irregular narrow tachycardia?
Afib
MAT
Aflutter with variable conduction
94
List the causes of regular narrow tachycardia?
```
Sinus tachycardia
atrial tachycardia
AVNRT
AVRT
Junctional tachycardia
aflutter
```
95
Causes of regular wide complex tachycardia?
Vtach
antidromic AVRT
SVT with aberrancy
96
Causes of irregular wide complex tachycardia?
Polymorphic vtach
| narrow complex tachycardia with aberrancy
97
What are the key features/ecg changes of WPW?
• WPW syndrome- kent bundle connects atria to ventricles
o Often see tachyarrythmias including paroxysmal reentrant SVT, afib, and aflutter
o Can have rapid ventricular response: therefore any pt with ventricular rate >300 beat/min should raise suspicion of preexcitation syndrome
o Narrow complex tx same as other SVTS
o Wide complex or afib tx with cardio version or procainamide (avoid b blockers, ccb, and adenosine)
ECG changes:
WPW triad: short pr (0.10) , delta wave
Delta wave equivalent can look like pathologic q wave
Wpw with tachy and Afib can be wide and narrow on same ECG- avoid bb/av blockers . Give procainamide.
Afib with prexcitation- shock!
98
What are the main categories of Afib?
* New onset
* Paroxysmal- short bursts, spontaneous cardioversion within 7 days, typically within 24 hrs
* Persistent ->7 days, needs pharm or electrical conversion
* Permanent – contious due to prolonged sx or refractory to cardioversion
99
List the causes of a junctional rhythm? (junctional escape beats are a rate between 40-60 without p wave preceeding it )
o Sustained may be seen with CHF, myocarditis, hypokalemia, dig toxicity
o If accelerated may be due to dig toxicity, acute rheumatic fever or inferior mi
100
List the key features of PVCs?
o P waves do not precede qrs complex
o Retrograde p waves may be present
o Qrs complex is premature and wide
o St segment and t wave are directed opposite major QRS deflection
o Pts with 3 or > are considered to have non sustained vtach and need tx accordingly (usually IV lidocaine)
o Otherwise tx underlying issue
101
List the key features of accelerated junctional rhythm?
```
o Wide and reg QRS complex
o Rate 40-100
o Rus of short duration3-30 bpm
o Begins with fusion beat
o Often in setting of AMI
o Some ass with vtach but not vfib
o If symptomatic may require atrial pacing, otherwise no tx
```
102
List the key features of Vtach?
• Vtach: (most common cause are AMI and ischemic heart disease)
o Wider qrs complex
o Rate >100 bpm (usually 150-200bpm)
o QRS axis usually constant
o Types; non sustained or sustained : monomorphic or polymorphic
o Torsade de pointe- type of polymorphic vtach
• Risk fxs: women, age >65, QT prlonging meds, electrolyte disturbance, genetic predisposition, CAD, CVA
o Vtach can be differentiated from SVT with abberance on the basis of clinical sx, BP, or hR
o tX: pts with polymorphic VT have high risk of degrading to pulseless arrest. Avoid CCB, or b blockers
103
What are some differentiating features of SVT and Vtach ectopic beats (key is if unsure tx all wide complex tachyarrythmias as vtach)
Favors SVT:
-preceeding ectopic P wave
Varying BBB
Varying coupling intervals
```
Favors Vtach:
AV dissociation
Fusion beats
QRS > 0.14 s
post ectopic pause
constant coupling intervals
```
104
What are the ECG Characteristics of a Left anterior fasicular block?
Normal QRS duration
QRS axis between -30 and -90 degrees (Left axis deviation)
R wave in lead 1 > R waves in II or III
Deep S wave leads II, III, and AvF
105
What are the ECG characteristics of a left posterior inferior fascicle block?
Normal QRS
QRS axis between 110 - 180 degrees (right axis devotion)
Small r and deep S waves in lead I
R wave in lead III larger than R wave in lead II
Qr complex in lead III
106
What are the ECG characteristics of a RBB?
Prolonged QRS (> 0.12 s)
RsR prime
wide S wave lateral leads
If
107
What are trifascicular blocks?
RBB + LAFB + first degree AV block
RBB + LPFB + first deg AV block
LBBB + first degree AV block
Alternating RBBB and LBBB
108
What are the features and tx of brugada syndrome
Brugada syndrome
• Genetic condition affecting sodium channels
• Pts present with syncope or sudden death
• ECG: J point elevation in v1-v3 and RBBB- may be normal initially but unmasked with anti arrythmics
• Tx ICD
109
What equals a prolonged QT? What are the causes?
> 470 in men
> 480 in women
QTc in men >0.44 in men and 0.45 sec in women. Ass with torsade. Will be prolonged BBB not pathologic.
Congenital or Acquired:
Drugs- Macrolides- clarith and erythro
Flouroquinolones
Psych meds
Anti emetics
Anti dysrryhthmics
Other causes: Hypokalemia, hypomg, hypocalcemia, hypothermia, cvd, ischemic heart disease, increased ICP
* Hypothermia and Hypocalcemia are due to prolonged ST segment, vs other causes have T wave changes
If stmpomatic Qt- slower rate it will be longer
Tx- overdrive pacing (high rate 100), 2g Mg BC can lt torsadde, replace lytes, tx cause
110
What are 4 pre- terminal rhythms?
• Four rhythms less likely to have survival pre/peri arrest
o PEA
o Idioventricular rhythm (rate
111
What are the Class I antiarrythmics?
o Class 1: (Fast sodium channel blockers)
• 1a: procainamide- has anticholinergic properties, negative iontropic effects, and at high levels can cause hypotension with reflex tachycardia. Can have proarrythmic effects. Can cause ANA antibodies and incre risk of lupus. Hematologic rxns can occur. CI in pts with myasthenia gravis as can cause increased weakness.
• 1b: lidocaine: little effect on peripheral vascular tone or cardiac contractility. Has CNS depression activity and can cause sedation, analgesic, and anticonvulsant effects
• 1C: Propafenone: ie pill in pocket for paroxysmal afib
112
What are the class II anti arrhytmics?
o Class II (beta blockers)
• Cardioselective (B1 receptor specific) include: acebutolol, atenolol, esmolol, and metoprolol: therefore may be better in pts with astma, COPD, DM
• Lose specfifity at high doses
• Labetolol has selective alpha blocking activity and is non cardioselective bb. Good for htn in AMI and in pts with with acute neurologic emergencies as it has little effect on cerebral erfusion pressure or ICP
• Decrease morb and mort in AMI (metoprolol and atenolol) and in CHF (bisoprolol, carvedilol, extended release metoprolol)
• Sotalol is effectie agent for suppression of life threatening ventricular arrythmias refractory to other antiarrhytmic drugs. Can also suppress SVT and afib. Can have proarrythmic effects.
113
What are the class III antiarrythmics?
o Class III (potassium channel inhibition)
• Amiodarone (has traits of class 1, ii, and iv)
• Impairs SA node function, AV conduction, etc.
• Used as 1st line in ACLS vfib and vtach pulseless, and used in SVT with impaired EF
• Short term SE: hypotension and bradycardia
• Long term effects: thyroid disorders, pulmonary fibrosis, skin discoloration, hepatic dysfunction, corneal infiltrates
• CI in pts with shellfish or iodine allergy d/t it contains iodine
• Coadmin with simvastatin is ass with incr risk rhabdo
114
What are the class IV antiarryhthmics?
o Class IV: (CCB) _Non dihyropuridine verapamil or diltiazem
• Diltiazem: minimal systemic vasodilation, preferentially dilates coronoary vasculature which makes it good for stable angina
• Use in afib or SVT to slow response, avoid in wide complex arrythmia suggesting accessory tract, angina,
• Verapamil: as effective as adenosine and diltiazem in termination narrow comples PSVT and controlling rate in vfib ro flutter. Also used in htn, angina.
115
List some "other" antiarrythmics
Digoxin-+ ionotrope, negative chrontrop, slow AV conduction velocity
• Inhibits na/k/atpase pump, therefore more na in cell and more k out of cell
• Aboid in WPW as may enhace pathways
• Half life 1.5-1.8 days, or up to 4-6 days in pts with renal impairment
• Uses: CHF (decr hosp not mortality), control of ventricular response in afib/flutter,
• Drug levels may incr with : amiodarone, verapamil, nifedipine, diltiazem, erythromycin, tetracycline
• Decr with: maxeran, cholestyramine, pcn, fibre
Adenosine- works at AV node. Half life 10 seconds. May induce bronchoconstriction in astmastics- this reponds to basic bronchodilator therapy
Mgs04 – use in torsade, or refractory vfib/tach. Also seen used in cardiac arrest, dig toxcitiy, pre eclampsia, acute asthma exacerbation
Atropine- blocks parasymp activity
116
List the causes of bradycardia?
```
Ddx: DIES (SS)
Drugs
Ischemia
Electrolytes
Sick sinus syndrome
```
117
List the basic points of cardiac pacing?
```
Pacing: VVI- ventricle only
DDD: atria and ventricles
Pacing:
1. Afib with slow VR- VVI
2. SSS- DDD
3. 3rd degree AV block-
4. transvenous ER pacing- VVI
```
118
How much TBW are adults? (split)
```
TBW 60%
Out of 100%
ICF 67%
ECF 33%
Interstial 25%
Other
```
119
What infusion rate fits with what gauge IV cath?
18 g- 120-180 ml/min
16 200-250
14 : 250-300
Central 400-500
120
What does low SCv02 indicate?
Global hypo perfusion leading to high tissue 02 supply - demand balance.
121
List the features of serum sickness?
- Caused by drug reaction
- usually 1-2 weeks after
- generalized malaise, arthralgias, arthritis, pruritus, urtaria, fever, adenopathy, hepatosplenomegaly
122
What are the causes of T wave inversion?
T waves:
Inversion DDx: ischemia, heart strain, intracranial pathology, Wellen's, persistent juvenile T wave pattern, Takyosubos
Persistent juvenile t wave pattern: inversion in leads v1-v3
More common in women
Wellen's syndrome: type of ACS, LAD T wave inversion (Deep symmetric T Inversions V1-V4)
prognosis is poor without PCI
Wellen's sign is just ECG findings and no clinical findings
ECG findings actually normalized with ischemia
123
What are the causes of Left axis deviation and Right axis deviation?
- Left axis deviation- causes: LAFB, LBBB, Inferior MI (inferior q waves), LVH, Ventricular ectopy, paced beats, WPW
- Right axis deviation: LPFB, lateral MI, RVH, acute or chronic lung disease, ventricular ectopy, hyperkalemia, Na channel OD, normal slender young adults, AvR and AvL lead misplacement
124
What are the ECG findings of LVH/RVH?
LVH- > 35 s in V1 and r in V5 or V6 Or AVL > 11, left axis deviation, strain (widened QRS T angle)
RVH- r/s ratio >1 in V1,r axis deviation, right atria peaked p in inferior leads, prominent S wave in V5 V6, RV strain- ST changes in V1 and inferior leads, incomplete RBB
-if you have biventricular hypertrophy findings can cancel out
125
What is the Ddx for wide WRS?
na channel blockade, hyper K, acidosis, Paced, block, WPW
126
What is the differential for Tall R wave > S in lead V1?
```
Ddx: RBBB
RVH
Posterior infarct (equivalent to posterior q waves)
Wpw (delta wave equivalent)
vtach or pvc
pediatric at some ages normal
```
127
What are the ECG findings of ischemia?
Ischemia: (st changes with t wave abn)
-St depression >1mm (use Tp as baseline not pr) (except Avr elevation) -+ t wave changes. Depression is usually downslope or horizontal (weaker correlation with ups loping happy face)
symmetrical t wave inversion is sign of LAD stenosis and is seen after clinical episode of ischemia
-criteria for emergency revascularization: sx up to 12 hrs, persistent sx up to 24 hrs, ST elev in 2 lead after nth
128
What are the ECF findings associated with Myocardial injury?
Myocardial injury:
St elevation: with transmural ischemia and MI. V1-v2 anteroseptal. V3-4 anteroapical. V5-6 anterolateral, 1-avl lateral, ii iii avf inferior.
Need st elevation in 2 contiguous leads. In v2- V3 need 2 mm (0.2mV) in all others you need 1 mm (2.5 mm in men II, R waves in V2-V3, V1-V3 St depression
- PAILS for reciprocal changes:
- Q wave more specific> reverese R wave progression> poor R wave progression
129
What are the ECG findings of LV aneurysm?
Persistent st elevation usually in leads that showed MI (suspicion of aneurysm is based on prolonged pattern)
Often coexistent evidence of Chronic MI such as q wave or inverted t wave or reciprocal St depression.
130
What are ECG findings of BER?
BER- not often found in AVR or V1, more prominent in precordial leads.
Absence of reciprocal changes found in ischemia
Absence of PR depression as in pericarditis.
131
Ecg findings hyperkalemia?
Levels correlate poorly with ECG findings
Mild-mod: decr p waves and peaked t waves
Sever- widening of PR Interval and QRS, high grade AV blocks, fasicular blocks, BBB
Sinusoidal is most severe
132
ECG findings hypothermia?
Hypothermia: Osborn j waves (positive deflection in terminal part of QRS), can also have QRS and QT prolongation
133
ECG findings of PE?
S1Q3T3 present in 10-15% of PEs
Often will have T wave inversion in inferior and anteroseptal leads (right precordial leads)- this is most specific
R axis deviation also commonly seen
134
ECG findings of Wellen's syndrome?
Wellens sign: biphasic T or t wave inversion mid precordial leads (sign of severe proximal LAD stenosis)
135
ECG findings of stroke?
```
Stroke:
Often transient abnormalities
Inverted T waves
ST segment changes
AV blocks
Tachydysrhythmias
```
136
List the key features of shock management?
Optimization of management :
1) Preload
2) Rate
3) Rythm
4) Contractility
5) Afterload
6) Content (of blood) (CO= (1.34xhgbxSa02) + 0.003 x PaO2) therefore optimize CO, hgb, sats
```
(I'd and treat cause
Optimize preload and fluids
Improve vascular tone with pressor
Improve contractilty with vasodilators /inotropes
Improve 02 carrying capacity )
```
If calcium low give calcium chloride may help with cardiac function and vessel squeeze
137
When does the biphasic rxn of anaphylaxis occur?
Peaks in 4-8 hrs
138
What is an anaphylactoid reaction?
Anaphylactoid reaction- autoimmune reaction, no previous sensitization
Vitamin K, Scromboid, protamine, IV contrast, NAC
Tx identically to anaphylaxis
139
What are the features of Angioedema?
Angioedema:
· Mostly second to ACE i
· Mgmnt supportive
· Airway control- ketamine, topical lidocaine, nebulized epi, possibly glycopyrrolate, double set up
· Can try anaphylaxis approach but little benefit
· Mild edema, observe and dc when swelling down- won’t have rebound unless take another ace
· Severe- admit
If secondary to C1 esterase deficiency- usually have own drugs
140
What are some "other" drug reactions?
Allergic drug reactions;
· Penicillin responsible for majority of true anaphylaxis reactions
· Serum sickness can occur – ie with sulpha containing drugs (septra, thiazides, lasix)
o First or second week after stopping drug, generalized malaise, arthralgias, arthritis, pruritis, uritacarial eruptions, fever, adenopathy, hepatosplenomegaly,
· Cytotoxic reactions- such as pcn induced hemolytic anemia
· Skin eruptions- erythema, pruritis, urticaria, angioedema, erythema multiforme, and photosensitivity, SJS, TENS
· Pulmonary complications such as bronchospasm and airways obstruction
