Random Flashcards
Push Dose Epinephrine:
- How to create
- Take 10mL syringe of saline with only 9mL of saline
- draw 1mL of cardiac epi (1:10,000 | 0.1mg/mL)
- This creates 10 mcg/mL
Push Dose Epinephrine:
- Onset
- Duration
- Dose
Onset: 1 minute
Duration: 5-10 minutes
Dose: 0.5-2mL (5-20mcg) q2-5 minutes
Convulsive Status Epilepticus:
1st Line Treatment
IM Versed (0.2-0.5mg/kg, max 10mg), single dose IV Ativan (0.1mg/kg, max 4mg), repeat x1 IV Valium (0.15-0.2mg/kg, max 10mg), repeat x1
Convulsive Status Epilepticus:
2nd Line Treatment
IV Fosphenytoin 20mg PE/kg, max 1500 mg PE / dose IV Valproate (40mg/kg, max 3000mg) IV Keppra (60mg/kg, max 4500mg) IV phenobarbital (15mg/kg)
Convulsive Status Epilepticus:
3rd Line Treatment
Repeat Second Line treatments
Anesthetic dosing thiopental, versed, pentobarb, propofol
Coronary Vessels to EKG Lead:
- LAD
- LCx
- RCA
Coronary Vessels to EKG Lead:
- LAD –> V1-V4
- LCx –> V5-V6, I, aVL
- RCA –> II, III, aVF
Coronary Vessels to EKG Lead:
- V1-V4
- V5-V6, I, aVL
- II, III, aVF
Coronary Vessels –> EKG Lead:
- V1-V4 –> LAD
- V5-V6, I, aVL –> LCx
- II, III, aVF –> RCA
Axis: Right on EKG
QRS down in I
QRS up in aVF
Axis: Left on EKG
QRS up in I
QRS down in aVF
If on AC, what’s the management for epistaxis?
If on AC, do RESORBABLE packing for epistaxis as per American Academy of Otolaryngology Jan 2020 guidelines.
New CHF. Cause most likely?
Valvular disease.
CHF + Prosthetic heart valve. Cause?
Valve thrombosis.
Seizure - physical exam findings that’s most specific.
Lateral tongue bite is 100% specific for seizure. But only 25% sensitive. (Using on population with transient LOC / syncope)
Tip of tongue and lips biting are more likely psychogenic than real seizure.
How to differentiate *cardiogenic pulmonary edema* from *noncardiogenic pulmonary edema* (pneumonia, fibrosis, TB, etc.)
Cardiogenic pulmonary edema: thin/regular pleural line
Non-cardiogenic pulmonary edema: thickened, irregular pleural line.
Myocardial injury
troponin I elevation; acute injury if there’s a rise/fall.
Myocardial infarction
acute myocardial injury + mycocardial ischemia signs (symptoms of ischemia, new EKG changes, pathologic Q-waves, imaging abnormality, finding coronary thrombus)
Cardiac necrosis progresses in what direction?
sub-endocardial (inside) –> sub-epicardial (outside)
Importance of Type II MI
- higher frequency of women > men
- higher mortality (short + long term) than Type I MI
(Obvious stuff): 3 reasons for
Type II elevation
Inadequate supply
Inc demand
can’t get the supply to the demand
Frequency of ST-elevation in Type II MI
3-24%
“Stable” troponin elevation definition
<20% variation of troponin values
Recurrent MI
Repeat MI AFTER 28 days
Re-infarction MI
Repeat MI BEFORE 28 days
Frequency of post-operative cardiac injury
35% of patients have elevation of troponin
17% have an elevation and rising pattern suggesting evolving myocardial injury.
Takotsubo’s syndrome: mortality
Inpatient mortality is same as STEMI (4-5%; from cardiogenic shock, ventricular rupture, malignant arrhthmias)
% of STEMI that is actually Takotsubo’s syndrome
1-2% of suspected STEMI; 90% are post-menopausal women
EKG findings in Takotsubo’s syndrome
STE: 44%
STD: <10%
TWI: 12-24 hours after, will develop deep, symmetric TWI and QTc-prolongation
Takotsubo’s resolves in what percent
85-90% have complete resolution.
Takotsubo’s vs Acute MI: 2 most important features for differentiation
QTC > 500 in acute phase for TTS
and
normalization of LV funciton after 2-4 weeks for TTS
Which is more important? Absolute changes in assay or relative changes in measurement
absolute changes are the most important.
Use a lower cut-off for women, higher for men.
Don’t use an age-related cutoff
This diffuse pattern is suggestive of
Left main disease
or
Multivessel disease
STD > 1mm in 6 leads
+/- STE in AVR or V1
Hemodynamic compromise
STD > 1mm in 6 leads
+/- STE in AVR or V1
Hemodynamic compromise
This diffuse pattern is suggestive of
Left main disease
or
Multivessel disease
EKG manifestations suggesting Acute MI (in the absence of LVH/BBB)
STE in 2 contiguous leads; >1mm in all leads except V2-V3. (use >2mm in male>40; >2.5mm in male <40; >1.5 in all females)
STD: new horizontal or down-slopping STD > 0.5mm in 2 continguous leads
or
TWI: >1mm in 2 continuous leads with prominent R-wave or R/S ratio > 1
Absence of STE in V1-V6
Tall, prominent, symmetric T-waves V1-V6
Upsloping STD > 1 mm V1-V6
STE > 1 mm in aVR
Symmetric, deep (>2 mm) TWI in V3-V4
Signs of LAD Occlusion
Signs of LAD Occlusion
Absence of STE in V1-V6
Tall, prominent, symmetric T-waves V1-V6
Upsloping STD > 1 mm V1-V6
STE > 1 mm in aVR
Symmetric, deep (>2 mm) TWI in V3-V4
STE in aVR > 1 mm
Anterior (LAD) or inferior STEMI
Sign of increased 30 day mortality in acute MI
Isolated STD > 0.5 mm in V1-V3 could be a sign of ____
Left circumflex occlusion
Left circumflex occlusion could be hinted at on an EKG by ___
Isolated STD > 0.5 mm in V1-V3
Locations for posterior EKG leads (V7-V9)
V7: left posterior axillary line
V8: left mid-scapular line
V9: left paraspina border
Cutpoint for STE in posterior leads
For V7-V9 use 0.5 mm STE
V7-V9 with >0.5 mm STE or
STD > 0.5 mm in V1-V3
Left circumflex occlusion or infero-basal ischemia / posterior MI
New name for posterior MI
Old name for infero-basal MI
Old name for infero-basal MI
New name for posterior MI
Left circumflex occlusion or infero-basal ischemia / posterior MI
EKG findings
V7-V9 with >0.5 mm STE or
STD > 0.5 mm in V1-V3
EKG changes associated with PRIOR MI
- Any Q-waves in V2-V3 > 0.02s or QS complex V2-V3
- [Q-wave > 0.03s and >1mm deep] or [QS complex]
in [Leads I, II, aVL, aVF, V4-V6] OR [in any 2 contiguous leads] - R-wave > 0.04s in V1-V2 and R/S>1 with a concordant positive T-wave in absence of conduction defect.
QS complex is normal in which lead
V1
LBBB Criteria
QRS duration of > 120 ms
Dominant S wave in V1
Broad monophasic R wave in lateral leads (I, aVL, V5-V6)
Absence of Q waves in lateral leads (I, V5-V6; small Q waves are still allowed in aVL)
Prolonged R wave peak time > 60ms in left precordial leads (V5-6)
Appropriate discordance on EKG
The ST segments and T waves always go in the *opposite* direction to the main vector of the QRS complex
Inappropriate concordance on EKG
J-point and ST-segment elevation in positive leads and J-point and ST-segment depression in negative leads
Normal Axis = QRS axis between
-30° and +90°
Left Axis Deviation = QRS axis
less than -30
Right Axis Deviation = QRS axis
greater than +90°
Extreme Axis Deviation = QRS axis between
-90° and 180° (AKA “Northwest Axis”)
Axis: Normal on EKG
QRS up in I
QRS up in aVF
Axis: extreme axis deviation on EKG
QRS down in I
QRS down in aVF
ECG Criteria for Left Anterior Fascicular Block (LAFB)
Left axis deviation
qR complexes in leads I and aVL
rS complexes in leads II, III, aVF
QRS duration normal or slightly prolonged (80-110 ms)
Prolonged R wave peak time in aVL > 45 ms
Increased QRS voltage in the limb leads
Features consistent with sodium-channel blockade
Interventricular conduction delay — QRS > 100 ms in lead II
Right axis deviation of the terminal QRS:
- Terminal R wave height > 3 mm in aVR
- R/S ratio > 0.7 in aVR
TCA Overdose: Usually sinus tachycardia 2/2 muscarinic (M1) receptor blockade.
TTP
Classic Pentad
Fever
Thrombocytopenia
Anemia (microangiopathic, hemolytic)
Neurologic findings (confusion, difficulty speakin,g headaches, vomiting, etc)
AKI
Hip dislocation
Which nerve damaged?
Loss of sensation in posterior leg and foot
Loss of dorsiflexion or plantarflexion
Loss of deep tendon reflex at ankle
Sciatic nerve injury
(occurs in 10% of hip dislocations)
Hip dislocation
Which nerve damaged?
Loss of sensation over thigh
Weakness of quadriceps
Loss of DTR at knee
Femoral nerve injury
Hip dislocation
Which artery is damaged?
Hematoma
Loss of pulses
Pallor
Femoral artery injury
Kanavel’s criteria
- Tenderness of flexor tendon
- Symmetrical / fusiform swelling of finger
- Flexed posture of finger
- Pain with passive extension
1st line oral medication
Raynaud’s phenomenon
nifedipine or amlodipine
(long-acting dihydropyridine CCB)
Fox’s sign
eccchymosis of upper lateral thigh; inferior to the inguinal ligament
The ecchymosis is parallel with, but distal to the inguinal ligament with a well demarcated upper border defined by attachment of the membranous layer of the superficial fascia (Scarpa’s fascia). Most often occurs in patients with retroperitoneal bleeding, usually due to acute haemorrhagic pancreatitis.
Stabler’s sign
ecchymosis over the inguinal ligament.
in neonates, think neonatal adrenal hemorrhage
Bryant’s sign
ecchymosis of the scrotum
Think retroperitoneal bleeding
Gold standard to dx
Placental Abruption
Tococardiography
What is this?
Epsilon wave
Altered Mental Status (AMS) Etiology
AEIOU TIPS Mnemonic
Alcohol, acidosis
Endocrine, epilepsy, electrolytes, encephalopathy
Infection
Opiates, overdose
Uremia
Trauma
Insulin
Poisoning, psychosis, pharmacology
Stroke, seizure, syncope
