FINAL Flashcards
3 WAYS TO CALCULATE HR FROM EKG
1) number of QRS complexes in 6 second strip x 10
2) 300 / 150 / 100 / 75 / 60 / 50
3) 1500 / number of small squares between R waves
WHAT ARE THE LIMB LEADS
WHAT ARE THE PRECORDIAL LEADS
LIMB LEADS = I II III AVR AVL AVF
PRECORDIAL LEADS = V1 V2 V3 V4 V5 V6
WHAT IS THE J POINT ON EKG
Transition from S wave to T wave
- changes from vertical to horizontal
LIMB LEAD PLACEMENTS
AVR = right arm
AVL = left arm
AVF = left leg
I = AVR (-) to AVL (+)
II = AVR (-) to AVF (+)
III = AVL (-) to AVF (+)
SEPTAL LEADS
ANTERIOR LEADS
INFERIOR LEADS
LATERAL LEADS
SEPTAL LEADS = V1 V2
ANTERIOR LEADS = V3 V4
INFERIOR LEADS = II III AVF
LATERAL LEADS = I AVL V5 V6
NORMAL DURATIONS OF EACH EKG SECTION
P WAVES
PR INTERVAL
QRS COMPLEX
QT INTERVAL
P WAVES < 0.12 (3 boxes)
PR INTERVAL = 0.12 - 0.20 (3-5 boxes)
QRS COMPLEX = 0.04 - 0.12 (1-3 boxes)
QT INTERVAL = 0.36 - 0.44 (9 - 11 boxes)
WHAT DOES THE P WAVE INDICATE?
WHAT DOES THE Q WAVE INDICATE?
WHAT DOES THE QRS COMPLEX INDICATE?
WHAT DOES THE T WAVE INDICATE?
P WAVE = atrial depolarization
Q WAVE = interventricular septum depolarization
QRS COMPLEX = ventricular depolarization (atrial repolarization is hidden in there)
T WAVE = ventricular repolarization
RBBB CRITERIA
o QRS > 0.12
o rsR in leads V1 - V3 - “bunny ears”
LBBB CRITERIA
o QRS > 0.12
o deep S wave in V1/V2
o broad R waves in I, AVL, V5, V6
o absent Q wave in I, V5, V6; may have a slight or narrow one in AVL
o inverted T waves (or going opposite direction of QRS)
if Q wave is >/= 1/3 the height of R wave = indicative of
transmural MI
U WAVE
can be normal or pathologic
prominent U waves = hypokalemia
repolarization of purkinje fibers
RATES FOR
- SINUS RHYTHM
- BRADYCARDIA
- TACHYCARDIA
- SVT
sinus rhythm = 60-100
bradycardia < 60
tachycardia > 100
SVT = 150-200
significance of a prolonged PR interval
caused by a blocking of the conduction from the SA node to the AV node
1st degree AV block
prolonged PR interval (> 0.20)
PR interval should be 0.12 - 0.20 (3-5 boxes)
2nd degree AV blocks (2 of them)
o Type I (Wenckebach) = longer longer longer drop = PR interval progressively gets longer, until QRS complexes drops (doesn’t show up)
o Type II (Mobitz II) = PR interval is fixed, but some QRS complexes don’t show up (if some p’s don’t get through)
IVCD vs RBBB/LBBB
Intraventricular Conduction Delay = QRS complex > 0.12, but other criteria for bundle branch blocks not met
AXIS = look at leads ________
axis should never both be _________
If I is positive and AVF is positive =
If I is positive and AVF is negative =
If I is negative and AVF is positive =
I / II / AVF (supposed to look at I & AVF, but can compare I to II also)
should never both be negative = indeterminate
If both leads are positive (upwards) = normal
If I is positive and AVF is positive = normal
If I is positive and AVF is negative = LAD (left axis deviation)
If I is negative and AVF is positive = RAD (right axis deviation)
P WAVE MORPHOLOGY
BIPHASIC vs P PULMONALE vs P MITRALE
mostly look at lead II for R/L atrial enlargement
Evaluate leads II, III, AVF and V1 for atrial deformities
may be biphasic P waves in V1 = normal
normal = < 2.5mm in limb leads & < 1.5mm in precordial leads
mostly look at lead II to find this
P PULMONALE = Right atrial enlargement = right atrial depolarization lasts longer than left = will see a tall P wave in lead II and a biphasic wave with increased height of the initial positive p wave deflection (>1.5mm)
P MITRALE = Left atrial enlargement = lasts longer (not taller, but wider), > 0.12s. Notch in lead II, and increased depth of second negative p wave deflection in V1
RVH (right ventricular hypertrophy)
look at the precordial leads (V1 - V6)
tall R waves in V1 / V2 (get smaller as it goes to V5/V6)
deep S waves in V5 / V6 (start smaller in V1/V2)
***RVH should accompany RAD (right axis deviation)
LVH (left ventricular hypertrophy)
look at precordial leads (V1 - V6)
deep S waves in V1 / V2
tall R waves in V5 / V6
Amplitude of S wave in V1 + R wave in V5 = > 35mm
may also have inverted / asymmetrical / depressed T waves in lateral leads
Hypokalemia on EKG
Hyperkalemia on EKG
Hypokalemia = U waves
Hyperkalemia = peaked T waves (> 5mm in II/III) (> 10mm in V3/V4); can also have flattened P waves
Hypocalcemia on EKG
Hypercalcemia on EKG
Hypocalcemia = prolonged QT interval (can also seen with hypomagnesemia & hypokalemia & hypothermia)
Hypercalcemia = shortened QT interval; may see J wave
Hypothermia on EKG
J waves
prolonged PR, QRS, and QT
PE on EKG
S1Q3T3
***Most common finding = Sinus Tachycardia
S wave in lead I
Q wave in lead III
inverted T waves in lead III
transient RBBB`
ventricular strain
- associated with ventricular hypertrophy
- strain results in depression of the ST segment
RV strain = V1
LV strain = V5, V6
THERE ARE MANY MARKERS OF ISCHEMIA
- Pathologic Q waves
- Poor R wave progression
- ST segment elevation or depression (make sure when looking at ST segment to look at where T wave is starting to tell if ST is elevated or depressed)
- T wave abnormalities (flattening, peaking, inverted)
Q waves
small Q waves = insignificant
can signify hypokalemia
pathologic Q waves = indicate necrosis or scarring
Criteria for abnormal/pathologic Q waves
> 1 mm wide OR
> 1/3 the height of QRS complex
Q waves = seen in STEMI, not NSTEMI
R wave progression
QRS complex should start out negative in V1 and end positive in V6
R wave should be tallest in V3/V4 = where the transition should occur
if the transition occurs in V1/V2 (early) = can be indicate of a previous posterior wall MI
Causes of poor R wave progression
- anterior MI (old if no other signs of ischemia, new if other signs of ischemia)
- lead misplacement (frequently in obese women)
- LBBB or Left anterior fascicular block
- LVH
- WPW
- Dextrocardia
- Tension pneumothorax with mediastinal shift
- CHD
EKG CRITERIA FOR STEMI
ST elevation at J point in 2 contiguous leads of >/= 1mm
ST elevation of >/= 2mm in men in leads V2 / V3
ST elevation of >/= 1.5mm in women in leads V2 / V3
ischemia = ST depression, peaked T waves, T wave inversion
Infarction = ST elevation & appearance of Q waves
Fibrosis = ST & T waves return to normal, Q waves may persist
NSTEMI EKG
ST depression & T wave inversion = infarction or ischemia
After injury = ST returns to normal, but inverted T wave persists
NSTEMI = could see ST depression or T wave inversion or both
infarction vs ischemia
Myocardial infarction (MI) denotes the death of cardiac myocytes due to extended ischemia.
ischemia –> infarction –> fibrosis
Hypomagnesemia EKG
prolonged QT
Torsades de pointes (give magnesium sulfate; reversed with calcium gluconate)
cranial nerves for eye muscles
CN IV = superior oblique
CN VI = lateral rectus
CN III = superior rectus, inferior rectus, medial rectus and inferior oblique
SMALL BOWEL OBSTRUCTION
MC cause = post-surgical adhesions
- other causes = incarcerated hernias, malignancy, IBD, Intussusception, volvulus
SIGNS/SYMPTOMS (cavo)
- cramping / abdominal pain
- abdominal distention
- vomiting
- obstipation (lack of stool / flatus)
PHYSICAL EXAM
- abdominal distention
- high pitched tinkling sounds (hyperactive bs with early obstruction)
- hypoactive bs with late obstruction
- may have tachycardia, peritoneal signs (guarding, etc)
- perform DRE to check for masses / blood
DIAGNOSTICS
- can do labs (BUN / CR elevated due to dehydration), serum LDH (due to lack of perfusion/oxygen to tissues –> breakdown)
IMAGING
- abdominal XRAY (flat & standing to check for perforation) - see dilated bowel loops & air-fluid line = initial test
- can do CT for better view of site / severity
TREATMENT
- IV fluids (NS)
- antiemetics (Zofran / Phenergan)
- analgesic (morphine)
- stool softeners (Colace)
- bowel decompression via NG tube
- may need abx / surgery
cranial nerves for eye muscles
CN IV = superior oblique
CN VI = lateral rectus
CN III = superior rectus, inferior rectus, medial rectus and inferior oblique
AMBLYOPIA
“lazy eye”
DECREASED VISION in one or both eyes due to abnormal development of vision in infancy or childhood.
Vision loss occurs because nerve pathways between the brain and the eye aren’t properly stimulated.
May not have obvious problem with the eye.
Brain favors one eye.
Brain is trained to ignore one eye (worse vision) and focus on the vision of the better eye - loses nerve connection with that other eye
STRABISMUS
Eye misalignment caused by an imbalance in the muscles holding the eyeball, or neuro involvement.
esotropia (in), exotropia (out), hypotropia (down), and hypertropia (up)
Can cause Amblyopia
DIAGNOSIS
- Hirschberg corneal light reflex testing
- cover-uncover test to determine the angle of strabismus, cover test, convergence testing
MANAGEMENT
- Patch therapy* - normal eye covered to stimulate & strengthen the affected eye
- corrective surgery if severe or unresponsive to conservative therapy
**If not treated before 2 years old, amblyopia may occur = where have decreased visual acuity that is not correctable by refractive means
TERMS
ANISOMETROPIA
APHAKIA
ASTHENOPIA
CONVERGENCE
DIPLOPIA
ACCOMMODATION
ANISOMETROPIA = one eye has much poorer vision than the other (aniso - uneven or unequal)
APHAKIA = no lens in the eye (congenital or due to trauma/ infection)
ASTHENOPIA = eye strain
CONVERGENCE = eye turned inwards so that they are aimed towards a near object
DIPLOPIA = blurry vision
ACCOMMODATION = ability to switch from near to far or far to near vision
EXOPHTHALMOS
COMMONLY SEEN WITH
bulging of the eye out
commonly seen in Grave’s disease
CYCLOPLEGIA
Paralysis of the ciliary muscle of the eye, resulting in a loss of accommodation (inability to switch from near to far or far to near objects) or a consistently dilated pupil
HEMIANOPSIA
a blindness or reduction in vision in one half of the visual field due to damage of the optic pathways in the brain.
decreased vision or blindness in half the visual field. can occur in one eye or both eyes
homonymous hemianopsia = both right sides or both left sides of visual fields are decreased/blind
(due to damage of optic tract on one side); if damage on the optic tract on the left side = goes to the left side of both eyes = then lose vision on right side of both eyes
if damage to optic tract on the right side = goes to the right side of both eyes = then lose vision in the left side of both eyes
if damage at the optic chiasm (where cross-over occurs) = goes to the inner vision of both eyes = then lose vision on lateral sides of both eyes = bitemporal hemianopsia
if damage at the optic nerve = supplies both the inner and outer vision of the same eye –> monocular blindness
HYPHEMA
blood in the anterior chamber
usually from trauma. Can sometimes fill up the anterior chamber so much that it impedes vision
HYPOPYON
Presence of leukocytes in the anterior chamber (white crescent instead of red crescent from hyphema - blood)
PAPILLEDEMA
Swelling of the optic disc caused by increased Intracranial Pressure
ECTROPION
EYELID & LASHES TURN OUTWARD
- due to relaxation of the orbicularis oculi muscle
- MC seen in elderly (tends to be bilateral) but can be congenital, scar tissue, infectious, or with CN 7 palsy
SIGNS/SYMPTOMS
- irritation
- ocular dryness
- tearing
- sagging of the eyelid
- increased sensitivity
TREATMENT
- surgical correction if needed
- lubricating eyedrops for symptom relief (artificial tears)
ENTROPION
EYELID & LASHES TURNED INWARD
- may be caused by spasms of the orbicularis oculi muscle
- MC seen in the elderly
SIGNS/SYMPTOMS
- eyelashes may cause corneal abrasion / ulcerations
- erythema
- tearing
- increased sensitivity
TREATMENT
- surgical correction if needed
- lubricating eye drops for symptom relief
DACROCYSTITIS
INFECTION OF THE LACRIMAL SAC
MC Etiology = STAPH AUREUS
others: GABHS, Staph epidermidis, H. flu, strep pneumo
SIGNS / SYMPTOMS
- **Tearing
- tenderness
- edema
- **Redness to medial canthal of lower lid (+/- purulent)
TREATMENT o Acute = Antibiotics, warm compresses - Clindamycin - Augmentin - Vancomycin + Ceftriaxone
o Chronic = Dacryocystorhinostomy
- can get infected –> cellulitis, cause sinusitis or brain infection…send to ophthalmologist if not getting better
BLEPHARITIS
INFLAMMATION OF THE LID MARGINS
- common in patients with down syndrome & eczema
ETIOLOGY
o Anterior = less common; involves the skin and base of eyelashes
- 1) infectious (STAPH AUREUS or staph epidermidis)
- 2) SEBORRHEIC
o Posterior = more common; Meibomian gland dysfunction
- associated with rosacea & allergic dermatitis
SIGNS/SYMPTOMS
- eye irritation / itching
- ***crusting, scaling, red rimming of the eyelid & eyelash flaking
- burning, erythema
- may or may not also have entropion or ectropion (especially with posterior blepharitis)
inflammation involving the lid margin
characterized by: erythema, crusting, & scaling
Often associated with systemic conditions such as rosacea & seborrheic dermatitis
RISK FACTORS = people who have a tendency towards oily skin, dandruff, and dry eyes
CLINICAL PRESENTATION = burning, watering, crusting of lashes and medial canthus, scaling, erythematous eyelids. Usually a chronic course with intermittent exacerbations
PHYSICAL EXAM = eyelids show erythema & crusting of lashes & lid margins. May be some injection of conjunctiva
TREATMENT = systematic/long term commitment to eyelid margin hygiene! = application of HEAT (warm compresses) - promotes evacuation/cleansing of secretory passages. Mechanical WASHING of eyelid margin - baby shampoo with warm water/gentle washing of eyelid margins, NOT just the skin of the lids.
ANTIBIOTIC SOLUTION OR OINTMENT applied to eyelid margin (azithro solution, erythromycin ointment) during exacerbations. In some stubborn cases = can be used nightly for prophylaxis
for posterior blepharitis = eyelid hygiene, regular massage / expression of Meibomian gland
- can give systemic abx in severe/unresponsive cases = Tetracyclines or Azithromycin
Patients should be educated/understand that this is a chronic condition with intermittent exacerbations
