I know the random fact throwing thread is very popular on here and I wanted to start a PCCN/CCRN edition to help those who are planning on taking the PCCN/CCRN study
Hyperacute (tall) T waves that are localized in the absence
of hyperkalemia could be an early sign of ischemia.
Ischemia: ST depression and/or T wave inversion in >/ 2 contiguous leads
Injury: ST-segment elevation >/ 1mm in >/ 2 contiguous limb or >/ 2mm in precordial leads
Infarction: pathological Q waves (>0.04sec wide, >25% amplitude of the R wave)
NSTEMI: subendocardial damage (doesn't go all the way through). Normal R wave progression, ST-segment depression, normal Q.
STEMI: transmural damage, loss of R wave progression, ST elevation with abnormal Q wave
Anterior MI (LCD, LAD)
- leads V3, V4
- tachycardia, pulmonary edema (dyspnea, orthopnea)
erior MI (RCA)
- leads II, III, aVF
(these leads are also at the bottom or inferior part on a printed 12-lead EKG which helps me remember)
- bradycardia, hypotension
- **do a right-sided EKG because there is a chance a patient with an inferior MI will have a RVMI.
ateral MI (LCA, Circumflex)
- Leads V5, V6, I, aVL
- ventricular dysrhythmias, heart failure, AV blocks
- Leads V1, V2
- Tachycardia, atrial fibrillation, septal rupture
Posterior MI (LCA, Circumflex, RCA)
- Pathological R waves in V1-V4
- ST depression in V1, V2
- You need to look through
the heart for reciprocal changes
- Bradycardia, junctional rhythms
- As mentioned above, you need to do a right-sided EKG in a patient with an inferior MI, incidence is about 40%!
- Lead V4R
- Hypotension, bradycardia, absence
of pulmonary edema in a true RVMI (clear lungs!)
Cardiogenic pulmonary edema (more common)
- increase in hydrostatic pressure (push) within the pulmonary-capillary bed due to heart failure. Third-spacing occurs in the INTERSTITIUM.
- bibasilar rales, vascular prominence, bilateral infiltrates
Non-cardiogenic pulmonary edema: third spacing into the ALVEOLI
Nov 10, '12
The oxyhemoglobin dissociation curve affects AFFINITY of oxygen to hemoglobin. Left shift = LOCKED and is bad for the patient. Shift to the left is caused by:
* low 2-3 DPG (seen in low phosphorus levels, hypothyroidism and blood tranfusions...so check your phos levels and make sure they are within range!)
Left shift increases affinity between O2 and Hgb HOWEVER the O2 does not get delivered at the tissue level. O2 stays bound to hemoglobin. LEFT = LOCKED.
* H/H, SaO2 normal. ScVO2 is elevated (poor cellular O2 consumption)
DI (diabetes insipidus)
* excessive polyuria
* low USG (<1.005)
* excessive dehydration
* high serum Na+ (remember dehydration = high Na+; overhydration = low Na+ due to dilution)
* DI = dehydration!
SIADH (syndrome of inappropriate ADH)
* oliguria (<0.5mL/kg/hr)
* high USG (>1.030)
* low Na+ (dilutional)...can be severe, </120mEq/L
* decreased BUN (dilutional), serum Osmo
DKA: hyperglycemic crisis resulting in metabolic acidosis and ketosis (type 1 diabetics)
HHNKS: hyperglycemic crisis with ABSENCE OF metabolic acidosis and ketosis...in patients with a relative insulin deficiency (i.e. type 2 diabetics)
* Serum glucose 300-800mg/dL
* normal serum Na+
* high serum K+ (d/t acidosis) that later becomes LOW once insulin is administered (insulin drives K+ back into the cell)
* Increased BUN/Cr
* increased serum osmo
* metabolic acidosis
* Serum glucose >600-2000mg/dL
* LOW serum Na+ due to hyperglycemia
* LOW serum K+ (no acidosis)
* Elevated BUN/Cr
* Increased serum osmo (more so than in DKA patients)
* NO acidosis...if there is an acidosis, consider lactic acidosis.
Causes of metabolic acidosis:
* DKA/ETOH ketoacidosis
* renal failure
* lactic acidosis
* ASA overdose
I hear the test can go pretty in-depth in differentiating between DI/SIADH and DKA/HHNKS, especially in regards to electrolyte imbalances. Hopefully this helps!
Last edit by turnforthenurse on Nov 10, '12