• Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

Card Range To Study

through

image

Play button

image

Play button

image

Progress

1/39

Click to flip

Use LEFT and RIGHT arrow keys to navigate between flashcards;

Use UP and DOWN arrow keys to flip the card;

H to show hint;

A reads text to speech;

39 Cards in this Set

  • Front
  • Back
What is the first sign of ischemia?
Swelling --> inflammation --> Na/K pump stops working
What happens when the Na/K pump stops working?
K still leaks out of the cell
Cell becomes more neg-->less likely to depolarize
What other ion gets trapped inside the cell when Na gets trapped inside the cell?
Ca also gets trapped in the cell - increases contractility
What is the first EKG change that is seen when the Na/K ATPase pump shuts down? Why?
ST wave depression because cells are more negative 2/2 K+ leaking out
What is an ST-wave depression indicative of? What is the treatment?
70% stenosis of vessel --> early ischemic changes

Stable angina (starts with exertion, stops with rest)

Tx: vasodilators
What are the steps to take in the management of angina?
If pain goes away -

-hospitalize for 24 hours
-serial EKGs and Card enzyme checks q6h for 24h
-If neg then send home
-Reg stress test in 6 wks
-If neg - Thallium stress test (look for cold areas = no flow)
What test can I do if I think my patient had an MI?
Ca-Pyrophosphate scan b/c cells that die take up calcium

-look for hot spot
What are the alternatives for a stress test if patient physically unable to do it?
Dobutamine stress test or dipyridamole stress test
What physiology causes MI symptoms in my patient? What changes do I expect to see on EKG?
Na gets trapped in the cell --> more likely to depolarize --> more positive at baseline therefore ST segment increases
What is the definition of unstable angina? What is the pathological cause of angina?
90% stenosis of vessel

rupture of plaque and clotting by platelets occluding the vessel
What angiogram findings result in taking patient straight to surgery?
70% or more stenosis of 3 vessels or 90% stenosis of 1 vessel
If angiogram findings aren't suggestive of surgery, what should I do?
Place stent +/- coated with clopidogrel
What events occur during inflammation from the first 24 hours to 6 months?
< 24h - swelling
24h - neutrophils arrive, peak at 3 days
4 days - macrophages and T cells show up, peak at 7 days
7 days - fibroblasts show up, peak at day 30, cause fibrosis until 6 months
What happens when too much Na+ gets trapped within a cell?
Na begins to leak out down it's concentration gradient using the Na/Ca pump --> pulls all Ca into cell

Cells needing extracellular Ca to depolarize, now can't b/c extracellular Ca is low
How long is a normal PR interval?
< 0.20 sec
What is the pathology causing 1st degree heart block? What is the treatment?
SA node dysfunction or dysfunction of tissue between SA and AV node
What is the pathology causing Wenckebach's heart block?
What is seen on EKG?
What is the treatment for it?
Early ischemia of AV node

progressive lengthening of the PR interval untili a QRS is dropped 2/2 K leaking out of cells so they repolarize more slowly
If asymptomatic - do nothing; if symptomatic - pacemaker
What are the two types of 2nd degree heart block?
Mobitz Type I: Wenckebach
Mobitz Type II
What is the pathology causing Mobitz II heart block?
What is seen on EKG?
What is the treatment for it?
Late ischemia at the AV node
PR interval "appears" normal b/c impulse is averaged by the lead recording it
All must have a pacemaker
What is the pathology causing 3rd degree heart block?
What does it look like on EKG?
What is the treatment for it?
Complete atrial/ventricular dissociation
QRS and p waves have no relationship
All must have a (dual chamber) pacemaker
What are the types of pacemakers? For what indication should each be used?
On demand - used for heart block
Overdrive (used for arrythmias)
What is the indication on EKG that patient is having premature ventricular complexes?
No p wave, wide QRS complexes, a pause following QRS complex
What is the definition of:
Bigeminy
Trigeminy
Ventricular Tachycardia
Ventricular fibrillation
Bigeminy: PVC every other beat
Trigeminy: PVC every third beat
V-tach: 3 consecutive PVCs and HR 150
V-fib: No recognizable QRS complexes
What protocol will be tested on the exam regarding treatment of patient with V-tach?
If patient stable - treat with meds
If patient unstable
- shock with 200 joules
- shock with 300 joules
- shock with 360 joules
- Lidocaine
- shock
- Bretylium or Amiodarone (intubate --> ICU)
What should I do for my patient who is in V-fib?
1 - O2
2 - Na-cahnnel blocker
3 - K+ channel blocker
Give epinephrine or ADH then treat like V-tach
What is the treatment protocol for atrial arrythmias
1 - O2
2 - Ca channel blocker
3 - Adenosine (blocks C-amp)
4 - B-blocker (blocks SA node B receptor)
5 - K channel blocker
6 - digoxin
How will I be able to discern a premature atrial contraction on EKG?
I'll see a pause afterwards
How do I treat A-fib?
If acute and stable: treat with medication
If acute and unstable: defibrillate
If chronic: put on coumadin and may defibrillate after 2 weeks
When should I use the synchronize button on the defibrillator?
When I see QRS wave
What is the CHADS score used for? What are the components of the score? When does my patient qualify for treatment?
Identifies which patients with A-fib should be on coumadin for the rest of their lives

C-CHF (1)
H-HTN uncontrolled (1)
A-Age>70 (1)
D-Diabetes (1)
S-Stroke (2)

Start tx if score is 2 or >
Will hypermagnesemia cause cells to be more/less likely to depolarize?

What is the treatment?
Less likely to depolarize

Tx: IVF to dilute, loop diuretic to pee it off
Will hypomagnesemia cause cells to be more/less likely to depolarize?

What is the treatment?
More likely to depolarize

Tx: IVF to dilute; replace Mg
Will hypercalcemia cause cells to be more/less likely to depolarize?

What is the treatment?
Less likely to depolarize at first (neuron), then more likely (muscle)

Tx: IVF to dilute, loop diuretics to pee it off, mithramycin - binds Ca in GI tract - poop it out
Will hypocalcemia cause cells to be more/less likely to depolarize?

What is the treatment?
More likely to depolarize at first (neurons), then less likely to depolarize (muscle)

Tx: CaCl, CaGluconate
Will hyperkalemia cause cells to be more/less likely to depolarize?

What is the treatment?

What will I see on EKG?
More likely to depolarize at first, then K will get stuck inside cells and repolarization will become slower

Tx: Push insulin-glucose

EKG: peaked T waves, widened T waves, prolonged QT interval
Will hypokalemia cause cells to be more/less likely to depolarize?

What is the treatment?

What will I see on EKG?
Less likely to depolarize b/c K will rush out of cells

Tx: Replete K

EKG: narrow T waves, flat T wave, flipped and inverted T wave, exaggerated flipped T wave = U wave
Will hypernatremia cause cells to be more/less likely to depolarize?

What is the treatment?
More likely to depolarize b/c Na rushes into cells but after a while Less likely b/c Na/K pump pumps it out

Tx: IV normal saline - correct slowly
Will hyponatremia cause cells to be more/less likely to depolarize?

What is the treatment?
More likely to deplarize b/c Na leaks out of cell using Na/Ca exchange and cell becomes more +

Tx: 3% saline - correct slowly
What tissues don't use insulin for uptake of glucose?
B - Brain
R - RBCs
I - Intestine
C - Cardiac
K - Kidney
L - Liver
E - Exercising muscle