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what's normal value for pH, CO2, HCO3?
- Couch homeostasis:
- pH 7.35-7.45
- CO2 = 35-45mm Hg
- HCO3 = 22-26 mmol/L
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What causes respiratory acidosis? give examples of some specific diseases.
- pulmonary disease causes respiratory acidosis - i.e.
- copd
- pulmonary edema
- pna
- asthma
- respiratory failure
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How to treat respiratory acidosis?
- You want to decrease CO2. You can do this through:
- 1. Medication (bronchodilator/steroid)
- 2. bipap
- 3. ventilator - increase respiratory rate / tidal volume.
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what causes respiratory alkalosis?
hyperventilation
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what is the treatment for respiratory alkalosis?
- You wanna try to get pt to stop hyperventilating:
- 1. have them breathe into a paper bag
- 2. if pt is on ventilator decrease tidal volume or respiratory rate
- 3. address anxiety
- 4. look at metabolic system to see if it is compensating (is bicarb going down)?
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most common causes of METABOLIC ACIDOSIS are:
- renal failure
- aspirin overdose
- antifreeze overdose
- diarrhea
- DKA
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How do you treat metabolic acidosis?
- You gotta treat the cause:
- i.e. consider renal failure (dialysis!)
- aspirin/antifreeze overdose (?pump stomach?)
- you can also give sodium bicarbonate IV
- and, look at the opposite system (respiratory) to see if it is compensating.
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What's metabolic alkalosis?
caused by LOSS OF ACID FROM STOMACH! Results in too much bicarbonate. - this'll happen if pt throwing up lots or if they are in constant NG suction. if you lose too much acid it'll throw the body into metabolic alkalosis.
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How do you treat metabolic alkalosis.
- 1. address underlying cause.
- 2. see if IV fluids are needed (to replace volume lost)
- 3. look at opposite system (respiratory) to see if it is compensating.
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what is the osmolality of plasma?
270-300 mOsm/L
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0.9% Normal Saline Sodium Chloride - give me a summary
- This is used to increase
- circulating volume (does not carry oxygen):
- Watch for fluid overload and hypokalemia/hypernatremia.
- Contains Na - be careful with renal disease, glucocorticoids!
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When do we use normal saline?
shock, dka, blood transfusion, metabolic ketoacidosis, hypercalcemia
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when do we use lactated ringer
as a fluid and electrolyte replenisher
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What do we need to watch for when it comes to lactated ringers?
- liver converts lactate to bicarbonate.
- patients with liver disease cannot metabolize lactate well.
- if patient has alkalosis, lactate will make it worse (i.e. bicarbonate).
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Give the names of MI by location.
- 1. Left circumflex occlusion (lateral or posterior MI)
- 2. Left anterior descending occlusion (anterior wall damage - highest mortality - "widow maker")
- 3. Right coronary artery occlusion - inferior wall damage
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What are the 4 classifications of MI
- subendocardial infarction (NSTEMI)
- intramural infarction (NSTEMI)
- transmural infarction (STEMI)
- subepicardial infarcton (NSTEMI)
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difference in ST segment between ischemia and NSTEMI
- In ischemia, minimal ST depression
- In NSTEMI, large ST depression
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What's a myocardial infarction
localized area of necrotic dead tissue caused by occlusion of a coronary artery that cuts off supply of oxygenated blood to the heart.
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Cardiac biomarkers what do they tell us?
whether there has been damage to tissue
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Name 4 cardiac biomarkers
- Troponin I or T
- High-sensitivity troponin
- Creatinine Kinase (CK) and CK-MB
- Myoglobin
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Troponin I and Troponin T - describe how long they take to peak and return to baseline
- rises in 3-6 hours
- peaks 24-48 hours
- back to baseline 5-14 days
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tell me about high sensitivity troponin
- approved by FDA in 2017
- more sensitive, positive results appear sooner
- may also be present in stable angina or no symptoms, indicate increased risk of future heart attack
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What is CK (CPK)
It's a measure of enzymes released by myocardial cells when they are damaged. Released within 30-60 minutes.
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What isoenzyme for CPK represents the heart
CK-MB
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Tell me about life cycle of CK-MB
- CK-MBspecific to myocardial damage in absence of skeletal damage
- rises in 4-8 hours
- peaks 18-24 hours
- back to. normal in 3 days
CK-MB must be > 5% total CK for definitive diagnosis of MI
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Other than enzymes, what tests are ordered to diagnose MI
- ABG
- CMP/BMP
- Electrolytes
- CBC
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chronic stable angina is associated with fixed stenosis of the blood vessel. Explain.
- in chronic stable angina, atherosclerotic plaques, not thrombus, are present in the vessel. this will lead to chest pain when the heart works harder and needs more oxygen (ie exercise).
- unstable angina, on the other hand, is associated with thrombus.
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describe common symptoms of unstable angina
- new onset exertional symptoms
- symptoms when client is at rest
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how can you tell if chronic stable angina is progressing to unstable angina
if the angina increases in intensity/duration OR occurs at rest, then this may signal increasing occlusion and the potential for infarction.
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Tell me about vasospastic angina, aka prinzmetal angina
- lasts 5-30 minutes
- caused by vasospasm, contraction of the vessel
- occurs at rest or during sleep[
- it's not a medical emergency, can be managed at home
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tell me about how to handle chronic stable angina
- this type of angina occurs during exercise, activity or stress
- usu subsides with rest or medication (nitroglycern)
- not a medical emergency
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how do beta blockers work
beta blockers block the effect of epinephrine -> this causes the heart to beat more slowly and with less force. this, in turn, reduces the amount of oxygen needed by the heart - and can prevent mi / death.
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Describe treatment for unstable angina
- unstable angina is a medical emergency. treatment consists of:
- 1. anti-ischemic therapy: nitroglycerin, beta blocker, oxygen, ace inhibiter, ARBs
- 2. anti-platelet therapy: i.e. aspirin
- 3. anti-coagulant therapy: LMW heparin, direct thrombin inhibitors, unfractionated heparin
- 4. consider thrombolytic after diagnosis and only after contraindications are ruled out.
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What does PaO2 measure?
The partial pressure of oxygen in the blood.
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FiO2 - what is taht?
The fraction of inspired oxygen.
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What is the range for FiO2
.21-1.0 (or, 21% - 100%)
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how much oxygen in room air?
21%
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What is ARDS?
- Acute respiratory distress syndrome - characterized by:
- 1. Severe hypoxemia
- 2. Bilateral infiltrates on chest radiograph - note infiltrates do not exchange Oxygen and Co2 well.
- 3. Reduced pulmonary compliance - cant get air in well, alveoli is jacked up
As a result PaO2/FiO2 is low.
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What is the Berlin Definition of ARDS
- First category - respiratory problems happen within first week of a known clinical insult (pna, injury, trauma). Plus you gotta rule out the following:
- 1. make sure the bilateral opacities on the xray is not due to effusion, lung collapse or nodule;
- 2. respiratory failure isn't due to cardiac failure or fluid overload; and,
- 3. you'll need an objective assessment to exclude hydrostatic edema if no risk factors are present (ie via echocardiography)
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SECOND Category - impaired oxygenation
1. Mild: PaO2/FiO2 200-300 w/ vent setting for PEEP or CPAP >= 5 cm H2O
2. Moderate: PaO2/FiO2 100-200 w/ PEEP >= 5 cm H2O
3. Severe: PaO2/FiO2 < 100 w/ PEEP >= 5 cm H2O
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