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General Concepts Flashcards

1
Q

Name the BLS steps for CPR including:

  • rate of compressions
  • depth of compressions in adults and chilren
  • when to give compressions in adults and children
  • how often to give breaths to adults and children
  • how often to give breaths if advanced airway is used
  • how soon to defibrillate
A
  1. Recognize: (not or abn. breathing/unresponsive)
  2. Activate: Call EMS and get AED
  3. Pulse: (carotid adult/child & brachial infant.
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2
Q

Name the general steps to manage choking

A

CHOKING

  1. Ask if they are choking
  2. Abd. Thrusts
  3. If unresp. = CPR algorithm + (check for FBO)
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3
Q

For a lone rescuer how does the BLS algorithm change for adults and children when collapse is witnessed? Not witnessed?

A

Witnessed: Adult: Activate EMS and get AED Then CPR. Child: 2 min. CPR then Activate and get AED.
Not witnessed or drowning: 1 cycle CPR, then Activate and get AED.

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4
Q

What is the basic ACLS algorithm for cardiac arrest given a monitor read of VF/VT? Asystole? PEA?

A
  1. Recognize
  2. ACTIVATE/AED
  3. ABC IV O2 Monitor
    a. SHOCK: VF/VT->shock #CPR2min+EPI(3-5min)1MG/Amio300mg,150mg. Airway, capno.#RPT.
    b. No SHOCK: Asyst/PEA-> #CPR2min+EPI(3-5min)1MG Airway, capno.#RPT.
  4. ROSC?->HR, BP, PETCO2>40= O2>94%, TX BP SBP>90 w/ 1-2 L fluid, Epi 0.1-.5mcg/kg/Dop 5-10mcg/kg/min.
    12-lead. A&O? Y: coronary repro, N: hypothermia.
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5
Q

What are the 3 main treatments for ROSC?

A

O2>94%,
TX BP SBP>90 w/ 1-2 L fluid, Epi 0.1-.5mcg/kg/Dop 5-10mcg/kg/min.
12-lead. A&O? Y: coronary repro, N: hypothermia.

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6
Q

What is bradycardia? What are symptoms of bradycardia and how is it treated for asymptomatic patients vs symptomatic patients?

A

BRADYCARDIA (<50/MIN)
1. ABC IV O2 Monitor
2. SX (BP, MS, Shock, Chest pain/disc, CHF)
If no SX: monitor,
If SX Atropine 0.5mg q3-5 mx3mg., TCP/Dop 2-10mcg/kg/min / EPI 2-10 mcg/min.

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7
Q

What is tachycardia? When is it symptomatic and what are the symptoms?

A

tachycardia >100 bpm. Symptoms often occur over 150 bpm. SX = BP, MS, Shock, Chest pain/disc, CHF

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8
Q

What is the treatment for symptomatic tachycardia with regular and narrow QRS and what are common rhythms found with this?

A

Try adenosine then 100J cardioversion. Atrial flutter and SVT.

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9
Q

What is the treatment for symptomatic tachycardia with regular and wide QRS and what are common rhythms found with this?

A

100 J cardioversion. V-tach, SVT

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10
Q

What is the treatment for symptomatic tachycardia with irregular and narrow QRS and what are common rhythms found with this?

A

200 J. A-fib

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11
Q

What is the treatment for symptomatic tachycardia with irregular and wide QRS and what are common rhythms found with this?

A

Defibrilation. V-fib.

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12
Q

What is the treatment for asymptomatic tachycardia with regular and narrow QRS?

A

QRS<.12 : Vagal/Adenosine 6mg,12mg/BB(atenolol5mg)/CC(diltiazem20mg)/Consult.

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13
Q

What is the treatment for asymptomatic tachycardia with regular and wide QRS?

A

QRS>.12 reg monomorphic: Adenosine. Polymorphic antiarrythmic (amiodarone 150mg for 10 min).

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14
Q

Name the basic steps in management of stroke

A 
Identify
Activate EMS
ABC IV O2 monitor, check blood glucose
Asses stroke and time of onset
Get to stroke center
CT
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15
Q

What is the plan for stroke if CT shows hemorrhage?

A

Send to neurosurgery

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16
Q

What is the plan for stroke if CT shows no hemorrhage?

A

Determine if candidate for fibrinolytics:

  • Yes: review Procedures, alternatives, risks and questions. If patient agrees then rtPA (no anticoagulant/anti-platelets for 24h)
  • No: give ASA and consult with neurosurgery.
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17
Q

What is the Cincinnati Pre-hospital Stroke Scale and what does it mean if one of the tests is right?

A
  1. Face droop.
  2. Arm drift.
  3. Abnormal speech.
    1/3 = 73% probability.
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18
Q

Describe the basics of the Glasgow Coma Score

A 
GCS: 
4E5V6M.  
4 levels of eye response
5 levels of verbal response
6 levels of motor response
>14 mild, >13 mod, </= 10 severe.  3 is the minimum.
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19
Q

Major inclusion criteria for fibrinolytic to treat stroke?

A

stroke occured /= 18 yoa.
- you can give it up to 4.5 hours if patient is not >80, not using anticoagulants and has no history of diabetes or ischemic stroke.

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20
Q

Major exclusion criteria for fibrinolytics to treat stroke?

A

Head trauma within 3 months, subarachnoid hem, hx intracran hem, BP>185/110, INR>1.7, PT>15, plt<100k

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21
Q

What is the basic treatment for someone with chest pain?

A

ABC, MONA (morphine, oxygen, nitro, asa), IV, Monitor

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22
Q

How does a STEMI show on ECG?

A

ST elevation> .1mm / t-wave inv in 2+ contiguous limb leads, or >2mm in 2+ contiguous precordial leads, new lbbb

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23
Q

If you see STEMI what is the criteria for reperfusion therapy?

A

has to be within 12 hours of STEMI, but you should actually do either PCI or fibrinolysis even it its over 12 hours given the chance you could save some of the heart.

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24
Q

Your patient has a confirmed STEMI what are the goals of reperfusion therapy? When is fibrinolysis indicated? PCI? What labs/tests are helpful?

A
  • If you can get the patient to PCI w/in 2 hours then PCI is the therapy of choice.
  • If no PCI in 2 hours and qualify for fibrinolysis, then TX w/ fibrinolysis…ideally w/in 30 minutes of medical contact.

Get, but don’t wait for:

  • cardiac markers
  • electrolytes
  • coags
  • chest x-ray
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25
Q

What if the STEMI happened 12 hours ago?

A

Same plan as for NSTEMI and unstable angina

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26
Q

What is acute coronary syndrome

A

STEMI, NSTEMI, Unstable Angina

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27
Q

What is the difference between NSTEMI and unstable angina?

A

Both are from ischemia, both can present with T wave inversion and ST depression, symptoms include heart failure and tachycardia.

NSTEMI has positive cardiac markers (troponin I/T)

YOU TREAT THEM THE SAME THOUGH

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28
Q

What is the treatment for NSTEMI and unstable angina?

A

Nitro, heparin, BB, clopidigril, glycoprotien inhibitors. Admit the patient and start on ACE + Statin.

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29
Q

If a patient with chest pain has no ECG findings what is the plan?

A

get markers, consider serial ECGs, stress test. If nothing then discharge w/ follow up

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30
Q

When do CKmb markers show up/leave? Troponin I/T?

A

CKmb: show up 3hrs, leave 3 days
Troponin: show up 3 hours, leave 6 days

(approximations)

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31
Q

What are exclusion criteria for treating ACS w/ fibrinolysis?

A

BP>185/110, or >15 mmhg difference b/t arms, trauma/surg/GI/GU past 3 weeks, stroke 3months, hx of intracranial hemorrhage

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32
Q

Name 4 types of shock, what the underlying problem is for each and an example.

A

Hypovolemic- low fluid: burns
Distributive- container got bigger: sepsis
Obstructive- pump blocked from the outside: tension pneumothorax
Cardiogenic- bad pump: MI

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33
Q

What are symptoms of .5 L blood deficit? 1 L? Severe deficit?

A

.5L: tachycardia, vasoconstriction
1L: tachycardia, dyspnea, diaphoresis, metabolic acidosis, oliguria.
Severe: end organ damage.

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34
Q

What is calcium’s role in the body?

A 
muscle contraction
nerve transmission
platelet activation
part of clotting cascade
bone
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35
Q

How is calcium regulated?

A
  • PTH: bone resorption
  • Kidney: controls excretion/resorption and produces D3 which causes GI absorption.
  • Parafollicular cells: produce calcitonin to stimulate bone deposition by stopping osteoclasts.
36
Q

Where is most of Ca in the blood?

A

45% bound to proteins, 40% ionized

-We typically measure protein bound Ca.

37
Q

What is pseudohypocalcemia?

A
  1. low albumin makes Ca look low, but ionized remains stable.
  2. Acidotic state makes Ca look low, but ionized remains stable. Low pH causes H+ to have more affinity to proteins and Ca to have less affinity to proteins so Ca gets booted off. (body’s way of buffering excess H+)
38
Q

What are two major causes of Hypocalcemia?

A
  • Hypoparathyroidism

- PTH is good, but bad Vit D. consumption, kidney disease, etc.

39
Q

Signs and Symptoms of Hypocalcemia….Acute and Chronic

A

Acute: trousseau sign, chvostek sign, spasms, tetany, papilledema, arrhythmia, HF, long QT and seizures. Chronic: calcification of basal ganglia->parkinsonism, dystonia, cataracts, abn dentition, dry skin.

40
Q

What are three major causes of Hypercalcemia?

A

Hyperparathyroidism
Malignancy
Drugs (thiazides, lithium)

41
Q

Signs and Symptoms of Hypercalcemia…

A

Often asx.

Stones: polyuria, polydipsia, moans: anorexia, nausea, and constipation ,-> tones: weak, depressed, alt ms, coma.

42
Q

Treatment for Hypocalcemia?

Treatment for Hypercalcemia?

A

Hypo: IV Ca, oral Ca, vitamin D.
Hyper: Fluids, calcitonin, bisphosphonates

43
Q

Role of magnesium in the body?

A

transports Ca across membranes (muscle/nerve function)
protein synthesis
glucose and BP control

44
Q

How is magnesium regulated?

A

Absorbed in small bowel, excreted in large bowel secretions and reabsorbed in kidney (No hormone control)

45
Q

Causes of hypomagnesemia

A

GI issues like diarrhea
Kidney issues
Drugs like thiazides and PPIs
High Ca since your body excretes mg when trying to pee out Ca

46
Q

Causes of hypermagnesemia

A 
Renal insufficiency (isn't filtered)
Infusion/diet
47
Q

Sx of hypomagnesemia

A

neuro: tetany, tremors, convulsions, weakness
cardio: widening PR/QRS peaked T’s, arrythmia

48
Q

Sx of hypermagnesemia

A

neuro: decreased reflexes, somnolence, paralysis

Hypocalcemia, nausea, vomiting, flushing.

49
Q

Causes of hypophosphatemia

A

movement from ECF to ICF: epinephrine, insulin, etc.
GI absorption impaired: antacids bind to it, diarrhea
Renal excretion increased: AKI

50
Q

Causes of hyperphosphatemia

A

Cell lysis: Tumor, rhabdomyolysis

51
Q

Role of phosphate in the body

A

Energy: ATP

Bone mineralization

52
Q

How is phosphate regulated?

A

Absorbed in GI, stored in cells and bones, excreted in kidneys.
Calcitriol/D3 increases to increase GI absorption/decreases to decrease absorption (PTH increases calcitriol)

53
Q

Sx of hypophosphatemia

A

increased bone resorption: rickets/osteomalacia

decreased atp: decreased cardiac contractility, proximal myopathy (dysphagia)

54
Q

Sx of hyperphosphatemia

A

ectopic calcification (lungs, eyes, arteries), hyperparathyroidism (increased PTH also decreases phosphate resorption in kidneys- body’s way of trying to lower phosphate)

55
Q

role of potassium in the body?

A

nerve conduction
muscle contraction
potassium/H+ buffer system (H and K exchange w/ changes in pH)

56
Q

regulation of potassium?

A
  • Na/K pumps in cells
  • Excretion in cortical collecting duct in response to aldosterone acting on Na/K (Na in K out)
  • anything that increases renal filtration (salt, diuretics…)
57
Q

Name three major causes of hypokalemia

A
  • Alkalosis (vomiting, etc)
  • Insulin, B adrenergic stimulation (increases Na/K activity)
  • diuresis
58
Q

Sx of hypokalemia?

A
  • weakness
  • arrhythmia
  • low T waves and u waves
  • glucose intolerance (get hyperglycemic quick)
59
Q

Tx for hypokalemia

A
  • BB if redistributive

- oral/IV k if depleted

60
Q

Major causes of hyperkalemia

A
  • Tissue breakdown (*could be bad blood draw)
  • impaired aldosterone (Ace inhibitor?)
  • Acidosis
  • low insulin, BB
61
Q

Sx of hyperkalemia

A

weakness
peaked T waves
arrythmias

62
Q

Tx hyperkalemia

A

Ca infusion

Insulin w/ glucose

63
Q

Role of Na in body?

A

Fluid balance
nerve conduction
muscle contraction
Na/K pumps

64
Q

How is Na regulated?

A
  • Levels detected by osmo and stretch receptors
  • Filtration and reabsorption in kidneys
  • Aldosterone (keeps salt and water: reabsorption)
  • ADH (retain water: dilution)
  • ANP (increase GFR and block renin and aldosterone: dilution)
65
Q

What are 3 types of hyponatremia?

A

*in all cases dilution is occurring
Hypovolemic: decreased H20, more decreased salt
Euvolemic: increased water, stable salt
Hypervolemic: increased salt, more increased water

66
Q

Give examples of each of the three types of hyponatremia

A

hypovolemic: salt lost through kidneys (diuretic) or salt lost from elsewhere (vomit, diarrhea…)
euvolemic: water retention (SIADH)

Hypervolemic: water and salt retention (edematous: AKI, CKD, Cirrhosis)

67
Q

Sx hyponatremia

A

low osmolality causes fluid to move into cells. This is bad in the brain: nausea, malaise, seizures, coma, resp. arrest.

68
Q

Tx hyponatremia

A

slow admin hypertonic saline. Too fast can cause demyelination and lead to irreversible damage.

69
Q

Two causes of hypernatremia

A

Unreplaced water losses

sodium overload

70
Q

Sx hypernatremia

A

high osmolality causes fluid to shift out of cells. In the brain it causes low cerebral volume: lethargy, weakness, irritability, seizure, coma.

71
Q

Tx hypernatremia

A

slow admin 5% dextrose w/ water. Too fast can cause swelling and herniation.

72
Q

what are the four steps to reading an ABG?

A
  1. Is pH acidic or alkalotic?
  2. what is the cause: metabolic or respiratory?
  3. Is it gap or non gap?
  4. Is compensation adequate?
73
Q

What is normal pH?

74
Q

what is acidic pH? alkaline?

A

acidic: < 7.35
alkalotic: > 7.45

75
Q

What changes with respiratory causes of acid-base disorders?

76
Q

What changes with metabolic causes of acid-base disorders?

A

Bicarb/HCO3-

77
Q

What is gap acidosis and how is it determined?

A
  • the gap is the amount of unmeasured anions.
  • It is calculated as the difference between measured cations (Na) and measured anions (HCO and Cl). Its normally between 8 to 16.
  • if its increased then there are more unmeasured anions, which indicates certain types of metabolic acidosis: gap metabolic acidosis.
78
Q

What is compensation and how is it determined in acid-base disorders?

A
  • compensation is the body’s way of countering acid/base disorders w/ respiratory or renal mechanisms.
  • if compensation is inadequate then disorder = mixed.
  • quick way: HCO and CO2 should move in same direction in compensation.
  • technical way: 1.5(HCO)+8=PCO2
79
Q

What are the 3 figures on the top line of an ABG? Bottom line? Far right?

A

Na/Cl/Bun
glucose
K /HCO/Cr

80
Q

name three causes of respiratory acidosis

A

TBI
COPD
Opiates
(dec. resp)

81
Q

name three causes of respiratory alkalosis

A

hyperventilation
ASA poisoning
Altitude sickness

82
Q

name three causes of metabolic acidosis

A

sepsis (increased production)
diarrhea (loss of bicarb)
CKD (dec. excretion)

83
Q

name three causes of metabolic alkalosis

A

vomiting (loss of acid)
H+/K shift in hypokalemia
fluid contraction that causes relative increase of HCO concentration.

84
Q

name three isotonic fluids and their general use and contraindications(*)

A
  • D5W- hypernatremia
  • NS- shock, general fluid replacement. *fluid overload if HF or edema
  • LR-burns. *renal failure, liver disease, hypothermia
85
Q

name one hypotonic fluid and its general use and contraindications(*)

A

1/2 NS- water replacement, DKA. *careful for cerebral edema. Liver disease, trauma, burns.

86
Q

name three hypertonic fluids and their general use and contraindications(*)

A

D5 in 1/2 NS- later in DKA after glucose s crisis.*Cardiac/renal failure
Hypertonic saline for hyponatremia.
D10W-when nutrition w/ glucose is required.

87
Q

PT has difficulty breathing, bronchoconstriction, hives and flushing after you give IV abx. What is happening and how will you treat this?

A 
Anaphylaxis
stop drug admin
EPI IM .3-.5 mg in thigh
Secure airway
O2 
1L NS bolus
elevate legs
25mg diphenhydramine IV
50mg ranitidine IV
125mg Solumedrol IV

E-MED (9 decks)

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