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CH 17 Cardiovascular Emergencies > Tables > Flashcards

Tables Flashcards

1
Q

Table 1

9 Modifiable risk factors for heart disease

A

Hypertension, cholesterol, smoking, diet, obesity, sedentary, oral contraceptives, hormone replacement therapy, stress

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2
Q

Table 2

4 nonmodifiable risk factors for heart disease

A

Age, Family history, carbohydrate intolerance, type A personality traits

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3
Q

Table 3

Sodiums role in cardiac function

A

Flows into the cell to initiate depolarization

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4
Q

Table 3

Potassium’s role in cardiac function

A

Flows out of the cell to initiate repolarization
Hypokalemia increases myocardial your ability
Hyperkalemia decreases automaticity conduction

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5
Q

Table 3

Calcium’s role in cardiac function

A

Maintains pacemaker cell depolarization and involved in contraction of heart muscle tissue
Hypocalcemia leads to decreased contractility and increased myocardial irritability
Hypercalcemia leads to increased contractility

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6
Q

Table 3

Magnesium’s role in cardiac function

A

Stabilizes the cell membrane acts with potassium and against calcium
Hypomagnesemia leads to decreased conduction
Hypermagnesemia leads to increased myocardial your debility

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7
Q

Table 5

P wave represents

A

Depolarization of the atria

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8
Q

Table 5

PR interval represents

A

Depolarization of the atria and delay at the AV node

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9
Q

Table 5

QRS complex represents

A

Depolarization of the ventricles

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10
Q

Table 5

ST segment represents

A

Time between ventricular depolarization and beginning of repolarization

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11
Q

Table 5

T-wave represents

A

Repolarization of the ventricles

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12
Q

Table 5

R-R interval represents

A

Time between two ventricular depolarization’s

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13
Q

Table 6
Primary chemical mediator of the…
1. parasympathetic
2. sympathetic nervous system

A
  1. acetylcholine

2. norepinephrine, epinephrine

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14
Q

Table 6
Primary nerves regulating cardiac function of the…
1. sympathetic
2. parasympathetic

A
  1. Vagus

2. Nerves of the thoracic and lumbar ganglia

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15
Q

Table 6
Primary effects of stimulation
1. Sympathetic
2. Parasympathetic

A
  1. positive inotropic, positive dromotropic, positive chronotropic, dilates pupils, constricts blood vessels, slows digestion, dilates the bronchi
  2. negative inotropic, negative dromotropic, negative chronotropic, constricts pupils, increases salivation, increases gut motility
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16
Q

Table 6
Prime agonists of the…
1. Sympathetic
2. Parasympathetic

A
  1. alpha: phenylephrine, beta: isoproterenol, beta-2: albuterol, alpha + Beta: norepinephrine, epinephrine, dopamine
  2. Neostigmine, Reserpine
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17
Q

Table 6
Prime antagonists of the…
1. sympathetic
2. Parasympathetic

A
  1. alpha: chlorpromazine, phentolamine, Beta: propranolol, metoprolol, labetalol, atenolol
  2. atropine
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18
Q

Table 9

Physiologic effects of dopamine at a dose of 1 to 2 µg per kilogram per minute

A

Increased renal perfusion

Dopaminergic receptor site

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19
Q

Table 9

Physiologic effects of dopamine at a dose of 2 to 10 micrograms per kilogram per minute

A

Positive chronotropic and inotropic effects

Beta-1 receptor site

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20
Q

Table 9 physiologic effects of dopamine at A dose of 10 to 20 µg per kilogram per minute

A

Vasoconstriction

Alpha receptor sites

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21
Q

Common beta-1 blockers

A

Atenolol
Bisoprolol
Metoprolol

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22
Q

Common nonselective beta blockers

A

Propranolol
Carvedilol
Labetalol

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23
Q

Common calcium channel blockers

A

Amlodipine
Felodipine
Diltiazem
Verapamil

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24
Q

Commonly used antidysrhythmic to drugs

A

Amiodarone
Digoxin
Lidocaine
Procainamide

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25
Q

Commonly prescribed diuretics

A 
Furosemide
Torsemide
Hydrochlorothiazide
Metolazone
Triamterene
26
Q

Commonly prescribed antihypertensive agents

A

Labetalol
Propranolol
Clonidine
Reserpine

27
Q

Commonly prescribed anticoagulant and antiplatelet drugs

A

Plavix
Aspirin
Warfarin

28
Q

What occurs during the S1 “lub” sound

A

Closure of mitral and tricuspid valves at the start of systole

29
Q

What occurs at S2 “dub” sounds

A

Closure of aortic and pulmonic valves at the end of systole

30
Q

What causes the S3 sound

A

Vibrations of the ventricular waltz into rapid filling.

Indication of heart failure in the elderly

31
Q

What causes S4 sounds

A

Turbulent filling of a stiff ventricle usually occurring in hypertrophy and possibly MI.
Heard just prior to S1

32
Q

13 common causes of cardiac dysrhythmias

A 
MI
Ischemia
Hypoxemia
Autonomic nervous system imbalance
Increased vagal tone
Increased sympathetic output
Heart failure (distention of cardiac chambers)
Electrolyte disturbances
Drug toxicity
Hypothermia
Metabolic imbalances
CNS damage
Trauma
33
Q

Leads II, III, and aVF “see” what part of the heart?

A

LV Inferior wall

RCA; Posterior Descending

34
Q

Leads V1, V2 “see” what part of the heart?

A

Septum

LCA; LAD, Septal

35
Q

Leads V3 and V4 “see” what part of the heart?

A

LV anterior wall

LCA; LAD, diagonal

36
Q

Leads V5 V6 and aVL “see” what part of the heart?

A

LV lateral wall

LCA; circumflex

37
Q

Lead V4R “sees” what part of the heart?

A

RV

RCA; proximal

38
Q

Possible complications found in leads II, III and aVF

A

Hypotension, LV dysfunction

39
Q

Possible complications found in V1 and V2

A

Infranodal blocks and BBB’s

40
Q

Possible complications found in V3 and V4

A

LV dysfunction, CHF, BBB’s, complete heart block, PVCs

41
Q

Possible complications found in V5 and V6, I and aVL

A

LV dysfunction, AV node block

42
Q

Possible complications found in V4R

A

Hypotension, Infranodal and AV Noble blocks, A-fib, PACs

43
Q

Looking at leads I and aVF, how can you tell axis deviation?

A

Right (axis deviation) together, left (axis deviation) apart
Normal = both upward
Extreme right = both downward

44
Q

The EKG changes commonly seen in ischemia

A

T-wave inversion
ST depression
Occurs at onset

45
Q

EKG changes commonly seen in injury

A

ST elevation

Occurs within minutes to hours

46
Q

EKG changes commonly seen in infarct

A

Q waves may appear, usually wide and deep

Occurs within several hours to days

47
Q

Step 1 of the bradycardia algorithm

A

HR >50

If yes go to step 2

48
Q

Step 2 of the bradycardia algorithm

A 
ABC's
O2 > 94%
Monitor BP
12 lead
IV
49
Q

Step 3 of the bradycardia algorithm

A 
If persistent bradycardia are the following present;
AMS
Acute heart failure
Ischemic chest pain
Hypotension
Shock
If no, continue to monitor vitals
If yes go to step 4
50
Q

Step 4 of the bradycardia algorithm

A

Administer atropine
.5mg every 3 to 5 min not to exceed total dose of .4mg/kg
If ineffective go to step 5

51
Q

Step 5 of the bradycardia algorithm

A

Perform TCP, or dopamine infusion, or FB infusion
2-10mcg/kg/min
If ineffective go to step 6

52
Q

Step 6 of the bradycardia algorithm

A

Consider transvenous pacing

53
Q

Possible causes of PEA to consider during cardiac arrest

A

Hypovolemia, hypoxemia, hypoglycemia, hypothermia, hyperkalemia, hypokalemia, hydrogen ions
Tension pneumo, cardiac Tamponade, toxins

54
Q

Clues to causes and treatment of hypovolemia

A

Patient history

Volume infusion

55
Q

Clues to causes and treatment of hypoxemia

A

Cyanosis, airway problem

Intubation and ventilation with O2

56
Q

Clues to causes and treatment of hypoglycemia

A

BG<60

D50 25g

57
Q

Clues to causes and treatment of hypothermia

A

History of cold exposure

Hypothermia algorithm

58
Q

Clues to causes and treatment of hyperkalemia, hypokalemia, hydrogen ions

A

Renal history, ECG changes

Immediate transport, consider sodium bicarb if certain of acidosis

59
Q

Clues to causes and treatment of tension pneumo

A

History, no pulse with CPR, unequal breath sounds with hyper resonance to percussion unaffected side
Needle decompression

60
Q

Clues to causes and treatment of cardiac tamponade

A

History, no pulse with CPR, JVD

Pericardiocentesis

61
Q

Clues to causes and treatment of toxicities

A

History

Narcan

CH 17 Cardiovascular Emergencies (3 decks)

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