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Critical Care > Exam 1 > Flashcards

Exam 1 Flashcards

1
Q

myocardial cells

A

muscle, property of contractility

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2
Q

Specialized cells

A

electrical activity, property of conduction

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3
Q

Conductivity

A

ability to transmit impulses from one area to another

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4
Q

Excitability (irritability)

A

capability of the cell to respond to a stimulus

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5
Q

Automaticity

A

capacity to initiate an impulse or stimulus

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6
Q

Rhythmicity

A

property of regularity of the intervals at which impulses are formed

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7
Q

Refractoriness

A

property of being unresponsive to an impulse

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8
Q

inside the cardiac cell

A

high K low Na, at rest (polarized)

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9
Q

outside the cardiac cell

A

low K high Na, at rest (polarized)

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10
Q

Absolute refractory period

A
  • the time during the cardiac cycle in which the heart cannot respond to a stimulus (during depolarization)
  • serves as a protective mechanism
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11
Q

Relative refractory period

A
  • cell can respond to a strong stimulus
  • The repolarization phase is in process but not quite completed (some cells are polarized and others are depolarized =vulnerable)
  • T wave on the ECG
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12
Q

Supernormal Period

A

during this period the cardiac cells will respond to a weaker than normal stimulus (just before the cells have completely repolarized)

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13
Q

Nonrefractory period

A

the time when the heart is completely repolarized and ready to adequately and efficiently respond to another stimulus

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14
Q

Normal pathway for cardiac electrical conduction

A

originates in the SA node, backup pacemaker is the AV node, Bundle of HIS and Purkinje Fibers

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15
Q

SA node

A

normally where impulses originate

60 to 100 times per minute

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16
Q

AV node

A
  • when the impulse reaches the A-V node, conduction is delayed 0.1 second allowing time for the atria to eject blood into the ventricle
  • if the S-A node fails, the A-V junction can assume control at a rate of 40 to 60 per minute
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17
Q

the His-Purkinje system

A
  • The Purkinje fibers allow a rapid spread of the impulse through the ventricular mass.
  • If the S-A node and A-V junction fail to initiate an impulse, the His-Purkinje system takes over and pace the heart at a rate of 20 to 40 beats per minute
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18
Q

Lead II

A
  • bipolar lead
  • positive electrode is placed over the apex of the heart (in the left midclavicular line at the 4th or 5th intercostal space).
  • negative electrode is placed beneath the clavicle to the right of the sternum near the 2nd intercostal space
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19
Q

Small box value

A

0.04 sec

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20
Q

Big box value

A

0.2 Seconds

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21
Q

P wave

A

Represents atrial depolarization

If present and upright in Lead II, normally indicates impulse originated in S-A node

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22
Q

PR interval (PRI)

A

Normal duration is 0.12- 0.20 second
Measured from the beginning of the P wave to the beginning of the QRS complex
Represents atrial depolarization and delay through the A-V node

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23
Q

QRS complex

A

Normal duration is less than 0.12 second
Measured from the beginning of the QRS to the end of the S wave
Represents ventricular depolarization

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24
Q

ST segment

A

Measured from the end of the QRS complex to the beginning of the T wave
Period between the completion of ventricular depolarization and beginning of ventricular repolarization

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25
Q

ST-segment elevation

A

acute myocardial injury, preinfarction, & pericarditis

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26
Q

ST-segment depression

A

myocardial ischemia

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27
Q

J-joint

A

end of QRS and beginning of ST segment

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28
Q

T wave

A

Represents ventricular repolarization (recovery phase)

Normally upright in Lead II

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29
Q

U waves

A

May or may not be visible.
Found after T wave
Prominent upright U waves are abnormal (Hypokalemia)

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30
Q

Method 1- 1500

A

1500 (number of small squares in 1 minute) divided by number of small boxes between 2 R waves

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31
Q

Method 2- 300

A

300 (number of large squares in 1 minute) divided by number of large boxes between 2 R waves

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32
Q

Method 3- 10

A

10 multiplied by number of Rs in 6 seconds

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33
Q

Artifact

A

ECG waveforms from sources outside the heart (interference seen on a monitor)
4 common causes: patient movement, loose or defective electrodes, improper grounding, faulty ECG apparatus

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34
Q

Normal sinus rhythm

A 
PP and RR interval (rhythm)- regular
PP  and RR rate- 60-100/min
P wave- upright in lead II
PRI- 0.12-0.20 second
QRS interval- less than 0.12 second
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35
Q

Sinus Dysrhythmias

A

Dysrhythmias originating in the sinoatrial (S-A) node.

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36
Q

Sinus Bradycardia looks

A 
PP  and RR interval (rhythm)- regular
PP and RR rate- less than 60/min
P wave- upright in lead II
PRI- 0.12-0.20 second
QRS interval- less than 0.12 second
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37
Q

Sinus Bradycardia Common etiology

A

damage to the S-A node, vagal stimulation, increased intracranial pressure, certain drugs (digoxin or beta-blockers), during sleep, normal in conditioned athletes

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38
Q

Sinus Bradycardia Clinical S&S

A

seldom symptomatic unless rate is markedly decreased, slow regular pulse, hypotension, dizziness, chest pain, or changes in level of consciousness

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39
Q

Sinus Tachycardia looks

A 
PP and RR interval (rhythm)- regular
PP  and RR rate- greater than 100/min
P wave- upright in lead II
PRI- 0.12-0.20 second
QRS interval- less than 0.12 second
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40
Q

Sinus Tachycardia Common etiology

A

exercise, pain, fever, CHF, shock, agitation, illicit drugs, caffeine, nicotine

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41
Q

Sinus Tachycardia Clinical S&S

A

vary with rate, rapid regular pulse, may sense palpitations, may experience dyspnea, may be asymptomatic

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42
Q

Sinus Arrhythmia looks

A 
PP and RR interval (rhythm)- irregular
PP  and RRrate- varies (usually 60-100/min)
P wave- upright in lead II
PRI- 0.12-0.20 second
QRS interval- less than 0.12 second
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43
Q

Sinus Arrhythmia Common etiology

A

common in children and young adults, increase in heart rate with inspiration, decrease in heart rate with expiration, usually considered benign

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44
Q

Sinus Arrhythmia Clinical S&S

A

irregular pulse, usually asymptomatic

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45
Q

Premature Atrial Complex (PAC)

A

Early beats from an ectopic focus in the atria
early, abnormally shaped P wave
P wave- may differ from sinus P wave; may be notched, peaked, diphasic, or lost in preceding ST segment or T wave
QRS interval- less than 0.12 second

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46
Q

Premature Atrial Complex (PAC) common etiology

A

atrial stretch (may be seen with valve disease, CHF, liver disease, pulmonary hypertension), mitral valve prolapse, emotional upheaval, nicotine, caffeine, digitalis

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47
Q

Premature Atrial Complex (PAC) clinical s &s

A

irregular pulse, patient usually unaware of PACs

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48
Q

what is Paroxysmal Supraventricular Tachycardia (PSVT)

A

A dysrhythmia originating in an ectopic focus anywhere above the bifurcation of the bundle of His
Often a PAC triggers a run of PSVT
Paraxysmal refers to an abrupt onset and termination

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49
Q

Paroxysmal Supraventricular Tachycardia (PSVT) looks

A

Heart rate 100-300 (some text say 140-250) beats/minute
Rhythm is regular or slightly irregular
P wave is often hidden in the T wave (such a fast rate)
QRS is usually normal

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50
Q

Paroxysmal Supraventricular Tachycardia (PSVT) common etiology

A

same as PACs

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51
Q

Paroxysmal Supraventricular Tachycardia (PSVT) clinical s&s

A

rapid regular pulse, may exhibit signs and symptoms of decreased cardiac output or CHF or even myocardial infarction (rapid rates decrease ventricular filling time, increase myocardial oxygen oxygen consumption, and decrease oxygen supply)

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52
Q

Atrial Flutter

A

PP intervals (rhythm)- regular
RR intervals (rhythm)- regular or irregular
PP rate- 250-350/min
RR rate- varies
P wave- sawtooth appearance (called F waves), more than one F wave is present for each QRS
PRI- unable to measure
QRS interval- less than 0.12 second (may be distorted by F wave)

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53
Q

Atrial Flutter common etiology

A

increased sympathetic tone, atrial stimulation, valvular disease, hyperthyroidism

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54
Q

Atrial Flutter Clinical S&S

A

depend on ventricular rate, may experience palpitations, angina, or dyspnea

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55
Q

Atrial Fibrillation looks

A

PP and RR interval (rhythm)- grossly irrregular
PP rate- greater than 350/min (unmeasurable)
RR rate- varies
P wave- no discernible P wave (atrial activity is characterized by undulations in the baseline)
PRI- unable to measure
QRS interval- less than 0.12 second

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56
Q

Atrial Fibrillation common etiology

A

ischemic heart disease, hypoxemia, hyperthyroidism, valvular disease

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57
Q

Atrial Fibrillation Clinical S&S

A

irregular pulse, may have pulse deficit (difference in apical rate and radial rate), depend on ventricular response, may experience palpitations, angina, or dyspnea, may cause decreased cardiac output, may develop emboli from atrial wall thrombus formation

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58
Q

Atrial Fibrillation treatment

A

Rate Control
-RVR treat with negative chronotropic agent (beta dig)
-Bradycardic, assess for negative chronotropes, Possible pacemaker
Prevent embolic events (Stroke)- Treat with anticoagulants

59
Q

Junctional Dysrhythmias

A

Originate at AV node
Sometimes are called “nodal”
Atrial kick lost- CO increases

60
Q

Premature Junctional Complex (PJC) looks

A

Rhythm is regular except for the early complex
P wave- pacemaker site is the junctional tissue, therefore, in Lead II the P wave may be inverted before QRS, buried in QRS, or inverted behind QRS
PRI- 0.12 second or less
QRS interval- less than 0.12 second

61
Q

Premature Junctional Complex (PJC) Common etiology

A

ischemia or insult to atrioventricular (A-V) junction, hypoxemia, valvular disease, digitalis toxicity

62
Q

Premature Junctional Complex (PJC) clinical S&S

A

seldom produces symptoms, patient may have an irregular pulse, serious only if occurs frequently

63
Q

Premature vs Escape

A 
Premature- Beat occurs early
Escape
- Back-up rhythm
-Rate is based on the origin of the impulse
-Junctional (nodal) 40-60 bpm
-Ventricular 20-40 bpm
64
Q

Junctional (Escape) Rhythm looks

A 
PP interval (rhythm)- regular or absent
RR interval (rhythm)- regular
PP  and RR rate- 40-60/min
P wave- pacemaker site is the junctional tissue; therefore, in lead II the P wave may be inverted before QRS, buried in QRS, inverted behind QRS
PRI- 0.12 second or less
QRS interval- less than 0.12 second
65
Q

Junctional Escape Rhythm common etiology

A

insult to S-A node, hypoxemia, digitalis toxicity

66
Q

Junctional Escape Rhythm clinical S &S

A

slow regular pulse, often a temporary dysrhythmia, if rate dramatically decreases cardiac output may drop

67
Q

Accelerated Junctional Rhythm looks

A 
PP interval (rhythm)- regular or absent
RR interval (rhythm)- regular
PP and RR rate- 61-100/min
P wave- pacemaker site is the junctional tissue; therefore, in lead II the P wave may be inverted before QRS, buried in QRS, or inverted behind QRS
PRI- 0.12 seconds or less
QRS interval- less than 0.12 second
68
Q

Accelerated Junctional Rhythm common etiology and S&S

A

Common etiology- digitalis toxicity (digoxin enhances automaticity of the AV node)
Clinical S&S- usually benign

69
Q

Junctional Tachycardia looks

A 
PP interval (rhythm)- regular or absent
RR interval (rhythm)- regular
PP and RR rate- 101-140/min
P wave- pacemaker site is the junctional tissue; therefore, in lead II the P wave may be inverted before QRS, buried in QRS, inverted behind QRS
PRI- 0.12 second or less
QRS interval- less than 0.12 second
70
Q

Junctional Tachycardia Common Etiology and S&S

A

Common etiology- digitalis toxicity (digoxin enhances automaticity of the AV node)
Clinical S&S- may decrease cardiac output

71
Q

First Degree A-V Block looks

A

PRI- greater than 0.20 second due to a prolonged delay at the A-V node; PRI IS CONSTANT AND PROLONGED

72
Q

First Degree A-V Block Common etiology and S&S

A

Common etiology- digitalis toxicity, MI

Clinical S&S- none, may progress into second or third degree A-V block

73
Q

Second Degree A-V Block(Type I, Wenckebach) looks

A

PRI- BECOMES PROGRESSIVELY LONGER UNTIL A QRS COMPLEX IS DROPPED; P WAVE PRESENT BUT NO QRS

74
Q

Second Degree A-V Block(Type I, Wenckebach) etiology and S&S

A

Common etiology- insult to the A-V node, commonly seen in inferior MI, hypoxemia
Clinical S&S- usually none, if heart rate dramatically decreases may produce S&S of decreased cardiac output, usually does not progress to higher degree heart blocks

75
Q

Second Degree A-V Block (Type II) (Mobitz II) looks

A

PP interval (rhythm)- regular
P wave- upright in lead II; more P waves than QRS complexes
Multiple dropped QRS

76
Q

Second Degree A-V Block (Type II) (Mobitz II) etiology and S&S

A

Common etiology- insult to A-V node, MI, hypoxemia, cardiac drugs
Clinical S&S- slow heart rate may produce S&S of decreased cardiac output, may suddenly progress to complete A-V block or ventricular standstill

77
Q

Third Degree A-V Block (Complete Heart Block- CHB) looks

A

RR and PP regular but independent of each other. More P waves than QRS complexes; P waves may fall inside QRS complex

78
Q

Third Degree A-V Block (Complete Heart Block- CHB) etiology and S&S

A

Common etiology- insult to A-V node, cardiac drugs, acute MI
Clinical S&S- considered extremely dangerous, rate usually very slow, dramatic drop in cardiac output, may progress to ventricular standstill

79
Q

What is Premature Ventricular Complex (PVC)

A

A single ectopic impulse originating in the ventricles is called a premature ventricular contraction
The complex will be early
QRS interval- usually 0.12 second or greater (different from the QRS complex in the underlying rhythm)
Can be unifocal (look the same) or Multifocal (look different, more serious= can lead to VT or VF)

80
Q

3 or more PVC in row

A

VT, salvo

81
Q

Premature Ventricular Complex (PVC) considered dangerous if

A

Frequent (greater than 6PVCs/min)
Bigeminy (every other) or trigeminy (every third)
Paired or runs
Multiformed
R on T phenomenon (during relative period)
In the presence of acute MI

82
Q

Premature Ventricular Complex (PVC) etiology and S&S

A

Common etiology- ischemia, MI, acidosis, low potassium level, drugs (digitalis)
Clinical S&S- patient may complain of palpitations or skipped beats, pulse will have pause followed by a strong beat, may lead to ventricular tachycardia or ventricular fibrillation

83
Q

Ventricular Tachycardia (VT) looks

A

PP interval (rhythm)- unable to determine
RR interval (rhythm)- usually regular
PP rate- unable to determine
RR rate- usually 150-250/min
P wave- if present, has no relationship to QRS complex (A-V dissociation)
PRI- unable to measure
QRS interval- usually 0.12 second or greater, wide and bizarre

84
Q

Ventricular Tachycardia (VT) etiology and S&S

A

Common etiology- MI, hypoxemia, acidosis, low potassium level, drugs (digitalis and catecholamines)
Clinical S&S- decreased level of consciousness; patient may complain of palpitations, dyspnea, dizziness, anxiety, diaphoresis, and/or angina; decreased B/P; if short burst, may be asymptomatic; patient may have a seizure due to cerebral ischemia; may have no cardiac output (pulseless VT)

85
Q

Ventricular Fibrillation (VF) looks

A

PP and RR interval (rhythm)- no discernible P waves
PP and RR rate- unable to determine
P wave- no discernible P wave
QRS interval- repetitive series of chaotic waves

86
Q

Ventricular Fibrillation etiology and S&S

A

Common etiology- usually preceded by ventricular irritability or a PVC on a T wave, MI, hypoxemia, electrolyte disturbances, electrical shock, drugs (digitalis, catecholamines)
Clinical S&S- loss of consciousness; no pulse, respirations, or blood pressure; possible seizure activity; cyanosis; death

87
Q

Idioventricular Rhythm looks

A

PP interval (rhythm)- most often absent
RR interval (rhythm)- usually regular
PP rate- if present, regular
RR rate- 40/min or less
P wave- if present, normal and upright in lead II
PRI- if present, varies (no relationship to QRS complex)
QRS interval- 0.12 second or greater, wide and bizarre

88
Q

Idioventricular Rhythm etiology and S&S

A

Common etiology- protective mechanism, failure of normal conduction, dying heart
Clinical S&S- slow heart rate, may have no pulse or blood pressure, decreased cardiac output, syncopal episode

89
Q

ECG Changes with Hypokalemia

A 
ST depression
Shallow, flat, or inverted T waves
Prominent U waves
Ventricular dysrhythmias (especially PVCs)
Bradycardia
Enhanced digoxin effect
90
Q

ECG Changes with Hyperkalemia

A 
Tall peaked T waves
Flat P waves, or loss of P wave
Widened QRS complex
Prolonged PR interval
ST segment depression
Ventricular fibrillation, ventricular standstill
91
Q

Pulseless Electrical Activity etiology and S&S

A

Common etiology- poor pumping action of the heart muscle, massive MI, pulmonary embolism, hypovolemia, cardiac tamponade, tension pneumothorax, entricular rupture, acidosis
Clinical S&S- no palpable pulses, no obtainable B/P, no respirations, unconsciousness, cyanosis, clinically dead

92
Q

Hs and Ts

A

Hypovolemia Hydrogen ions (acidosis) Hyper/hypokalemia Hypoxia Hypothermia
Tension pneumothorax Tamponade (cardiac) Toxins Thrombosis (cardiac) Thrombosis (pulmonary)

93
Q

Cardiac tamponade

A

increased pressure around the heart from fluid in sac

94
Q

life-threatening dysrhythmias

A

av block, v fib, v tach

95
Q

If a patient is experiencing altered mental status, chest pain, dyspnea, lightheadedness, hypotension, or ventricular ectopy, treatment should be instituted:

A

For bradycardia:
Atropine 0.5 mg IV (drug of choice) (every 3-5 minutes with maximum dose 3 mg)
Transcutaneous pacing (if available)
Dopamine (2-10 mcg/kg/min), or Epinephrine (2-10 mcg/min) (if a transcutaneous pacemaker is unavailable and patient not responsive to atropine)

96
Q

If persistent tach dysrhythmia is causing hypotension, changes in mental status shock chest discomfort or acute AF (UNSTABLE)

A

Perform immediate synchronized cardioversion (when the rate greater than or equal to 150)
Establish IV access and give sedation if patient is conscious
Consider expert consultation
(if regular narrow QRS consider adenosine)

97
Q

In Tach dysrhythmia if stable with narrow QRS:

A 
Narrow QRS
IV access and 12 lead ECG
Attempt vagal maneuvers
Give adensoine 6 mg rapid IV push.  If no conversion, give 12 mg rapid IV push
Consider expert consultation
Control rate- diltiazem, beta-blockers
98
Q

In Tach dysrhythmia if stable with wide QRS:

A

If VT or uncertain rhythm, give amiodarone 150 mg IV over 10 minutes. Repeat as needed if VT recurs
Amiodarone maintenance infusion of 1mg/min for 6 hours followed by 0.5 mg/min
Prepare for synchronized cardioversion
Consider expert consultation

99
Q

Treatment of Dysrhythmias-Pulseless Arrest (VF/VT)

A

Give 1 shock (biphasic 120 to 200 joules)Resume CPR immediately for 2 minutes
Check rhythm & if shockable , give 1 shock (continue CPR while defibrillator is charging)
When IV is ready, give vasopressor during CPR before or after the shock
-Epinephrine 1 mg IV- repeat every 3 to 5 minutes or Vasopressin 40 units IV to replace 1st or 2nd dose of epinephrine
Consider advanced airway and capnography
Consider antiarrhythmics- amiodarone (1ST dose 300 mg, second dose 150 mg), lidocaine, magnesium (for torsades de pointes)

100
Q

torsades de pointes

A

polymorphic v-tach, hypomagnesia

101
Q

Asystole/PEA treatment

A

CPR
When IV is ready, give vasopressor
Epinephrine 1 mg IV- repeat every 3 to 5
minutes or
Vasopressin 40 units IV to replace 1st or 2nd
dose of epinephrine (1 dose)

102
Q

Indications for pacemakers

A

Bradydysrhythmias- drug toxicities, electrolyte imbalances, MI
Tachydysrhythmias (For SVT not Afib)- “Overdrive” pacing can decrease the rate of a rapid rhythm

103
Q

Noninvasive temporary pacing

A

used as an emergency measure or when a client is being transported and the risk of bradydysrhythmia exists

104
Q

transvenous invasive temporary pacing

A

pacing lead wire is placed through antecubital, femoral, jugular, or subclavian vein into the right atrium for atrial pacing, or through the right ventricle, and positioned in contact with the endocardium

105
Q

Epicardial invasive temporary pacing

A

applied by using a transthoracic approach; the lead wires are loosely threaded on the epicardial surface of the heart after cardiac surgery

106
Q

pacemaker code 1st letter

A

identifies which chamber(s) of the heart are paced by the pacemaker- “A” refers to atrium, “V” to ventricle, and “D” to both atrium and ventricle (also called “dual”)

107
Q

pacemaker code 2nd letter

A

refers to which chamber, if any, the pacemaker can sense electrical activity-”A” for atrial sensing, “V” for ventricular sensing, “D” for dual sensing, “O” is used for no sensing

108
Q

pacemaker code 3rd letter

A

describes the pacemaker’s response to sensed electrical activity in the heart- “O” for no response, “I” refers to inhibited, “T” to triggered, and “D” for dual triggered and inhibited response

109
Q

pacemaker code 4th letter

A

commonly used to indicate the presence of a rate responsive feature in the pacemaker. If the pacemaker is capable of increasing heart rate based on the body’s metabolic demands, the 4th letter is coded “R” for rate responsive.
Example- increase rate for fever

110
Q

Pacemaker spikes

A

When a pacing stimulus is delivered to the heart, a spike (straight vertical line) is seen on the monitor or ECG strip
If the electrode is in the ventricle, the spike is in front of the QRS complex
If the electrode is in the atrium, the spike is before the P wave
If the electrode is in both the atrium and the ventricle, the spike is before both the P wave and QRS complex

111
Q

Failure to capture

A

pacemaker initiates an impulse, but the stimulus is not strong enough to produce depolarization
Spike with no QRS

112
Q

Failure to pace

A

occurs when the pacemaker should deliver a pacing impulse but does not
no spike, pause

113
Q

Failure to sense

A

occurs when the pacemaker fires randomly at any point during the cardiac cycle instead of at the indicated or appropriate time
random all over spikes

114
Q

Implantable Cardioverter Defibrillator (ICD)

A

An electrical device used in the treatment of tachydysrhythmias
Capable of identifying and terminating life-threatening ventricular dysrhythmias
type of pacemaker that can shock and pace

115
Q

ICD two or more shocks in 24 hours

A

seek medical attention

116
Q

Acute Coronary Syndrome

A

Occurs when the myocardial tissue has an oxygen deficit (ischemia) long enough that injury occurs.
Ischemia is prolonged and not immediately reversible, acute coronary syndrome (ACS) develops

117
Q

ACS encompasses:

A

Unstable angina (UA) also known as Non ST segment elevation acute coronary syndrome (NSTE-ACS)
Non–ST-segment-elevation myocardial infarction (NSTEMI)
ST-segment-elevation (STEMI)

118
Q

Myocardial Infarction

A

Occurs with myocardial tissue is abruptly and severely deprived of oxygen

119
Q

Sustained ischemia

A

Result of sustained ischemia (>20 minutes), causing irreversible myocardial cell death (necrosis)
Necrosis of entire thickness of myocardium takes 4 to 6 hours

120
Q

Necrosis of entire thickness of myocardium takes

A

4 to 6 hours

121
Q

Development of Atherosclerosis

A

endothelial injury, Inflammatory process, Macrophages accumulate= more inflammation, oxidize the Low Density Lipoproteins, Macrophages engulf the oxidized LDL and foam cells are formed, Foam cells accumulate and form fatty streaks, growth of smooth muscle cells, development of fibrofatty lesions= can become fibrous plaques

122
Q

Partial (Severe but not total) occlusion of coronary artery

A

Unstable Angina

Non ST segment elevation Myocardial Infarction (NSTEMI)

123
Q

Total occlusion of coronary artery:

A

ST segment elevation Myocardial Infarction ( STEMI)

124
Q

ECG Changes associated with ACS

A

Ischemia- inverted T waves/and or ST depression (1 mm below isoelectric line)
Injury-ST elevation (at least 1 mm above the isoelectric line)
Infarction- pathologic Q wave (deep and > 0.03 second in duration)

125
Q

Troponin

A

protein found in striated muscle (skeletal and myocardial)
Levels elevate as early as 3 hours after myocardial injury
Troponin I levels stay elevated for 7-10 days

126
Q

CK – Creatine Kinase

A

enzyme found in muscle and brain tissue
Isoenzymes
CK-MB (Cardiac) – found mainly in cardiac muscle
Begins to elevate within 6 hours of damage, peaks at 18 hrs and returns to normal in 2-3 days.

127
Q

Myoglobin

A

protein found in cardiac and skeletal muscle.
Any release to skeletal muscle will cause increase
Levels rise as early as 2 hours after injury and decline rapidly after 7 hours (not specific to cardiac muscle)

128
Q

Homocysteine

A

Elevated levels may increase the risk of cardiovascular disease. Levels should be less than 14 mmol/dL

129
Q

C reactive Protein (CRP)

A

Detects inflammation . A level less than 1 mg/dl is considered low risk and a level over 3mg/dl is considered high risk for heart disease.

130
Q

Coagulation Studies

A

An increase in coagulation factors can occur during and after MI which places the patent at greater risk for thrombophlebitis and extension of clots in the coronary arteries

131
Q

Anterior/septal MI

A

Occlusion of the LAD
Pump problems
Ventricular dysrhythmias (PVC’s, VT, V fib)
ST elevation in V leads

132
Q

Inferior MI

A

Occlusion of the RCA
Rhythm issues due to supplying blood to SA and AV Node (Bradycardia , AV Blocks)
ST elevation in lead II, III, and AVF

133
Q

Posterior and Lateral MI

A

Occlusion of the circumflex
Sinus dysrhythmias
Circumflex feeds some of the SA and AV Node

134
Q

Dysrhythmias and MI

A

Most common complication
Present in 80% of MI patients
Most common cause of death in the prehospital period
Life-threatening dysrhythmias seen most often with anterior MI, heart failure, or shock

135
Q

HF and MI

A

A complication that occurs when the pumping power of the heart has diminished
Can occur with anterior MI
See dyspnea, restlessness, agitation, tachycardia
Later see JVD, decreased CO, pulmonary congestion, S3/S4

136
Q

Cardiogenic shock

A

Occurs when inadequate oxygen and nutrients are supplied to the tissues because of severe LV failure
Requires aggressive management

137
Q

Papillary muscle dysfunction

A

Causes mitral valve regurgitation

Condition aggravates an already compromised LV

138
Q

Ventricular aneurysm

A

Results when the infarcted myocardial wall becomes thinned and bulges out during contraction

139
Q

Acute pericarditis

A

An inflammation of visceral and/or parietal pericardium
May result in cardiac compression, ↓ LV filling and emptying, heart failure
Pericardial friction rub may be heard on auscultation
Chest pain different from MI pain

140
Q

Dressler syndrome

A

Characterized by pericarditis with effusion and fever that develop 4 to 6 weeks after MI
Pericardial (chest) pain
Pericardial friction rub may be heard on auscultation
Arthralgia, elevated WBC count and sedimentation rate

141
Q

Acute Coronary Syndrome Emergency Manangment

A 
Restore oxygenation to myocardium
Door to Balloon time
Less than 90 minutes
Thrombolytic therapy
Thrombolytic therapy is indicated in patients with evidence of ST-segment elevation MI (STEMI) presenting within 12 hours of the onset of symptoms if there are no contraindications to fibrinolysis
142
Q

Emergent PCI (Percutaneous Intervention)

A

Treatment of choice for confirmed MI
Balloon angioplasty + drug-eluting stent(s)
Athrectomy
Ambulatory 24 hours after the procedure

143
Q

PTCA : Percutaneous Transluminal Coronary Angioplasty

A

Completed in the cardiac catheterization lab under fluoroscopy with the client slightly sedated (Versed or Valium)
Access is usually via the right femoral artery
Hollow catheters (sheaths) are inserted into the femoral artery and a balloon-tipped dilation catheter is inserted through the sheath and directed to the area of stenosis. The balloon is repeatedly inflated to compress the plaque and stretch the vessel
Heparin or low molecular weight heparin will be administered to keep the vessel open

144
Q

Treatment of NSTEMI or UA with negative cardiac markers

A

Aspirin
Heparin or low molecular weight heparin
Glycoprotein IIb/IIIa inhibitor (Eptifibitide (Integrelin))
Possible PCI

Critical Care (4 decks)

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