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Adult Nursing - 225 > Cardiac Rhythm Disturbances > Flashcards

Cardiac Rhythm Disturbances Flashcards

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1
Q

***What does MAP stand for? What MAP value is necessary to maintain perfusion of major body organs, such as the kidneys and brain. What happens when the map is decreased?

A
  • Mean Arterial Pressure
  • 60 to 70 mm Hg
  • When map is below 60 the heart hurts
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2
Q

What is Cardiac output ? What is the equation for Cardiac output?

A

Amount of blood pumped out in a given time.

Cardiac Output = Stroke volume X heart rate

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3
Q

What does the SA NODE do? Where is it located? What is the intrinsic rate of the SA node? How is the SA NODE reflected on the ECG?

A
  • Chief Pacemaker - generates electrical impulses and conducts them throughout the muscle of the heart, stimulating the heart to contract and pump blood
  • SA Node Upper portion of the Right Atrium
  • 60 - 100 bpm
  • P wave - atrial depolarization - contraction of the atria
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4
Q

What does the AV node do? How is the slowing process of the AV node reflected on the ECG? What is the AV node’s intrinsic rate? In the case that the SA nodes fails, impulses may start at the level of the AV node, What are rhythms called that begin at the AV node?

A

The AV node serves as an electrical relay station, slowing the electrical current sent by the SA node before the signal is permitted to pass down through to the ventricles. Short delay allows atria to contract and ventricles to fill.

  • Reflected in the PR segment
  • 40-60 bpm
  • Junctional rhythms- they start at the “junction” between the atria and ventricles. The actual pacer cells in this area are in the bundle of his just below the av node
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5
Q

What is the intrinsic rate of the Bundle of His ? What does the bundle of his do? What makes up the bundle of his, bundle branches and terminal purkinje fibers?

A
  • 40-60 bpm
  • The bundle of His connects with the distal portion of the AV node and continues through the interventricular septum branching to the right (one branch) and left ventricle (2 branches).

-

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6
Q

What do Purkinje fibers do? What is the intrinsic rate? What is it called when the purkinje fibers initiate the heart beat and when would this occur?

A
  • Provide electrical conduction to the ventricles, causing the cardiac muscle of the ventricles to contract at a paced interval.
  • 20 - 40 bpm
  • Ventricular rhythms - In the case that both the SA node and AV node stop working.
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7
Q

Normal Cardiac output

A

4 to 8 L/min

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8
Q

**What is PRELOAD? What drugs are aimed at decreasing preload?

A
  • degree of myocardial fiber stretch at the end of diastole and just before contraction- Vasodilators, Diuretics
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9
Q

****What is AFTERLOAD? What determines afterload? Disease states that affect Afterload? Drugs used to improve?

A

Amount resistance that the ventricles must overcome to eject blood through the semilunar valves and into the peripheral blood vessels.

  • Systemic arterial resistance
  • More resistance makes it harder for the heart to pump blood
  • Hypertension, aortic stenosis, blood viscosity, arteriolar constriction

**Antihypertensives - Beta Blockers, Vasodilators

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10
Q

What is a normal stroke volume?

A

70ml/beat

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11
Q

*****What is ATRIAL KICK ? What happens when Atrial Kick is lost? What percent of cardiac output is Atrial Kick is responsible for? What are the manifestations when Atrial Kick is lost?

A
  • Contraction of the Atria that helps fill the ventricles
  • Atrial Kick is lost when the SA Node is not the chief dominant pacemaker in the heart (afib, aflutter)
  • 25 - 30% of CO
  • When Atrial Kick is lost Manifestations Hypotension, shortness of breath, chest pain, increase pulse rate (to make up for cardiac output)
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12
Q

How do Baroreceptors affect blood pressure?

A
  • Located in the aorta arch and carotid sinus. They recognize a change in tension and pressure and will kick in to help raise or lower BP according to need
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13
Q

Chemoreceptors

A

Increased carbon dioxide or decreased pH level causes the chemoreceptors to signal the heart to beat faster.

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14
Q

*** How do the kidneys help regulate cardiovascular activity?

A
  • When renal blood flow or pressure decreases, the kidneys retain sodium and water. BP tends to rise because of fluid retention and activation of the renin-angiotensin-aldosterone mechanism. This mechanism results in vasoconstriction and sodium retention (and thus fluid retention).
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15
Q

** External factors that also affect BP ? Emotional , physical activity, temperature

A
  • Emotional behaviors (e.g., excitement, pain, anger) stimulate the sympathetic nervous system to increase blood pressure (BP) and heart rate (HR).
  • Increased physical activity such as exercise also increases BP and HR during the activity.
  • Hypothermia, tissues require fewer nutrients and blood pressure falls.
  • Hyperthermia, the metabolic requirement of the tissues is greater and BP and pulse rate rise.
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16
Q

What is Automaticity?

A

-the ability of cardiac cells that alone can generate and create an electrical discharge

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17
Q

What is EXCITABILITY?

A

Excitability is the ability of non-pacemaker heart cells to respond to an electrical impulse that begins in pacemaker cells and to depolarized.

  • All cardiac cells have the ability to respond to electrical stimulation.
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18
Q

What is CONDUCTIVITY?

A

the ability to send an electrical stimulus from one cell to another.

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19
Q

What is Depolarization? What is the hearts to response to Depolarization?

A
  • Depolarization occurs when the normally negatively charged cells within the heart muscle develop a positive charge.
  • Contraction
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20
Q

Purkinje cells

A
  • make up the bundle of His, bundle branches, and terminal Purkinje fibers. These cells are responsible for the rapid conduction of electrical impulses throughout the ventricles, leading to ventricular depolarization and the subsequent ventricular muscle contraction.
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21
Q

What is the immediate priority for patients in VF or pulseless VT?

A

Defibrillate, then CPR is resumed

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22
Q

PR INTERVAL

A
  • Measurement from the beginning of the P wave to the end of the PR segment.
  • Time required for atrial depolarization as well as the impulse delay in the AV node and the travel time to the Purkinje fibers.

** It normally measures from 0.12 to 0.20 second (five small blocks).

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23
Q

ST SEGMENT

What does an elevate ST mean?
What does depression mean?

A
  • Measures time between ventricular depolarization and early VENTRICULAR REPOLARIZATION (rest).
Elevation = Injury or death to myocardial tissue
Depression = ischemia
  • Its length varies with changes in the heart rate, the administration of medications, and electrolyte disturbances.
  • The distance from the S wave to the beginning of the T wave.
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24
Q

T WAVE

A

VENTRICULAR REPOLARIZATION. It is usually positive, rounded, and slightly asymmetric.

** PEAKED T WAVE IS AN INDICATION FOR HYPERKALEMIA (INCREASED POTASSIUM)

  • T waves may become tall and peaked, inverted (negative), or flat as a result of myocardial ischemia, POTASSIUM or calcium imbalances, medications, or autonomic nervous system effects.
  • The T wave follows the ST segment and represents
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25
Q

U WAVE

A

The U wave, when present, follows the T wave and may result from slow repolarization of ventricular Purkinje fibers.

** Hypokalemia

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26
Q

What does the QRS INTERVAL represent? What is the normal time frame?

A
  • Time required for depolarization of both ventricles.

***It normally measures from 0.04 to 0.12 second (up to three small blocks).

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27
Q

Rhythm Interpretation Steps

A
  1. Determine heart rate - Atrial - P waves; Ventricular - QRS
  2. Determine heart rhythm
  3. Analyze P waves
  4. Measure PR interval
  5. Measure QRS
  6. Identify the rhythm
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28
Q

Digoxin

A
  • increases vagal tone, slowing AV nodal conduction.

Uses: Chronic Afib

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29
Q

Sinus Bradycardia can be normal in which patients?

A

Athletes during sleep; increase vagal tone (vomiting , valsalva maneuver); beta blockers

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30
Q

Treatment for Bradycardia (if symptomatic)?

A
  • Atropine 0.5mg IV
  • IV Fluids
  • Oxygen
  • temporary pacing - increase conduction
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31
Q

Sinus Tachycardia can be normal in which patients?

A

Increased sympathetic tone, CHF, hypoxia, fever, pain, stimulants, Increased myocardial workload and 02 demand

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32
Q

Causes of Sinus Tachycardia?

A

Caffeine, narcotics, amphetamines, cocaine, or thyroid issues

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33
Q

What are PREMATURE ATRIAL CONTRACTIONS? How does it affect the rhythm, rate, P waves?

A
  • Ectopic atrial tissue fires a n impulse before sinus impulse is due. May signify impending AFIB
  • HR is normal but rhythm is irregular
  • Inconsistent P wave - may occur rarely or be buried in prior T wave
  • Significance - PT should avoid caffeine, anxiety, could lead to more serious dysrhythmias

**

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34
Q

What happens in ATRIAL FLUTTER? How is the P WAVE affected? What role does the AV node play? What are patients with ATRIAL FLUTTER at risk for? Classic sign of A Flutter on a EKG?

A
  • SA NODE is no longer in charge thus we end up with a very high atrial rate
  • Atrial rhythm is normal (occur in a rhythmic fashion) but the P waves resemble a “saw-tooth pattern,
  • A/V node protects the ventricles from beating at the same increased rate as the atrium
  • At risk for thrombi due to the pooling of blood. etc. pulmonary embolism and embolic stroke
  • Treatment - Antidysrhythmics, anticoagulants, if unstable cardioversion.
  • SAW TOOTH
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35
Q

***What is ATRIAL FIBRILLATION? Rhythm? P waves? What is AFib usually associated with? Signs and Symptoms ?

A
  • No P waves and a very irregular rhythm (wavy baseline)
  • Treatment - Antidysrhythmics, anticoagulants, beta blockers, if unstable cardioversion. (Lifetime medicine = anti coagulant)
  • Associated with Heart disease or COPD, can precipitate decreased cardiac output

***Assess for thromi,

Signs and Symptoms: irregular rapid heart rate, lower blood pressure, ortho-hypotension, low 02 stat, anxious, change in level of consciousness

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36
Q

Radiofrequency Catheter Ablation

A

Invasive procedure that may be used to destroy an irritable focus causing a supraventricular or ventricular tachydysrhythmia.

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37
Q

What is a 1st Degree HEART BLOCK? How does this appear on the strip? Typical cause? Treatment?

A
  • Conduction delay from the Atria to the Ventricle which is evidenced by the PR interval being longer than .20 sec
  • Rhythm is regular, P waves are normal, QRS normal, PR intervals prolonged, rate is typically normal
  • More than likely caused by medications that prolong AV conduction such as digoxin, calcium channel blockers, and beta blockers.
  • See if patients are symptomatic, find cause and reviewing patient medication
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38
Q

What are ECTOPIC BEATS? PAC’s ? PJC’s? PVC’s ?

A
  • Small changes in a heartbeat that is otherwise normal
  • PACs are generated in the atria and have a P wave (full contraction right after a full contraction)
  • PJCs are generated from the AV node and usually have a short PR or no P at all (contraction (heartbeat) with a narrow QRS complex, less than 0.12 sec, but you have no P waves.)
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39
Q

*******What are PREMATURE VENTRICULAR COMPLEXES? How does it appear on the EKG? What are the typical causes when OVC is frequent and sustained? PVC may be a warning for the impending onset of ….? Treatment

A

Results from increased irritability of ventricular cells and are seen as early ventricular complexes followed by a pause. - PVC’s are generated from the ventricles and are wide (Contraction (heartbeat) with a wide QRS complex that is greater than 0.12 seconds.)

Rate = variable; 
Rhythm=  atrial regular, ventricular irregular; 
P waves= normal with sinus 
QRS wide (.12 sec or more), bizarre appearance (uniform or multiform)
  • Frequent and sustained PVC often indicates ventricular irritability due to hypoxia, heart disease or drug toxicities; may result in decreased cardiac output , may be a warning for the impending onset of, or precipitate V-tach or V-fib
  • Treatment = antidysrhythmics if symptomatic (amiodarone, lidocaine, procainamide, B-blockers)
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40
Q

What is VENTRICULAR TACHYCARDIA? What does it look like on the strip? Causes? What does the patient look like? Treatment ?

A
  • Repetitive firing of ventricular (MAJOR IRRITABILITY)
  • 100 - 250 bpm, regular rhythm, P waves usually obscured by QRS complex, no PR interval, QRS wide, bizarre appearance
  • Almost always occurs in diseased hearts especially with acute MI, drug toxicities, heart failure, hypoxia, acidosis, ventricular aneurysms
  • Pt is often symptomatic w/ sudden , profound heart failure; VT is unstable and may deteriorate into VF
  • Treatment
    Pharm: antidysrhythmics amiodarone, procainamide, lidocaine
    Pulse present: cardiovert
    Pulseless: defibrillation
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41
Q

What is VENTRICULAR FIBRILLATION? What is happening in the heart? How long can VF go on before death? Causes? What does the pt look like? Priority care

A
  • Electrical chaos in the ventricles; totally disorganized ventricular contractions; ventricles are quivering
  • HEART = ventricles merely quiver, consuming a tremendous amount of oxygen, No cardiac output or pulse thus no cerebral, myocardial, or systemic perfusion.
  • This rhythm is rapidly fatal if not successfully ended within 3-5 minutes
  • Pt’s with coronary artery disease, MI, hypokalemia, hypomagnesemia, hemorrhage, drug therapy, rapid SVT, shock or Trauma
  • Pt presentation: Faint, lose consciousness, pulseless, apneic, not BP
  • Priority care = DEFIBRILLATE THE PATIENT IMMEDIATELY. Do CPR until defibrillation is ready (heart needs to be shocked into some kind of rhythm)
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42
Q

Polarization

A

Cardiac cells at rest, no electrical activity.

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43
Q

Repolarization

A

Return of the ions to a resting state, causing relaxation of cardiac muscle.

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44
Q

NA+ - What is the normal range? Intracellular ion or extracellular?

A
  • 135-145 - extracellular
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45
Q

K+- Normal range? What cells are particularly sensitive to potassium? Intracellular ion or extracellular?

A
  • 3.5-5; Intracellular

- pacemaker cells

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46
Q

Ca++ Normal range? Intracellular ion or extracellular?

A
  1. 5 to 10.2 mg/dL

- extracellular

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47
Q

When do you DEFIBRILLATE (Asynchronous) ?

A

-Asynchronous countershock that depolarizes critical mass

  • Pulseless VTACH
  • VFIB
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48
Q

What is Asystole? How do you Verify Asystole? Priority Care?

A
  • Complete absence of any rhythm.

Verification: Check the leads and check the patient; Consider another EKG monitor to determine if asmystole or fine V-FIB.

Treatment: CPR; External temporary pacing, epinephrine, atropine

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49
Q

*****When do you do CARDIOVERSION (synchronized) ? What test should you do before cardioversion on a pt with AFIB, AFLUTTER?

A
  • VTACH with pulse ; Unstable AFIB or AFLUTTER electively for stable tachydysrhythmias
  • Trans Esophageal Ecocardiogram - (TEE) - check to see if there are any clots that can be dislodged
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50
Q

What is TEMPORARY PACING? INDICATIONS? What are the two basic types? What are the modes of pacing?

A

WHAT: Used to maintain heart rate and perfusion until more permanent method of pacing is used

INDICATIONS: Symptomatic Bradydysrhythmias, 2nd or 3rd degree heart block, Asystole

TYPES: Transcutaneous (temporary - used until better method of pacing can be done) of Transvenus

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51
Q

What is PERMANENT PACING? INDICATIONS?

A

WHAT: Device inserted to treat conduction disorders that are not temporary?

INDICATIONS: Complete heart block, Unstable AFIB

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52
Q

What INFORMATION ABOUT A PERMANENT PACER do you want to collect from a patient?

A
  1. Which chamber is being paced? (atria, ventricle, both)
  2. Which chamber is being sensed (atria, ventricle, both)
  3. Type of response (inhibit or trigger)
  4. Rate adaptiveness ( Can it fluctuate as needed based on metabolic demands)
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53
Q

Types of IMPLANTABLE DEVICES?

A
  1. Single Chamber (how many chambers of the heart)
  2. Dual Chamber
  3. Rate Responsive (responds based on rate)
  4. Tachyarrhythmia modes
  5. ICD (Implantable Cardiac Defibrillator) - for people at high risk for cardiac death
  6. Bi-Ventricular (coordinates right and Left Ventricle contractions)
  7. Reveal Implantable Loop Recorders - used to diagnose and treat dysrhythmias
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54
Q

What are the two MODES OF PACING?

A
  1. Synchronous (demand)

2. Asynchronous (fixed-rate)

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55
Q

***Pacemaker/ICD EDUCATION:

A
  • Report skin irritation at pacemaker site, report fever,
  • Don’t apply pressure over your generator. Avoid tight clothing
  • Follow activity restrictions
  • Avoid external electrical fields
  • Record daily pulse (1min) at the same time every day. (or if they patient is having symptoms of P/M failure)
  • Teach patient S/S of pacemaker failure
  • Report hiccups, weight gain, difficulty breathing, dizziness, fainting, chest pain.
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56
Q

Post - OP PACEMAKER CARE INSTRUCTIONS?

A
  • Avoid getting incision wet for 1st week (no shower/steam)
  • Don’t raise arm on the side of the device above shoulder for 3 weeks
  • No lifting more than the weight of a Gallon of milk for 3 weeks
  • Report twitching sensations in the chest
  • Report Strong jolt to chest
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57
Q

What should a person with a PACEMAKER AVOID do to INTERFERENCE?

A
  • Arc welding
  • MRI scans
  • Magnetic anti-theft exits at stores
  • Airport security (hand wand as well)
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58
Q

What should a person with a PACEMAKER AVOID do to INTERFERENCE which at HOME ?

A
  • Keep small hand held appliances 6 inches from device while in use
  • Use and store cell in opposite side of device
  • Keep 12 inches between P/M and power tools or small running engines
  • Ground all power tools
  • Try to avoid chain saws (if necessary use ELECTRIC)
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59
Q

How can you stop the pacemaker from working during an EKG to figure out what the patients intrinsic rate is?

A

Placing a magnet on the Pacemaker will temporarily stop the P/M from working

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60
Q

Where will you see the pacing spike on the EKG of a patient being A PACED versus a patient being V PACED?

A

In an A PACED patient, the spike will be before the P wave while in a V PACED patient the Pacer spike will be before the QRS wave (wave will be deflected down which is a normal finding)

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61
Q

What is Undersensing? Causes?

A
  • Pacemaker fails to sense the patients intrinsic beat. PACING CAN’T OCCUR WHEN IT IS SUPPOSED TO IF THE PACEMAKER CAN’T SENSE INTRINSIC BEAT
  • Results in asynchronous pacing
  • increased stimulation threshold at electrode site (exit block), poor lead contact, new bundle branch block or programming problems.
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62
Q

What is? Failure to Capture? Causes?

A
  • Failure to capture occurs when paced stimulus does not result in myocardial depolarization. Not responding to a pacing stimulus

CAUSES: electrode displacement, wire fracture, electrolyte disturbance, MI or exit block.

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63
Q

What might you NOTICE if the patient is experiencing inadequate oxygenation and tissue PERFUSION as a result of dysrhythmias?

A
  • Report of chest discomfort or pain
  • Report of dizziness or syncope
  • Shortness of breath
  • Weakness and fatigue
  • Decreased urine output
  • Pale, cool skin
  • Diaphoresis
  • Anxiety or restlessness
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64
Q

What should you assess when a patient is experiencing inadequate oxygenation and PERFUSION as a result of dysrhythmias?

A
  • Taking vital signs (may have hypotension and weak pulse)
  • Checking for pulse deficit
  • Asking if patient has palpitations
  • Checking capillary refill (decreased)
  • Listening to lung and heart sounds
  • Assessing cognition
  • Taking an ECG
  • Checking oxygen saturation
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65
Q

How should you RESPOND to a patient experiencing inadequate oxygenation and PERFUSION as a result of dysrhythmias?

A
  • Apply Oxygen and get the MONITOR on
  • Keeping the head of the bed elevated unless patient is very hypotensive
  • Maintaining or starting an IV line
  • Notifying the health care provider or Rapid Response Team
  • Giving drug therapy as prescribed
  • Initiating CPR for asystole
  • Defibrillation if the patient in VF
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66
Q

How do we measure the EKG?

A
  • little box = 0.04

- big box = 0.20

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67
Q

Atrial kick is lost when you are not in a ______ rhythm?

A

Sinus rhythm

68
Q

Difference between a Premature Ventricular Contraction and Premature Atrial Contraction

A

PVC wide and ugly

69
Q

**Medications to slow the heart down? Non medications that slow down the heart?

A
  • Amioderone, Lidocain, digoxin, cardiosim

- Vaso maneuver

70
Q

What does PTT test for?

A

Test blood level for Heparin

71
Q

PT or INR tests for?

A

coumadin and warfin

72
Q

Which anticoagulant can affect hearing?

A

coumadin

73
Q

Antidote for COUMADIN ? Antidote for Heparin?

A 
Coumadin = vitamin K
Heparin = Protamine Sulfate
74
Q

****What speeds up the heart? Medications? Non medications that speed up heart?

A

Atropine
Epinephrine
Inotropic - Dopamin,

  • Caffeine - stimulants
75
Q

Digoxin overdose reversal agent?

A

Digivine

76
Q

What is the single largest killer of american men and women in all ethnic groups?

A

Coronary Artery Disease

77
Q

Coronary Artery Disease is commonly caused by? CAD is a broad term that includes _________ & _____?

A

Atherosclerosis - impairs perfusion

  • Stable angina and acute coronary syndromes
78
Q

***What is ANGINA PECTORIS? Difference /b/ stable and unstable?

A
  • Temporary imbalance /b/ the coronary arteries ability to supply oxygen and the cardiac muscles demand for oxygen. “strangling of the chest”
  • Chronic stable angina is predictable and familiar to patient, it last over several months and pain episodes last less than 15 min. Usually associated with a fixed atherosclerotic plaque. Exacerbations are usually brought on by physical and emotional stress or exposure to cold. Treatment= nitro, or drug therapy. Does not cause permanent damage
  • Unstable angina falls under Acute Coronary Syndrome. Evidence by unpredictability, increased number of attacks, duration and intensity of pressure. Pain/pressure may last longer than 15 min. Pain occurs at rest or w/ exertion & causes severe activity limitation. Treatment = pain not relieved by nitro or rest. * Often seen as pre-infarction b/c the occlusion is larger and begins to block oxygen flow to the tissues
  • Variant - chest pain or discomfort resulting from coronary artery spasm and typically occurs after rest. EKG = ST changes but no changes in troponin or CK levels b/c no tissue has be damaged yet. * begins to block oxygen flow to the tissues
79
Q

Ischemia ?

Infarction?

A
  • Ischemia - lack of oxygen

- Infarction - cell death or necrosis due to severe/ prolonged ichemia

80
Q

ATHEROSCLEROSIS

A
  • plaque and inflammation
  • Labs - Homocysteine & C-Reactive Protein. These can tell us if someone is at risk based on their level of inflamation
81
Q

Manifestations of ANGINA (chronic) ?

A

TYPICAL COMPLAINTS

  • Substernal chest pain
  • Radiates to left arm
  • Precipitated by exertion or stress
  • Relieved by nitro or rest
  • Last less than 15 min
  • Few associated symptoms
82
Q

What happens in ACUTE CORONARY SYNDROME?

A
  • Atherosclerotic plaque in the coronary artery ruptures, resulting in platelet aggregation (clumping), thrombus (clot), formation and vasoconstriction.
  • Used to describe people who have unstable, variant angina or an acute myocardial infarction.
  • Amount of plaque = degree of blockage = occlusion of blood flow ( artery has to have at least 40% plaque accumulation before it starts to block blood flow)
83
Q

What happens with a MYOCARDIAL INFARCTION?

A

Myocardial tissue is abruptly and severely deprived of oxygen (80%-90%)

  • Treatment = clot busters or surgery
84
Q

SUBENDOCARDIAL INFARCTION (NSTEMI)

A
  • Less severe of MI b/c it does not effect all the layers of the heart. Less effect on Cardiac output
  • ischemic necrosis is limited to the endocardium or to the endocardium and myocardium
85
Q

What is VENTRICULAR REMODELING? What are the outcomes?

A
  • Over a 2- to 3-month period, the necrotic area eventually develops into a shrunken, thin, firm scar. Scar tissue permanently changes the size and shape of the entire left ventricle, called ventricular remodeling.
  • Outcome = decrease left ventricular function, cause heart failure, and increase morbidity and mortality. This area is often the cause of chronic ventricular dysrhythmias surrounding the infarcted zone
86
Q

TRANSMURAL MI

A
  • Devastating b/c it goes through all 3 layers of heart.
  • Effects Cardiac output and Wall function.
  • At risk for Left Ventricular failure
87
Q

*****What is the result of a NSTEMI ? EKG appearance?

A
  • Myocardial ischemia due to coronary vasospasm, spontaneous dissection, and sluggish blood flow due to narrowing of the
  • ST depression or T wave Inversion
88
Q

*******STEMI is the result of ? What is the treatment and goal time of treatment? Cause? EKG appearance?

A
  • happens as a result of a complete blockage in a coronary artery. A STEMI attack carries a great risk of death and disability. Typically indicates myocardial infarction/ necrosis. * Most severe
  • Treatment = cath lab in 90 mins or less- -
  • STEMI is attributable to rupture of the fibrous atherosclerotic plaque leading to platelet aggregation and thrombus formation at the site of rupture
  • ST elevation in two leads on a 12-lead ECG.
  • Typically go through all 3 layers of the heart
89
Q

Manifestations of an MI

A

▪ Occurring without cause, usually in the morning
- Heavy chest
▪ Pain Relieved only by opioids
▪ Lasting 30 min or more
▪ Weakness, Nausea/ vomiting, Diaphoresis
▪ Feelings of fear and anxiety
▪ Dysrhythmias
▪ Pain radiates to jaw, arms, shoulders, teeth, /b/ scapula
▪ Disorientation/ acute confusion
▪ Feeling “short of breath”

90
Q

Why are women more prone to delay seeking treatment for an MI?

A
  • Women have more generalized/subtle symptoms
  • indigestion
  • pain between the shoulders,
  • aching jaw,
  • choking sensation that occurs with
  • Vague GI symptoms
91
Q

What populations are known for having silent MI’s? Why?

A
  • Diabetics & Elderly

- Elderly have long-term atherosclerosis while Diabetics have long term nerve damage

92
Q

Priority Nursing Care for a MI

A
  • 02
  • IV line
  • EKG monitor
  • ASA (aspirin) to chew
  • Notify health care provider
93
Q

**PAIN MANAGEMENT for MI? What does MONA stand for?

A
  • Morphine, O2, Nitro, Aspirin
  • Morphine sulfate - vasodilates coronary arteries, relaxes/decreases anxiety. ease pain, increases oxygenation, lowers BP, decreases demand of 02
  • O2 - body is deprived
  • Nitro - vasodilator (sublingual, spray, IV) - should bring more 02 to the heart. I
  • Position of comfort; semi-fowlers
94
Q

Side effects of NITRO? Nursing intervention?

A

Hypertension and headache

Pain relief

95
Q

Function of GLYCOPROTEINS inhibitors

A

Target platelet formation

96
Q

Drug therapy for MI - ANTICOAGULANTS

A

Prevents clotting but their is a risk of bleeding so pt should be monitored for bleeding

97
Q

Function of BETA BLOCKERs? Side effects?

A

Decreases occurrence of ventricular dysrhythmias and helps reduce workload of the heart

  • Bradycardia, hypotension
98
Q

Function of ACE INHIBITORS/ ARBS? When are they given in relation to a MI? What are you trying to prevent? What organ can Ace Inhibitors protect in addition to the heart? Side effects?

A
  • Blocks conversion of Angiotensin I to angiotensin II which causes vasodilation, lowers BP and decreased workload on the heart. *Ace Inhibitors can increase the potassium level b/c it decreases aldosterone which causes body to retain Potassium and excrete sodium
  • Give within 48hrs especially if ejection fraction is less than 40 %.
  • Prevent ventricular remodeling and development of heart failure
  • Kidney’s
  • Hypotension, cough
99
Q

Function of CA CHANNEL BLOCKERS

A
  • antianginal and anti-ischemic properties

- Decrease workload of the heart

100
Q

Function of ANTIARRHYTHMICS

A
  • Decrease risk of dysrrthymias
101
Q

Function of DIURETICS

A
  • Given to reduce pulmonary edema or , fluid volume overload
102
Q

**Function of THROMBOLYTIC THERAPY? Examples of Thrombolytic therapy? Time frame of giving thrombolytics post MI? How are they administered? Contraindications? Patient monitoring?

A

Dissolve thrombi in coronary arteries, restore myocardial blood flow.

  • TPA, Alteplase, Tenecteplase TNK,
  • Withing first 6 hrs of cardiac event
  • Given during cardiac catheterization but they can be given via IV
  • Monitor INR and PTT, not invasive procedures
103
Q

What is CARDIAC CATHETERIZATION ? How is it done? Patient ed? Pre-procedure? Risks?

A
  • Most definite test in the diagnosis of heart disease and come up with a treatment plan.
  • Teach about risks; Potentials sensations during procedure such as palpitations, a feeling of heat or a hot flash (contrast dye), and a desire to cough (as the medium is injected into the right side of the heart).
  • Hydration (fluids) and admin of acetylcysteine pre- and post study to protect kidneys from contrast.
  • MI, Stroke, Arterial bleeding, Thromboembolism, Lethal Dysrhythmias, Arterial Dissection
104
Q

PRE CATHETERIZATION CARE ?

A
  • Fluids for renal protection
  • administration of acetylcysteine before and after
    LABS = baseline of kidney function, Analysis of electrolytes, blood urea nitrogen (BUN), creatinine, coagulation profile, and complete blood count (CBC)
105
Q

POST CATHETERIZATION CARE

A
  • Bed rest (2-6) depending vascular closure device
  • Keep extremity straight
  • Monitor vitals
  • Assess insertion site
  • Assess peripheral pulses
  • Monitor Urinary output and encourage fluids to rid body of contrast dye
106
Q

What is a ANGIOPLASTY? What do you look for post op?

A

Angioplasty opens blocked arteries and
restores normal blood flow to your heart
muscle. It is not major surgery. It is done
by threading a catheter (thin tube) through a small puncture in a leg or arm artery to the heart. The blocked artery is opened by inflating a tiny balloon in it.

  • post op - dysrhythmia , reaction to the die, bleeding
107
Q

Coronary Artery Sent

A
  • metal mesh tube that expands inside a coronary artery. A stent is often placed during or immediately after angioplasty. It helps prevent the artery from closing up again.
108
Q

What can a EKG detect ?

A
  • Ischemia
  • Old and new infarctions
  • Dysrhythmias
  • Electrical activity and heart rate
109
Q

**What is the Ejection Fraction? What is it measuring? What is the normal range? What kind of failure occurs as EF decreases? Patients with a an EF less than __% are a candidate for an ICD? What must the EF be to diagnose heart failure?

A
  • Percent of the blood ejected from the heart during systole
  • Measures contractility
  • 50-70%
  • Forward failure - tissue perfusion decreases
  • 33%
  • 40%
110
Q

What is an Exercise Tolerance Test (Stress Test) ? What drug is used to induce heart stress that mimics exercise in patients that are unable to exercise?

A
  • EKG during exercise

- Dobutamine

111
Q 
Normal ranges
Total lipids ? 
Cholesterol?
Triglycerides? (female & male)
LDLs?
HDL?
A
  • 400-1000mg/dL
  • Less than 200mg/dL
  • Female= 35 - 135mg/dL; Male= 40-160mg/dL
  • Less than 130
  • Greater than 55mg/dL
112
Q

What are the cardiac markers?

A
  • TROPONIN
  • Creatine Kinase -MB
  • Myoglobin
113
Q

What is an angiography?

A

Catheter angiography uses a catheter, x-ray imaging guidance and an injection of contrast material to examine blood vessels.

114
Q

What is an electrophysiologic study (EPS) ?

A

an invasive procedure during which programmed electrical stimulation of the heart is used to cause and evaluate lethal dysrhythmias and conduction abnormalities.

115
Q

What is Troponin? Who are Troponin T & I found in and what does it indicate? What his the diagnosis time frame?

A
  • Myocardial muscle protein released into the bloodstream with injury to myocardial muscle
  • Not found in healthy patients and indicates cardiac necrosis or acute MI
  • Wide diagnosis time frame making them useful for patients who present several hours after the onset of chest pain
116
Q

What is Creatine Kinase? What does the appearance of CK in the blood indicate? What Isoenzyme of CK is found in myocardial muscle? Diagnosis time frame?

A
  • An enzyme specific to cells of the brain, myocardium and the skeletal muscle
  • tissue necrosis or injury
  • CK-MB
  • Rises in 3hr; Peaks in 24 hrs; Back to norm in 3 days
117
Q

What is Myoglobin? When is it detected? Clinical usefulness?

A
  • A low-molecular-weight heme protein found in cardiac and skeletal muscle
  • Earliest marker detected; rises in 2hrs, declines after 7
  • B/c myoglobin is found in skeletal and cardiac muscle it is not as useful as toponin
118
Q

What is HOMOcysteine? What does an elevated level indicate? What are causes of elevation? What helps control it?

A
  • Byproduct of amino acid breakdown.
  • Increased values help predict CAD
  • Causes vessel inflammation = endothelial toxicity, formation of plaque, frequency of clots
  • Controlled by folic acid, B6, B12
119
Q

C-Reactive Protein is a marker for _______ ? Where is it produced? Detection time frame? Levels in pt’s with autoimmune disease? A C-reactive protein over __ means your at a high risk for heart disease?

A
  • Inflammation
  • Liver
  • Appears/disappears quickly
  • Normally increased with autoimmune disease
  • 3
120
Q

What is BNP: Brain Natriuretic Peptide ?

A

hormone secreted by cardiomyocytes in the heart ventricles in response to stretching caused by increased ventricular blood volume.

121
Q

Reversal agent from benzodiazepine

A

Flumazenil

122
Q

Reversal agent for a Thrombolytic/fibrolutic

A

Fresh frozen platelets

123
Q

What is the antidote to acetaminophen overdose?

A

N-acetylcysteine

124
Q

Morphine

A
  • Pushed very slow
  • Start with the lowest dose
  • Antidote = Narcan
125
Q

What assessment questions would you ask regarding disorders of the valves?

A
  • Ask about attacks of rheumatic fever, infective endocarditis; ask about possibility of IV drug abuse
126
Q

What happens during MITRAL VALVE STENOSIS? Most common cause? Does this happen more in women or men? What is the result? What are the effects of the heart structures? What do the manifestations resemble?

A

What’s happening - Leaflets fibros, thicken and calcify (Fuse and become stiff), the chordae (heart strings) contract and shorten. All these events cause narrowing which forces blood to flow through at a very slow rate increasing left atrial pressure causing the atrium to dilate.

Common Causes: Rheumatic fever

Dominate sex: Women

Effects on Heart structure: Left atrial pressure increase, left atrium dilates, pulmonary artery pressure increase
Right ventricle become enlarged

Results of MVS

  • Decrease cardiac output
  • increase in Left Atrial Pressure
  • Pulmonary congestion
  • Right sided heart failure
  • Later left side fails

Manifestations: will be of Pulmonary and right heart failure

127
Q

What happens with Mitral Valve Regurgitation? Main causes? How does this affect preload? Signs and Symptoms?

A

Whats happening: Fibrotic/calcific changes in THE mitral Valve leaflets prevent the valve from properly closing during systole

Main causes: are degenerative due to aging and infective endocarditis

Preload: Blood eventually causes L ventricular failure due to chronic blood volume overload from the constant regurgitation

Signs and Symptoms: Fatigue, chronic weakness, decrease CO, dyspnea on exertion, orthopnea

Rheumatic heart disease #1 cause in developing nations

Does not close completely during systole
Allows back flow of blood to left atrium when left ventricle contracts

128
Q

What happens in Mitral Prolapse? MP is associated with what ?

A

What happens: Leaflets enlarge and prolapse back into left atrium during systole

Associated: with congenital cardiac defects and has a familial tendency

129
Q

What is AORTIC STENOSIS? Significance in the US? Effect on the Afterload? What kind of Cardiac Output does AS cause? Effect on heart structures? Signs and Symptoms?

A

What: Aortic valve opening is narrowed

Significance: Most common valve dysfunction in US

Afterload : Increased resistance to ejection = Ventricular hypertrophy and eventually left ventricular failure

CO: Cardiac output becomes fixed and cannot increase to meet demands during exertion

Heart Structures: Left side fails and eventually right side can fail

Symptoms: Typically related to fixed Cardiac Output
Dyspnea, angina, syncope
**Can progress to fatigue, debilitation, and peripheral cyanosis later

130
Q

What happens in AORTIC REGURGITATION? How is the left ventricle affected? Causes? Presentation?

A

What happens: Allows blood flow to go from the Aorta back into the Left ventricle

L Ventricle: dilates with larger amount of blood

Causes: Infective endocarditis, congenital defects, hypertension

Presentation: slow progression - asymptomatic for years

Manifestations: Dyspnea, orthopnea, PND, diastolic murmur, bounding arterial pulse

131
Q

How is Valvular disease diagnosed? Triad of symptoms for Valvular disease?

A

Diagnosis: ECHOCARDIOGRAM diagnostic procedure of choice, EKG—watch for afib, Exercise tolerance testing (Stress test)

  • Chest pain
  • SOB
  • Light headedness
132
Q

When is SURGERY necessary for valvular disease management? What are the surgical options?

A

Surgery: CO is bad;

Options: 
 - Valvuloplasty  with balloon, 
 - Reconstruction/replacement of valve; 
 - Prosthetic or xenografts(biologic pig or cow) 
   replacement valves
133
Q

Advantages and disadvantages of prosthetics vs that of Xenografts(biologic)?
What lifelong Treatment is necessary with biological valves? Which valve lasts longer? Which would be used to replace the aortic valve and why?

A
  • Prosthetic last longer, but need lifelong anticoagulants
  • Aortic valve only replaced by prosthetic valve
  • Xenografts (biologic) do not need life long
    anticoagulants
  • Xenografts (biologic) not as durable as prosthetics
134
Q

****What is INFECTIVE ENDOCARDITIS? Ports of entry of Infective Agents? Who is at high risk?

A

What: Microbe has infected the endocardium

Infective Agents: Oral cavity

  • Skin rash
  • Lesion/abscess
  • Infection
  • Surgery or invasive procedure

Those at high risk:

  • IV drug abusers
  • Valve replacement recipients
  • People who have had systemic infections
  • People with structural cardiac defects
135
Q

First lab you want to get when Endocarditis is expected? What heart sound could be present? What would an echocardiography be looking for?

A

First test you want to do: Positive blood cultures

Heart sound: New regurgitant murmur

Echocardiography:

  • heart failure
  • Arterial embolization
136
Q

Non-surgical VALVULAR DISEASE MANAGEMENT

Drug therapy? What treatment is necessary prior to invasive procedures or dental work? What dysrhythmia is common and should be managed? Patient education?

A

Nonsurgical management focuses on drug therapy and rest
Drug therapy: including diuretics, beta blockers, vasodialators, digoxin, oxygen, and sometimes nitrates, anticoagulants

Prophylactic: antibiotics before invasive procedures and tests

Dysrhythmia: AFIB

PE: Encourage Rest with limited activity, educate patients on the S&S of heart failure

137
Q

Manifestations of Endocarditis?

A
  • Arterial embolization
  • Murmur
  • Heart failure
  • Splenic infarction
  • Neurologic changes
  • Petechiae
  • Splinter hemorrhages
138
Q

Surgical management of ENDOCARDITIS? Non-surgical management?

A
  • Removal of infected valve
  • Repair or removal of congenital shunts
  • Repair of injured valves and chordae tendineae
  • Draining of abscesses in heart or elsewhere
  • Antimicrobials
  • Activities balanced with adequate rest
139
Q

What is PERICARDITIS? Potential problems of the Pericardium? Pericarditis is commonly associated with?

A

What: inflammation or alteration of the pericardium (the membranous sac that encloses the heart).

Associated: with
: • Infective organisms (bacteria, viruses, or fungi) (usually respiratory)
• Post– myocardial infarction (MI) syndrome (Dressler’s syndrome)
• Post-pericardiotomy syndrome
• Acute exacerbations of systemic connective tissue disease

140
Q

What is Chronic constrictive pericarditis? What are some causes? Definitive treatment?

A

What: occurs when chronic pericardial inflammation causes a fibrous thickening of the pericardium.

Causes: tuberculosis, radiation therapy, trauma, renal failure, or metastatic cancer.

Definitive treatment: for chronic constrictive pericarditis is surgical excision of the pericardium (pericardiectomy).

141
Q

Manifestations of Pericarditis?

A

Manifestations:

  • Substernal precordial pain radiating to left side of neck, shoulder, or back
  • Grating, oppressive pain, aggravated by breathing, coughing, swallowing
  • Pain worsened by supine position; relieved by sitting up and leaning forward
  • Pericardial friction rub
142
Q

Complications of Pericarditis?

A

Complications: pericardial effusion and pericardial tamponade

Monitor all patients for pericardial effusion, which occurs when the space between the parietal and visceral layers of the pericardium fills with fluid. This complication puts the patient at risk for cardiac tamponade, or excessive fluid within the pericardial cavity.

143
Q

****Manifestations of Cardiac Tamponade? Treatment ?

A

Cardiac tamponade findings:

  • JVD
  • Paradoxical pulse
  • Decreased CO
  • Muffled heart sounds
  • Circulatory collapse
  • Hypotension

Treatment
-Pericardiocentesis - removes fluid

  • Pericardial window - involves removing a portion of the pericardium to permit excessive pericardial fluid to drain into the pleural space.
  • Pericardiectomy
144
Q

Pericarditis treatment

A
  • Pain management
  • NSAIDs
  • Antibiotics for bacterial form
  • Pericardiectomy
145
Q

What is RHEUMATIC CARDITIS? Which layers of the heart does inflammation occur in? What happens to the heart structures?

A

WHAT: Sensitivity response that develops after an upper respiratory tract infection with group A beta-hemolytic Streptococci.** It occurs in almost half of patients with rheumatic fever.

INFLAMMATION: All layers

HEART STRUCTURE:

  • Impaired contractile function of myocardium
  • Thickening of pericardium
  • Valvular damage
146
Q

RHEUMATIC MANIFESTATIONS

A
  • Tachycardia
  • Cardiomegaly
  • New or changed murmur
  • Pericardial friction rub
  • Precordial pain
  • Changes in ECG
  • indications of heart failure
  • Existing streptococcal infection
147
Q

What is hypovolemic shock? Causes?

A

occurs when too little circulating blood volume decreases MAP, resulting in inadequate total body PERFUSION and oxygenation.

  • Hemorrhage and dehydration ex. trauma, surgery, vomiting/diarrhea, severe burns
148
Q

****Cardiogenic Shock? When you have pump failure what happens?

A
  • occurs when the heart muscle is unhealthy and pumping is impaired.
  • Myocardial infarction is the most common cause of direct pump failure.
  • Everything is going to decrease (perfusion, BP etc)
149
Q

Distributive Shock? What are the two causes of Distributive Shock? What are the difference between the two causes?

A

occurs when blood volume is not lost from the body but is distributed to the interstitial tissues where it cannot perfuse organs.

Causes- Loss of sympathetic tone, blood vessel dilation, pooling of blood in venous and capillary beds, and increased capillary leak.

-neural-induced and chemical-induced

150
Q

Adequate blood flow requires what 3 things?

A
  1. Adequate cardiac pump
  2. Effective vasculature/circulatory system
  3. Sufficient blood volume
151
Q

Factors that influence MAP?

A
  1. Total blood volume
  2. Cardiac output
  3. Size of the vascular bed
152
Q

What is the difference /b/ Relative vs. Absolute Hypovolemia?

A

Relative = Decrease tissue perfusion caused by a relaxed (vasodilation) vascular bed; ex. neurogenic shock

Absolute = true volume loss; ex. hemorrhage

153
Q

Hemodynamic monitoring? What are some examples?

A

-Monitoring of vital signs using invasive measures

  • Pulmonary artery catheter
  • Invasive arterial catheter and monitoring
  • Pulmonary capillary wedge pressures
154
Q

Neural-induced DISTRIBUTIVE shock? Causes?

A
  • Loss of MAP due to loss of sympathetic tone * SNS impulses decreased, smooth muscles relax and cause vasodialation

Causes: Pain, Anesthesia, Spinal cord injury, Head trauma

155
Q

Chemical-induced DISTRIBUTIVE shock?

A

-has three common origins:
1. anaphylaxis - Anaphylaxis - Widespread loss of blood vessel tone, with decreased blood pressure and cardiac output after extreme
allergic reaction

  1. Sepsis - Wide spread infection triggers whole body inflammation
  2. capillary leak syndrome - Capillary leak syndrome - response of capillaries to the presence of body chemicals that enlarge capillary pores and allow fluid to shift from the capillaries into the interstitial tissues.
156
Q

How do Colloids affect the body?

A

Pull fluids from the tissues into intravascular space

-

157
Q

What is SEPTIC SHOCK (DISTRIBUTIVE SHOCK)? What 2 important things are happening internally? Death rate with appropriate intervention?

A
  • Widespread infection coupled with a general inflammatory response(SIRS); triggered when infection escapes local control
  • Multiple organ failure and uncontrolled bleeding occurs
  • Death rate exceeds 50%
158
Q

What is SIRS?

A

is triggered as a result of INFECTION escaping local control.

159
Q

What is MODS?

A

multiple organ dysfunction syndrome (MODS) when organ failure is evident and poor CLOTTING with uncontrolled bleeding occurs

160
Q

Swanz-ganz

A

Catheter goes directly into heart

Good for monitoring fluid balance

161
Q

What valve problem sounds like a washing machine?

A

Stenosis

162
Q

Acronym for heart sounds?

A 
A - American 
P - People 
E - Eat
T - To 
M - Much
163
Q

How does cardiac tamponade affect the heart?

A

Decreased cardiac output

164
Q

Medications for Valvular disease?

A
  • ACE inhibitor - blood pressure
  • Digoxin- decrease contractility
  • Beta Blockers - protects the heart
  • Antibiotics
  • Anticoagulant
  • Diuretics
  • Vasodialators
165
Q

Medications for shock?

A

Insulin
Steroids
Antibiotics
Vasopressors

Adult Nursing - 225 (9 decks)

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