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Medsurg 3 > Exam 2 > Flashcards

Exam 2 Flashcards

1
Q
  1. Describe sinus bradycardia:
  2. What diseases might cause sinus bradycardia (4)?
  3. T or F, increased vagal tone causes sinus bradycardia? Can hypothermia cause bradycardia?
  4. If condition is bad enough, what drugs or apparatus might be necessary?
  5. What are the clinical manifestations of sinus bradycardia?
A
  1. SA nodes fires <60 beats/min
    Normal in aerobically trained athletes & during sleep
    Can occur in response to parasympathetic nerve stimulation and certain drugs
    Associated with some disease states
  2. Hypothyroidism
    Increased intracranial pressure
    Obstructive jaundice
    Inferior wall MI
  3. T. Yes
  4. Atropine, epi or dopamine, pacemaker
  5. Hypotension
    Pale, cool skin
    Weakness
    Angina
    Dizziness or syncope
    Confusion or disorientation
    Shortness of breath
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2
Q
  1. Describe sinus tachycardia. Is it caused by vagal inhibition? Is sinus tachy associated with stress?
  2. Name the classic reason for sinus tachycardia and then all the other clinical associations:
  3. Will the heart use more or less O2 in sinus tach? What can this mean in an acute MI?
  4. What are the meds or tx for sinus tach?
  5. How does sinus tachycardia present (other than the hr)?
A
  1. SA node discharge rate of >100. Yes. Yes
  2. Hypovolemia (classic)
    Exercise
    Hypotension (also /bradycardia)
    Myocardial ischemia
    CHF
    Anxiety
  3. more. May cause angina or increase size of infarct
  4. Vagal maneuver
    β-blockers, adenosine, or calcium channel blockers
    Synchronized cardioversion
  5. Dizziness
    Dyspnea
    Hypotension
    Angina in patients with CAD
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3
Q
  1. Describe premature atrial contractions:
  2. What are PACs associated with?
  3. Are PACs significant?
  4. Do we treat these?
  5. How do these manifest?
A
  1. Contraction starts from ectopic focus in atrium (location other than SA node)
    Travels across atria by abnormal pathway - distorted P wave
    Impulse may be stopped, delayed, or conducted at AV node
  2. stress, fatigue, caffeine, tobacco, alcohol, hypoxia, electrolyte imbalance, and disease states
  3. In otherwise healthy heart, no. But they can warn of SVT or other problems in a diseased heart
  4. Usually not. But stop causative factors. Beta blockers can be used if needed.
  5. Described as palpitations or skipping a beat
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4
Q
  1. Describe SVTs:
  2. Clinical associations of SVTs:
  3. What are the manifestations of SVTs?
  4. How do we treat paroxysmal SVTs?
A
  1. Originates in ectopic focus anywhere above bundle of His
    Paroxysmal means “an abrupt onset & termination”
    Can be triggered by a preceding PAC
  2. Overexertion
    Stress
    Deep inspiration
    Stimulants, disease
    Digitalis toxicity
    Can occur in presence of Wolff-Parkinson-White syndrome (Onset during childhood)
  3. HR 151 to 220 beats/min
    Hypotension
    Palpitations
    Dyspnea
    Angina
  4. Vagal stimulation
    IV adenosine
    IV β-blockers
    Calcium channel blockers
    Synchronized cardioversion
    Ablation
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5
Q
  1. Describe Atrial flutter:
  2. What are the clinical associations of a-flutter?
A
  1. Atrial tachyarrhythmia
    Identified by recurring, regular, sawtooth-shaped flutter waves
    From single ectopic focus
    Associated w/slower ventricular response
    Atrial rate 200-350, Ventricular rate generally <100
    Ventricular rate may be regular or irregular
    1. CAD
      Hypertension
      Mitral valve disorders
      Cardiomyopathy
      Pulmonary embolus
      Chronic lung disease
      Cor Pulmonale
      Hyperthyroidism
      Drugs: Digoxin, Quinidine, Epinephrine
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6
Q
  1. Describe atrial fibrillation
  2. Clinical associations of A-fib:
A
  1. Total disorganization of atrial activity w/out effective atrial contraction
    Chronic or intermittent; Paroxysmal or Persistent
    Most common dysrhythmia
    Prevalence increases with age
    Usually occurs in patients with underlying heart disease
    Atrial Rate 350-600, Ventricular Response Variable/Irregular (CVR, RVR)
  2. CAD and/or Cardiac Surgery
    Hypertension
    Valvular Heart Disease
    Cardiomyopathy and/or Heart Failure
    Pericarditis
    Thyrotoxicosis
    Alcohol intoxication and/or Caffeine
    Electrolyte disturbances
    Stress
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7
Q
  1. How do a-flutter and a-fib manifest? What is the greatest risk?
  2. What are the treatments for these conditions?
A
  1. Symptoms result from high ventricular rate & loss of atrial “kick”
    Decreased CO
    Can cause heart failure
    Increased risk of stroke
    AFIB up to 20% of strokes
  2. Anticoagulate for Aflutter or AFib lasting > 48h
    Drugs to control ventricular response and/or convert to sinus rhythm (calcium channel blockers, beta blockers, antidysrhythmics most common)
    Electrical cardioversion (Anticoagulate for 3-4 weeks prior)
    Radiofrequency ablation
    Refractory AFib: AV nodal ablation w/Pacemaker or Maze
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8
Q
  1. Describe 1st degree heart block:
  2. Are these serious? Are patients asymptomatic?
  3. How do we treat?
A
  1. AV is moody and delays conduction. PR interval prolonged (>0.20)
    Associated with increasing age, disease states, and certain drugs
  2. Usually not serious
    Patients asymptomatic
  3. No treatment
    Monitor for changes in heart rhythm
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9
Q

1, Descrie 2nd degree, type 1 (Wenchebach)

  1. Are these usually transient and well-tolerated?
  2. What are the treatments if necessary?
A
  1. AV lets them in irregularly and eventually not at all (dropped beat). Gradual lengthening of PR interval until QRS complex eventually dropped
    Occurs because of prolonged AV conduction time
    May result from drugs or CAD
    Typically associated with ischemia
  2. yes
  3. Treat if symptomatic
    Atropine
    Pacemaker
    If asymptomatic, observe closely
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10
Q
  1. Describe the 2nd degree, type 2 AV block?
  2. Almost always occurs when ……. ……… ……… is present
  3. What is this associated with?
  4. Why are these dangerous?
  5. How do we treat?
A
  1. Certain number of SA node impulses not conducted to ventricles
    Sudden dropped QRS complexes.
    No gradual lengthening of PR interval
    P wave not conducted.
  2. bundle branch block
  3. Associated with heart disease and drug toxicity
  4. Often progress to 3rd degree heart block w bad prognosis
  5. Pacemaker
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11
Q
  1. Describe 3rd degree AV heart block:
  2. What are these associated with?
  3. What drugs might cause these?
  4. What is the treatment?
A
  1. Complete heart block
    P waves & QRS complexes have nothing to do with each other (divorced)
    No impulses from atria conducted to ventricles
  2. Severe heart disease
    Some systemic diseases (CAD, MI, myocarditis, cardiomyopathy, scleroderma)
    Certain drugs
  3. digoxin, beta-blockers, calcium channel blockers
  4. Pacemaker, dopamine, epi, (atropine wont work)
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12
Q
  1. Describe PVCs:
  2. clinical associations:
  3. Are these harmful?
  4. How do we treat?
A
  1. Contraction originating in ectopic focus of ventricles
    Premature occurrence of QRS complex
    Multifocal, unifocal, ventricular bigeminy, ventricular trigeminy, couplets, and triplets
  2. Stimulants, electrolyte imbalances, hypoxia, heart disease, exercise
    May occur following acute MI and/or following reperfusion of coronary arteries
  3. not in a normal heart. Possible in a diseased heart
  4. Assess hemodynamic status
    Correct cause
    β-blockers, lidocaine, or amiodarone
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13
Q
  1. Describe V-tach
  2. Is this life threatening? Why?
  3. What is this associated with?
  4. What is torsade des pointes?
  5. How do we treat?
A
  1. Ectopic foci in ventricles take over as pacemaker
    Monomorphic, polymorphic, sustained, and nonsustained
  2. Yes because reduced cardia Output and possibility to progress to V-fib
  3. Heart disease
    Long QT syndrome
    Electrolyte imbalances
    Drug toxicity
    CNS disorders
    Has been observed in individuals with no evidence of heart disease
  4. polymorphic v-tach
  5. Precipitating causes must be identified and treated
    VT with pulse (stable) treated with antidysrhythmics and/or rapid cardioversion
    Pulseless VT (unstable) treated with CPR and rapid defibrillation
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14
Q
  1. Describe v-fib:
  2. What is this associated with?
  3. Why is this significant?
  4. How do we treat?
A
  1. chaotic firing of multiple ectopic foci (rave in the strip club)
  2. Acute MI, Myocardial Ischemia
    Electrolyte imbalances Hypoxia, Acidosis
    Chronic diseases (CAD, HF, Cardiomyopathy)
    Cardiac procedures
    Electrical Shock
    Durg Toxicity
  3. No cardiac output
    Unresponsive, pulseless, and apneic
    If not treated rapidly, death will result
  4. Immediate CPR then ACLS when available
    Defibrillation
    Drug therapy (epinephrine, amiodarone)
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15
Q
  1. Describe asystole
  2. Usually a result of …..
  3. How do we treat?
  4. What is the prognosis?
A
  1. Total absence of ventricular electrical activity
    No ventricular contraction
    Patient unresponsive, pulseless, apneic
    *Must assess in more than one lead
  2. advanced cardiac disease, severe conduction system problem, or end-stage HF
  3. Treat with immediate CPR and ACLS measures
    Epinephrine
    Intubation
  4. Poor prognosis
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16
Q
  1. What is pulseless electrical activity?
  2. What is the prognosis?
  3. Potential underlying causes of this (6H’s and 5 T’s):
  4. Treatment?
A
  1. Electrical activity can be observed on the ECG, but no mechanical activity of the heart is evident
    Patient has no pulse
  2. Prognosis is poor unless underlying cause quickly identified and treated
  3. Hypovolemia
    Hypoxia
    Hydrogen ion (acidosis)
    Hyper-/hypokalemia
    Hypoglycemia
    Hypothermia
    Toxins
    Tamponade (cardiac)
    Thrombosis (MI and pulmonary)
    Tension pneumothorax
    Trauma
  4. CPR followed by intubation and IV epinephrine
    Treatment is directed toward correction of the underlying cause
17
Q
  1. When do we defibrillate (with which rhythms)?
  2. When is it most effective?
  3. What does it do?
  4. Difference between monophasic and biphasic defibrillators:
A
  1. Treatment of choice for VF and pulseless VT
  2. Within 2 minutes of dysrhythmia onset
  3. Passage of electrical shock through the heart to depolarize myocardial cells

Allows SA node to resume pacemaker role

  1. Monophasic delivers energy in one direction. Biphasic delivers energy in 2 directions. Uses lower energies and less post shock dysrhythmias.
18
Q
  1. Describe synchronized cardioversion (which dysrhythmias, how does it work):
  2. Does this use higher or lower energy than a defibrillator?
  3. Do we sedate patient prior?
  4. If patient becomes pulseless, what do we do?
A
  1. Therapy of choice for ventricular or supraventricular tachydysrhythmias (VT with a pulse)
    Synchronized delivery of a shock on the R wave of the QRS complex of the ECG
    Intent is to allow SA node to resume role
  2. lower energy
  3. If patient stable, sedate prior
  4. turn sync button off and defibrillate
19
Q
  1. What patients benefit from an implanted cardioverter defibrillator?
  2. What do these devices do?
A
  1. Have survived SCD
    Have spontaneous sustained VT
    Have syncope with inducible ventricular tachycardia/fibrillation during EPS
    Are at high risk for future life-threatening dysrhythmias
  2. decreases mortality by delivering 25 J or less to heart when detects lethal dysrhythmia

Medsurg 3 (2 decks)

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