Download 3Rd degree block

~ Maria’s notes Cardiac/EKG Page 1 ~
CHF—left ventricle failure with pulmonary edema.
Acute Failure

Impaired emptying of both ventricles.

Risk: CAD or MI both alters perfusion to cardiac muscle.
Diabetes, smoking and HTN

Results in low forward flow = output
Types:
1. Left sided failure—Blood backs up into lungs—congestion, pulmonary edema.
2. Rt. Sided failure—backup of blood peripherally—jugular distention,
hepatosplenomegally, acites, edema peripherally
* Drug that decreases afterload—Nitroprusside/Nipride
Chronic CHF—Both sides are impaired—fatigue, SOB with exertion, dyspnea at night
Nocturia, edema, weight gain.
Thrombolytic therapy
Expected outcomes: CK increase ST segment decreases. Reperfusion arrhythmias.
* Stop therapy if mental state changes.
Oozing from gums and IV site= normal
Complications—re-occlusion, form another clot—Heparin is used to prevent
Common complication of MI—Arrhythmia
CAD, HX of stable Angina—first line drug at home is ASA or Plavix
After MI start rehabilitation immediately there are 4 steps and 4-6 months. Look at METS
(Cal/min).
CHF—failure of ventricles
Acute failure—something changes left side MI or PE—look for lung crackles.
Chronic failure—symptoms always there
paroxysmal nocturnal
Increase urinary output
~ Maria’s notes Cardiac/EKG Page 2 ~
Pulmonary edema—Drug nitropruside
Treatment of collaborative care for CHF—
1. Decrease intravascular volume
diuretics—Lasix PO or IV SE: ototoxic and nephrotoxic—push very slowly
2. Decrease preload (venous return)—sit pt up in fowler’s position
3. Decrease afterload—Nipride (Nitroprusside)—a vasodilator or dubutrex (inotropic)
4. Improve gas exchange
 Give O2
 For PE—ventilator
 Give morphine for pain, anxiety and dyspnea
5. Improve Cardiac function—give digitalis (or linoxin)
CAUTION: toxic with hypokalemia—Lasix that are K wasters
S/S of dig toxicity—yellow vision, N/V, anorexia
Can cause arrhythmias, Toxic with Ca channel blockers
6. Ace inhibitors—Vasotec, lotensin, prinivil, zestril
Decreases afterload, and Decreases workload
FIRST LINE TX.
7. Diet—low Na only 2 g of Na a day.
CardioMyopathy
1. Primary—cause unknown
2. Secondary—identifiable cause
Types:
1) Dilated
 Most common
 Congestive
 Ventricular and atrial dilation
 Causes: diabetes, chemo, Nutritional def. (anorexia nervosa) and cocaine
 Results—grave prognosis
2) Hypertrophic—hypertrophy without dilation
Familial—genetic
~ Maria’s notes Cardiac/EKG Page 3 ~
Valvular surgery—replace heart valve
a) Mechanical—metal will always need anticoagulants for entire life, Lasts
longer. PT 2-3
b) Biological—pig heart, valve—no anticoagulants.
Arrhythmia—telemetry strip—regular how fast—not diagnostic
Leads:
Lead II expect upward deflection of P wave, baseline
MCL-I modified chest lead P upright and QRS is downward.
EKG—1 mm tiny box—0.04 sec.
5 mm Big box—0.2 sec.
QRS—ventricular response—pulse (depolarization of heart)
Assessing a strip:
1.
Is there a P for every QRS?
2.
Is it regular?
3.
Rate 60-100 normal
4.
P—R interval, count from P to Q. Should be less than 0.20, one big box, 5
little boxes
5.
How big is QRS interval? Should be less than 0.12—less than 3 little boxes.
If it is wider there is a ventricular block
6.
What is it? Sinus rhythm is normal
Pacemaker of the heart—SA node 60-100. AV node—40-60
Sinus Rhythm—60-100 bpm
AV node—40-60 bpm and no P wave
Purkinji fibers in ventricles—20-40 bpm and no P wave
Sinus Bradycardia—Check Pulse and BP 70/40
TX: Give atropine—speeds up HR and increases firing of SA node
Symptomatic-atropine and/or pacemaker
~ Maria’s notes Cardiac/EKG Page 4 ~
Sinus Tachycardia—Causes hypoxia, increased temperature, CHF, and hypoglycemia
NORMAL K levels = 3.5 – 5.
I. Junctional rhythm:
 Originates in the A-V node.
 May move retrograde
 No P wave
 Rate should be 40-60.
 No 1:1 conduction
TX: Don’t slow down the heart, give Atropine or inderal
II. First degree A-V Block
 PR interval > 0.20 sec.
 Causes MI, rheumatic fever, digoxin toxicity
 1:1 conduction
 No specific treatment, look at pt.
III. 2nd degree A-V block Type I—Wenkebach
Progressive lengthening of P-R interval until QRS is dropped and then pattern repeats.
No 1:1 Conduction
Causes: Drug Digoxin and Beta Blockers, MI, CAD or ischemic changes.
TX: give Atropine to speed up may need temp. pacemaker.
IV. 2nd degree A-V block Type II
QRS is dropped without warning
No lengthening of P-R interval
No 1:1 conduction
Almost always occurs with bundle branch block
Wide QRS
Scariest there is NO warning.
~ Maria’s notes Cardiac/EKG Page 5 ~
TX: Atropine increase rate, and pacemaker, Epinephrine—increase HR, contractility, BP is
also a bronchodilator.
V. 3Rd degree block
 Complete block
 No relationship between P and QRS, They fire independently.
 Ventricles pace itself—rate 20-40.
 No relationship between the atria and ventricles.
 Ventricle tries to pace itself
 Caused from Ischemia, MI,
 Will have bradycardia, syncope, Decreased CO.
TX: Atropine, If collapse—epi. Dopamine and pacemaker.
1. Premature ventricular contractions: (PVCs)
 ectopic beat originates in the ventricle.
 T wave moves in opposite direction
 Wide, ugly and bizarre.
 Normal beat, wide ugly bizarre and then upside down T.
Causes of PVC: Caffeine, alcohol and HypoKalemia and hyperkalemia, MI, Mitral valve
prolapse.
3 or more in a row –ventricular tachycardia.
TX: Lidocaine (in acute situation) if PVC turns into V-tach use defibrillator and shock them
ASAP.
Pulseless electrical activity—caused from severe hypovolemia conduction is still normal but no
output. Monitor looks great but pt looks dead.