CRC 431 ECG Basics. Bill Pruitt, MBA, RRT, CPFT, AE-C
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1 CRC 431 ECG Basics Bill Pruitt, MBA, RRT, CPFT, AE-C
2 Resources White s 5 th ed. Ch 6 Electrocardiography Einthoven s Triangle Chest leads and limb leads Egan s 10 th ed. Ch 17 Interpreting the Electrocardiogram Wilkin s 7 th ed. Ch 11 Interpretation of Electrocardiogram Tracings
3
4 Normal ECG
5 Anatomy and the electrical signal 1-2: SA Node- normal pacemaker (~ 65 bpm) SA node fires (too small to see on EKG) and wave of depolarization travels through the atria (P wave). Atria contracts ( atrial kick to preload the ventricles)) 3: AV node causes a delay in the impulse (P-R interval) AV fires ~ 55 bpm
6 Anatomy and the electrical signal 4-5: Bundle of His then R & L bundle branches carries the impulse to the purkinje fibers in the ventricles (purkinje firse ~45 bpm) Ventricles depolarize and contract (QRS complex) Delay occurs again (S-T segment) then ventricles repolarize (T wave)
7 Exclusive characteristics of cardiac cells Cardiac muscle cells are found ONLY in the heart (myocardium) Automaticity Cells that generate an impulse intrinsically (no external or nerve stimulation) Location: SA node, AV junction, purkinje fibers Excitability Cells respond to an electrical stimulus (irritability) Location: All cardiac cells Conductivity Ability of a cell to receive an electrical stimulus and transmit it to other cells Location: All cardiac cells Contractility Ability of a cell to contract in response to an electrical stimulus Location: myocardial muscle cells
8 Factors on Cardiac Output 1) Preload: 2) Afterload: 3) Contractility: 4) Heart Rate:
9 Factors on Cardiac Output 1) Preload: Preload cardiac output (Starling-Frank Mechanism)
10 Factors on Cardiac Output 1) Preload: More out Preload cardiac output (Starling-Frank Mechanism) More in
11 Factors on Cardiac Output 1) Preload: R 2) Afterload: afterload CO R resistance (ie HTN)
12 Factors on Cardiac Output 1) Preload: 2) Afterload: 3) Contractility: contractility CO
13 Factors on Cardiac Output 1) Preload: 2) Afterload: 3) Contractility: 4) Heart Rate: dual effects CO = Heart Rate x Stroke Volume
14 Factors on Cardiac Output 1) Preload: Stoke Volume less out 2) Afterload: 3) Contractility: 4) Heart Rate: dual effects less in Heart Rate CO = Heart Rate x Stroke Volume
15 Normal ECG
16 EKG recording details The EKG paper is made of a grid of big boxes and small boxes. Each big box is 10 mm in length has five small boxes and covers a total of 0.20 sec. Each small box is 1 mm and represents 0.04 sec. The EKG paper moves at a standard speed of 25 mm/sec
17 Einthoven s triangle Positive to negative electrode Lead I - Left arm to right arm Lead II Left leg to right arm Lead III Left leg to left arm
18 ECG Limb Leads As the ECG signal travels toward the arrow, the QRS deflection is upward
19 ECG Augmented Limb Leads
20 ECG Precordial Leads
21 Normal Sinus Rhythm Rhythm - Regular Rate - ( bpm) QRS Duration - Normal P Wave - Visible before each QRS complex P-R Interval - Normal (<5 small squares). Anything above 5 squares would be 1st degree block) Indicates that the electrical signal is generated by the sinus node and travelling in a normal fashion in the heart.
22 Rate: Quick Count ( )
23 Interpretation of ECG: 3 Options for calculating the rate
24 Normal ECG Quick rate just above 60 beats/min (~24 mm 1500/24 = 63 bpm)
25 Normal sinus rhythm Quick rate between 75 and 100 (or ~18 mm: 1500/18= 83 bpm)
26 Premature ventricular contractions (PVCs)
27 Describing PVC s Couplets = 2 abnormal (ectopic) beats in a row Triplet = 3 beats in a row Bigeminy = every other beat is ectopic Trigeminy = every third beat is ectopic
28 Ventricular tachycardia danger!
29 V tach to shock to normal rhythm
30 Monomorphic Ventricular Tachycardia V Tach (Quick rate between 300 and 150. or ~ 8mm 1500/8 = 188 bpm)
31 Torsades de pointes, or simply torsades (polymorphic V Tach) Twisting of points very unstable, may be linked to electrolytes or to some antiarrhthymic drugs. Estimated to occur in ~ 5% of the 300,000 sudden cardiac deaths each year
32 Polymorphic ventricular tachycardia
33 Ventricular fibrillation- Deadly! Pathophysiology/ECG criteria Quivering cardiac muscle, no organized beat (no P, QRS, or T wave) Clinical signs Sudden collapse, unresponsive, no pulse or blood pressure, may have agonal breathing, death Common etiologies Ischemia leading to stable then unstable ventricular tachycardia (VT) Drug, electrolyte imbalance, or acid-base issues that prolong the relative refractory period Electrocution, hypoxia, many more
34 V-tach moving into ventricular fibrillation
35 V-fib
36 Pulseless electrical activity (PEA) Deadly! Pathophysiology/ECG criteria Cardiac conduction (electrical activity) looks fairly normal but there is no pulse, no blood pressure. Clinical signs Sudden collapse, unresponsive, no pulse or blood pressure, may have agonal breathing, death Common etiologies Ischemia leading to stable then unstable ventricular tachycardia (VT) Drug, eleoctrolyte, or acid-base issues that prolong the relative refractory period Electrocution, hypoxia, many more
37 PEA 6 H s Hypovolemia Hypoxia Hydrogen ion (acidosis) Hypo or hyperkalemia Hypoglycemia Hypothermia and 5 T s Toxins Tamponade Tension pneumothorax Thrombosis Trauma EKG is present on monitors but there is no blood pressure, no pulse
38 Asystole - dead
39 Supraventricular tachycardia (SVT) Rhythm - Regular Rate beats per minute QRS Duration - Usually normal P Wave - Often buried in preceding T wave P-R Interval - Depends on site of supraventricular pacemaker Impulses stimulating the heart are not being generated by the sinus node, but instead are coming from a collection of tissue around and involving the atrioventricular (AV) node
40 Supraventricular tachycardia (SVT) Quick rate between 300 and 150 (versus normal tracing 75 to 100) or. 8 mm 1500/8 = 188 bpm
41 Supraventricular tachycardia (SVT) Quick rate between 300 and 150 or 8 mm ~ 188 bpm
42 Sinus tachycardia Rhythm - Regular Rate - > 100 beats per minute QRS Duration - Normal P Wave - Visible before each QRS complex P-R Interval Normal, less than 0.20 sec The impulse generating the heart beats are normal, but they are occurring at a faster pace than normal. Seen during exercise
43 Sinus tachycardia Quick rate between 150 and 100 or 12 mm ~ 125 bpm
44 Atrial flutter Rhythm - Regular Rate P Ventricles have slower response ~ around 110 beats per minute QRS Duration - Usually normal P Wave - Replaced with multiple F (flutter) waves, usually at a ratio of 2:1 (2F - 1QRS) but sometimes 3:1 P Wave rate beats per minute P-R Interval - Not measurable May be asymptomatic
45 Atrial flutter saw tooth
46 Atrial flutter saw tooth
47 Atrial fibrillation Rhythm - Irregularly irregular Rate - usually beats per minute but slower if on medication QRS Duration - Usually normal P Wave - Not distinguishable as the atria are firing off all over P-R Interval - Not measurable The atria fire electrical impulses in an irregular fashion causing irregular heart rhythm May be asymptomatic A-fib and A flutter: increased risk of clots, loss of atrial kick and potential drop in C.O.
48 Atrial fibrillation (irregular not saw tooth )
49 Atrial fibrillation (irregular not saw tooth )
50 Sinus bradycardia Rhythm - Regular Rate - less than 60 beats per minute QRS Duration - Normal P Wave - Visible before each QRS complex P-R Interval - normal Usually benign (asymptomatic) and often caused by patients on beta blockers
51 Sinus bradycardia Quick rate between (or 28 mm ~ 53 bpm)
52 AV Blocks First degree AV block Second degree AV block Type I (Wenckebach/Mobitz I) Type II (Mobitz II) Third degree block
53 1st Degree AV Block Rhythm Regular Rate Normal QRS Duration Normal (< 0.12 sec or 3 small squares) P Wave :QRS - Ratio 1:1 with P rate Normal P-R Interval - Prolonged (>5 small squares) or in other words P-R > 0.20 sec. and fixed (no variation) Just a long P-R interval Usually benign (asymptomatic) and often caused by patients on beta blockers
54 1st Degree AV Block Quick rate (or 24 mm ~ 62 bpm)
55 2 nd degree type I (Mobitz type I or Wenckebach) Rhythm - Regularly irregular Rate - Normal or Slow QRS Duration - Normal P Wave - Ratio 1:1 for 2, 3 or 4 cycles then 1:0 (no QRS) P Wave rate - Normal but faster than QRS rate P-R Interval - Progressive lengthening of P-R interval until a QRS complex is dropped
56 2 nd degree type I (Mobitz type I or Wenckebach) Progressively longer P-R interval until a QRS is dropped
57 2 nd degree block type II (Mobitz II) Rhythm - Regular Rate - Normal or Slow QRS Duration - Prolonged P Wave - Ratio 2:1, 3:1. P to QRS P Wave rate - Normal but faster than QRS rate P-R Interval - Normal or prolonged but constant Constant steady P but disappearing QRS
58 2 nd degree block type II (Mobitz II) You often see 2 P waves for every QRS, or 3 P s for every QRS. Steady, constant P rate, but QRS disappears
59 2 nd degree block type II (Mobitz II)
60 3rd Degree Block Rhythm Regular Rate Slow QRS Duration Prolonged P Wave Unrelated to the QRS P Wave rate - Normal but faster than QRS rate P-R Interval Variation Complete AV block. No atrial impulses pass through the atrioventricular node and the ventricles generate their own rhythm
61 3rd Degree Block
62 3rd Degree Block
63 Heart Blocks Type of block PR interval QRS complex 1 st degree Constant, longer than normal None dropped, no changes 2 nd degree Type 1 (Wenckebach) Gradually longer each time Some dropped, regular pattern 2 nd degree Type 2 Constant 2:1 or 3:1 association with QRS Some dropped 3 rd degree Extremely variable Complete dissocation
64 Bundle Branch blocks Delay through the bundle branches cause a longer, wider QRS Normal QRS is less than.10 seconds or within 2 ½ small boxes on the EKG Sometimes shows up as rabbit ears on the QRS
65 Bundle branch block wide QRS, may have rabbit ears
66 Cardiac ischemia, injury, infarction Ischemia tends to show up as ST segment depression Seen in the corresponding lead for the injury Resolves if perfusion and O 2 delivery is restored
67 Cardiac ischemia, injury, infarction Infarction tends to show ST segment elevation Time is muscle
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