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EKG CARDIOVASCULAR ANATOMY & PHYSIOLOGY. Basic Heart Anatomy ▪ The heart is a muscle made of 3 layers ▪ Pericardium aka= pericardial sac is a connective.

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Presentation on theme: "EKG CARDIOVASCULAR ANATOMY & PHYSIOLOGY. Basic Heart Anatomy ▪ The heart is a muscle made of 3 layers ▪ Pericardium aka= pericardial sac is a connective."— Presentation transcript:

1 EKG CARDIOVASCULAR ANATOMY & PHYSIOLOGY

2 Basic Heart Anatomy ▪ The heart is a muscle made of 3 layers ▪ Pericardium aka= pericardial sac is a connective tissue layer around the heart 1.Epicardium is the smooth outer surface of the heart 2.Myocardium is the muscular middle layer of heart tissue ▪ It is made of cardiac muscle cells that give the heart the ability to contracts to push out blood 3. Endocardium is the innermost layer of the heart  made up of smooth thin connective tissue  This smooth layer allows blood to flow easily throughout the heart

3 Basic Heart Anatomy ▪ The heart is a muscle ▪ Referred to as a 2 sided PUMP ▪ Right side ▪ Left side ▪ Each side has 2 hollow chambers ( total of 4 chambers ▪ 2 upper chambers are called=Atrium ( singular) Atria ( plural) ▪ 2 lower chambers are called = Ventricle(s)

4 Heart Anatomy- CONTINUED ▪ Both upper chambers receive blood back to the heart ▪ RA- receives blood from the superior & inferior vena cava ▪ LA- receives blood from the lungs ▪ Both lower chambers pump blood away from the heart ▪ RV – pumps blood to the lungs for re-oxygenation ▪ LV- pumps blood into the systemic circulation

5 Basic Heart Anatomy ▪ Valves of the Heart ♥The 4 valves of the heart allow blood to flow only in one direction ♥There are 2 sets of valves ♥Atrioventricular valves ♥Are located between the atria and the ventricles ♥Right sided valve is the tricuspid valve ♥Left sided valve is the bicuspid valve or the mitral valve ♥Semilunar valves ♥Serve to prevent blood from flowing back into the ventricles ♥Right sided semilunar valve = Pulmonary valve is located between the right ventricle and the pulmonary artery ♥Left sided semilunar valve = Aortic valve is located between the left ventricle and the trunk of the aorta

6 Heart Anatomy- CONTINUED Atria Are the 2 upper chambers (LEFT & RIGHT) Upper chambers are located in what is called the BASE of the heart Ventricles Are the 2 lower chambers (LEFT & RIGHT ) Lower chamber are located in what is called the APEX of the heart

7 Heart Anatomy- CONTINUED Blood flow through the heart Refer to handout on cardiac/pulmonary circulation Heart Blood Flow Animation Heart Blood Flow Animation

8 Basic Physiology of the Heart CARDIAC CYCLE STROKE VOLUME CARDIAC OUTPUT AUTONOMIC NERVOUS SYSTEM

9 Cardiac Cycle ♥ The heart functions as a unit: ♥ Both atria contract simultaneously then both ventricles contract ♥ Blood is ejected into both the pulmonary and systemic circulation when the ventricles contract ♥ Both the tricuspid and mitral valves will also close during ventricular contraction ♥ The cardiac cycle=Represents the time sequence between ventricular contraction and ventricular relaxation ♥ Systole is ventricular contraction ♥ Diastole is ventricular relaxation ♥ SO--- One cardiac cycle is equal to one systole and one diastole of the ventricle or one heart beat ♥ In a normal heart the cardiac cycle lasts for 0.8 seconds

10 Stroke Volume ♥ Stroke volume (SV)= is the amount or volume of blood pumped out of the one ventricle in a single beat or contraction ♥ Normal SV is 70 cubic centimeters (cc) per beat ♥ The number of contractions or beats per minute is known as the heart rate ♥ The normal heat rate in an adult is 60-100 beats per minute

11 Cardiac Output ♥ Cardiac output is the amount of blood PUMPED by the LEFT VENTRICLE in ONE MINUTE ♥ The formula for Cardiac Output is: ♥ CARDIAC OUTPUT(CO) = STROKE VOLUME (SV) X HEART RATE (HR) HR= 80 SV= 70 cc What is the Cardiac Output of this patient in cc’s_______ and in _______liters????

12 Cardiac Output ▪ Inadequate, CO will result in patients having any of the following symptoms: ▪ Shortness of breath ▪ Dizziness ▪ Drop in blood pressure ▪ Chest pain ▪ Cool and clammy skin

13 PRELOAD and AFTERLOAD ♥ PRELOAD ▪ Pre-load is the filling pressure of the heart, the pressure the heart has when it is relaxing. (Volume- In) ♥ Afterload ▪ is the RESISTANCE against which the heart must pump ▪ After-load is the pressure of the contracting heart. (Resistance- push- Out) ▪ This pressure will greatly affect the stroke volume and the cardiac output

14 Autonomic Nervous System ▪ ANS regulates functions of the body that are INVOLUNTARY ▪ Both HR and BP are regulated by this component of the nervous system ▪ There are 2 major divisions of the nervous system: ▪ sympathetic and parasympathetic ▪ The major organs of the body are innervated by both systems with the exception of blood vessels which are only innervated by the sympathetic system

15 Sympathetic Nervous System ▪ Sympathetic nervous system (or Adrenergic) ▪ 1. Accelerates the heart ▪ 2. Two chemicals are influenced by the sympathetic system – ▪ epinephrine & norepinephrine ▪ 3. These chemicals increase heart rate, contractibility, automaticity, and AV conduction

16 Parasympathetic Nervous System ▪ Parasympathetic nervous system ( or Cholinergic) ▪ 1. Slows the heart ▪ 2. The vagus nerve is one of this systems nerves, when stimulated slows heart rate and AV conduction.

17 Basic Electrophysiology Basic Cell Groups ▪ The heart is made up of thousands of myocardial cells ▪ There are 2 basic myocardial cell groups: ▪ myocardial working cells ▪ pacemaker cells of the electrical conduction system ▪ MYOCARDIAL CELLS responsible for generating the physical contraction an d relaxation of the heart muscle ▪ PACEMAKER CELLS ▪ do not contain contractile fragment and can not contract ▪ Responsible for controlling the rate & rhythm of the heart by regulating depolarization

18 Characteristics of Cardiac Cells Cardiac cells possess primary cell characteristics:  Extensibility  Ability to be stretched ▪ Excitability ▪ Ability of cardiac cells to respond to electrical stimulation ▪ Conductivity ▪ Ability of cardiac cells to receive electrical stimulation and transmit the stimulus to other cells ▪ Contractility ▪ Ability of cells to shorten and cause a muscle contraction ▪ Automaticity ▪ Ability of cardiac pacemaker cells to make their own electrical impulses

19 ELECTRICAL CELLS OF THE HEART ▪ Electrical cells ▪ a) Make up the conduction system of the heart ▪ b) Are distributed in an orderly fashion through the heart ▪ c) Possess specific properties ▪ (1) automaticity – the ability to spontaneously generate and discharge an electrical impulse ▪ (2) excitability – the ability of the cell to respond to an electrical impulse ▪ (3) conductivity – the ability to transmit an electrical impulse from one cell to the next

20 MYOCARDIAL CELLS ▪ Myocardial cells ▪ a) Make up the muscular walls of the atrium and ventricles of the heart ▪ b) Possess specific properties ▪ (1) contractility – the ability of the cell to shorten and lengthen its fibers ▪ (2) extensibility – the ability of the cell to stretch

21 Major Electrolytes that Affect Cardiac Function An electrolyte is a substance with charged components producing positive and negative charged ions ▪ a positive ion is called a cation ▪ a negative ion is called a anion  3 major cations that affect heart muscle are:  Potassium K+  Sodium Na+  Calcium Ca+  Magnesium Mg

22 DEPOLARIZATION & REPOLARIZATION ▪ Depolarization and Repolarization ▪ 1. Cardiac cells at rest are considered polarized, meaning no electrical activity takes place ▪ 2. The cell membrane of the cardiac muscle cell separates different concentrations of ions, such as sodium, potassium, and calcium. This is called the resting potential ▪ 3. Electrical impulses are generated by automaticity of specialized cardiac cells ▪ 4. Once an electrical cell generates an electrical impulse, this electrical impulse causes the ions (Na+ rush into the cell making inside more +) cross the cell membrane and causes the action potential, also called depolarization

23 Depolarization & Repolarization Continued ▪ 5. The movement of ions across the cell membrane through sodium, potassium and calcium channels, is the drive that causes contraction of the cardiac cells/muscle ▪ 6. Depolarization with corresponding contraction of myocardial muscle moves as a wave through the heart ▪ 7. Repolarization is the return of the ions to their previous resting state, which corresponds with relaxation of the myocardial muscle ▪ 8. Depolarization and repolarization are electrical activities which cause muscular activity ▪ 9. This electrical activity is what is detected on ECG, not the muscular activity

24 Conduction System THE PATH OF AN ELECTRICAL SIGNAL ▪ Step One: The S-A node creates an electrical signal ▪ The S-A node controls your heart rate, it is called your heart's "natural pacemaker." Electrical signals created by the S-A node travel down pathways to the A-V node creating the P WAVE ▪ It has as inherent rate of 60-100 bpm ▪ Step Two: The signal follows natural pathways through both atria. This causes the blood to contract, pushing blood into the ventricles ▪ Step Three: The signal reaches the A-V node. There, the signal pauses very briefly to give the ventricles time to fill with blood. ▪ This delay is seen as the PR interval ▪ Step Four: The signal spreads through the His-Purkinje system. This makes the ventricles contract, pushing blood out to your lungs and body. ▪ This generates the QRS complex ▪ Bundle of His have pacemaker cells that can self-initiate a rate of 40-60 bpm ▪ Purkinje pacemaker fibers are normally within 20-40 bpm

25 Electrical Conduction VIDEO ▪ Electrical Flow in the Heart Electrical Flow in the Heart

26 EKG Conduction Animation ▪ Conduction and EKG Waveform Animation Conduction and EKG Waveform Animation

27 The Electrocardiogram EKG or ECG ▪ Graphic representation of the electrical activity of the heart ▪ It is a tracing of the electrical activity of the heart NOT the mechanical activity ▪ The machine used to record the activity is called an: electrocardiograph ▪ It is a diagnostic tool

28 Information Obtainable from EKG RHYTHM ANALYSIS ▪ Heart Rate ▪ Rhythm & regularity ▪ Impulse conduction time intervals ▪ Abnormal conduction pathways ▪ WE CANNOT HOWEVER determine: ▪ Pumping action ▪ Cardiac output ▪ Blood pressure ▪ Cardiac muscle hypertrophy

29 EKG Machine ▪ An EKG machine is a voltmeter– it reads electrical energy from the body ▪ The heart uses electrical energy to contract muscles

30 EKG LEADS and ELECTRODES ▪ ELECTRODE is the adhesive pad that contain conductive gel and is placed on the patients skin ▪ LEADS are the wires that are then connected to the electrode – they are color coded to be user-friendly ▪ In order for the machine to give a clear picture– there must be a positive, negative and ground lead ▪ EKG will look at the heart from the positive lead to the negative lead and gives a different view of the heart ▪ The exact portion of the heart being visualized depends on lead placement ▪ This allows for observation of electrical activity in many different parts of the heart

31 3 Lead EKG- Used for continuous patient monitoring ▪ A 3 lead ECG is considered non-diagnostic so it does not provide a clear view of the entire heart, but instead a basic view of the electrical pathway of the heart triangulated between the 3 leads. ▪ The 3 lead ECG is usually simple to use and most have standardized color coded placement of the 3 electrode leads. These are the most common 3 lead ECG placements: ▪ 3-electrode system - Uses 3 electrodes (RA, LA and LL). - Monitor displays the bipolar leads (I, II and III) - To get best results – Place electrodes on the chest wall equidistant from the heart Will give us a view of the lateral, and inferior portion of the heart

32 AUGMENTED LEADS: PLEASE NOTE THE FOLLOWING: ▪ EKG Augmented Limb Leads ▪ The same three leads that form the standard leads also form the three unipolar leads known as the augmented leads. These three leads are referred to as aVR (right arm), aVL (left arm) and aVF (left leg) and also record a change in electric potential in the frontal plane. ▪ These leads are unipolar in that they measure the electric potential at one point ▪ We can get additional contiguous (adjoining) views of the heart: ▪ aVL- Lateral ▪ aVF- Inferior

33 5 Lead EKG ▪ This configuration refers to the standard Holter monitor or the 5 lead rhythm setup White lead=right sternum/clavicle area Black lead=left sternum/clavicle area Red lead=left lower thoracic area Green lead=right lower thoracic area Brown lead= just below and to the right of the bottom of the sternum

34 12 LEAD EKG ▪ Definition- A representation of the heart’s electrical activity recorded from 10 electrodes placed in standard positions on the body surface. ▪ Analogy- Envision the heart as an object placed on a pedestal around which a person can move while taking photographs (different views) from all angles.

35 12 Lead EKG Provides a Cross Sectional View of the Heart ▪ 12-lead ECG - 10 electrodes required to produce 12- lead ECG. - Electrodes on all 4 limbs (RA, LL, LA, RL) - Electrodes on precordium (V1–6) V1 @4 th IC right of sternum V2 @ 4 th IC left of sternum V3@ between V2/V4 V4 @ 5 th IC midclavicular V5 5 th IC between V4/V6 V6 @ 5 th IC midaxillary Leads I,II,II are bipolar= this means they have one positive and one negative electrode ( limb leads) -Allows the best interpretation of specific areas of the heart - Inferior (II, III, aVF) - High Lateral Wall(I, aVL) -Lower Lateral Wall( V5, V6) -Septal View (V1-V2) -Anterior View (V3-V4)

36 Precordial LEAD Placement of the 12 lead EKG V1 @4 th IC right of sternum V2 @ 4 th IC left of sternum V4 @ 5 th IC midclavicular V3 @ between V2/V4 V6 @ 5 th IC midaxillary V5 5 th IC between V4/V6 Lead Placement Visual 12 LEAD EKG PLACEMENT VIDEO

37 EKG Graph Paper ▪ Arranged in a series of horizontal and vertical lines and squares ▪ Standard in all health care settings ▪ Moves at a constant speed of 25 millimeters per second ▪ Both time and amplitude are measured on EKG graph paper ▪ Time is measured on the HORIZONTAL line ▪ Amplitude is measured on the VERTICAL line ▪ Divided into small squares, each of which is 1 mm in width and equals a time interval of 0.04 second ▪ Darker lines further divide every 5 th square, both vertically and horizontally ▪ Each larger square measures 5 mm in height and 5 mm in width and represents a time interval of 0.20 second

38 EKG Paper and Markings ▪ Divided into small squares, each of which is 1 mm in width and equals a time interval of 0.04 second ▪ Darker lines further divide every 5 th square, both vertically and horizontally ▪ Each larger square measures 5 mm in height and 5 mm in width and represents a time interval of 0.20 second ▪ 5 of the large squares all equal one second noted by the small line on the very top of the paper ▪ Most practitioners will print a 6 second strip to interpret a patients rhythm ▪ The squares of on the EKG paper represent the measurement of the length of time required for the electrical impulse to traverse a specific time in the heart

39 EKG Paper and Markings

40

41 EKG Waveforms P Wave ▪ P wave ▪ Impulse fired by the SA node ▪ The p wave is a smooth rounded upward deflection ▪ Represents depolarization of the atria ▪ It is 0.1 second in duration

42 PR Interval  Represents the time interval for the impulse to travel for the SA node through the internodal pathway toward the ventricle  Normal PR interval is 3-5 small boxes or 0.12 – 0.20 second in length

43 QRS Complex ▪ Represents the conduction of the impulse from the Bundle of His through the ventricle muscle or ventricle depolarization ▪ QRS measures less than 0.12 second or less than 3 small boxes on the EKG graph paper

44 ST Segment ▪ Represents the time interval which the ventricles are depolarized and ventricular repolarization ▪ ST segment is ISOELECTRIC or at baseline

45 T Wave ▪ Represents ventricular repolarization ▪ Resting phase of the cardiac cycle

46 U Wave ▪ The U wave is a wave on an electrocardiogram that is not always seenelectrocardiogram ▪ typically small, and, by definition, follows the T waveT wave ▪ U waves are thought to represent repolarization of the Purkinje fibers. [1]Purkinje fibers [1]

47 How is an EKG Interpreted? ▪ Read strip from left to right ▪ Apply the 5 step approach that you will learn ▪ Ask and answer each question in the 5 step approach ▪ You must master the accepted parameters for each dysrhythmia and then then apply those parameters to each of the 5 steps when analyzing the strip.

48 FIVE STEP APPROACH ▪ Step 1: What is the rate? ▪ Step 2: Is it regular? ▪ Step 3 : Is the complex narrow? ▪ Step 4: Is there a P WAVE? ▪ Step 5: Do all the complexes look the same?

49 STEP ONE & the 6 Second Method ▪ What is the rate? ▪ Count the number of QRS complexes or number of ventricular beats in one minute -- ▪ Normal heart rate is 60-100 bpm ▪ 6 second method ▪ Simply count the number of QRS complexes in either 3 or 6 second strip ▪ If a 3 second strip is used– X by 20 ▪ If a 6 second strip is used – X by 10

50 6 Second Strip

51 3 And 6 second Illustrations

52 STEP 2 ▪ Asks if the rhythm is regular? ▪ Rhythms that originate from the normal pacemakers in the heart will be regular ▪ IRREGULAR rhythms indicate extra or abnormal beats ▪ Looks at the patterns of your QRS complexes ▪ All heart rhythms are classified as regular or irregular ▪ You should use EKG calipers or use a piece of paper and mark r-r wave distance 1.Measure your R-R interval to determine Ventricular regularity 2.Measure your P-P waves for atrial regularity

53 STEP 3 ▪ Is the complex narrow? ▪ Narrow complexes are normal ▪ Wide QRS complexes indicated a conduction abnormality ▪ Normal QRS width is 0.12 second or less than 3 small boxes ▪ Wide QRS or greater than 0.12 second or more than 3 small boxes ( ventricular in origin) ▪ Narrow QRS less than 0.12 second may indicate a supraventricular rhythm

54 NARROW & WIDE QRS Complexes

55 Step 4 ▪ ASK– IS THERE A P WAVE????????? Preceding the QRS complex? ▪ A P-wave before the QRS represent normal conduction from the atria to the ventricles ▪ If there is NO P wave---- the impulse is being generated from ELSEWHERE IN THE HEART AND IS NOT A SINUS RHYTHM

56 Step 5 ▪ Do all the complexes look the same?

57 5 STEP APPROACH to EKG Interpretation 1.What is the rate? 2.Is it regular? 3.Are the QRS complexes narrow? 4.Is there a P WAVE? ( Is there a P WAVE before each complex?) Is the PRI normal ? 5.Do all the QRS complexes look the same?

58 Normal P wave, Absence of P wave, Abnormal P Wave

59 Step 5 ▪ Do all the complexes look the same? ▪ Normal conductions follows the same pathway with each beat ▪ Different looking complexes indicate that some impulses are following alternative or aberrant pathways

60 Conclusion of the 5 STEP METHOD ▪ If you can answer affirmatively to all of the 5 steps then your patient has a Normal Sinus Rhythm or NSR

61 Normal Sinus RHYTHMS ▪ Normal Sinus Rhythm or NSR ▪ Rate 60-100 ▪ Sinus Bradycardia--- ▪ Rate is LESS THAN 60 ▪ Sinus Tachycardia– ▪ Rate is GREATER THAN 100 but not more than 140

62 Atrial RHYTHMS ATRIAL FIBRILLATION ATRIAL FLUTTER SVT/PSVT

63 Rhythms That Originate in the Atria ▪ Atrial Fibrillation ▪ Atrial Fibrillation with Rapid Ventricular Response ▪ Atrial Flutter ▪ Supraventricular Tachycardia

64 EKG Findings Common to ATRIAL RHYTHMS ▪ P wave absent or has an abnormal shape ▪ Fibrillatory waves present– commonly called f waves ▪ Flutter waves present ▪ QRS is narrow

65 Atrial Fibrillation ▪ Atrial fibrillation produces a rapid and irregular heartbeat ▪ The atria (the upper two chambers of the heart that receive blood) quiver, or fibrillate, instead of beating normally ▪ impulses come from all over the atria, triggering 300 to 500 contractions per minute within the heart’s upper chambers ▪ the atrioventricular node becomes overwhelmed by impulses ▪ the result is an irregular and rapid heartbeat (80 to 160 beats per minute versus normal 60 to 100 beats per minute). ▪ Atrial Fibrillation Atrial Fibrillation

66

67 ▪ P wave---none or fibrillation waves ▪ PR interval—none ▪ QRS—less than 0.12 seconds ▪ Ventricular rate—60-100 bpm ▪ Atrial rate( if different than the ventricular rate)– 300-600/min ▪ Complexes look similar ▪ RHYTHM__ IS IRREGULAR ▪ FYI- if the rate is less than 100 = controlled ▪ If the rate is greater than 100= rapid ventricular response or RVR

68 TREATMENT ▪ Medications ▪ Cardioversion ▪ Ablation surgical procedures

69 Atrial FLUTTER ▪ Typical atrial flutter results from a single “short-circuit” in the right atrium. ▪ This short-circuit causes the atria to beat at about 300 beats per minute while the lower chamber of the heart (the ventricles) beat at a slower rate (often 75 to 150 beats per minute ▪ Atrial flutter is similar to Atrial fibrillation ▪ It differs from atrial fibrillation (AF) in that the heartbeat is regular, not irregular. ▪ Will see characteristic FLUTTER waves that are saw-tooth in shape

70 Atrial Flutter ▪ P wave- none– Flutter waves ▪ PR interval– NONE ▪ QRS -- less than 0.12 seconds ▪ Ventricular rate– 60-100 – but can be as high as 130-160 ▪ Atrial rate– 240-320/ min ▪ Complexes will look similar ▪ RHYTHM is REGULAR

71 Atrial Flutter

72 Atrial FLUTTER Treatment ▪ Medications ▪ Ablation Therapy

73 Supraventricular Tachycardia - PSVT ( Paroxysmal SVT) ▪ Most episodes of SVT are caused by faulty electrical connections in the heartelectrical connections in the heart ▪ Supraventricular tachycardia (SVT) is a rapid heart rhythm originating at or above the AV node. ▪ SVT rates are above 100 beats per minute and are typically 150- 250 bpm. ▪ SVT’s rapid heart rate does not allow the ventricles to completely fill with blood, decreasing cardiac output.

74 SVT/PSVT ▪ P-wave- hard to find– if present there is one per QRS ▪ PR interval-usually not measurable ▪ QRS- 0.04-0.10 seconds NARROW ▪ All complexes look the same ▪ Ventricular rate- 150-240/min ▪ RHYTHM is REGULAR

75 SVT/ PSVT

76 Treatments for SVT/PSVT ▪ Carotid Massage ▪ Vagal Maneuvers ▪ Valsalver maneuver & Holding breath, Cold immersion, coughing ▪ Innervated by parasympathetic NS ▪ Medications ▪ Synchronized Cardioversion ▪ Ablation interventions

77 VIDEO on SVT/ A FIB & A Flutter ▪ THE Atrial and SVT RHYTHMS THE Atrial and SVT RHYTHMS

78 JUNCTIONAL RHYTHMS

79 Junctional RHYTHMS ▪ Junctional rhythms are named such because their impulse originates from the AV node (AV junction) instead of the SA node. ▪ ▪The SA node may be impaired secondary to drug toxicity or underlying cardiac disease. ▪ ▪When the AV node does not sense an impulse coming down from the SA node, it will become the pacemaker of the heart

80 Junctional RHYTHM ▪ Rate- 40-60 bpm ▪ RHYTHM is REGULAR ▪ P wave are ABSENT OR INVERTED ▪ ▪PR interval of <0.12 seconds (remember normal is 0.12-0.2) ▪ Narrow complexes ( 0.06 seconds on average) ▪ All complexes look the same

81 Junctional RHYTHM

82 ▪ Junctional Bradycardia ▪ Rate=less than 40 ▪ Accelerated Junctional RHYTHM ▪ Rate=greater than 60 ▪ Junctional Tachycardia ▪ rate= greater than 100

83 Junctional Treatment ▪ If the patient has NO symptoms--- they will just will observe the patient ▪ If symptomatic ----a permanent pacemaker may be needed ▪ If the junctional rhythm is due to digitalis toxicity, then the medication atropine, digoxin immune Fab (Digibind), or both may be necessary.

84 Heart BLOCKS FIRST DEGREE SECOND DEGREE THIRD DEGREE

85 Heart Blocks ▪ Heart blocks are arrhythmias caused by an interruption in the conduction of impulses between the atria and the ventricles. ▪ ♥The AV block can be total or partial or it may simply delay conduction.

86 The Heart Block Rhythms  First Degree AV Block ▪ ♥Second Degree AV Block ▪ ♥Type I (Wenckebach) -----also called Mobitz I ▪ ♥Type II---- also called Mobitz II ▪ ♥Third Degree AV Block

87 First Degree Heart Block ▪ First Degree AV Block ▪ ♥Is the most common form of heart block ▪ ♥Looks similar to sinus rhythm ▪ ♥Impulse conduction between the atria and the Bundle of His is delayed at the level of the AV node ▪ ♥The PR interval will be prolonged (> 0.20)

88 5 STEPS to Interpret First Degree HB ▪ 1.What is the rate? 60-100 bpm ▪ 2. What is the rhythm? Usually regular ▪ 3. Is there a P wave before each QRS? YES Are P waves upright and uniform? Yes ▪ 4. What is the length of the PR interval? >0.20 seconds ▪ 5. Do all QRS complexes look alike? Yes ▪ What is the length of the QRS complexes? Less than 0.12 seconds (3 small squares)

89 Causes and S/S of First Degree AV Block ▪ ▪Can occur in healthy hearts ▪ ▪May be temporary ▪ ▪Myocardial infarction or ischemia ▪ ▪Medications – digitalis, calcium channel blockers, beta blockers ▪ ▪Myocarditis ▪ ▪Degenerative changes in the heart

90 Medical Tx of First Degree AV Block ▪ ▪No treatment is usually necessary if the patient is asymptomatic ▪ ▪Treat the underlying cause ▪ ▪Monitor closely to detect progression to a more serious form of block

91 2nd Degree AV Block Mobitz Type I (Wenckebach) ▪ ♥The delay of the electrical impulse at the AV node produces a progressive increase in the length of the PR interval (> 0.20 seconds) ▪ ♥ The PR interval continues to increase in length until the impulse is not conducted or the QRS complex is “dropped”

92 2nd Degree AV Block Mobitz Type I (Wenckebach) The PR interval continues to increase in length until the impulse is not conducted or the QRS complex is “dropped”

93 5 Steps to Identify 2nd Degree AV Block Mobitz Type I (Wenckebach) ▪ 1. What is the rate? Varies ▪ 2. What is the rhythm? Ventricular: irregular ▪ 3. Is there a P wave before each QRS? ----------------------------Yes ▪ Are P waves upright and uniform? ------------------------------- Yes, for conducted beats ▪ 4. What is the length of the PR interval? ▪ Progressively prolongs until a QRS is not conducted ▪ 5. Do all QRS complexes look alike? ---------------------------------YES ▪ What is the length of the QRS complexes? ▪ Less than 0.12 seconds (3 small squares)

94 Causes of 2nd Degree AV Block Mobitz Type I (Wenckebach) ▪ ▪May occur normally in an otherwise healthy person ▪ ▪Coronary artery disease ▪ ▪Inferior wall MI ▪ ▪Rheumatic fever ▪ ▪Medications – propanolol, digitalis, verapamil ▪ ▪Increased vagal stimulation

95 Medical Tx of 2nd Degree AV Block Mobitz Type I (Wenckebach) No treatment is usually necessary if the patient is asymptomatic ▪ ▪Treat the underlying cause ▪ ▪Monitor closely to detect progression to a more serious form of block, especially if the block occurs during an MI ▪ ▪If symptomatic ▪ ▪Atropine may improve AV node conduction ▪ ▪Temporary pacemaker may help with symptom relief until the rhythm resolves itself

96 BIGGEST RISK WITH 2nd Degree AV Block Mobitz Type I (Wenckebach ) ▪ ▪Reduced cardiac output, although this is uncommon ▪ ▪Progression to 3rd degree block

97 2nd Degree AV Block Mobitz Type II ▪ Occurs when there is intermittent interruption of conduction ▪ ♥Less common that a 2nd Degree Type 1 block, but more dangerous ▪ ♥PR intervals are regular for conducted beats ▪ ♥The atrial rhythm is regular ▪ ♥The ventricular rhythm is irregular due to dropped or nonconducted (blocked) beats

98 2nd Degree AV Block Mobitz Type II FIXED PR interval with randomly dropped QRS complexes

99 5 Steps to Identify 2nd Degree AV Block Mobitz Type II ▪ 1.What is the rate? Varies ▪ 2. What is the rhythm? Ventricular: irregular ▪ 3. Is there a P wave before each QRS? More than one can precede the QRS ▪ Are P waves upright and uniform? Yes, some not followed by a QRS -----Yes, for conducted beats ▪ 4. What is the length of the PR interval? ------------ Constant for conducted beats ▪ 5. Do all QRS complexes look alike? -----------------------Yes, but may be intermittently absent ▪ What is the length of the QRS complexes? --------Less than or greater than 0.12 seconds

100 Causes and S/S of 2nd Degree AV Block Mobitz Type II ▪ Anterior wall MI ▪ ▪Degenerative changes in the conduction system ▪ ▪Severe coronary artery disease ▪ uses and S/S of 2nd Degree AV Block Mobitz Type II

101 Medical Tx of 2nd Degree AV Block Mobitz Type II ▪ May choose to just observe an asymptomatic patient ▪ ▪Bedrest to reduce myocardial oxygen demands ▪ ▪Oxygen therapy ▪ ▪Focus on raising the heart rate to improve cardiac output ▪ ▪Medication ▪ ▪Permanent pacemaker ▪ RISK: ▪ Reduced cardiac output ▪ ▪Progression to 3rd degree AV block (complete)

102 3rd Degree AV Block Complete heart block, AV dissociation Is the most serious type of heart block ▪ ♥May progress to asystole, because ventricular rate is usually very slow and ineffective ▪ ♥Impulses from the atria are completely blocked at the AV node and can’t be conducted to the ventricles ▪ P waves are usually march consistently through….NO correlation between P’s & QRS’s ▪ Loss of all communcation between atria & ventricles

103 3rd Degree AV Block Complete heart block, AV dissociation P waves are usually march consistently through….NO correlation between P’s & QRS’s

104 5 Steps to Identify 3rd Degree AV Block 1.What is the rate?----------------------less than 60 ▪ 2. What is the rhythm?------------Regular ▪ 3. Is there a P wave before each QRS?--- NO --No relationship to QRS complexes ▪ Are P waves upright and uniform?----Yes What is the length of the PR interval?-Totally variable, no pattern 4. Is the complex narrow?– No- they are WIDE ▪ 5. Do all QRS complexes look alike? -------------------Yes

105 Causes and S/S of 3rd Degree AV Block ▪ ▪Congenital condition ▪ ▪Coronary artery disease ▪ ▪Anterior or inferior wall MI ▪ ▪Degenerative changes in the heart ▪ ▪Digitalis toxicity ▪ ▪Surgical injury

106 Medical Tx of 3rd Degree AV Block ▪ ▪ Aim to improve the ventricular rate ▪ ▪Atropine ▪ Isopreterenol ▪ ▪Permanent pacemaker

107 Heart Block Video ▪ Heart Blocks Heart Blocks

108 Heart Blocks Made EASY- GOLDEN RULES ▪ Perform a normal interpretation on the tracing ▪ If you find more P waves than QRS complexes do the following: 1.Measure your R-R interval 2.Measure your PR interval If the R-R interval is CONSTANT, the block must be second degree type 2 or third degree. If the PR interval VARIES– HOW DOES IT VARY?? If it elongates, the block must be second degree type 1 If there is NO association, the block must be third degree

109 Ventricular Rhythms ▪ Objective ▪ Recognize ventricular dysrhythmias on EKG and relate cause, significance, symptoms, and treatment

110 Ventricular Rhythms ♥ ▪ When the sinoatrial (SA) node and the AV Junctional tissues fails to generate an impulse the ventricles will assume the role of pacing the heart ▪ ♥ There is an absence of P waves because there is no atrial activity or depolarization ▪ ♥Ventricular rhythms will display QRS complexes that are wide (greater than or equal to 0.12 seconds) and bizarre in appearance

111 Ventricular Rhythms ▪ These 8 rhythms are the lethal ones: KNOW THESE ▪ ♥Idioventricular rhythm (ventricular escape rhythm; rate usually >20 – <40 bpm) ▪ ♥Accelerated Idioventricular rhythm (>40 bpm) ▪ ♥Agonal rhythm (20 or less bpm) ▪ ♥Ventricular tachycardia (>150 bpm) ▪ ♥Ventricular fibrillation ▪ ♥Torsades de Pointes ▪ ♥Pulseless Electrical Activity (PEA) ▪ ♥Asystole - Cardiac Standstill

112 Ventricular Rhythms Premature Ventricular Contractions ▪ A PVC is not a rhythm, but an ectopic beat that arises from an irritable site in the ventricles. ▪ ▪PVCs appear in many different patterns and shapes, but are always wide and bizarre compared to a “normal” beat

113 PVC Patterns Ventricular ▪ Ventricular bigeminy PVC occurs every other beat ▪ Ventricular trigeminy PVC occurs every third beat ▪ Ventricular quadrigeminy PVC occurs every fourth beat ▪ Couplets Two PVC’s together ▪ Runs of ventricular tachycardia (VT) Three or more PVC’s in a row

114 Causes and S/S of PVC’s ▪ Causes ▪ ▪Exercise ▪ ▪Stress ▪ ▪Caffeine ▪ ▪Heart disease: MI, CHF, Cardiomyopathy, Mitral valve prolapse ▪ ▪Electrolyte imbalances ▪ ▪Hypoxia ▪ ▪Tricyclic antidepressants ▪ ▪Digitalis toxicity

115 Idioventricular Rhythm Idioventricular arrhythmia is also termed ventricular escape rhythm. It is considered a last-ditch effort of the ventricles to try to prevent cardiac standstill. ▪ ▪The SA node and AV node have failed ▪ ▪Rate usually between 20 to 40 beats per minute (bpm) ▪ ▪Cardiac output is compromised!! Keys to identifying: rhythm is SLOW, no P wave, wide & bizarre QRS!

116 5 Steps to Identify Idioventricular Rhythm ▪ What is the rate? Ventricular: 20-40 bpm ▪ 2. What is the rhythm? Usually regular ▪ 3. Is there a P wave before each QRS? Absent ▪ Are P waves upright and uniform? Absent ▪ 4. What is the length of the PR interval? Not measureable ▪ 5. Do all QRS complexes look alike? ▪ What is the length of the QRS complexes? Wide and bizarre (>0.12 sec), with T wave deflection

117 Causes and S/S of Idioventricular Rhythm Causes ▪ Causes ▪ Drugs- Digitalis ▪ MI ▪ Metabolic imbalances ▪ Hyperkalemia ▪ Cardiomyopathy

118 Treatment ▪ Medical Treatment ▪ ▪Atropine ▪ ▪Pacing ▪ ▪Dopamine when hypotensive ▪ ▪CPR

119 Agonal Rhythm Agonal rhythm is when the Idioventricular rhythm is 20 beats or less per minute. Frequently is seen as the last-ordered semblance of a heart rhythm when resuscitation efforts are unsuccessful

120 5 Steps to Identify an Agonal Rhythm ▪ What is the rate? Ventricular: <20 bpm VERY SLOW!! ▪ 2. What is the rhythm? Usually regular ▪ 3. Is there a P wave before each QRS? Absent ▪ Are P waves upright and uniform? Absent ▪ 4. What is the length of the PR interval? Not measureable ▪ 5. Do all QRS complexes look alike? ▪ What is the length of the QRS complexes? Wide and bizarre (>0.12 sec), with T wave deflection

121 Signs and TX of Agonal Rhythm ▪ Signs and Symptoms ▪ ▪Loss of consciousness ▪ ▪No palpable pulse or measurable BP ▪ Medical Treatment ▪ ▪CPR/ACLS Protocol ▪ ▪If life saving efforts have already been attempted no further treatment

122 Ventricular Tachycardia ▪ ▪ Ventricular tachycardia almost always occurs in diseased hearts. ▪ ▪Rhythm in which three or more PVCs arise in sequence at a rate greater than 100 beats per minute. ▪ ▪V-tach can occur in short bursts lasting less than 30 seconds, causing few or no symptoms. ▪ ▪Sustained v-tach lasts for more than 30 seconds and requires immediate treatment to prevent death. ▪ ▪V-tach can quickly deteriorate into ventricular fibrillation.

123 Ventricular Tachycardia

124 5 Steps to Identify Ventricular Tachycardia (V-Tach) ▪ 1. What is the rate? 101-250 bpm ▪ 2. What is the rhythm? Atrial rhythm not distinguishable Ventricular rhythm usually regular ▪ 3. Is there a P wave before each QRS? No ▪ 4. What is the length of the PR interval? Not measureable ▪ 5. Do all QRS complexes look alike? ▪ What is the length of the QRS complexes? Wide and bizarre (>0.12 sec)

125 Causes of V TACH ▪ Causes ▪ ▪Usually occurs with underlying heart disease ▪ ▪Commonly occurs with myocardial ischemia or infarction ▪ ▪Certain medications may prolong the QT interval predisposing the patient to ventricular tachycardia ▪ ▪Electrolyte imbalance ▪ ▪Digitalis toxicity ▪ ▪Congestive heart failure

126 Medical Treatment of V Tach ▪ ▪ If there is no pulse, begin CPR and follow ACLS protocol ▪ ▪If there is a pulse and the patient is unstable - cardiovert and begin drug therapy ▪ ▪Amiodarone ▪ ▪Lidocaine ▪ ▪With chronic or recurrent VT ▪ ▪Give antiarrhythmics ▪ ▪Ablation may be used for reentry

127 Ventricular Fibrillation ▪ V-Fib (coarse and fine) ▪ ♥Occurs as a result of multiple weak ectopic foci in the ventricles ▪ ♥No coordinated atrial or ventricular contraction ▪ ♥Electrical impulses initiated by multiple ventricular sites; impulses are not transmitted through normal conduction pathway

128 Course and Fine V. FIB

129 5 Steps to Identify Ventricular Fibrillation ▪ 1. What is the rate? Not discernible ▪ 2. What is the rhythm? Rapid, unorganized, not discernable ▪ 3. Is there a P wave before each QRS? No ▪ Are P waves upright and uniform? No ▪ 4. What is the length of the PR interval? None ▪ 5. Do all QRS complexes look alike? ▪ What is the length of the QRS complexes? None

130 Causes of V FIB ▪ ▪AMI ▪ ▪Untreated VT ▪ ▪Electrolyte imbalance ▪ ▪Hypothermia ▪ ▪Myocardial ischemia ▪ ▪Drug toxicity or overdose ▪ ▪Trauma

131 Medical treatment ▪ ▪CPR with immediate defibrillation ▪ ▪Initiate ACLS algorithm ▪ IF not patient will DIE

132 Torsades de Pointes Rhythm ▪ ▪ Torsades de pointes is associated with a prolonged QT interval. Torsades usually terminates spontaneously but frequently recurs and may degenerate into ventricular fibrillation. ▪ ▪The hallmark of this rhythm is the upward and downward deflection of the QRS complexes around the baseline. The term Torsades de Pointes means “twisting about the points.”

133 Torsades Rhythms

134 5 Steps to Identify Torsades de Pointes ▪ 1. What is the rate? Ventricular: 150-250 bpm ▪ 2. What is the rhythm? Regular or irregular ▪ 3. Is there a P wave before each QRS? No ▪ 4. What is the length of the PR interval? Not measurable ▪ 5. Do all QRS complexes look alike? ▪ What is the length of the QRS complexes? Wide and bizarre, some deflecting downward and some deflecting upward

135 Medical Treatment for Torsades ▪ Treatment ▪ ▪Begin CPR and other code measures ▪ ▪Eliminate predisposing factors - rhythm has tendency to recur unless precipitating factors are eliminated ▪ ▪Administrate magnesium sulfate bolus ▪ ▪Synchronized cardioversion is indicated when the patient in unstable if possible or defibrillate

136 Asystole Ventricular standstill

137 5 Steps to Identify Asystole ▪ 1. What is the rate? none ▪ 2. What is the rhythm? none ▪ 3. Is there a P wave before each QRS? ▪ Are P waves upright and uniform? none ▪ 4. What is the length of the PR interval? none ▪ 5. Do all QRS complexes look alike? ▪ What is the length of the QRS complexes? none

138 Treatment of Aysytole ▪ ▪CPR ▪ ▪ACLS protocol

139 Pulseless Electrical Activity (PEA) Electricity is working, but the mechanics and plumbing are not. ▪The absence of a palpable pulse and absence of myocardial muscle activity with presence of organized electrical activity on the cardiac monitor. The patient is clinically dead despite some type of organized rhythm on monitor.

140 The H’s ▪ Hypovolemia #1 cause ▪ Hypoxia ▪ Hydrogen ions (acidosis) ▪ Hypo / Hyperkalemia ▪ Hypothermia ▪

141 The T’s ▪ Toxins ▪ Tamponade (cardiac) ▪ Tension pneumothorax ▪ Thrombosis (coronary or pulmonary) ▪ Trauma ▪ Massive MI ▪ Overdose of tricyclic antidepressants

142 Medical Treatment ▪ ▪Determine cause & treat ▪ ▪CPR ▪ ▪Initiate ACLS protocol

143 Ectopic and Escape Beats

144 Ectopic Beats ----aka Ectopy or Arrhythmias ▪ A. Any cardiac impulse originating outside the SA node is considered abnormal and is referred to as an ectopic beat- WILL OCCUR EARLIER DUE TO INCREASE AUTOMATICITY ▪ B. Ectopic beats can originate in the atria, the AV junction, or the ventricles, and are named according to their point of origin ▪ Ectopic beat (or cardiac ectopy) is a disturbance of the cardiac rhythm frequently related to the electrical conduction system of the heart, in which beats arise from fiber or group of fibers outside the region in the heart muscle ordinarily responsible for impulse formation (i.e., the sinoatrial node). Depending upon the origins of the ectopic beat within the myocardium, an ectopic beat can be further classified as either:electrical conduction system of the heartheart musclesinoatrial node ▪ a premature ventricular contraction, orpremature ventricular contraction ▪ a premature atrial contractionpremature atrial contraction

145 Causes for ectopic beats include: ▪ 1. Failure or excessive slowing of the SA node ▪ 2. Premature activation of another cardiac site ▪ 3. Abnormal conduction system

146 Escape Beats ▪ An escape beat is a heart beat arising from an ectopic focus in the atria, the AV junction, or the ventricles – WILL OCCUR LATER DUE TO DELAYED SA NODE FIRING ▪ The usual pacemaker fails, so a slower pacemaker fires at its inherent rate.inherent rate ▪ Causes: ▪ sinus node fails in its role as a pacemaker ▪ when the sinus impulse fails to be conducted to the ventricles as in complete heart block ▪ The ectopic impulse in this instance is always late, appearing only after the next anticipated sinus beat fails to materialize

147 Videos of Heart Rhythms ▪ Heart Rhythms Heart Rhythms


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