A Review of Cardiac Pathophysiology and EKG Jamie Dyson PT, DPT Kathy Swanick PT, DPT, OCS
Cardiac Pathophysiology Coronary Artery Disease Congestive Heart Failure Valvular Heart Disease Athletic Heart Syndrome
Coronary Artery Disease (CAD) Arteries on the walls of the heart are vital to the heart muscle s survival, providing oxygen and necessary nutrients The disease process begins when atherosclerotic plaque begins to build up in the arteries
Coronary Artery Disease Atherosclerosis Begins with trauma to the intima of the arterial wall Trauma related to list of risk factors Media (consists of smooth muscle is exposed to circulation Thought to be the origin of lesion.
Atherosclerosis Platelet agitation at lesion site induce smooth muscle and endothelial replication Fatty streaks low density lipoproteins (LDL) develop in smooth muscle of media Fibrous Plaque then develop impinging lumen Plaque consists of connective scar like tissue, smooth muscle, and fat.
CAD Overtime, build-up of plaque can lead to arterial occlusion, which can cause a devastating blockage which will decrease or cut off oxygen to the myocardium Major risk factors for CAD: Smoking High blood pressure Diabetes > 45 years old (men) > 55 years old (women) Family history
Angina Pectoris Chest pain related to myocardial ischemia May be referred to left shoulder, neck, jaw, or between scapula. Anywhere above umbilicus could be anginal pain Three types
Stable Angina Brought on by physical effort or stress Usually substernal nonradiating pain Last 5 to 15 minutes after stopping stressor Subsides completely with treatment Sublingual nitrate (nitro)
Unstable Angina Brought on by same triggers as stable angina Occurs more frequently Duration greater than 15 mins Intensity of pain more severe Indication of progression of CAD Increased risk for MI Less responsive to treatment can require hospitalization with IV nitrates.
Variant Angina Occurs at rest- during waking hours Not influenced by exertion Dysrhythmias occur Caused by stenosis and coronary artery spasm Treated with Ca Channel Blockers
Myocardial Infarction (MI) Necrosis of a portion of the myocardium Characterized by location, size and degree of involvement Location-anterior, posterior, lateral, inferior Size- large, small Transmural (full wall), subepicardial, subendocardial.
Myocardial Infarction Uncomplicated- small infarction, inferior portion of heart partial wall thickness = full recovery Complicated MI- one or combination of dysrhythmia, heart failure, thrombosis, damage to heart structure. Prognosis is dependent on extent of damage to the ventricles
Congestive Heart Failure The inability of the heart to produce adequate cardiac output due to a structural or functional problem- impairing the ability of the heart to fill and pump blood adequately
Prevalence Estimated 23 million in the world Most common cause of hospital admission in the U.S. for patients older than 65 5.3 million in the United States alone (Dupree) 600,000 cases diagnosed each year 1 million hospitalizations Records 1 out of 8 deaths $34.8 million a year (2008)
CHF More prominent in: Older population (>65) More men than women 4-6x more likely to die of heart disease than breast cancer Kills more women over 65 than all cancers combined Reported depression in 25-50%
Risk Factors Coronary artery disease It affects the heart by restricting or blocking the flow of blood Strongest risk factor in both men and women Smoking
Main Risk Factors Cont... Hypertension Preexisting hypertension is present in 75% of heart failure cases in the United States Previous MIs Diabetes More in women; associated with a 2-5 fold increase in heart failure Obesity Valvular disease
Other Risk Factors Anemia Thyroid Toxic agents: cocaine, alcohol, nonsteroidal agents Albuminuria Viruses/Infections Allergic reactions Blood clots in the lungs Dyslipidemia Chronic kidney disease Sleep-disordered breathing
Valvular Heart Disease Congenital or Acquired Acquired- bacterial or viral infection of the heart valves Common over age of 65 Some do not require treatment Mitral Valve prolapse common in women vs men
Athletic Heart Syndrome Cardiovascular adaptation to intense exercise can mimic disease process Sudden cardiac death in athletes usually caused by hypertrophy, dysrhythmia or both. Can be manifestation of congenital abnormalities in electrical or mechanical function of the heart.
Cardiac Action Potential Phase 0- depolarization- Na+ channels open Phase 1-prolonged action potential due to slow and extended opening of Ca channels - repolarization begins. Phase 2-outward flow of K+ and prolonged opening of Ca lead to a plateau phase Phase 3- closure of Ca channels and opening of K channels completes repolarization. Phase 4- resting phase Na and Ca are pumper out K is pumped in.
EKG 12 Lead (view) of the heart Six Leads record frontal plane Six Leads record transverse plane
Frontal Plane Leads 3 Bipolar limb leads I, II, III Single positive and single negative electrode 3 augmented unipolar limb leads avr (right arm) avl (left arm) avf (left leg) Have single positive lead derive negative from a combination of other electrodes.
Einthoven s Triangle
Bipolar Leads
Bipolar Limb Leads Lead Negative Electrode Positive Electrode Angle (degrees) Lead I RA LA 0 Lead II RA LL 60 Lead III LA LL 120
Augmented Leads
Augmented Leads Lead Formula Angle (degrees) avr RA (LA+LL) / 2-150 avl LA (RA+LL) / 2-30 avf LL (RA+LA) / 2 90
Axis Deviation
Axis Deviation
Precordial (transverse plane) Leads V 1-6 V1 and V2 look at R Ventricle V3 and V4 look at the intraventricular septum V5 and V6 look at L Ventricle
EKG Evaluation What is the rate and pattern (regularity) is R-R interval equal for each beat? Is the a P wave before each QRS? = atrial Is the a QRS after every P wave?= conduction of atria to the ventricles P-R interval? Normal= 0.12-0.2 seconds > 0.2 seconds= conduction delay or block QRS normal duration (0.1 sec) and shape?
Calculating Rate
Calculating Rate Count the number of small boxes between two R waves and divide into 1500. Count the number of R waves in a six second strip and multiply by 10.
Lets try it
Sinus Rhythms Sinus Rhythm- 60-100 bpm Sinus Bradycardia- < 60 bpm Sinus Tachycardia- > 100 bpm These rhythms have normal P waves, PR int and QRS int
Supraventricular Dysrhythmias Atrial and junctional Mechanisms SVT Atrial tachycardia Atrial Flutter Atrial Fibulation Junctional Rhythm
SVT Rate- 150-250- regular rhythm- no visible P waves- PR not measurable- QRS.12 or less
Atrial Tachycardia Rate 150-250- regular- 1 P per QRS- PR may be shorter, QRS.12 or less
Atrial Flutter Atrial rate 250-450- ventricular varies- Atrial is regular- ventricular can be irregular- P wavesaw tooth- PR not measurable- QRS <.12.
Atrial Fibrillation Rate can vary- Irregularly Irregular- P waves chaotic- PR not measured- QRS <.12.
Junctional Rhythm Rate- 40-60- regular- P waves inverted-before or after QRS or absent- PR if present <.12- QRS.12 or less.
Ventricular Dysrhythmias Premature Ventricular Contraction (PVC) Bigiminy Ventricular couplet Multifocal PVC (>1 etopic focus) Ventricular Tachycardia Ventricular Fibrillation
PVC Rate varies- Can be regular or irregular- P wave will be absent- unmeasurable PRI- QRS >.12.
Bigiminy 1 PVC every other beat- regular-irregular rhythm
PVC occurs twice Ventricular Couplet
Multi-Focal PVC Can be both positive and negative since there are different etopic origins
Ventricular Tachycardia 3 or more PVC with rate >100 bpm- patient can be asymptomatic- symptomatic or unconscious and pulseless.
Ventricular Fibrillation No organized rhythm- needs immediate defibrillation
Atrioventricular Blocks First Degree AV Block Second Degree AV Block Mobitz Type 1- Wenckebach Mobitz Type 2 Third Degree AV Block
First Degree Heart Block PR interval >.20
Mobitz Type 1 PR interval progressively get longer than QRS drops
Mobitz Type 2 Regular dropped QRS every 2 nd third or 4 th P wave- consistent PR interval
Third Degree Heart Block No conduction between A and V- both will have regular rates- Ps can be hidden in QRS
Story of the AV block Family
Bundle Branch Blocks Right Bundle Branch Block RBBB Left Bundle Branch Block LBBB
Left Bundle Branch Block Increased QRS >.10s Once a widened QRS > 0.10s is identified, we look at leads closest to the LV to identify a LBBB. Leads V5,V6, I, and avl are in close proximity to the left ventricle, and as such, are the best location to identify a LBBB. Characterized by an RSR segment or notched QRS
Right Bundle Branch Block Look at Right chest Leads V1 and V2
Myocardial Infarction ST segment elevation ST segment depression Inverted T wave
ST segment elevation Transmural MI Use precordial leads to localize
ST segment depression Myocardial ischemia- can be diagnostic during exercise
Inverted T wave Myocardial ischemia (can be old)
Lets Give it a Try EKG Slides
Case 1
Case 2
Case 3
Case 4
Case 5
Answers EKG # Rate Regularity Axis Name of Rhythm Would you work with them? Why/Why not 1 105 regular RAD 2 48 regular Normal Sinus Tachycardia Junctional Rhythm Yes if stable BP and no report of SOB or CP will monitor closely Depends on condition- would be very concerned about BP 3 60 Irregular Normal A-fib with bradycardia- ST depression No- there is ischemia would stop all activity 4 60 Regular LAD STEMI No way 5 75 Regular Normal 1 st degree heart block Yes- unless symptomatic