1. 1. Regular or Irregular Rhythm?
1.1. Regular
1.1.1. Regular Rhythm
1.1.1.1. If the distance of the R-R intervals or P-P intervals is the same, the rhythm is regular
1.1.1.1.1. Can use the 300-150-100-75-60-50 Method
1.1.2. P wave before each QRS complex
1.1.3. Normal PR interval
1.1.4. Normal QT interval
1.1.5. Normal Heart Rate (60-100)
1.2. Irregular
1.2.1. If the distance differs, the rhythm is irregular.
1.2.1.1. Must use the 6 Sec Interval x 10 Method
1.2.2. Sick Sinus Syndrome
1.2.2.1. Dysfunction of the SA node; inability to generate a heart rate that meets the physiologic needs of an individual.
1.2.2.2. Can result in; profound bradycardia, sinus pauses, sinus arrest, and can be accompanied by paroxysmal supraventricular tachycardia as part of tachycardia-bradycardia syndrome (tachy/brady syndrome)
1.2.3. Ectopic Rhythms
1.2.3.1. Rhythms that arise from elsewhere, other than the sinus node. (impulse formation)
1.2.3.2. Sustained rhythms
1.2.3.3. Enhanced automaticity of a non-sinus site
1.2.3.4. Abnormal acceleration of the depolarization such that it can over-ride the normal sinus mechanism
1.2.3.5. Often caused by medication
2. 2. Determine Rate
2.1. 300-150-100-75-60-50 Method
2.1.1. Rule of Thumb: • Two large squares = 150 bpm • Three large squares = 100 bpm • Four large squares = 75 bpm • Five large squares = 60 bpm • Six large squares = 50 bpm
2.1.1.1. Easier way?
2.1.1.1.1. Or just divide 300 by the number of squares between R waves
2.2. 6 Sec Interval x 10 Method
2.2.1. 1) Remember 5 boxes = 1 sec - draw 2 lines on blank paper to show this 2) Count out 6 seconds with extra paper 3) Add number of QRS in 6 seconds 4) Multiply that number by 10 (since 6 beats in 6 secs = 60 beats in 60 secs) SO FOR EX. 8 beats in 6 seconds = 80 beats in 60 seconds 5) 60secs = 1min...80 beats in 1 min = 80bpm
2.2.2. multiply by 6 for std???
3. 3. Axis?
3.1. Normal
3.1.1. 2 thumbs up!
3.1.1.1. Positive in Leads 1 and avF
3.2. Left Ventricular Hypertrophy
3.2.1. 1. Left Axis Deviation (it’s ok if this is not present)
3.2.1.1. Left Axis Deviation?
3.2.1.1.1. Left thumb up, right thumb down
3.2.2. 2. Increased R wave amplitude in leads overlying the left ventricle 3. Increased S wave length in leads overlying the right ventricle 4. Common to see repolarization abnormalities (ST elevations and depressions) (All three will be present for pure LVH but many patients also have some element of RVH so they don’t have a left axis deviation)
3.2.2.1. Count V1 and V2 for S and V4 and V5 for R, and. if they are greater than 35 mm (7 boxes)
3.2.2.1.1. The waves look like they are kissing
3.3. Right Ventricular Hypertrophy
3.3.1. 1. Right Axis Deviation
3.3.1.1. Right Axis Deviation?
3.3.1.1.1. Right thumb up, left thumb down
3.3.2. 2. Poor R wave progression (the R wave is larger than the S wave in V1 whereas the S wave is larger than the R wave in V6) (must have both 1 and 2 for pure RVH)
3.4. Extreme Right Axis Deviation
3.4.1. Both thumbs down!
3.4.1.1. Negative in both leads
3.4.1.1.1. Northwest axis
4. 4. QRS complexes; (narrow vs. wide)
4.1. Narrow
4.1.1. Comes from above the ventricles
4.2. Wide
4.2.1. -Either because the impulse is generated in the ventricle -Or because it takes an aberrant pathway through the ventricle
4.2.1.1. Narrow is better than Wide...
4.2.1.2. >0.1sec is considered a wide QRS complex
4.2.2. Right Bundle Branch Block (RBBB)
4.2.2.1. QRS wide b/c of right ventricular delay depolarization
4.2.2.2. bunny ear pattern in V1 V2 and V3
4.2.2.3. wide S in V4- V6
4.2.2.4. Pulmonary Embolism
4.2.3. Left Bundle Branch Block (LBBB)
4.2.3.1. Delay in the left ventricular depolarization
4.2.3.2. prolongation in the rise of R waves in overlying Left ventricle (broard or notched QRS complex)
4.2.3.3. wide in V1-V3
4.2.3.4. Notched, not really bunny ears is V6
4.2.3.5. Associated wth coronary artery dz, it's a STEMI equivalent if new and an indication for lyrics or emergent Cath
5. 5. Intervals (PR interval, QT interval)
5.1. PR Interval
5.1.1. Normal
5.1.1.1. 0.12 to 0.2 seconds (up to one big box)
5.1.1.2. Normal QT interval = < 440 milliseconds
5.1.2. Heart Block
5.1.2.1. If >one large box, then you’re dealing with some type of heart block.
5.1.2.1.1. First Degree AV Block
5.1.2.1.2. Second Degree AVB Mobitz Type I AKA Wenckebach
5.1.2.1.3. Second Degree AVB Mobitz Type II
5.1.2.1.4. Third Degree AVB (Complete Heart Block)
5.1.2.1.5. P waves hidden between QRS, P waves will always be equidistant so you can use that to find the others
5.2. QT Interval
5.2.1. Normal
5.2.1.1. < 1⁄2 WAY BETWEEN TWO QRS COMPLEXES
5.2.1.1.1. • The duration of the QT interval is proportionate to the heart rate. • The faster the heart beats, the faster it must repolarize to prepare for the next contraction; thus the shorter the QT interval.
5.2.2. Prolonged QT
5.2.2.1. MEN
5.2.2.1.1. Greater than 450ms
5.2.2.2. WOMEN
5.2.2.2.1. Greater than 470ms
5.2.2.3. Hypocalcemia
5.2.2.3.1. EKG: Hard to see QT prolongation with flat T wave. But there's also shortened PR.
5.2.2.3.2. Increase risk of Torsade de Pointe
5.2.2.3.3. Also have R on T phenomenon where T wave happens the same time you are supposed to get Rwave, so heart is trying to relax and contract at the same time
5.2.2.3.4. Causes: • Malaborption • Vitamin D deficiency • Hypoparathyroidism
5.2.3. Shortened QT
5.2.3.1. Hypercalcemia
5.2.3.1.1. Causes: Malignancies Granulomatous diseases Medication induced Primary Hyperparathyroidism • Increased bone resorption • Decreased renal excretion • Increased gastrointestinal absorption
5.2.3.1.2. EKG: T wave is also gonna come right after QRS
5.3. QTc
5.3.1. the QT interval corrected for heart rate (EKG machine will calculate this for you)
5.3.1.1. know**QTc >500 starts to get into danger zone -->increased risk of Torsades de Pointe (dangerous cardiac arrhythmia)
6. 6. Assess wave forms
6.1. a. P waves; are they present, morphology, does a P wave precede each QRS complex?
6.1.1. Normal
6.1.1.1. SHOULD PRECEDE EACH QRS COMPLEX by more than 0.2 sec. and:
6.1.2. Sinus Bradycardia
6.1.2.1. if <60 bpm with predictable P waves
6.1.2.2. Normal (expected) or pathologic
6.1.2.3. Normal – well conditioned athletes, meds-i.e. Atenolol (for BP also lowers HR)
6.1.2.4. Pathologic – vasovagal syncope, conduction disturbances
6.1.2.4.1. Vasovagal syncope occurs when you faint because your body overreacts to certain triggers, such as the sight of blood or extreme emotional distress.
6.1.2.4.2. Hypothermia
6.1.3. Sinus Tachycardia
6.1.3.1. if >100 bpm with predicable P waves
6.1.3.2. Normal (compensatory)or pathologic
6.1.3.3. Normal- exercise, anxiety
6.1.3.4. Pathologic- hyperthyroidism, pulmonary embolism (most common rhythm associated with PE
6.1.3.4.1. Pulmonary Embolism
6.1.3.4.2. PE- Reduced blood flow to one or both lungs can cause shortness of breath and a rapid heart rate
6.1.3.4.3. When I was in PE class, my heart raced (ST), but not too fast (SVT)
6.1.4. Supraventricular Tachycardia (SVTs)
6.1.4.1. Originate in the atria or the AV node (above the ventricles)
6.1.4.2. regular rhythm, rapid rate (150-250 bpm, P wave not present
6.1.4.3. Atrial arrhythmias can consist of a single beat or a sustained rhythm disturbance (lasting seconds to years)
6.1.4.4. Types of SVTs
6.1.4.4.1. 1. Paroxysmal supraventricular tachycardia (PSVT), i.e. AV nodal reentrant tachycardia
6.1.4.4.2. 2. Multifocal atrial tachycardia(MAT)
6.1.4.4.3. 3. Paroxysmal atrial tachycardia (PAT), also called ectopic atrial tachycardia
6.1.4.5. How to break an SVT
6.1.4.5.1. Vagal Maneuver: Carotid massage
6.1.4.5.2. Adenosine conversion
6.1.4.6. Clinical Features (symptoms)
6.1.4.6.1. Sudden onset, can cease on its own
6.1.4.7. Very Common
6.1.4.8. Can occur in normal heart without pathology
6.1.4.9. Usually initiated by a premature supraventricular beat (atrial or junctional)- narrow complex
6.1.4.10. Usually driven by a reentrant circuit looping within the AV node (AVNRT)
6.1.4.11. Can be caused by alcohol, coffee, excitement Regular rhythm, rapid rate (150-250bpm)
6.1.4.11.1. is svt Just no clear pwave with fast hr???
6.1.4.12. No discernable P wave
6.1.4.13. with Retrograde p waves
6.1.4.14. Wolff-Parkinson White Syndrome
6.1.4.14.1. Early signs: shortened PR interval and the upscoping of the base of QRS: Delta Wave
6.1.4.14.2. Can result in Orthodromic or antidromic AVRT
6.1.5. Atrial fibrillation
6.1.5.1. not usually referred to as SVT
6.1.5.2. Common (more common than aflutter)
6.1.5.3. Atria activity is completely chaotic
6.1.5.4. AV node may be bombarded with >500 impulses/minute
6.1.5.5. Multiple reentrant circuits whirl around in totally unpredictable fashion.
6.1.5.6. No true p waves can be seen
6.1.5.6.1. No truth (p) as he fibs too much, causing him to be inconsistent (irregular rhythm) his hands to get sweaty and not able to think straight (light headed)
6.1.5.7. irregularly irregular ventricular rate unlike in SVT
6.1.5.8. AV node allows variable impulses to pass through creating an
6.1.5.9. Has a propensity to go fast (as you can imagine). Typical HR 120-180.
6.1.5.10. Slow AFIB
6.1.5.11. Conditions Associated with Atrial Fibrilation
6.1.5.11.1. Cardiac conditions (especially high prevalence) • HTN • Mitral valve disease Acute Precipitants • Pulmonary embolism (but not as common as sinus tach) • Thyrotoxicosis • Pericarditis
6.1.5.12. if AFIB w/ RVR
6.1.5.12.1. Pulmonary edema or Tachy Induced Cardiomyopathy or Demand Ischemia (if ACS)
6.1.5.13. Risk
6.1.5.13.1. Puts patients at risk of stroke
6.1.6. Atrial flutter
6.1.6.1. not usually referred to as SVT
6.1.6.2. Fairly common
6.1.6.3. Best seen in leads 2, 3, AVF
6.1.6.4. irregular rate but very rapid
6.1.6.5. “Rapid-fire” atrium (250-350 p waves per minute)
6.1.6.6. P waves are called ‘flutter wave” and have a “saw-toothed pattern”
6.1.6.7. Not all of the p waves are conducted through the AV node (this is called AV block -2:1 is most common)
6.1.6.8. Common Conditions associated with Flutter
6.1.6.8.1. Hypertension (HTN) Electrolyte abnormalities Alcohol intoxication Drug abuse (stimulants) Pulmonary disease Thyrotoxicosis Cardiac conditions
6.1.7. Ventricular Tachycardia
6.1.7.1. tall and fast QRS waves
6.1.7.2. Greater / = 120 bpm
6.1.7.3. Episode of Paroxysmal Ventricular Tachycardia
6.1.7.3.1. short run of PVCs (Premature Ventricular Contractionss
6.1.7.4. Ventricular Arrhythmia
6.1.7.4.1. risk @ 500 ms
6.1.7.4.2. Medications that prolong QTc
6.1.7.5. Sustained V Tach
6.1.7.5.1. > 30 secs
6.1.7.5.2. can lead to V fib --> death
6.1.7.6. Non-sustained V Tach
6.1.7.6.1. < 30 secs
6.1.7.6.2. common in the elderly with medical problems
6.1.7.6.3. aymptomatic
6.1.7.6.4. benign if not structural heart dz
6.1.7.7. Torsade de Pointe
6.1.7.7.1. usually seen with prolonged QT interval
6.1.7.7.2. QRS spiral around baseline with changing axis and amplitude
6.1.7.8. Ventricular Fibrillation
6.1.7.8.1. V-tach degenerates into this
6.1.7.8.2. No discernable QRS complexes
6.1.7.8.3. no cardiac output
6.1.7.8.4. immediate CPR and defibrilation required
6.1.7.8.5. short amplitudes in V3 --> fib not tach
6.1.8. Premature Atrial Contraction (PAC)
6.1.8.1. Also called atrial premature beat. Note the morphology of the p wave in front of the premature beat is different from others.
6.1.8.1.1. the PPPPACkage is weirdly shaped
6.1.8.1.2. can look like the p wave is merged with t wave or that p wave is inverted
6.1.9. Blocked Atrial Contraction
6.1.9.1. P wave arrived too early, during refractory period, before ventricular depolarization could occur
6.1.9.2. P wave can't conduct ventricular contraction
6.1.9.3. First Degree AVB
6.1.9.3.1. Rhythm gets longer, with the same p wave throughout?
6.1.10. Sinus Pause
6.1.10.1. Sinus node stops firing
6.1.10.2. Causes a flat line
6.1.10.2.1. Sinus Pause with Sinus Recovery
6.1.10.2.2. Sinus Pause with Junctional Escape Rhythm
6.1.10.2.3. Sinus Pause with Ventricular Escape
6.1.10.3. Length of line depends if and when rescue beat occurs
6.1.11. Asystole (Sinus Arrest)
6.1.11.1. Sinus Arrest or exit block
6.1.11.1.1. getting arrested stops you from living your regular life
6.1.12. Rescue Beats (Escape Beats)
6.1.12.1. Escape beats originate from
6.1.12.1.1. Atria 60-100bpm
6.1.12.1.2. AV node (most common) 40- 60bpm (called junctional pacemakers)
6.1.12.1.3. Ventricular 20-40bpm
6.1.13. Left atrial enlagement
6.1.13.1. Wide P wave (often notched) (lead II)
6.1.13.2. Wide biphasic wave in V1
6.1.13.3. Amplitude normal or increased
6.1.14. Right Atrial Enlagement
6.1.14.1. P wave taller than 2.5mm (lead II)
6.1.14.2. Initial component of biphasic P wave taller in Lead V1
6.1.14.3. Normal P wave duration (0.06- 0.10sec)
6.1.15. Biatrial Enlargement
6.1.15.1. combo of tall and wide (often notched)
6.2. b. Q waves; are they pathologic
6.2.1. Normal
6.2.1.1. Q WAVE = NEGATIVE DEFLECTION AT BEGINNING OF QRS COMPLEX REPRESENTS SEPTAL DEPOLARIZATION L--> R
6.2.2. Pathologic
6.2.2.1. IRREVERSIBLE MYOCARDIAL DAMAGE HAS OCCURRED (MI) hours or days prior
6.2.2.1.1. *Note: Don’t be fooled by AVR. The negatively deflected QRS complex is NOT a Q wave. • Duration ≥ 0.04 seconds • Depth ≥ 1/3rd the height of R wave
6.3. c. Height of R and length of S waves. Is there normal R wave progression?
6.3.1. R wave Progression
6.3.1.1. pattern of progressively increasing R wave amplitude moving right to left in the precordial leads
6.4. d. T waves; are they up-going; flat or inverted?
6.4.1. Normal
6.4.1.1. Typically same deflection as QRS complex
6.4.2. Pathologic
6.4.2.1. Peaked T waves
6.4.2.1.1. Hyperkalemia
6.4.2.2. Flattened T waves
6.4.2.2.1. Hypokalemia
6.4.2.2.2. Digitalis (Digoxin) Effect
6.5. e. Normal or Pathologic Voltage
6.5.1. Normal
6.5.2. Low Voltage
6.5.2.1. Pericardial Effusions
6.5.2.1.1. because of the fluid around the heart, it's hard to pick up signal when fluid is in the way
6.5.2.1.2. EKG: also electrical alternans: Heart rotates freely within fluid-filled sac. Amplitude of waveform varies from beat to beat.
6.5.2.1.3. Can cause cardiac tempanade (effusion is so big that the pericardium can't even stretch). This puts pressure on the heart itself, squeezing it, and leading to low cadiac output. Very dangerous and will need an emergency Aspiration to pull the fluid out.
6.5.2.2. COPD (Emphysema and Chronic Bronchitis)
6.5.2.2.1. EKG: Low voltage Right axis deviation Poor R wave progression R atrial enlargement
6.5.2.2.2. Cause: Mainly from Cigarette smoking
7. 7. Segments; are they elevated, depressed or normal? (PR segment, ST segment)
7.1. Elevated
7.1.1. ST elevation myocardial infarction (STEMI)
7.1.1.1. • Must be at least 1mm in height in limb leads • Must be at least 2mm in height in precordial leads
7.1.1.1.1. “Tombstone appearance” “Frown face appearance”
7.1.1.2. Clinically??
7.1.1.3. MI Heart Attack
7.1.1.3.1. Infarction = death of tissue Usually progressive narrowing of coronary artery from atherosclerosis Sudden total occlusion or near total occlusion usually from thrombosis (ruptured plague) Myocardium loses blood supply & is therefore deprived of oxygen & other nutrients
7.1.1.4. Localizing the Infarct
7.1.2. Acute Pancreatitis
7.1.2.1. EKG: Diffuse ST Elevation, T wave change, and PR depressions
7.1.2.2. Cause, Course and Treatment: Inflammation of pericardium Often post-infectious Patient’s present with chest pain EKG may show diffuse ST elevations, T wave changes & PR depressions in multiple leads Usually self-limited Occasionally associated with pericardial effusion Treatment is NSAIDs
7.1.2.2.1. inflammation around the sac that wraps the heart. But from that can rules in fluid build up, thus separating the pericardium, from the heart.
7.1.2.2.2. Patient's pain depends on their position (supine position gets affected)
7.1.2.2.3. Pt won't typically have a history of coronary artery disease
7.1.2.2.4. Tx: Moltrin (look like a superhero!) or Toradol (Ketorolac) in emergency cases
7.1.2.2.5. Increase of ST in Itis
7.1.3. Brugada
7.1.3.1. Causes: Inherited autosomal dominant trait More common in men Affects young men 20s-40s Pt present with syncope EKG shows RBBB & ST elevation in V1, V2 and V3 Risk of V-tachsudden death
7.1.3.1.1. see RBBB + STEMI
7.1.3.1.2. Looks like hypecalcemia or Osborne wave, but context of abrupt falling and facial trauma is indicative of dz in males
7.1.3.1.3. BRo we GADA BBBuild and Elevate each other
7.2. Depressed
7.2.1. Cardiac Ischemia
7.2.1.1. ST segment below the isoelectric line
7.2.1.1.1. iSchemia-Sub - Depressed
7.2.1.1.2. Looks like a cool signature
7.2.1.2. Digoxin
7.2.1.3. Oxygen Deprivation: An issue of supply/demand mismatch
7.2.1.3.1. Deprivation of oxygen and nutrients to the myocardium Heart needs more oxygen than arteries can deliver Exercise Tachycardia Hypotension Anemia
7.2.1.4. Symptom
7.2.1.4.1. ANGINA Chest pain resulting from diminished blood flow to a region of the heart from CAD or coronary vasospasm Stable angina – exercise induced, predictable Unstable angina – at rest