Cardiac Part II- Arrhythmias and Ischemia Flashcards

(138 cards)

1
Q

What HR is the AV node beating at?

A

40-60 bpm

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2
Q

What HR are the Purkinje fibers beating at?

A

20-40 bpm

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3
Q

What length of time is a little box in an EKG?

A

0.04 secs

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4
Q

What length of time is a big box in an EKG?

A

0.2 secs

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5
Q

What does a p-wave represent?

A

Atrial depolarization

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6
Q

What does a QRS segment represent?

A

Ventricular depolarization

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7
Q

What does a T-wave represent?

A

Ventricular repolarization

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8
Q

Sinus tachycardia

A

Upright P wave in lead II preceding every QRS with a ventricular rate >100/min

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9
Q

Causes of sinus tach

A
Exercise
Anemia
Dehydration or shock
Fever
Sepsis
Infection
Hypoxia
Chronic pulmonary disease
Hyperthyroidism
Pheochromocytoma
Medications/stimulants
Heart failure
Pulmonary embolus
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10
Q

What is the rate when you count the boxes for the next QRS segment?

A
1st box: 300
2nd box: 150
3rd box: 100
4th box: 75
5th box: 60
6th box: 50
7th box: 43
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11
Q

Sinus bradycardia

A

Upright P wave in lead II preceding every QRS with a ventricular rate <60/min

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12
Q

Causes of sinus bradycardia

A
AV blocking meds
Heightened vagal tone
Sick sinus syndrome
Hypothyroidism
Hypothermia
Obstructive sleep apnea
Hypoglycemia
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13
Q

Sinus arrhythmia

A

Changing sinus node rate with resp cycle
Common in young healthy individuals
HR increases with inspiration and decreases with expiration

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14
Q

Premature atrial contractions (PAC)

A

Occurs when a focus in the atrium (not the SA node), generates an action potential before the next scheduled SA node action potential

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15
Q

Characteristics of premature atrial contractions (PAC)

A
Premature
Ectopic
P-wave looks morphologically different
Narrow QRS
Compensatory pause
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16
Q

Atrial fibrillation

A

Occurs when action potentials fire very rapidly within the pulmonary veins or atrium in a chaotic manner resulting in a VERY fast atrial rate (300-600 bpm)
Ventricular rate is usually 100-200 due to the AV node that becomes intermittently refractory
No P-waves

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17
Q

Risk factors for A fib

A
HTN
Valvular heart disease
CAD
Cardiomyopathy
COPD
Obesity
Sleep apnea
Excessive EtOH
DM
Thyrotoxicosis
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18
Q

S/Sx of A fib

A
Asymptomatic
Palpitations
Fainting
SOB
CP
CVA
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19
Q

Classifications of A fib

A
First detected
-Only one diagnosed episode
Paroxysmal
-Recurrent episodes that stop on their own in <7 days
Persistent
-Recurrent episodes that last >7 days
Permanent
-An ongoing long-term episode
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20
Q

Management of A fib

A

Rate control- beta blockers, calcium channel blockers, digoxin
Rhythm control
Anticoagulation
-Warfarin, heparin, dabigatran, rivaroxaban, apixaban
-ASA
Cardioversion
-Electrical or chemical (amiodarone, etc.)
Ablation/MAZE procedure

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21
Q

Atrial flutter

A

Occurs when a “reentrant circuit” is present causing a repeated loop of electrical activity to depolarize the atria at a fast rate of ~250-350 bpm
Produces a “sawtooth” pattern of the P waves with lack of P waves
A narrow complex tachycardia at a ventricular rate of exactly 150 bpm is very commonly atrial flutter

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22
Q

Supraventricular tachycardia (SVT)

A

Any tachycardia that begins above the ventricles (at or above the AV node)
-Paroxysmal (comes and goes) supraventricular tachycardia (PSVT)

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23
Q

Mechanisms of supraventricular tachycardia (SVT)

A

Re-entry: often quick acceleration to 200 bpm

Automaticity: atrial tachycardia, junctional ectopic tachycardia

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24
Q

Antidromic

A

Going in a clockwise direction

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25
Orthodromic
Going in a counterclockwise direction
26
S/sx of supraventricular tachycardia (SVT)
``` Palpitations SOB CP Tachypnea Dizziness Loss of consciousness ```
27
EKG findings in supraventricular tachycardia (SVT)
Narrow QRS complex | Tachycardia
28
Tx for supraventricular tachycardia (SVT)
``` Physical maneuvers -Valsava, coughing, carotid massage, drinking ice water, plunging the face into cold water Medications -Adenosine Cardioversion -Synchronized ```
29
Junctional rhythm
Occurs when the electrical activation of the heart originates near or within the AV node instead of from the SA node
30
Characteristics of junctional rhythm
Narrow QRS complex P wave frequently is not seen (may be buried) P waves sometimes seen after QRS May be slow or fast
31
What does accelerated indicate if it precedes the words junctional bradycardia?
>60 bpm HR
32
Premature ventricular contraction (PVC)
Occurs when a focus in the ventricle generates an action potential before the next schedule SA nodal action potential
33
Characteristics of premature ventricular contractions (PVC)
Premature Ectopic Wide complexes Compensatory pause
34
V tach
Wide QRS complex (>120 ms) originating in the ventricles at a rate >100 bpm Considered to be hemodynamically unstable life-threatening -May or may not have a pulse
35
Tx for v tach
ACLS (defibrillation, epi, antiarrhythmics)
36
Classifications of v tach
Sustained- lasts more than 30 secs or symptomatic Non-sustained VT: lasts less than 30 secs and is asymptomatic Monomorphic- same pattern Polymorphic- changing pattern
37
What electrolyte finding occurs with Torsades de Pointes?
Hypomagnesemia
38
Steps of pulseless V-tach
1. No pulse 2. IV, O2, monitor 3. Start CPR (2 min), hook up AED 4. Evaluate rhythm and pulse 5. Defibrillation 6. Continue CPR (2 mins) 7. Evaluate rhythm and pulse 8. Defibrillation 9. Continue CPR (2 mins) and epinephrine q3-5 mins 10. Evaluate rhythm and pulse 11. Continue CPR (2 mins) and Amiodarine 300 mg bolus
39
V-tach tx
Treat with IV Mg
40
Clinical pearl about V-tach
Pts with a prolonged QT interval have a higher risk of developing polymorphic VT
41
Idioventricular rhythm
It is very similar to ventricular tachycardia (VT) except the ventricular rate is <60 Often called "slow VT" When ventricular rate is between 60-100, it is referred to as an accelerated idioventricular rhythm or AIVR (common with MI)
42
V fib
Quivering of the ventricles with virtually NO forward CO | Main cause of sudden death in pts with MI
43
Tx of V fib
1. No pulse 2. IV, O2, monitor 3. Start CPR (2 min), hook up AED 4. Evaluate rhythm and pulse 5. Defibrillation 6. Continue CPR (2 min) 7. Evaluate rhythm and pulse 8. Defibrillation 9. Continue CPR (2 min) and epi q3-5 min 10. Evaluate rhythm and pulse 11. Continue CPR (2 min) and amiodarone 300 mg bolus
44
Tx of asystole
High-quality CPR, epi
45
First-degree AV block
Fixed prolonged PR interval (>0.20 sec)
46
Causes of 1st degree AV block
Medications Ischemia Lyme disease
47
2nd degree AV block | Mobitz Type I (Wenckebach)
Progressive PR interval prolongation with each beat until a QRS wave is not conducted Longer, longer, longer...drop QRS
48
Mobitz type II
Extra P waves with dropped QRS Usually associated with bradycardia PR interval may be nl or prolonged
49
Tx for Mobitz type II
Pacemaker
50
3rd degree heart block
No communication between atria and ventricle P waves: equal distance between all QRS: WIDE, slow, and equal distance between all Usually symptomatic
51
Tx for third degree heart block
Pacemaker
52
What is an EKG finding in hypokalemia?
U wave
53
What are EKG findings in hyperkalemia?
Peaked T waves Widening of the QRS Increase in PR interval Bradycardia
54
What is an EKG finding in hypocalcemia?
Prolonged QT interval
55
What is an EKG finding in hypercalcemia?
Shortened QT interval
56
Long QT syndrome
May lead to potentially fatal arrhythmia polymorphic ventricular tachycardia (torsades de pointes)
57
S/sx of long QT syndrome
Palpitations Fainting Sudden death
58
Nl range of QT
<0.440
59
Prolonged QT interval causes
``` Congenital Acquired -Medications -Disease states -Electrolyte abnormalities ```
60
Medication causes of prolonged QT interval
``` Macrolides FQs TCA Antipsychotics Ondanstron ```
61
Diseases that cause prolonged QT interval
Intracranial hemorrhage
62
Electrolyte abnormalities that cause long QT syndrome
Hypocalcemia Hypomagnesemia Hypokalemia
63
Brugada syndrome
Genetic disorder that results in sudden cardiac death from polymorphic ventricular tachycardia or ventricular fibrillation in the setting of a structurally nl heart -Most commonly from a mutation in the Na channel gene SCN5A QT interval is nl
64
Type I EKG findings in Brugada syndrome
Lead V1 has a "covered" ST segment elevation of at least 2 mm followed by a neg T wave
65
Type II EKG findings in Brugada syndrome
There is a "saddleback" appearance of the ST segment in lead V1 with ST elevation of at least 2 mm. This can be present in nl individuals as well
66
Type III EKG findings in Brugada syndrome
Features of type I or type II with a <2 mm of ST segment elevation
67
Wolff-Parkinson-White (WPW)
Accessory pathway that connects the electrical system of the atria directly to the ventricles allowing conduction to avoid passing through the AV node Shortened PR interval Delta wave
68
Tx for Wolff-Parkinson-White
Procainamide +/- electrical cardioversion
69
Class I Vaughan-Williams classification- antiarrhythmic meds
Block membrane sodium channels
70
Class II Vaughan-Williams classification- antiarrhythmic meds
Beta-blockers that decrease automaticity, prolong AV conduction, and prolong refractoriness
71
Class III Vaughan-Williams classification- antiarrhythmic meds
Block potassium channels and prolong repolarization, widening the QRS and prolonging the QT interval
72
Class IV Vaughan-Williams classification- antiarrhythmic meds
Calcium channel blockers that decrease automaticity and AV conduction
73
Class I | Ia
Quinidine, Procainamide, Disopyramide | -SVT, VT, prevention of VF, symptomatic ventricular premature beats
74
Class I | Ib
Lidocaine, Mexiletine | -VT, prevention of VF, symptomatic ventricular beats
75
Class I | Ic
Flecinide, Propafenone | -Life-threatening VT or VF, refractory SVT
76
Class II MOA
Slows AV conduction
77
Class II indications
SVT, may prevent VF - Esmolol - Propranolol - Metoprolol
78
Side effects of Class II
Fatigue Bradycardia AV block Decreases LV function
79
Class III- Amiodarone
Refractory VT, SVT, prevention of VT, A fib, VF
80
Side effects of Amiodarone
``` Hypotension Corneal micro-deposits Thyroid dysfunction -Hypothyroidism > Hyperthyroidism Pulmonary fibrosis Blue-gray skin discoloration ```
81
Class III- Dronedaron
Side effects: - QT prolongation - Contraindicated in severe heart failure
82
Class III- sotalol
VT, A fib | Side effects: Torsades de pointes, bradycardia
83
Class III- Dofetilide
A fib and flutter | Side effects: Torsades de pointes in 3% of pts
84
Class III- Ibutilide
Conversion of A fib and flutter | Side effects: Torsades de pointes in 5% of pts
85
Class IV indications
SVT
86
Class IV- Verapamil
Side effects: - Constipation - Decreases LV function
87
Class IV- Diltiazem
Side effects: - Hypotension - Decreases LV function
88
Class V indications
SVT
89
Class V adenosine MOA
Blocks AV nodal conduction and shortens atrial refractoriness
90
Class V- adenosine SEs
Transient flushing Dyspnea AV block Sinus bradycardia
91
Class V- digoxin MOA
Inhibits the Na, K, ATPase pump and prolongs AV nodal conduction and AV nodal refractory period
92
Class V- digoxin SEs
AV block Arrhythmias GI Visual changes
93
Tx for Brugada syndrome
Implantable cardioverter-defibrillator (ICD)
94
Tx for long QT syndrome
Beta blockers | Implantable cardioverter-defibrillator (ICD)
95
Coronary artery disease
MOST pts have identifiable and modifiable risk factors
96
Risk factors of CAD
``` Aging Male gender/post-menopausal women FHx of premature CAD DM HTN Hyperlipidemia Smoking- #1 preventable cause Obesity and inactivity ```
97
What is responsible for almost all cases of coronary heart disease?
Atherosclerosis -Insidious process: Begins with fatty streaks that are first seen in adolescence- progress into plaques into early adulthood- culminate in thrombotic occlusions and coronary events in middle age and later life
98
Ischemic heart disease
Often associated with other ischemic disease: - PAD - Coronary artery stenosis - Cerebrovascular disease/stroke/TIA - Renal artery stenosis - Mesenteric ischemia
99
Angina pectoris
Precordial CP precipitated by stress or exertion and relieved by rest or nitrates Angina is the term used when CP is thought to be attributable to myocardial ischemia Occurs whenever myocardial oxygen demand exceeds oxygen supply
100
Most common cause of angina pectoris
Atherosclerotic obstruction of one or more coronary arteries | -Other causes: coronary artery vasospasm, congenital anomalies, emboli, arteritis, LVH, dissection
101
Sx of angina pectoris
``` Pressure, pain, squeezing, tightness, heaviness Exertion and relieved with rest Atypical sx: -Dyspnea -Indigestion -Arm or jaw pain -Exertional SOB -Nausea -Diaphoresis -Fatigue ```
102
Activities that promote angina pectoris
``` Physical activity Cold Emotional stress Sexual intercourse Meals Lying down More commonly in the morning Generally lasts for 2-5 minutes ```
103
Stable angina pectoris
Pattern to the pain, predictable Chest discomfort can be reproduced at a certain level of exertion and is relieved with rest or nitro Lasts 5-15 minutes
104
Workup for stable angina pectoris
EKG Stress test +/- coronary angiography
105
Labs for angina pectoris
Negative troponins
106
EKG for angina pectoris
Usually nl at rest Ischemic changes: T wave flattening or inversion, ST depression Exercise EKG is the most commonly used noninvasive procedure for evaluating for inducible ischemia
107
Precautions and risk for exercise EKG for angina pectoris
1 infarction or death per 1,000 tests | Symptomatic aortic stenosis is a relative contraindication
108
Indications for exercise EKG for angina pectoris
Comfirm dx of angina, determine severity of limitations of activity due to angina, assess prognosis in pts with known CAD, evaluate responses to therapy
109
Exercise EKG positive test for angina pectoris
1 mm horizontal or downsloping ST-segment depression measured 80 msec after the J point 60-80% of pts with anatomically significant coronary dz will have a pos test
110
Tx for angina pectoris
SL nitro
111
Prevention of further attacks for angina pectoris
Beta blockers- prolongs life ASA or alternative clopidogrel Ranolazine- may prolong QT Calcium channel blockers- generally used as last line agent
112
Printzmetal's or variant angina
``` Angina pain at rest (often b/w midnight-early morning) Most common in early women Each episode generally lasts 5-15 mins Coronary artery vasospasm ST segment elevation Treated with CCBs Avoidance of nicotine, caffeine, ergots ```
113
Unstable angina and non-ST elevation MI
"Preinfarction" acute coronary syndrome New or worsening sx of myocardial ischemia -Angina may come on at rest or with minimal exertion and may last >30 min Changing pattern: -Frequency, duration, intensity -Requires longer rest periods/more nitro
114
Labs for unstable angina and NSTEMI myocardial infarction
Troponin neg with unstable angina Troponin pos with NSTEMI Check BMP for K and Crt
115
EKG for unstable angina and NSTEMI myocardial infarction
Unstable angina- usually ST depression | NSTEMI- non ST elevation MI (+ troponins)
116
Tx for unstable angina and non-ST elevation MI
``` MONA-B -CCB if BB contraindicated Antiplatelet and anticoagulation therapy Hospital admission Risk-stratification tools Early invasive coronary catheterization Statins ```
117
MONA-B components- Nitro
1st line therapy SL tablet, spray or paste Contraindicated if PDE-5 inhibitors used in past 24 hrs
118
MONA-B components- ASA
162-325 mg loading dose | Then 81-325 mg daily for at least one month
119
MONA-B components: Beta blockers, morphine, and oxygen
Oral or IV Morphine-chest discomfort Oxygen- supplemental
120
P2Y12 inhibitors
Antiplatelet therapy for unstable angina and NSTEMI Clopidogrel Prasugrel Ticagrelor
121
Glycoproetin IIB/IIIA inhibitors
Antiplatelet therapy from unstable angina and Tirofiban, Eptifibatide, Abciximab Usually started in cath lab
122
Heparin
Anticoagulant therapy for unstable angina and STEMI | Enoxaparin (LMWH) or unfractionated heparin
123
Fondaparinux
Anticoagulant therapy for unstable angina and NSTEMI | Slightly better for high risk bleeders
124
Direct thrombin inhibitors
Anticoagulant therapy for unstable angina and NSTEMI | Bivalirudin + glycoprotein IIb/IIIa inhibitor
125
Risk stratification tools for unstable angina and NSTEMI- GRACE risk score
BP ST-segment deviation Cardiac arrest at presentation Serum Crt Elevated troponin or CK-MB HR
126
Risk-stratification tools for unstable angina and NSTEMI: TIMI risk score
``` Age 65 or older 3 or more risk factors Prior coronary stenosis 50% or more ST-segment deviation Two anginal events in prior 24 hrs ASA in prior 7 days Elevated cardiac markers ```
127
Indications for cardiac catheterization and PCI in unstable angina and NSTEMI
``` Recurrent angina/ischemia at rest or with low-level activity Elevated troponin ST-segment depression Recurrent ischemia with evidence of HF EF <40% Hemodynamic instability Sustained VT PCI within 6 mos Prior CABG ```
128
PCI
``` AKA: coronary angioplasty Balloon angioplasty Implantation of stents -Bare metal or drug eluding Rotational or laser atherectomy Brachytherapy -Radioactive source to inhibit restenosis ```
129
STEMI
EMERGENCY Acute episode of chest discomfort that results in most cases, from an occlusive coronary thrombus at the site of a preexisting atherosclerotic plaque Other causes: prolonged vasospasm, inadequate myocardial blood flow, emboli, coronary dissection, cocaine
130
STEMI risk
Risk of cardiac biomarkers with at least one value above the 99th percentile of the upper reference limit together with evidence of myocardial ischemia with at least two of the following: - Sx of ischemia - EKG changes of new ischemia - New Q waves - Imaging evidence of new loss of viable myocardium or new wall motion abnormality
131
Sx of STEMI
Worsening in the pattern of angina or at rest -May occur with minimal exertion Pain may be more severe -Nitro also has little effect Associated sx -Cold sweat feel weak and apprehensive, and move about trying to see a position of comfort -Light-headedness, syncope, dyspnea, orthopnea, cough, wheezing, nausea, vomiting, abdominal bloating
132
Painless infarction in STEMI
Older pts Women Pts with diabetes
133
Sudden death and early arrhythmias in STEMI
50% of deaths occur before the pts arrive at the hospital | Death is presumably caused by v fib
134
General signs of STEMI
Anxious, resp distress, sweating Bradycardia, tachycardia, arrhythmias Hypertension, hypotension
135
Heart signs of STEMI
Murmurs, S3, pericardial friction rubs
136
Extremity signs of STEMI
Usually nl | Cyanosis, peripheral pulses, edema
137
Labs for STEMI
Pos troponin or CK-MB
138
EKG of STEMI
``` Peaked hyperacute T waves ST-segment elevation Q wave development T wave inversion NEW LBBB ```