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Educational Development and Resources The Ohio State University Medical Center
CHEST PAIN
Characteristics Onset Location Radiation Quality STABLE ANGINA Crescendo Mid retrosternal Radiation inside of left arm, both arms Pressing, Squeezing, Tightness, Heaviness UNSTABLE ANGINA Occurs with less exertion than stable or at rest or with exertion Mid retrosternal Radiation inside of left arm, both arms Heaviness (more serve) Severe Pressure Hard pain Choking Short of Breath Nausea & Vomiting Severe Distressing Up to 30 minutes (SL) NTG {May require IV} Rest, Beta Blockers, ASA, Heparin Occurs at rest or minimal exertion less than if stable before Anxious VARIANT ANGINA Occurs early AM or night - cyclic Mid retrosternal MYOCARDIAL INFARCTION Protracted Retrosternal radiates to neck, jaw, shoulder, arm (left > right), back, may be epigastric Crushing Terrible Heaviness (elephant on chest) Pressing Constricting Short of Breath , Tachypnea Nausea, vomiting, Diaphoresis Severe
Mild to Moderate Discomfort Gradual worsening with stress removed 2-5 minutes after precipitating factor removed Rest NTG Effort, Stress, Cold environment Vague anxiety
Severe
Greater than 5 min. (SL) NTG, Calcium Channel Blockers for prevention Occurs at rest or with ordinary activity Anxious
Protracted Thrombolytics, Narcotics, IV NTG, Calcium, Beta Blockers, ASA Often NONE
S. Walden, September 1993; Revised June 1999; Edited by M.B. Fontana, MD 3/00
Reciprocal Changes
Leads that are opposite the damage (May or May not be present)
8 ST Segments
2mm V Leads > 1mm Frontal Leads Significant Q Waves
9 ST Segments
Tall R Waves
! V1 ! I, aVL ! Reciprocal changes only V1 - V3 ! R > S V1 V2 ! Usually associated with Inferior (High incidence of Right Ventricular Involvement) and Lateral Infarctions. ! None
Right Ventricular
! RCA (proximal)
! !
8ST
9B/P
+ JVD
+S3
+S4 3
Why (Action)
O2 supply to ischemic tissues Pain in ischemic tissue Venous dilation Preload & O2 consumption Dilates coronary arteries Collateral flow in MI area Pain of ischemia Anxiety Venous capacitance Systemic vascular resistance Catecholamines leading to in demand and infarction reduction
When (Indications)
Routinely in AMI Suspected ischemic pain Unstable angina Acute Pulmonary Edema Routinely in AMI B/P with AMI Continuing Pain after NTG Evidence of vascular congestion ( preload) B/P > 90mmHg No Hypovolemia
How (Dosing)
Start with 4L/m via nasal cannula & titrate to O2 Sat of 97-98% 0.3- 0.4 mg subling. q 5 min Spray inhaler q 5min 1-2 paste locally IV infusion 12.5-25 mcg bolus 10-20 mcg/min - titrated 2-4 mg titrated to effect Titrate to eliminate pain
NTG
Morphine
Aspirin
Heparin
Prevents platelet aggregation by blocking thromboxane A2 Mortality Non-fatal infarction Non-fatal stroke Coronary thrombosis results from ruptured plaque Residual thrombi + vascular injury persists after thrombolysis Maintains patency of infarct-related artery Prevents mural thrombus in anterior MI Automaticity & Dysrhythmias SA Node discharge Heart rate
PTCA or CABG Fibrin specific lytics High risk for emboli Anterior MI A-Fib LV thrombus
5000 IU IV Bolus 1000 IU/hr IV Infusion x 24-48 hrs Maintain PTT 1.5-2 x nml
Beta Blockers
Drug
Why (Action)
AV Node conduction B/P Myocardial contractility Block catecholamine stimulation Incidence of primary VF
When (Indications)
sympathetic tone Tachycardia or B/P Treat large M.I.s early Refractory chest pain
How (Dosing)
min x2 Propranolol 1 mg IV 1q 5min x5
ACE Inhibitors
Fibrinolytic Therapy
Reduces BP by inhibiting angiotensin-converting enzyme Alters post-AMI LV remodeling by inhibiting tissue ACE Lowers peripheral vascular resistance by vasodilatation mortality and CHF from AMI Breaks up the fibrin network that binds clots together
ST elevation >1 mm in 2 or more contiguous New LBBB or new BBB that obscures ST Time of symptom onset must be <12 hours ACS with NO ST elevation: NonQ-wave MI Unstable angina managed medically UA undergoing PCI
Antiplatelet Agents
Blocks glycoprotein IIb/IIIa receptors on platelets Blocked receptors cannot attach to fibrinogen Fibrinogen cannot aggregate platelets to platelets
Agents differ in their mechanism of action, ease of preparation and administration; cost; need for heparin! 5 agents currently available: alteplase (tPA, Activase), anistreplase (Eminase), reteplase (Retavase), streptokinase (Streptase), tenecteplase (TNKase) Abciximab (ReoPro), eptifibitide (Integrilin), tirofiban (Aggrastat
Source: American Heart Association 2000 Textbook of Advanced Cardiac Life Support. American Heart Association, Dallas Texas. Educational Development and Resources, The Ohio State University Medical Center, 2001
! Previous Tracings - qRs morphology of Tachycardia is similar to PVCs on previous tracings ! Valsalva maneuver does not slow the Tachycardia
qRs Morphology
Ventricular Tachycardia
! V1 monophasic positive R or ! V1 monophasic notched positive R (2 peaks) with left peak taller than right V1 ! V1 biphasic qR or ! V1 biphasic Rs and ! V6 rS with r<S V1 V1 V1 V6 ! V1 negative rS with narrow r < 0.04 sec & straight downstroke or ! V1 negative QS
V1
V1
V1
V1
V6
! V1 negative QS ! Small r > 0.04 sec ! Notched or slurred S ! S broad and slurred > 0.06 sec on left side V1 ! V1 right peak taller than left occurs with both Ventricular Tachycardia and SVT with aberrancy ! V1 right peak taller than left occurs with both Ventricular Tachycardia and SVT with aberrancy
V1
V1