AHA Acute Coronary Syndromes

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AHAAcute Coronary Syndromes

• Spring 08

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Why is this important?

• 1.1 million Americans are diagnosed with AMI
  annually
• 460,000 are fatal
• ½ of these deaths occur within 1 hour of onset of
  symptoms (outside of hospital)

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Acute Coronary Syndromes

• Recognition, appropriate and timely care can have
  a big impact on outcome.
• ACSs include
• Unstable angina
• NSTEMI
• STEMI
• SCD

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Acute Coronary Syndromes

• Critical actions for ACLS providers Immediate
  assessment lt10 min
• Immediate treatment lt10 min
• Assess 12-lead ECG classify into 1 of 3
  algorithm branches
• Recognizes ECG changes that indicate
  fibrinolytics
• Knows indications/contraindications for
  fibrinolytics
• Knows use of adjunctive agents
• Knows basic approach to infarct localization

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Pathology

• Usual cause of ACS is rupture of an
  atherosclerotic plaque.
• Arteries have 3 layers
• Tunica adventitia flexible connective tissue
  helps hold vessel open.
• Tunica media smooth muscle tissue and elastic
  connective tissue innervated by fibers of
  autonomic nervous system. Maintains vascular tone
  and regulate local blood flow.

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Pathology, cont.

• Tunica intima endothelium lines the vascular
  system a single layer of cells indirect contact
  with blood. At risk of damage from HTN, high
  cholesterol, smoking, diabetes.

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Terminology

• Arteriosclerosis a chronic disease characterized
  by abnormal thickening and hardening of vessel
  walls.
• Atherosclerosis a form of arteriosclerosis
  thickening and hardening of vessel is caused by
  build up of fat-like deposits.

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Pathology, cont.

• Any artery can develop atherosclerosis
• Coronary arteries CAD angina may result.
• Leg arteries PVD, leg pain (claudication) may
  result.
• Cerebral arteries (carotid artery disease) TIA
  or CVA

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Pathology, cont.

• Oxidation the bodys inflammatory response
  contribute to atherosclerosis heart disease.

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Pathology, cont.

• Oxidation is normal chemical process caused by
  release of free radicals.
• Oxygen atoms created during normal metabolism.
• Conditions causing overproduction of free
  radicals
• Cigarette smoke
• Stress
• Pesticides
• Air pollution
• Ultraviolet light
• radiation

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Pathology, cont.

• Antioxidants
• I.e., Vitamin C E
• Bind to free radicals and transform them into
  nondamaging substances or repair cellular damage.

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Pathology, cont.

• Oxidation causes injury to inner lining of
  arteries.
• LDL become damaged when reacting with free
  radicals.
• May be responsible for buildup of fat-like
  material on cell walls.
• Injury to inner lining starts inflammatory
  response.
• Leukocytes are released and oxidize LDL. Converts
  LDL to foamy material that sticks to arterial
  smooth muscle cells. Over time, foamy material
  builds up and forms hard plaque.
• Cytokines are also released and trigger
  inflammatory response, raise BP, increase
  clotting tendencies.

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And more pathology

• Stable plaques (mostly collagen-rich tissue)
  unlikely to rupture.
• Arterial walls remodel until plaque fills 40
  of inside.
• Complete blockage may cause MI
• Collateral circulation may provide alternative
  pathway for circulation.
• Vulnerable plaques mostly soft and have a thin
  cap.
• Platelets stick within 1 5 seconds and form a
  plug.

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Still more pathology

• sticky platelets secrete chemicals incl.
  Thromboxane A2 stimulates vasoconstriction
• Aspirin blocks production of thromboxane A2
• When platelets are activated, glycoprotein
  IIb/IIIa receptors necessary for platelet
  clumping appear on surface of platelet.
• Fibrinogen molecules bind to these receptors,
  allowing clumping.
• A clot is ultimately produced.

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• Vulnerable plaque rupture may follow extreme
  physical activity, severe stress, sexual
  activity, drug use, cold exposure, or infection.
• Blockage of a coronary artery
• Complete blockage may STEMI or sudden death
• Incomplete blockage may silent MI, unstable
  angina, NSTEMI, or sudden death.

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Initiating Events

• Vasoconstriction
• Plaque rupture
• Thrombus formation

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Prognosis

• Pt. S/s and outcome depend on
• Amount of heart muscle supplied by affected
  artery
• Severity and duration of myocardial ischemia
• Electrical instability of ischemic myocardium
• Degree and duration of coronary vessel blockage
• Presence and extent or absence of collateral
  coronary circulation.

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Angina

• Chest discomfort that occurs when heart muscle
  does not receive enough oxygen.
• A symptom, not a disease.
• CAD
• Uncontrolled high BP
• Valvular heart disease

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What does it feel like?

• Heaviness
• Bursting
• Pressing
• Burning
• Suffocating
• Grip-like
• Strangling
• constricting

• Squeezing
• a band across my chest
• a weight in the center of my chest
• A vise tightening around my chest

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Treatment for angina

• Early assessment including a focused history
• Rapid emergency care
• Serial ecgs
• Continuous ecg monitoring
• Community education call within 5 minutes of
  onset of sx.

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Stable angina

• Remains relatively constant and predictable
• Brief episodes of chest discomfort related to
  activity
• Sx typically last 2 15 min.

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Unstable angina

• Occurs most often in men and women 60 80 y/o.
  with major risk factors.
• Sx occur at rest and usually last gt 20 min.
• Sx are severe and/or of new onset.
• Sx are more severe in pt with hx of stable angina
• Discomfort more likely to be described as
  painful.
• Pt is at high risk of MI or death.

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• Vasoconstriction
• Plaque rupture
• Thrombus formation

Unstable angina
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Prinzmetals angina

• Uncommon form of angina.
• Result of intense spasm of coronary artery.
• May occur in otherwise healthy people (usually 40
  50 y/o) with no hx CAD.
• Almost always occurs at rest, in early morning
  hours may wake pt. From sleep.
• Episodes usually last only a few minutes. But may
  cause serious dysrhythmia.

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AMI

• Relates to dead myocardial tissue.
• Applies to the process that results in death of
  myocardial tissue.
• AMI usually from a thrombus. May occur from
  coronary spasm or embolism.
• 10 MIs occur in pt lt 40 y/o 45 occur in pt. lt
  65 y/o.

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H P

• Precipitating factors
• Present in 50 of pt.
• Pts at risk for SCD may have typical cardiac s/s
  or nonspecific complaints
• Pts successfully resuscitated following
  out-of-hospital cardiac arrest
• 28 - new or changing angina or dyspnea in 4 wks
  prior to arrest

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5 most important factors to assess

• The nature of the anginal symptoms
• Previous history of CAD
• Gender
• Age
• Number of risk factors present

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• If pt has STEMI, goal is for fibrinolytics within
  30 min. arrival at ED or percutaneous coronary
  intervention (PCI) within 90 min. arrival at ED.
• Chest discomfort is present in 75 80 of pt.
  With AMI.
• Typically lasts gt 30 min.

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Atypical Presentation

• Chest discomfort absent in 20.
• 2000 study 33 admits for AMI did not have chest
  pain on presentation.
• These pts less likely to be dx with AMI, and less
  likely to receive definitive care.

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Atypical presentaiton, cont.

• Atypical chest discomfort is localized to chest,
  but has musculoskeletal, positional, or pleuritic
  features.
• Pts most likely to present atypically
• Elders, diabetics, women

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• Elders
• Altered mentation
• Generalized weakness
• Syncope
• SOB
• Diabetics
• Generalized weakness
• Syncope
• Lightheadedness
• Altered mentation

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• Women
• Aching, tightness, pressure, sharpness, burning,
  fullness, or tingling
• Location often back, shoulder, neck
• Vague chest discomfort intermittant.
• SOB
• Weakness, dizzy
• Unusual fatigue
• Cold sweats
• N/V

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Where does the MI occur?

• Most in the left ventricle
• Obtain a 12-lead ecg ASAP

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Cardiac Ischemia
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What changes do we look for?

• ST-segment depression suggest myocardial ischemia
• ST-segment depression is significant if 0.5 mm
  below baseline

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12-Lead ECG Findings
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ECG Lead Changes Due to Injury or Infarct With
Coronary Artery, Anatomic Area of Damage, and
Associated Complications
LCA indicates left coronary artery LAD, left
anterior descending artery RCA, right coronary
artery LV, left ventricle (left ventricular)
RV, right ventricle BBB, bundle branch block
CHF, congestive heart failure PVC, premature
ventricular complex AV, atrioventricular and
PAC, premature atrial complex.
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Treatments to Consider for Acute Coronary
Syndromes

• Oxygen/airway
• Nitroglycerin
• Analgesia
• Aspirin
• ?-Blockers
• Glycoprotein IIB-IIIA

• Clopidogrel (Plavix)?
• Heparin (UFH or LMWH)
• Reperfusion therapy
• PTCA
• Fibrinolytics

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Nitroglycerin

• Mechanism of action
• Dilates Coronary Arteries
• Particularly in region of plaque disruption
• Increases Collateral Flow
• Reduces Myocardial Oxygen use
• Reduces LV Workload
• Decreases Afterload
• Analgesic ( but is not a substitute for
  narcotics)
• Suppresses Coronary Artery Spasm

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Nitroglycerin

• Indications ( without contraindication)
• ACS and ongoing ischemic pain
• Unstable Angina
• Acute Pulmonary Edema
• Hypertension in AMI

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Nitroglycerin

• Administration
• SL, Spray, Topical for stable patients
• IV for precise control
• Cautions
• Use carefully if hypotensive (lt 90) or
  bradycardic (lt50)
• Right sided MI
• Viagra, Cialis, etc. 24-48 hours
• Hypovolemic patients are prone to hypotension

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Narcotic Analgesia- Morphine

• Effects
• Relieves pain and anxiety not relieved by
  nitroglycerin
• Dilates arteries and veins
• Reduces myocardial oxygen needs, preload and
  pulmonary edema
• Administration
• 2 to 4 mg IV q 5 minutes (slow)
• Caution
• N V, low BP, respiratory depression

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Aspirin

• Aspirin inhibits platelet aggregation to reduce
  coronary re-occlusion
• Aspirin benefits
• Reduces overall mortality in AMI
• Reduces incidence of nonfatal re-infarction
• Dose 160 to 325 mg PO ASAP
• Unless true allergy
• If allergic Consider Clopidogrel

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?-BlockersFor all patients without
contraindications

• Mechanism of action
• Blocks sympathetic nervous system
• Reduce HR, BP, myocardial contractility, and
  oxygen consumption
• Decrease oxygen consumption
• Increases myocardial salvage in area of infarct
  and can reduce incidence of
• Ventricular ectopy
• VF

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?-Blockers

• Recommendations
• All patients with ACS ( unless contraindicated)
• Patients with Tachyarrhythmia's (AF with Rapid
  Ventricular Response)

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?-Blockers

• Benefits
• 23 reduction in long-term mortality
• Risks
• CHF
• Cardiogenic Shock
• High Degree AV block

Relative Contraindications

• Heart rate lt60 bpm
• Hypotension (SBP lt100 mm Hg)
• Moderate or severe LV failure and Pulmonary Edema
• 2nd- or 3rd-degree AV block
• Acute Asthma or Reactive Airway Disease
• Signs of hypo-perfusion
• PR interval gt.24 second

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?-Blockers

• ?-1 ?-2 Non-Selective Agents
• Inderal
• Betapace
• Levatol
• Visken
• Labetalol (Normodyne)
• Nadolol (Corgard)

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?-Blockers ?-1 Selective Agent

• Atenolol (Tenormin)
• Esmolol (Brevibloc)
• Metoprolol (Lopressor, Toprol)
• Acebutolol (Sectral)
• Betaxolol (Kerlone)
• Bisoprolol (Zebeta)

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UnFractionated Heparin (UFH)

• Mechanism of action
• Indirect thrombin inhibitor (with AT III)
• Indications
• Adjunctive therapy in AMI
• Begin heparin with fibrin-specific lytics
• Alteplase
• Retephase
• TNK

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Low Molecular Weight Heparin (LMWH)

• Mechanism of Action
• Inhibit thrombin generation
• Not neutralized by heparin binding proteins
• Indications (Lovenox)
• ACS with NSTEMI/unstable angina ( oral)
• Can be used with STEMI (IV)

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Heparin

• Effective ( supported by evidence)
• PTCA or CABG
• With fibrin-specific lytics (eg, alteplase,
  reteplase, TNK)
• IV UFH for patients treated with non selective
  fibrinolytic (Strepto and APSAC) who are at
• High risk for systemic emboli
• Large anterior MI, atrial fib, LV thrombus
• IV UFH for or sub-q LMWH for NSTEMI

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Heparin

• Effective with strong support
• UFH or LMH in patients with STEMI not receiving
  fibrinolytics

• Effective with less support
• LMWH in STEMI with lytics
• gt75 yrs
• No renal dysfunction (creatininegt 2.5 men and gt
  2.0 women) page 33
• DVT prophylaxis with sub-q UFH

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Fibrinolytic Therapy
Relative contraindications

• Previous hemorrhagic stroke any time
• Other stroke, CVA within 1 year IC neoplasm
• Active internal bleeding(not menses)
• Suspected aortic dissection
• LMWH in STEMI age gt75 years or renal dysfunction

• Severe uncontrolled hypertension (gt180/110)
• Current use of anticoagulants
• Recent trauma (2 to 4 wk) major surgery lt3 wk
• Recent internal bleeding, active peptic ulcer
• Pregnancy

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Fibrinolytic Therapy

• Fibrinolytic Agents
• Activase
• Retavase
• Streptase
• Tenectaplase (TNKase)

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Percutaneous Transluminal Coronary Angioplasty

• Direct treatment
• Mechanical reperfusion of infarct-related
  coronary artery

• Best outcome achieved for patients with AMI plus
  cardiogenic shock

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PTCA
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PTCA
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PTCA STENT
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ECHOCARDIAGRAM
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ECHOCARDIOGRAM
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ECHOCARDIOGRAM

• WATCH FOR CARDIAC WALL MOTION
• LOOK FOR HEART VALVE FUNCTION

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IntraAorticBallonPump
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IABP

• RECOMMENDATIONS
• STABILIZE CARDIOGENIC SHOCK FOR ANGIOPLASTY AND
  REVASCULARIZATION
• HEMODYNAMIC INSTABILITY
• POOR LV FUNCTION
• PERSISTENT ISCHEMIA WITH A LARGE AREA OF THE
  MYOCADIUM AT RISK

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IABP

• EFFECTS OF IABP DURING INFLATION
• INCREASE AORTIC DIASTOLIC PRESSURE
• INCREASE CORONARY ARTERY PERFUSION
• INCREASE OXYGEN SUPPLY

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CABG
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The Five Quadrads Approach to ACLS-EP

• 1. Primary ABCD Survey
• 2. Secondary ABCD Survey
• 3. OxygenIVmonitorfluids
• 4. TempBPHRRR
• 5. Tankpumprate

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ST elevation or new or presumably new
BBBStrongly suspicious for injury

• ST Elevation MI (STEMI)

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Case Study 1
Profile55 year old male, no cardiac history,
CP for 2 hours, calls 911
sinus rhythm in lead IIIV, O2 , ECG monitor
during transport
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AssessmentFive Quadrads Approach

• Primary Survey
• Airway adequate
• Breathing present with equal chest rise,
  adequate tidal volume
• Circulation pulse present carotid and radial
• Defibrillation not needed

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AssessmentFive Quadrads Approach

• Secondary Survey
• Airway adequate
• Breathing lung sounds clear
• Oxygen sat 97 with NRB
• Circulation sinus rhythm
• BP 126/84 mm Hg IV access present
• Differential diagnosis AMI. Others?

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What Coronary Artery is involved?
Case Study 1
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Prehospital Course

• Oxygen, Monitor, IV (OMI)
• Administer
• Aspirin
• Nitro (if not contraindicated)
• Morphine
• Obtain 12 lead
• Read 12 lead - If STEMI
• Notify receiving hospital
• Transmit 12 lead..
• STEMI blood draw Fibrinolytic Screening

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ED Course

• MONA
• Fibrinolytic Screening Completed
• Send EMS STEMI lab draw for initial cardiac
  markers, electrolyte and Coagulation studies
• Direct to PTCA Cath Lab
• Door to balloon (90 min goal)
• Door to needle Fibrinolysis (30 min goal)
• Patient Pain free post treatment
• Admitted to CCU

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Case Study 2

• Profile
• 72 year old female
• Complaining of being short of breath
• No cardiac history
• Atypical chest pain
• Risk factors smoker, family hx

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AssessmentFive Quadrads Approach

• Primary Survey
• Airway adequate
• Breathing labored with equal chest rise
• Circulation pulse present carotid and radial
• Defibrillation not needed

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Approach to ACS Patients(Acute Coronary
Syndromes)

• Follow the Secondary ABCD Survey
• Airway observe air movement, noise of breaths
• Breathing listen to lungs, watch level of
  distress
• JVD Rales suggests CHF
• Circulation Elevated BP
• Differential diagnosis 12-lead ECG

Ischemic Chest Pain Algorithm combined with
Acute Pulmonary Edema Algorithm followed.
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Treatment ConsiderationsAcute Pulmonary Edema
(high risk)
Second-line Actions

• Furosemide
• Dopamine
• Dobutamine
• CPAP
• Glycoprotein IIB-IIIA (if troponins )

• Morphine
• Oxygen
• Nitroglycerin
• Aspirin
• Heparin (UFH or Enoxaprin)

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Case Study 2

• After ED Stabilization
• UFHeparin bolus/heparin drip started
• Glycoprotien IIB-IIIA infusion (if Triponins )
• Patient had run of V-Tach
• V-Tach cardioverted to sinus rhythm after 2nd
  shock

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Case History

• Mr. Murphy, age 45, complains of chest
  discomfort, nausea, severe fatigue
• Past Med Hx hypertension (poor control), 2 to 3
  pack/day cigarettes, high stress job
• Refuses coworkers assistance
• States Its just the flu
• Goes to break room to rest

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Case Progression

• One hour later a coworker finds Mr. Murphy
  lethargic, pale, profusely diaphoretic
• Coworker offers to drive Mr. Murphy to ED, only
  15 minutes away

Should Mr. Skimmer go to ED byALS ambulance?WHY?
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Case Progression

• EMS treatment
• O2 via NRB
• IV NS _at_ KVO in the field
• Received Nitro
• BP dropped alarmingly, near syncope

What would you like to do NOW?
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Immediate EMS treatment

• IV fluids
• Grade chest pain character, intensity
• Fibrinolytic screening
• VS frequent recordings
• Multilead ECG
• Transmit and notify receiving hospital
• STEMI Blood Draw
• TriponinsElectrolytes coagulation studies

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Immediate ED Assessments

• Grade chest pain character, intensity
• H P focus on fibrinolytic screening
• VS frequent recordings
• Next Multilead ECG? (12, 15, or 22 leads)
• Send lab for triponins
• Electrolytes coagulation studies
• Portable chest film

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Mr. Murphy 12-lead
Time 901 AM
What is your interpretation of this 1st ECG?
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Posterior View of the Heart
NOTE 1 Inferior wall supplied by either the
right (85 to 90 of people) or left coronary
artery. NOTE 2 If there is acute injury in
inferior leads (II, III, aVF), unknown whether
left or right coronary artery is blocked. NOTE 3
KEY you must obtain a RIGHT-SIDED ECG at once.
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Summary ACLS Drugs

• Vasopressin
• Positive epy effects (augment CPP) without epy
  side effects
• 1 dose 40 unit to replace first or second dose of
  epinephrine
• Studies show most effectiveness in Asystole, PEA
  and VF/VT no pulse.
• Higher BP and HR post arrest if used
• Can be given ET ( not preferred)
• Amiodarone
• Handicapped by extreme difficulty in giving for
  emergencies
• Most Effective in cardiac arrest with heart
  history
• Only 2 doses in cardiac arrest (300mg, 150mg)
• Must ALWAYS be diluted
• DO NOT administer with other drugs that prolong
  QT
• Cannot go down the tube
• 150mg over 10 minutes every 10 minutes as needed
• Maint. Drip _at_ 1 mg/min

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Summary ACLS Drugs

• Atropine
• Relieves bradycardia,
• Ineffective if bradycardia is from
• Hypoxia
• Ischemia
• 1 mg for patients without pulse
• 0.5mg for patients with a pulse
• Lidocaine
• Effective in cardiac arrest with NO heart history
• Increases the electrical energy required to
  defibrillate by more than 50
• Used if Amiodarone is contraindicated
• Can be given by ET

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Summary ACLS Drugs

• Magnesium
• Must be diluted
• Given over 5-20 minutes in cardiac arrest
• 5- 60 minutes in Torsades with a pulse
• Life threatening ventricular arrythmias due to
  digitalis toxicity
• Tricyclic OD, Torsades, hypomagnesemia
• Caution in renal failure patients
• ET drugs discouraged
• IO or IV preferred
• Glucagon
• TX Betablocker and Ca Channel Toxicity

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Summary ACLS Drugs

• Adenosine
• 6, 12, 12 mg stable patient
• 12,12,18 for stable patient on theophyllin or
  caffeine OD
• 3 mg for dipyridamole (persantine), tegretol,
  heart transplant (denervated heart)
• Monophasic versus Biphasic

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New Post-Resuscitation Care

• Optimize tissue perfusion, especially for the
  brain
• Induction of mild hypothermia (33-34 C for 12-24
  hours
• During resuscitation spontaneous cooling occurs
  to 35 C
• Improves neurologic recovery
• Low blood pressure within 2 hours
• Associated with poor neuro outcomes

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Questions?