acute coronary syndrome presentation with bivalirudin
TRANSCRIPT
Acute Coronary Syndrome
Hollis Guenther RN
The downward spiral• As a plaque develops, white blood cells (notably,
lymphocytes and macrophages) collect underneath the endothelial cells, and their reaction to the material they encounter is to begin releasing inflammatory molecules (e.g., cytokines, proteolytic enzymes). The macrophages also ingest the excess lipoproteins in the vicinity, and these macrophages become bloated foam cells.
• Many of the processes in the inflammatory response weaken the structure of an atherosclerotic plaque. The foam cells do not hold together strongly. The secreted inflammatory molecules destabilize the plaque by breaking bonds between extracellular matrix molecules. In these and other ways, inflammation makes a plaque prone to rupture
• CAD 2012 Michael Katz MD/PhD, Wild Iris Medical Education INC
Acute Coronary Syndrome includes the following diagnoses
• ST elevation MI (STEMI)
• Non ST elevation MI (NSTEMI)
• Unstable Angina (UA)
Stable Angina
• Stable Angina is not included in ACS• It is predictable, is associated with such
things as physical activity or exposure to cold
• Usually lasts for 1-5 minutes and is relieved by rest
• May result in transient ST depression but will disappear with pain relief
• Doesn’t mean you don’t have a problem
ACS Symptoms
• Non-traumatic chest pain/discomfort• Left arm/shoulder/neck or jaw pain unrelated to
injury• Syncope (passing out)• Rapid heart beat/Palpitations (skipped heart
beats)• Difficulty breathing/Shortness of breath• Epigastric discomfort• Diaphoretic (sweating)• Weakness• *Diabetics and women may have atypical
presentations such as weakness, shortness of breath or epigastric discomfort
Gender related differences in the symptoms of ACS
• Women are more likely than men to experience shortness of breath with or without chest pain, nausea/vomiting, upper back or jaw pain as presenting symptoms of a heart attack.
• Other symptoms include epigastric pain, dizziness, or syncope
• American Heart Association
Rapid EKG Criteria
• Anyone 30 years of age or older presenting with the signs of ACS (previous slide) need to have an EKG performed within 10 minutes and rapidly interpreted by a physician.
• These patients should be triaged according to the 5 Level ESI triage system
• ACS patients should be triaged Level 2
Unstable Angina
• Considered to be unstable if it is expressed in any of the following 3 ways:
• Angina at rest lasting greater than 20 minutes
• New onset angina that markedly limits physical activity
• Increasing angina that is more frequent, lasts longer or occurs with less exertion than previous angina episodes
NSTEMI vs Unstable Angina
• NSTEMI is determined by the presence of positive serum biomarkers such as CPK-MB or Troponin
• NSTEMI not observed on EKG because it does not extend damage through the entire myocardium.
Cardiac Enzymes
Test Onset Peak Duration
CPK-MB 3-12 hours 18-24 hours 36-48 hours
Troponin I 3-12 hours 18-24 hours Up to 10 days
Creatine Kinase (CK)
• Creatine Kinase - Total: – The total CK is a simple and inexpensive test
that is readily available using many laboratory instruments. However, an elevation in total CK is not specific for myocardial injury, because most CK is located in skeletal muscle, and elevations are possible from a variety of non-cardiac conditions. (Chattington et al, 1994)
Creatine Kinase-MB (CKMB)• Creatine Kinase - MB Fraction:
– Creatine kinase can be further subdivided into three isoenzymes: MM, MB, and BB. The MM fraction is present in both cardiac and skeletal muscle, but the MB fraction is much more specific for cardiac muscle: about 15 to 40% of CK in cardiac muscle is MB, while less than 2% in skeletal muscle is MB. The BB fraction (found in brain, bowel, and bladder) is not routinely measured.
– The creatine kinase-MB fraction (CK-MB) is part of total CK and more specific for cardiac muscle that other striated muscle. It tends to increase within 3 to 4 hours of myocardial necrosis, then peak in a day and return to normal within 36 hours. It is less sensitive than troponins. (Saenger and Jaffe, 2007) (Kumar and Cannon, Part I, 2009)
– The CK-MB is also useful for diagnosis of reinfarction or extensive of an MI because it begins to fall after a day, so subsequent elevations are indicative of another event. (Chattington et al, 1994)
Patients that have skeletal muscle injury (motor vehicle accident or rhabdomyolysis) often have elevations in CKtotal and elevations in CK-MB. Attempting to exclude a noncardiac source of CK-MB often leads to furthertesting such as echocardiography, stress testing, or coronary angiography. Troponin I has been demonstrated tohelp identify patients with false positive CK-MBs in this setting. In a study of 215 patients without clinical or ECGevidence of cardiac disease, 59% of patients with skeletal muscle injury and 3.8% with renal failure had increasedCK-MB levels whereas none of these patients had increased troponin I levels
Because Troponin I increases to a first peak value 40 times the detection limit vs CK-MB only 6-9 times there arenot the borderline cases where although the CK-MB has started to rise early it has not yet exceeded the upper limitof normal. (hence the need for the 3rd (16 hour) CK-MB measurement). By 6 hours after symptom onset usingtroponin I there is a 95-99% detection of patients who are ultimately shown to have a myocardial infarction
Troponin I Diagnostic Module, UCLA Medical CenterDeveloped by Gregg C. Fonarow, M.D., UCLA Division of Cardiology
Conditions in which troponin levels may be elevated without overt ischemic heart disease
• Trauma (contusion, ICD firing, cardioversion etc)
• Congestive heart failure (acute or chronic)• Hypertension• Pulmonary embolism, severe pulmonary
hypertension• Sepsis
Babuin L , Jaffe A S CMAJ 2005;173:1191-1202
ST segment Elevation Myocardial Infarction (STEMI)
• The AHA classifies a STEMI as ST segment elevation or new left bundle branch block (LBBB)
• STEMI is characterized by ST segment elevation of greater than 1mm in 2 or more contiguous leads
Contiguous LeadsArea of Involvement
Associated Leads
Vessel Involvement
Inferior II, III, AVF
ST elevation
Right coronary artery
Posterior V1, V2, V3 ST depression
Proximal right coronary
Anterior V1, V2, V3, V4
ST elevation
Left Anterior Descending
Lateral I, AVL, V5, V6
ST elevation
Left circumflex
Antero-Lateral V1-V6, I, AVL
ST elevation
Left Main
Coronary Arteries
Normal EKG
• The P wave is caused by atrial depolarization. The P wave is usually smooth and positive. The P wave duration is normally less than 0.12 sec.
• The PR interval is the portion of the EKG wave from the beginning of the P wave ( onset of atrial depolarization) to the beginning of the QRS complex ( onset of ventricular depolarization). It is normally 0.12 - 0.20 seconds
Normal EKG
• The QRS complex represents the time it takes for depolarization of the ventricles. - due to ventricular depolarization. The normal QRS interval range is from 0.04 sec - 0.12 sec measured from the first deflection to the end of the QRS complex
• The ST Segment represents the period of ventricular muscle contraction before repolarization. The ST segment is normally isoelectric (no electrical activity is recorded). however, the ventricles are contracting.
Ischemia seen as ST depression or T wave inversion, which represents lack of oxygen to the myocardial tissue
Upsloping" ST depression is not an ischemic abnormality
Note: "horizontal" ST depression in lead V6
What is J point elevation• J-point is the point at which the QRS complex
meets the ST wave.
ST segment elevation with an upward convexity is usually benign, especially when seen in healthy, asymptomatic individuals
• ST segment elevation with a downward concavity is more likely to be due to acute coronary syndrome
• Although ST elevation with an upward concavity and J-point notching often reflects a normal variant, this is only true if the patient is asymptomatic. The same ST pattern in a patient with chest pain is due to acute coronary syndrome until proven otherwise.
Early Repolarization
• Normal Variant "Early Repolarization" (usually concave upwards, ending with symmetrical, large, upright T waves)
• Early Repolarization": note high take off of the ST segment in leads V4-6; the ST elevation in V2-3 is generally seen in most normal ECG's; the ST elevation in V2-6 is concave upwards, another characteristic of this normal variant.
Contiguous LeadsArea of Involvement
Associated Leads
Vessel Involvement
Inferior II, III, AVF
ST elevation
Right coronary artery
Posterior V1, V2, V3 ST depression
Proximal right coronary
Anterior V1, V2, V3, V4
ST elevation
Left Anterior Descending
Lateral I, AVL, V5, V6
ST elevation
Left circumflex
Antero-Lateral V1-V6, I, AVL
ST elevation
Left Main
What part of the heart is affected ?What part of the heart is affected ?
II, III, aVF = II, III, aVF =
Inferior WallInferior Wall
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
Inferior Wall MIInferior Wall MI
What is the most common location for STEMI?
• An inferior MI is most common due to the
smaller diameter of the right coronary artery
Based on the EKG, which vessel in the heart is Based on the EKG, which vessel in the heart is blocked?blocked?
• V1 - V4 = Anterior WallV1 - V4 = Anterior Wall
(Left Ventricle) =(Left Ventricle) =
Left Anterior Left Anterior
Descending Artery Descending Artery
BlockageBlockage
Anterior Wall MIAnterior Wall MI
What part of the heart is affected ?What part of the heart is affected ?
I, aVL, V5 and V6I, aVL, V5 and V6
Lateral wall of left Lateral wall of left ventricleventricle
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
Based on the EKG, which vessel in the heart is Based on the EKG, which vessel in the heart is blocked?blocked?
• I, aVL, V5 + V6 = I, aVL, V5 + V6 =
Lateral Wall = Lateral Wall =
Circumflex ArteryCircumflex Artery
BlockageBlockage
Antero-Lateral Wall MIAntero-Lateral Wall MI
STEMI Treatment
• 324 mg Aspirin unless documented allergy
• Nitroglycerin oral dosage of 0.4mg q 5 min. Or IV nitro, titrate to effect being careful to monitor BP
• Use nitrates with caution in Inferior MI due to decreased or inadequate preload
Ticagrelor (Brilinta trade name)
• Reversible inhibition of platelet ADP P2Y(12) receptor
• Reaches max blood concentration 90 minutes after oral intake
• Active metabolite has 9hr ½ life• 180 mg oral loading dose
Bivalirudin (Angiomax, trade name)
• Reversible direct thrombin inhibitor• Inhibits both circulating and clot-bound
thrombin while also inhibiting thrombin-mediated platelet activation and aggregation
• No risk for Heparin Induced Thrombocytopenia (HIT)
• Half life 25 minutes in normal renal function
• Half life 3.5 hours in dialysis dependent patients
Bivalirudin mechanism of action• Bivalirudin exhibits direct and reversible binding to thrombin
(Gly)4
D-Phe-Pro-Arg-Pro(active-site-binding portion)
C-terminal dodecapeptide(Substrate recognition / Exosite 1-binding portion)
Thrombin
Bivalirudin binds to active site and substrate recognition site of thrombin
Bivalirudin is slowly cleaved by thrombin; allowing thrombin to resume its hemostatic function
Maraganore J et al Biochemistry 1990;30:7095-101
PLEASE SEE IMPORTANT SAFETY INFORMATION AND ACCOMPANYING FULL PRESCRIBING INFORMATION
Heparin
• Indirect inhibitor of thrombin• Consult pharmacy for initial bolus dosing• Risk of HIT• Does activate platelets
Effects of heparin or bivalirudin on platelets
All scanning electron micrographs were acquired at a magnification of 4,000x with the investigator blinded to treatment. Platelets from healthy volunteers treated with 30 min
bivalirudin (12μg/mL) or 0.1 to 1.0 U/mL of heparin.
Control platelets
Anand SX et al. Am J Cardiol. 2007;100:417-424. Reproduced with permission.
Platelets treated with UFH
Platelets treated with bivalirudin
PLEASE SEE IMPORTANT SAFETY INFORMATION AND ACCOMPANYING FULL PRESCRIBING INFORMATION
Platelets incubatedwith bivalirudin did not demonstrate ultrastructural
change consistent with platelet activation; platelets remainedin a discoid state reflecting platelet inactivation
In contrast, UFH-treated platelets lost their normaldiscoid shape at rest and formed pseudopodia extendingfrom the platelet central body, a morphology associated
with platelet activation
PCI
• Percutaneous Coronary Intervention has been shown to be superior to fibrinolysis
• Fibrinolysis results in reperfusion 75% of the time
• PCI is the intervention of choice for CMC-NE
What else could it be?
• Cardiopulmonary• Aortic
aneurysm/dissection• Pericarditis• Pneumonia• Pneumothorax• Pulmonary embolism
• Musculoskeletal/GI• Chest wall injury• Costochondritis• Esophageal spasm• Reflux• Gall bladder disease• Pancreatitis• Herpes
Zoster/Shingles
CODE STEMI- 22 MinutesFebruary 24, 2012
• Direct admit from EMS to Cath Lab
• 911 Call: 1131 First Medical Contact: 1137 EMS EKG Time: 1143
• EMS STEMI activation time: 1142 Page: 1152
• Mode of transportation: Cabarrus County EMS
• EMS Team: Scott Hess, Christopher Goenner
• Arrived at NEMC Cath Lab: 1200
• Code STEMI activated: Yes ECG transmitted: Yes
• Interventional Cardiologist: Dr. Campbell
• Cath Lab: Ruth Russell, Dia Dulin, Beth Johnson, Ed Messer, Barbara Reynolds, Carla Bitler
• Cath Lab Begin Time: 1210
• Door to Balloon: 1222, 22 minutes CMS GOAL: 90 MINUTES
• 911 Call to balloon: 51 minutes
• First Medical Contact to Balloon: 45 minutes
• Access: Femoral
• Intervention: BMS to Mid RCA
CODE STEMI- 46 MinutesMarch 5, 2012
• ECC Team: Dr. Cox, Julie Dibias
• Mode of transportation: Self
• Arrived at NEMC: 1733
• Door to ECG: 1736, 3 minutes (goal 10 minutes)
• Code STEMI activated: Yes
• Interventional Cardiologist: Dr. Kruse
• Cath Lab Team: Ruth Russell, Eric Hartsell, Melody Correll, Gina Young
• Door to cath lab: 1808, 35 minutes (Goal 30 min)
• Cath Lab Begin time: 1811
• Door to Balloon: 1918, 46 minutes CMS GOAL: 90 MINUTES
• Access: Femoral
• Intervention: DES to RCA
STEMI Goals
• Door to EKG within 10 minutes• Door to Cath Lab within 30 minutes• Door to reperfusion within 90 minutes• As a Emergency Department Triage
Nurse, you are the first line of detection for the STEMI patient. Your vigilance saves lives and reduces morbidity.
EMS Responding to 911 through Delivery of Patient to ECC 5.5.6.0
4/09Revised 4/12
ECGs Consistent with STEMI 5.8.0.05.8.5.0
4/09Revised 4/12
4/09Revised 4/12