scary coronary eventsnormal coronary anatomy – no cad severe hypokinesis to akinesis of the distal...

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Scary Coronary EventsScary Coronary Events

Cheryl Herrmann, APN, CCRN, CCNS-CSC/CMCCardiac Clinical Nurse Specialist

www.cherylherrmann.com

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49 y/o male with crushing chest pain is 49 y/o male with crushing chest pain is

enrouteenroute to your facility via ambulanceto your facility via ambulance

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Time Is MuscleTime Is Muscle

Door to PCI time = 49 minutesDoor to PCI time = 49 minutesAmbulance EKG to PCI time = 66 minutesAmbulance EKG to PCI time = 66 minutes

♥ Occluded RCA ♥ RCA post stent

Door to PCI time = 49 minutesDoor to PCI time = 49 minutesAmbulance EKG to PCI time = 66 minutesAmbulance EKG to PCI time = 66 minutes

♥ Initial – CK = 72 IU/L– CK MB = 1.0 ng/ml – Troponin = < 0.4 ng/ml

♥ 8 hours later – CK MB = 2.8 ng/ml– Troponin = 0.58 ng/ml

♥ 12 hours later – CK MB = 3.3 ng/ml– Troponin = 0.51ng/ml

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Time Is MuscleTime Is Muscle

Muscle is Ejection Fraction

Ejection Fraction isQuality of Life

Scary Coronary EventsScary Coronary EventsCase StudiesCase Studies

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Case Study #1Case Study #1

♥ 69 y/o female comes to ED with c/o of severe chest discomfort

♥ PMH: mild HTN and hyperlipidemia♥ B/P 173/89, HR 91, RR 21

SpO2 98% on 2 l/np

16:59

EKG on admissionEKG on admission

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♥ NTG 0.4 mg SL x 3 in 30 minutes♥ ASA 81 mg po♥ Metoprolol 25 mg po♥ Retavase

More historyMore history ……..

♥ A few hours earlier in the same ED, her husband came in full arrest and was not able to be resuscitated

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No relief of symptomsNo relief of symptomsRepeat EKGRepeat EKG

No improvement No improvement InferolateralInferolateral leadsleads

Transported via helicopter to hospital with cardiac cath

Labs on admissionLabs on admission

♥ CK = 156

♥ CKMB = 10.7 ↑♥ Myoglobin = 298 ↑♥ Troponin I = 2.91 ↑♥ BNP = 35

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Cardiac Cardiac CathCath findingsfindings

♥ Normal coronary anatomy – No CAD♥ Severe hypokinesis to akinesis of the

distal 2/3 anterolateral, apical, and inferior walls.

♥ The basal segments contract vigorously giving it very Japanese amphora shape suggestive of Takotsubo cardiomyopathy

♥ Markedly depressed LV function with ejection fraction = 5 – 10%

ManagementManagement

♥ Transferred to CVICU♥ No IABP due to

hemodynamicallystable and recent Retavase

♥ Diagnosis: Broken Heart Syndrome or Transient Apical Ballooning

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Discharged the next day so she Discharged the next day so she could attend her husbandcould attend her husband’’s funerals funeral

♥ Discharge medications♥ Aldactone 25 mg every day♥ Alprazolam 0.5 mg prn♥ Altace 2.5 mg every day♥ ASA 81 mg every day♥ Coreg 6.35 mg every 12 hours♥ Coumadin 5 mg po every day♥ Lasix 20 mg every other day♥ Lipitor 40 mg po at hs

3 3 –– 6 weeks later6 weeks later

♥ EF 50 – 60%♥ Patient doing good

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Broken Heart SyndromeBroken Heart Syndrome

♥ A specific syndrome of stress-related reversible cardiomyopathy

♥ Mimics acute myocardial infarction without obstructive disease

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Precipitating factorsPrecipitating factorsMarked psychosocial or physical stress

Transient Left Ventricular Apical BallooningTransient Left Ventricular Apical BallooningTakotsubo CardiomyopathyTakotsubo Cardiomyopathy

♥ 1st Described in Japanese literature in early 1990

♥ Was first attributed to simultaneous spasm of multiple coronary arteries

♥ Original name given “Takotsubo cardiomyopathy”

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♥ Takotsubo is the narrow-necked bulging container used by Japanese fisherman to trap octopus

♥ The shape of the takotsubo pot resembles the distorted ballooning ventricle.

EtiologyEtiology

♥ Unclear etiology♥ 1 – 2% of patients who have S/S AMI have

apical ballooning (Japan & USA)♥ 6-9 times more common in women♥ 6% of women with AMI have apical

ballooning♥ Most often in postmenopausal women

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PathophysiologyPathophysiology

♥ Marked systolic ballooning of the ventricular apex

♥ Hypercontractility of the base of the heart♥ Most common in LV ---can occur in RV♥ Initial reports thought it was due to spasm♥ Now thought to be related to stunning of

the myocardium related to excessive catecholamines

♥ Since preceded by increased psychosocial or physical stress suggest an association with ↑ SNS activity

♥ Catecholamines have a toxic effect on the myocardium

♥ Catecholamine levels reported to be 7 –34 times as high as the normal 2 – 3 elevation in classic AMI patients

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Other possible pathophysiology Other possible pathophysiology mechanismsmechanisms

♥ Rupture of a nonobstructive plaque followed by spontaneous thrombolysis

♥ Microvascular coronary spasm or dysfunction

♥ Transient obstruction to left ventricular outflow

♥ Acute myocarditis

Other findingsOther findings

♥ Abnormally long left anterior descending artery that courses along the diaphragmatic surface of the left ventricle

♥ But not consistent finding

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Signs & Symptoms (not consistent)Signs & Symptoms (not consistent)

♥ Chest pain♥ ST segment changes♥ Release cardiac biomarkers♥ Syncope or near syncope♥ Fatigue/malaise♥ Palpitations♥ Dyspnea♥ Hypotension♥ Pulmonary edema♥ Cardiogenic shock♥ Lethal ventricular arrhythmias

12 Lead EKG12 Lead EKG

♥ Variable findings♥ ST segment elevation or depression usually in

the precordial leads (V2 – V5)♥ Reciprocal changes in the inferior leads may not

occur♥ Q waves usually do not develop

or Q waves V3 – V6♥ Deeply inverted T waves are common in the

recovery period♥ Markedly prolonged QT interval

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Cardiac biomarkersCardiac biomarkers

♥ Only moderately elevated♥ Do not follow the typical rise-fall-pattern

seen with AMI

Echocardiogram/Cardiac Echocardiogram/Cardiac CathCath

♥ Systolic ballooning of the ventricle, akinetic or dyskinetic left ventricle

♥ Ejection fraction markedly decreased in the acute phase – as low as 14 – 40%

♥ No significant coronary artery disease to account for the marked left ventricular dysfunction

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Normal LVNormal LV

♥ Systole ♥ Diastole

Left Left ventriculogramventriculogram in systole (3a) and diastole (3b) to illustrate in systole (3a) and diastole (3b) to illustrate the ballooningthe ballooning

6565--yearyear --old woman was admitted to a local ED due to chest p ain in the old woman was admitted to a local ED due to chest p ain in the retrosternalretrosternal region associated with region associated with severe severe dyspneadyspnea . Before the onset of the symptoms, the patient rep orted a signi. Before the onset of the symptoms, the patient rep orted a signi ficant stress episode following ficant stress episode following

a serious quarrel with her husband.a serious quarrel with her husband.

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Metzl MD et al. (2006) A case of Takotsubo cardiomyopathy mimicking an acute coronary syndromeNat Clin Pract Cardiovasc Med 3: 53–56 doi:10.1038/ncpcardio0414

Left ventriculogram of the patient during systole showing mid, distal and apical left ventricular ballooning, with vigorous contraction of the basal segment as

seen in Takotsubo cardiomyopathy

The echocardiogram revealing apex expansion, The echocardiogram revealing apex expansion, akinesiaakinesia of some segments of the of some segments of the left ventricle, with a severe reduction in the ejec tion fractionleft ventricle, with a severe reduction in the ejec tion fraction

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Nuclear stress testingNuclear stress testing

♥ Evidence of reversible myocardial injury

DiagnosisDiagnosis

♥ Immediately difficult to differentiate between STEMI caused by thrombosis

♥ Suspect Takotsubo cardiomyopathy when obstructive CAD is not present to explain the LV dysfunction

♥ Confirmation of diagnosis: typical octopus morphology of LV

♥ Stressor considered supportive evidence♥ Complete resolution of LV dysfunction weeks

after the event

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Mayo Clinic CriteriaMayo Clinic Criteria

♥ New ECG finds (not evident on previous ECGs or are acute changes) such as T-wave inversionor ST-segment changes

♥ Absence of any CAD♥ Transient akinesis of the left ventricular

apical and midventricular segments, including wall motion abnormality

♥ All other possible caues of the changes have been ruled out


♥ Prompt recognition of apical ballooning prevents unnecessary administration of fibrinolytics with the ST segment elevation

♥ Specific guidelines do not exist♥ Mostly managed per NSTEMI and STEMI

guidelines

♥Proceed with STEMI treatment & emergent cardiac cath

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Management of Management of CardiogenicCardiogenic shockshock

♥ Vasopressors♥ Pacemaker♥ Intraaortic balloon pump (IABP)♥ Support until LV recovers

Supportive ManagementSupportive Management

♥ Arrhythmias � antiarrhythmic drugs♥ Diuretics � pulmonary congestion♥ B Blockers, vasodilators, ACEI,

vasocontrictors, IABP � left sided HF♥ Short term anticoagulant � prevent LV

thrombus

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PrognosisPrognosis

♥ Left ventricular function improves rapidly♥ Often within 7 – 30 days♥ EKG changes may be slower to resolve♥ Generally favorable prognosis♥ Mortality of 0 – 8%

Scary Coronary EventsScary Coronary EventsCase Study # 2Case Study # 2

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♥ 74 y/o female POD #2 rectal prolapserepair & cholecystectomy

♥ PMH: 2 coronary stents three years ago, & iliac stents. Quit smoking 4 years ago. Smoked 1 ½ packs x 50 years

♥ Clear lung sounds, uneventful post op course. SpO2 97% on room air

3/6 POD #2 14503/6 POD #2 1450

♥ Patient abruptly has respiratory distress.♥ Respirations 36 labored♥ SpO2 drops to 78% on 3 liters♥ UAT called

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UAT assessmentUAT assessment

♥ O2 increased to 7 l/min. SpO2 81%♥ BP 197/111, HR 139, Resp Rate 36

labored♥ Lungs rhonci throughout♥ Color dusky

♥ ABGs:– Ph 7.45– pC02 30– pO2 45– TCO2 21.8– O2% 83– BE -3.1– Lactic Acid 1.9

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♥ O2 increased to 100% nonrebreather. SpO2 increased to 91%

♥ Transferred to ICU @ 1505

EKG at 1509EKG at 1509

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CXR at 1535CXR at 1535

CathCath results: Normal LAD & other results: Normal LAD & other coronary arteriescoronary arteries

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♥ Anterobasal & basal 2/3 of inferior wall contracts normally

♥ Rest of LV is akinetic & perhaps dyskinetic

♥ EF = 20%♥ Findings are consistent

with “broken heart syndrome/Takotsubo cardeiomyopathy”

♥ Physical stressor-surgery

♥ Patient started on Cardizem♥ Placed on BiPap 12/6♥ Given Lasix 40 mg IV♥ Albuterol/Atrovent & Pulmicort nebulization♥ Supportive management of Cardiogenic

shock

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12 Lead EKG 48 hours later12 Lead EKG 48 hours later

CXR 4 days laterCXR 4 days later

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10 days later 3/2010 days later 3/20

♥ Back on telemetry unit♥ Patient abruptly goes into respiratory

distress and is diaphoretic.♥ BP 97/45, HR 131, RR 40 SpO2 92%♥ Placed back on BiPAP 14/10

3/20 16003/20 1600

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♥ Started on Cardizem @ 10 mg/hour♥ ABGs

– Ph 7.53– PCO2 23– pO2 60– TCO2 20– O2% 94– BE – 3.3– Lactic Acid 4.7 (Abdomen tender)

CXR on 3/20CXR on 3/20

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♥ Transferred back to ICU♥ Supportive Care of Cardiogenic Shock♥ Started having Ventricular Tachycardia --

defibrillated several times over the next several hours. Then made DNR & expired shortly thereafter

Scary Coronary EventsScary Coronary EventsCase Study #3Case Study #3

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♥ 49 y/o white female came to ED because of two episodes of resting palpations associated with tightness across the midchest and in the throat SOB and diaphoresis

♥ Symptoms subsided by the time patient arrived at ED

EKG in ED. EKG in ED. TroponinTroponin NormalNormalSent home to follow up with cardiologist next daySent home to follow up with cardiologist next day

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Cheryl Cheryl –– Note Left axis deviationNote Left axis deviation

EKG during stress test in Cardiologist officeEKG during stress test in Cardiologist officeSent directly to Sent directly to CathCath LabLab

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Cardiac Cardiac CathCath: Normal Coronary Arteries: Normal Coronary ArteriesLV apical LV apical balloningballoning, EF = 40%, EF = 40%

StressorsStressors

♥ Aunt died one month ago♥ Just told father has terminal illness♥ Significant other – 3 stents last week

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TS: EKG day later TS: EKG day later Note: Deep T wave inversion & prolonged QT intervalNote: Deep T wave inversion & prolonged QT interval


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♥ 52 y/o presents with onset of left sided and sternal area chest pressure with some SOB

♥ Previous episodes of anxiety♥ Under significant amount of stress

because of ongoing divorce

Admission EKG Admission EKG ----TroponinTroponin bumped to 2.0 bumped to 2.0 ngng/ml /ml Taken emergently to Taken emergently to CathCath lablab

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♥ No occlusive CAD♥ EF 25 % ♥ Basal and anterobasal

wall of LV contract normally.

♥ Rest of LV akinetic♥ Findings consistent with

Takotsubo

EKG next dayEKG next dayNote: T wave inversion & prolonged QT intervalNote: T wave inversion & prolonged QT interval

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Broken Heart SyndromeBroken Heart SyndromeSummary: Clinical features Summary: Clinical features

♥ Onset of s/s often preceded by emotional/physical stressor

♥ Most common in postmenopausal women♥ ST-segment abnormalities that mimic those of AMI♥ Mild to moderate increase in levels of cardiac enzyme

compared with the increase in AMI♥ No significant coronary artery disease to account for the

left ventricular dysfunction♥ Left ventricular “ballooning” wall motion at the apex with

hypercontractility at the base♥ Transient and reversible left ventricular changes with

favorable prognosis

Source: McCulloch B 2007: Critical Care Nurse 27(6): 20 - 27


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♥ 54 y/o black male calls 911 and comes to ED via ambulance

♥ c/o crushing chest pain♥ BP 210/110, HR 140, RR 18, Temp 102.2♥ HR “racing earlier”♥ Pupils dilated

DxDx STEMI STEMI Taken emergently to EDTaken emergently to ED

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Normal Coronary Arteries & EFNormal Coronary Arteries & EF

♥ RCA ♥ LAD & Circumflex

♥ Now admits to using Cocaine 3 hours ago

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CocaineCocaine--Associated Chest Pain & Associated Chest Pain & Myocardial InfarctionMyocardial Infarction

♥ Scientific Statement from the AHA & Acute Cardiac Care Committee of the Council on Clinical Cardiology 2008

EpidemiologyEpidemiology

♥ Cocaine is the 2nd most commonly used illicit drug in the USA – next to marijuana

♥ Cocaine related visits increased by 46% from 1999 to 2002

♥ 2005: 448,481 cocaine-related visits to EDs♥ Cocaine associated myocardial infarction

occurs after cocaine ingestion in 0.7 – 6% of individuals

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Cocaine Effects: Cocaine Effects: Other Names: Coke, snow, nose candy, flake, Other Names: Coke, snow, nose candy, flake,

blow, big C, lady, white, snowbirdsblow, big C, lady, white, snowbirds

♥ Addiction ♥ Pupil dilation ♥ Elevated blood

pressure and heart rate♥ Increased respiratory

rate ♥ Increased body

temperature♥ Paranoia ♥ Seizures ♥ Heart attack ♥ Respiratory failure ♥ Constricted peripheral

blood vessels

♥ Restlessness, irritability, anxiety

♥ Tactile hallucinations ♥ Insomnia ♥ Increased risk of

exposure to HIV, hepatitis, & other infectious diseases if injected

♥ Death from overdose

Cardiovascular Effects of CocaineCardiovascular Effects of Cocaine

♥ Accumulation of catecholamines �Acts as a powerful sympathomyometic agent

♥ ↑ Heart rate, ↑ blood pressure, ↑contractility � ↑ myocardial demand

♥ Chronotropic effects are intensified in the setting of alcohol use

♥ ↓ LV function♥ ↑ end-systolic wall stress

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Cardiovascular Effects of Cocaine Cardiovascular Effects of Cocaine contcont

♥ Vasoconstriction of coronary arteries � more accentuated in patients with preexisting CAD

♥ Combination of cocaine & smoking results in greater increases in heart rate & vasocontriction

♥ ↓ oxygen supply induces myocardial ischemia by the above methods

♥ Also causes premature coronary atherosclerosis & thrombosis

Hematologic Effects of CocaineHematologic Effects of Cocaine

♥ ↑ plasminogen-activator inhibitor♥ ↑ platelet count♥ ↑ platelet activation♥ Platelet hyperaggregability

♥ ↑ C-reactive protein♥ ↑ von Willebrand factor♥ ↑ Fibrinogen♥ May lead to acute thrombosis of coronary

arteries shortly after cocaine use

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MultifactorialMultifactorial Ways Cocaine causes Ways Cocaine causes myocardial ischemia or MI myocardial ischemia or MI

♥ ↑ myocardial oxygen demand by ↑ heart rate, blood pressure, and contractility

♥ ↓ oxygen supply via vasoconstriction♥ Inducing a prothrombotic state by

stimulating platelet activation & altering the balance between procoagulant & anticoagulant factors

♥ Accelerating atherosclerosis

Clinical PresentationClinical Presentation

♥ Chest pain (pressure-like in quality) – 56%♥ Dyspnea♥ Anxiety♥ Palpitations♥ Dizziness♥ Nausea♥ Diaphoresis♥ Chest pain can be due to AMI or aortic

dissection (0.5%)

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Other symptomsOther symptoms

♥ Pulmonary Hypertension♥ Dyspnea♥ “Crack Lung”

– Hypoxemia– Hemoptysis– Respiratory Failure– Diffuse pulmonary inflitrates

Timing Between Cocaine Use and AMITiming Between Cocaine Use and AMI

♥ Usually occurs soon after ingestion♥ 2/3 occur within 3 hours (Hollander, Hoffman, 1992)

♥ Another study showed 24-fold higher risk of MI in the 1st hour after cocaine ingestion with a rapid decrease in risk after this time (Mittleman, Mintzer, 1999)

♥ Ischemic symptoms can still occur hours up to 4 days after ingestion

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Patient CharacteristicsPatient Characteristics

♥ Male (87%)♥ Young – mean age 38 – 44 y/o♥ Nonwhite (72 – 84%)♥ Smokers (84 – 91%)♥ History of cocaine use within the

preceding 24 hours (88%)♥ Few cardiac risk factors

Note: Cocaine associated MI is low volume so percentages are from a small population

Complications & PrognosisComplications & Prognosis

♥ Cardiac Complications (38%)– Arrhythmias (43%)

• Ventricular Tachycardia• Supraventricular tachycardia• Bradyarrhythmia

– Heart Failure (7%)– 90% of these complications occurred with in 12

hours after presentation and did not lead to significant adverse events

♥ 58% incidence of recurrent ischemic events after cocaine-associated AMI

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Diagnostic StrategiesDiagnostic Strategies

♥ Self reporting of cocaine use♥ Urine analysis for cocaine metabolite

benzoylecgonine– > 300 mg/ml– Urinary half-life of 6 – 8 hours– Can be detected for 24 – 48 hours– For long term cocaine use, may be detected

up to 22 days

Evaluation of AMIEvaluation of AMI

♥ Evaluate same as ACS without cocaine use– ECG– Serial cardiac biomarkers– Stress testing

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♥ 56 – 85 % abnormal EKG♥ Early repolarization patterns (32%)♥ Left ventricular hypertrophy pattern (16%)♥ Typically ST segment Elevation MI (2%)♥ Acute ischemia changes (6%)

ST Elevation PatternsST Elevation Patterns

♥ ST segment elevation for STEMI

♥ Early RepolarizationST Elevation

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♥ Elevated take-off of ST segment at the j point♥ Concave upward ST elevation ending with a symmetrical upright T

wave – often of large amplitude♥ Gently upsloping and curving downward or sagging of the ST

segment , producing the so called “smiley face”♥ Contrasted with the junctional elevation and horizontal or straight ST

segment & the curving upward of “sad face” of the STEMI examples♥ No reciprocal ST segment depression

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♥ RCA ♥ LAD & CX

LAD & CXLAD & CX

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RCARCA

Type of AMIType of AMI

♥ Anterior (45%)♥ Inferior (44%)♥ Non Q wave (61%)

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Cardiac BiomarkersCardiac Biomarkers

♥ ↑ myoglobin & creatine kinase due to rhabdomyolysis

♥ Creatine Kinase ↑ in 75% patients – 65% did not have MI

♥ Troponin I is preferred marker

EchocardiographyEchocardiography

♥ Higher left ventricular mass index & thickness of the posterior wall

♥ Left ventricular hypertrophy

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Coronary AngiographyCoronary Angiography

♥ 50% had no significant stenosis♥ 32% single vessel disease♥ 10% 2 vessel disease♥ 5.6% triple vessel disease♥ Coronary artery disease

– 77% significant CAD patients with proven MI– 35% significant CAD in patients without MI

Evaluation of chest painEvaluation of chest painNo obvious AMINo obvious AMI

♥ Manage in a chest pain observation unit for 9 – 12 hours

♥ Serial EKGs, cardiac markers♥ Risk Stratification

– High risk patients have a 23% incidence of MI– Another 23% will be diagnosed with unstable

angina

♥ Stress test based on risk factors & clinical status

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Therapeutic StrategiesTherapeutic StrategiesTreat as ACS exceptTreat as ACS except……

♥ Avoid B-blockers acutely � due to the unopposed alpha-adrenergic effect, which may lead to worsening coronary vasoconstriction, increased blood pressure, and risk of exacerbating coronary spasm. (Class III, C)

♥ IV NTG, Nitroprusside for persistent hypertension (phentolamine – alternative).


♥ IV Benzodiazepines to relieve chest pain & lead to beneficial effects on cardiac hemodynamics. Also relieves anxiety. (Class I, B)

♥ Calcium channel blockers should not be used as first-line therapy but may be considered in patients not responsive to benzodiazepines or NTG. (Class IIb/C)

♥ Phentolamine decreases coronary vascular resistance and blood pressure after cocaine ingestion, and may be considered in patients not respnsive to NTG or calcium channel blockers. (Class IIb,C)

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♥ In patients with chest pain of unclear origin, hypertension & tachycardia should be treated conservatively.

♥ Cautious use of fibrinolytic therapy for STEMI � higher rate of cranial hemorrhage with cocaine use.

Therapeutic StrategiesTherapeutic Strategies

♥ Ventricular Tachycardia occurring immediately after cocaine ingestion– Sodium Bicarbonate as VT is caused by the

local anesthetic (sodium channel) effects on the myocardium

♥ Ventricular arrhythmias occurring hours after ingestion are usually due to ischemia– Treat ischemia & then treat per arrhythmia

protocols

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Discharge therapy AMIDischarge therapy AMI

♥ ASA, clopidogel, statin, ACE I♥ Consider B-blocker especially if high risk

features (systolic dysfunction, dysrhythmia)♥ Drug abuse counseling♥ Recurrent chest pain is less common and

MI & death are rare in patients who discontinue cocaine

CASE REPORTCASE REPORT

♥ Transient Left Ventricular Apical Ballooning After Cocaine Use: Is Catecholamine Cardiotoxicity the Pathologic Link?

♥ MAYO CLINIC PROCEEDINGS. 2006;81:829-832♥ SANDEEP ARORA, MD; FADI ALFAYOUMI, MD; VENKATRAMAN SR INIVASAN, MD

♥ 55 y/o Postmenopausal women admitted to ED with severe squeezing-type retrosternal chest pain that had begun 2 to 3 hours before presentation. She admitted smoking “crack” cocaine in progressively increasing amounts during the preceding few months and reported that her most recent use was 2 to 3 hours before the onset of symptoms.Admitted with STEMI. Cardiac Cath: Left apical ballooning with EF 25%.

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42 y/o white male male42 y/o white male male

♥ Came to ED due to c/o substernal burning pain that radiates up chest to both arms.

♥ Becomes SOB with chest pain♥ Episodes last approx 10 minutes at a time.♥ Episodes occur more when lying flat. This

occurs several times during the night so he is not able to sleep

♥ Episodes have been occurring for last 4 months.

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More HistoryMore History

♥ Had a negative stress test & normal GI workup.

♥ Denies any drug use of cocaine or other medications

♥ Quit Smoking 4 months ago. No other past medical history

♥ Father had some cardiac problems when he was in his 50s or 60s --- history unclear.

♥ Pain free on arrival to ED♥ Alert, Oriented♥ Skin Warm/dry

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Feb 24 at 1331Feb 24 at 1331

♥ When laid down for EKG developed chest pain

♥ BP 122/77, HR 87, RR 20 SpO2 99%♥ Chest pain 7/10♥ Weight: 70 kg

♥ This 12 Lead was done when he was lying down and complaining of chest pain on Feb 24 at 1333.

♥ Patient is SOB & in severe pain at the time of the EKG.♥ First time EKG done during chest pain

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♥ Chest pain resolved when sat up♥ BP 118/56, HR 74, RR 20

♥ At 1339 on 2-24 (6 minutes later), the chest pain was gone. Pt was sitting up at the time. This is the 12 Lead EKG.

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♥ Serial troponin levels & lipid levels ordered♥ Troponin < 0.4 ng/ml♥ CK = 71♥ Total Cholesterol = 161♥ Triglycerides = 66♥ HDL = 35♥ LDL = 113

♥ Called cardiologist♥ 1st EKG STEMI that resolved after a few

minutes.♥ Admit patient to CVICU. Started on ASA,

plavix, heparin drip, nitroglycerin drip, and lopressor

♥ Hold cardiac cath for now as pain free with normal EKG

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Cardiac Cardiac CathCath Feb 25Feb 25Initial Injection of RCAInitial Injection of RCA

70% Occlusion

Cardiac Cardiac CathCath Feb 25Feb 25RCA after administration of RCA after administration of Intracoronary NitroglycerinIntracoronary Nitroglycerin

10 % Occlusion after NTG

EF = 70%

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Cardiac Cardiac CathCath on Feb 25on Feb 25

♥ The RCA is a dominant vessel giving off the PDA and posteriolateral branches, and appears to have a dynamic stenosis to the distal RCA.

♥ The first injection (RCA) shows a narrowing of around 50%, the subsequent injection shows narrowing closer to 70 – 80%, and after administration of NTG, there was perhaps a narrowing of around 10%.

♥ LAD and Circumflex showed no occlusion ♥ Impression: Dynamic stenosis of the distal RCA.

Intense coronary spasm causing transient ST elevation.

♥ EF = 70%


♥ Diltiazem 180 mg ♥ Nitroglycerin 0.4 mg Transdermal patch.

Apply at bedtime and remove at 10 am.♥ Two days later, stated, “ I am finally sleeping

at night!”♥ Discharged with

– Diltiazem 180 mg daily – Nitroglycerin 0.4 mg Transdermal patch at HS

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Unstable AnginaUnstable Angina

♥ Result of partial occlusion of a coronary artery without the presence of elevated cardiac biomarkers

PrinzmetalPrinzmetal or Variant Unstable or Variant Unstable AnginaAngina

♥ Caused by a dynamic obstruction from intense vasoconstriction

♥ Unstable angina represents a transition from stable angina to an unstable state

♥ One or more of the coronary arteries are more than 60% obstructed or the symptoms have become more frequent , more severe, or occur at rest

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♥ Modification of risk factors♥ Vasodilators to decrease spasms

– Nitroglycerin– Calcium Channel Blockers


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Case Study Case Study –– 37 y/o white male37 y/o white male

♥ Came to cardiologist office as he developed rapid palpations associated with some shortness of breath while exercising with weight lifting.

This patientThis patient’’s s ““normalnormal”” EKGEKG

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Family history positive for CADFamily history positive for CAD

♥ One uncle died suddenly of AMI♥ Three uncles -- CAD, AMI, CABG, and

angioplasty♥ Mother & all grandparents = hypertension♥ Grandfather – stroke♥ One aunt -- CAD, CABG, and stenting♥ One cousin died of cardiac arrhythmia

PMHPMH

♥ Moderate drinker – 6 beers per week♥ Does not smoke♥ Average BMI♥ 1st seen by cardiologist one year ago for three

episodes of resting palpitations which resided spontaneously.

♥ 12 Lead at that time: Findings consistent with left posteroseptal WPW syndrome

♥ 24 hour holter – no arrhythmia♥ Stress test: negative for ischemia♥ ASA 81 mg daily

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At cardiologist officeAt cardiologist office

♥ BP 120/70♥ Heart rate 160 irregular


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Direct admit to CVICUDirect admit to CVICU

♥ Walks to bed & placed on monitor!

♥ Tambocor 150 mg given po♥ Does not convert and BP dropped to 76/sys.♥ Cardioverted (moderate sedation) with 100

joules.

Post Post CardioversionCardioversion

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DischargeDischarge

♥ Tambocor 150 mg po bid♥ Baby ASA 81 mg daily♥ Follow up with electrophysiologist for

catheter ablation of the left posteroseptalpathway

♥ Shortened PR interval < 0.12 sec with a normal p wave

♥ Wide QRS complex > 0.11 sec

♥ The presence of a delta wave♥ ST-T wave changes or abnormalities

♥ Association with paroxysmal tachycardias – can be fatal

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59 y/o white male59 y/o white malePMH: GERD & AsthmaPMH: GERD & Asthma

♥ Sitting at table after breakfast – Started feeling hot, flushed, and sweaty and heartburn sensation

♥ Passed out for 2 minutes♥ Eyes rolled back♥ Then became alert, no suggestion of

postictal state. No seizures

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♥ Cardiac Markers = Negative♥ Cardiology Consult - Cardiac Cath due to chest pain to

r/o cardiac disease♥ Neruology Consult - Suggested MRI and sleep study

Cardiac Cardiac CathCath = Normal except while = Normal except while holding his breath, this was his rhythmholding his breath, this was his rhythm

♥ Unable to reproduce the asystole♥ Carotid Massage gave bradycardia but not

significant bradycardia♥ Admitted for observation overnight ♥ Plan to schedule Echo and possibly tilt table

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Patient returns to room and then Patient returns to room and then when he turned his headwhen he turned his head……

Returned to Returned to CathCath Lab for PacemakerLab for Pacemaker

Quiz time:Quiz time:What type of pacemaker does he need?What type of pacemaker does he need?

A. VVIB.

C. DDDD. DDD with ICD

AAI

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Quiz time:Quiz time:What type of pacemaker does he need?What type of pacemaker does he need?

A. VVI ♥ Will cause Pacermaker Syndrome due to loss of

atrial kick from no SA node conduction

B. AAI ♥ Will stimulate sinus node

C. DDD♥ No problem with AV node so don’t need

venticular support

D. DDD with ICD♥ No ventricular arrhythmias

Sick Sinus SyndromeSick Sinus Syndrome

♥ Degenerative changes in and around the sinus node result in a marked decline in the number and effectiveness of sinus node pacemaker cells in older adults

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Manifestations of SSSManifestations of SSS

♥ Inappropriate resting bradycardia,♥ Chronotropic incompetence – the inability

to increase HR in response to increased demands imposed by normal activities

♥ Sinus pauses♥ Sinus arrest♥ Tachy-brady syndrome

Sick Sinus Syndrome FeaturesSick Sinus Syndrome Features♥ Persistent, severe, inappropriate sinus bradycardia♥ Sinoatrial block and/or sinus arrest episodes♥ Long pauses with failure of secondary pacemakers or

failure of sinus rhythm♥ Ectopic atrial or junctional pacemaker rhythm as

replacement for NSR♥ Prolonged suppression of sinus rhythm after electrical or

spontaneous cardioversion from atrial tachydysrhythmiasor bradycardia alternation with tachycardiac

♥ AF that may be paroxysmal, persistent, or permanent and may have slow ventricular rate caused by permanent silence from sinus node and other AV node disease

Source: Moser, D. Riegel B (2008) Cardiac Nursing

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DiagnosisDiagnosis

♥ Electrophysiology studies♥ Age – Peak incidences in 70s♥ No gender difference♥ 40 – 60 % also have SVT♥ May be reversible and self limiting IF

associated with cardiac disease or medications that involves the sinus node

TreatmentTreatment

♥ Temporary Pacemaker♥ Review medication list♥ Treat underlying cardiac disease♥ Permanent pacemaker

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Case Study #9Case Study #986 y/o white female admitted for syncope86 y/o white female admitted for syncope

♥ States that while standing and talking, she suddenly felt, “different”

♥ Then she had an attack and thought she was going to die

♥ Her eyes rolled back in her head and LOC for 20 seconds – she does not remember this

♥ No loss of bowel or bladder control

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PMHPMH

♥ Hypertension♥ Hypothyroidism♥ Osteoarthritis,♥ Diastolic Heart failure – EF 60% on Echo 4

months ago♥ Hx lower GI bleed♥ Hx CVA with Left sided weakness♥ Hx sinus bradycardia♥ Nursing home resident who signed a full code

status paper one week ago

LabsLabs

♥ CT = old right parietal infarct♥ CXR = cardiomyopathy♥ UA = suggestive of UTI♥ Cardiac markers = negative♥ WBC 6.7♥ Monitor in ED showed Sinus Bradycardia,

Rate 30 which responded to Atropine 1 mg IV

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12 Lead EKG on Admission12 Lead EKG on Admission

12 Lead EKG after 12 Lead EKG after AtrpoineAtrpoine

2 hours later from previous EKG2 hours later from previous EKG

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This is her admission rhythm on the This is her admission rhythm on the telemetry unit.telemetry unit.

♥ What is the rhythm?

As you are admitting her, the rhythm changes to….

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♥ EKG strips are over a 2 minute time period

MedicationsMedications

♥ Aricept♥ Aspirin 325 mg daily♥ Benicar 40 mg daily♥ Lanoxin 0.25 mg daily♥ Lipitor 80 mg daily♥ Nitroglycerin patch 0.4 mg every day♥ Toprol XL 25 mg daily♥ Lanoxin Level = 1.1

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♥ Patient was placed on external pacemaker Rate 60 MA 60 with frequent paced beats

♥ Atropine 0.5 mg IV given ♥ Rhythm changed to Atrial Flutter with

occasional to frequent paced beats♥ The external pacemaker is working well,

the patient says it feels like a tickle

♥ Cardiology at the bedside and suggesting a temporary pacemaker

♥ Patient states, “ I am a nurse. I have lived a good life. I do not want heroic measures done. I do not want to go to cath lab for a pacemaker.”

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♥ The atropine has worn off♥ External pacemaker is pacing occasionally

to frequently♥ Do you turn off the external pacemaker?

♥ Additional information♥ Daughter notified and says, “it doesn’t

matter to her what is done” and is not planning to come in.

♥ Only “family” present is “nursing home nurse

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Mutual agreement between patient Mutual agreement between patient and cardiologistand cardiologist

♥ To leave external pacemaker on for 24 hours to let the effect of the beta blocker and digoxin to go out of her system

♥ To treat with Atropine 0.5 mg IV if needed during the next 24 hours

♥ Provide sedation if external pacemaker uncomfortable

♥ Re-evaluate in 24 hours and then make further decisions

♥ If develops lethal arrhythmias, will not resuscitate

♥ Rhythm after Atropine x 3 and Isuprel drip♥ Once Beta blocker wore off, rhythm was

stable and patient discharged to nursing home

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♥ 49 y/o white male♥ Railway Conductor – fairly strenuous

activity♥ PMH: Mild Hypertension, Non smoker♥ Family Hx: Father died suddenly in early

50’s presumably of cardiac disease

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Presentation at MD OfficePresentation at MD Office

♥ c/o SOB with mowing lawn♥ Whenever tried to exert himself, he would

get just mildly SOB, would rest, and then continue

♥ No chest discomfort, jaw pain, shoulder or back pain. No sweating

♥ c/o more lightheadness than SOB♥ Has been occurring for a couple of weeks

if not months

Sent for Stress TestSent for Stress Test

♥ Pt later stated, “They got so excited during my stress test. I felt fine. They made me sit down and kept asking me if I was okay. I think I scared them!”

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Now for the rest of the storyNow for the rest of the story……ST depression and then thisST depression and then this……..

Stress Test #1 0800

Stress Test #2 0801Stress Test #2 0801

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75 75 –– 80% Proximal LAD, mid LAD 80% Proximal LAD, mid LAD stenosisstenosis75 75 -- 80% Two long tandem lesions & a distal at the bifurcation80% Two long tandem lesions & a distal at the bifurcation

LVEF NormalLVEF Normal

LAD with one stent deployedLAD with one stent deployed

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LAD post three (DES) stentsLAD post three (DES) stentsNote: diagonal 2 lost with stent over bifurcationNote: diagonal 2 lost with stent over bifurcation

Discharge medsDischarge medsTroponinTroponin normalnormal

♥ Plavix 75 mg daily – probably for lifetime♥ ASA 325 mg daily♥ Tropol 50 mg daily♥ Crestor 40 mg daily♥ Lisinopril & Hydrochlorothiozide 10/12.5

mg daily♥ NTG SL prn

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Anterior AMIAnterior AMILAD occlusionLAD occlusion

♥ Arrhythmias = VT or VF♥ Usually have the lowest EF


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At 2 pm, a 68 y/o white male comes to the ED per private At 2 pm, a 68 y/o white male comes to the ED per private transportation because, transportation because, ““he isnhe isn’’t feeling wellt feeling well””

♥ Last night at midnight, he developed chest pain, radiating to both arms, with belching.

♥ Concerned about urinary infection as his urostomy is draining darker urine than normal.

♥ Chest pain started one day again and has had more than 3 episodes of chest pain in last 24 hours.

♥ Most recent episode of chest pain started more than three hours ago. He has known angina but is unable to distinguish if this is typical angina chest pain

♥ This recent chest pain is described as quite severe, like a tightening in the chest, dull aching pain that radiates to the left shoulder. He became diaportic with the chest pain.

♥ No pain at the present time.

♥ BP 114/54, HR 47, RR 20, SpO2 93% RA♥ Alert, Oriented x 3, Skin Warm/dry♥ Pain 0/10♥ Home Meds

– ASA 81 mg po daily– Metoprolol Tartrate 12.5 mg bid

♥ PMH– Bladder cancer (resection – urostomy)– Hypertension– Nonsmoker

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Initial 12 Lead EKGInitial 12 Lead EKG

♥ Rhythm: 3rd Degree (Complete) Heart Block with Junctional Escape Rhythm

♥ Cath lab called, External pacer available, prep for angiogram and temporary pacer

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Occluded RCAOccluded RCA

Export Export CathCath used to aspirate thrombus in RCA used to aspirate thrombus in RCA Rhythm changed to Rhythm changed to MobitzMobitz IIII

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Stent to RCAStent to RCARhythm changed to Sinus Rhythm with 1Rhythm changed to Sinus Rhythm with 1stst degree AV Blockdegree AV Block

♥ PCI time = 68 minutes

Normal Sinus Rhythm post stentNormal Sinus Rhythm post stent

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Inferior AMIInferior AMIRCA occlusionRCA occlusion

♥ Arrhythmias= Blocks♥ Involves right ventricle – may also get right

ventricular infarct♥ Need lots of fluids to increase preload since RV is

involved♥ RCA wraps around the back of the heart and

changes to PDA. Typically have inferior –posterior AMI.

♥ Inferior- Posterior AMI: – ST Elevation: II, III, AVF and

– ST depression V1, V2, V3

♥ Anterior AMI -- LAD – VT♥ Inferior AMI --- RCA -- Blocks

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48 y/o white male comes to ED48 y/o white male comes to ED

♥ Chest pain that awoke him from a nap♥ Pressure type across the chest♥ Some diaphoresis♥ BP 149/108

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EKG on admissionEKG on admission

24

♥ Pt wants to go home♥ Had a stress Echo 4 months ago due to

hypertension. Stress echo was normal

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Occluded Diagonal Post StentOccluded Diagonal Post Stent

Normal AortaNormal Aorta

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♥ Also on angio 6 cm ascending thoracic aortic aneurysm

♥ Repaired 1 week later

Normal

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41 year presents to ED with SOB 41 year presents to ED with SOB for past 2 for past 2 –– 3 days3 days

♥ BP 157/95♥ HR 108♥ RR 28♥ T 96.2♥ SpO2 95% on 5 liters/NP

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♥ No history of smoking♥ No cardiac or pulmonary history♥ Family history: Grandmother- heart

disease. Mother – aneurysm♥ Two days ago was in the ED with BNP

700, received IV lasix with good response.♥ Sent home on Lasix 20 mg bid♥ Improved for one day and then increasing

SOB

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Pulmonary Embolus CriteriaPulmonary Embolus Criteria

♥ S1, Q3 or S1,Q3, T3♥ RBBB♥ Inverted T waves secondary to RV strain may be seen in the right

precordial leads and can last for months

Admission LabsAdmission Labs

♥ Na 141♥ K 3.8♥ Bun 16♥ Creatinine 0.9♥ Glucose 106

♥ WBC 12.1♥ HBG 11♥ HCT 33.4♥ Platelets 268♥ BNP 938♥ CK 71♥ Troponin 0.01

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♥ CT negative for PE

More HistoryMore History

♥ 1 week post partum ♥ 1st pregnancy, 48 hours in labor, vaginal

delivery ♥ Diet controlled gestitational diabetes♥ On day of discharge – post delivery,

noticed swelling of her lower legs and then had � SOB and orthopnea that brought her to the ED two days ago

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DxDx–– Postpartum CardiomyopathyPostpartum Cardiomyopathy

♥ Received IV Lasix in ED with 2 liter response and significant improvement of symptoms of congestive heart failure

♥ EF = 20%

♥ 1st CXR

♥ CXR 6 hours after IV Lasix

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♥ BNP reached 1233♥ Discharged with the following medications:

– Lasix– Potassium supplement– Enapril– ASA

♥ Patient wants to breast feed???

♥ Breast feeding – Okay for Enapril

• Do not give ACEI/ARBs during pregnancy!

– Unknown for Lasix

♥ Encouraged not to breast feed♥ Added Coreg 3.625mg later♥ Five months later Coronary angiogram

– no occlusive coronary disease– Moderate global LV dysfunction– EF 20 – 30%

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ICD inserted due to low EF & high ICD inserted due to low EF & high risk for sudden cardiac deathrisk for sudden cardiac death

PeripartumPeripartum CardiomyopathyCardiomyopathy

♥ Cardiomyopathy in the last month or the first five months after pregnancy – EF < 45%– m-mode fractional shortening <50%– LVED dimension > 2.72 cm/m2

♥ Incidence 1:3000 – 4000♥ Risk Factors

– Advancing maternal age– Multiparity– Multi-fetal gestation,– Preeclampsia– Black race

Source: Moser & Riegel. 2008. Cardiac Nursing

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PeripartumPeripartum Cardiomyopathy Cardiomyopathy ConcernsConcerns

♥ Increased risk of thrombotic emboli – start anticoaguation therapy

♥ As high as 85% risk of death associated with peripartum cardiomyopathy in women with persistent LV dysfunction 6 months after pregnancy

Source: Moser & Riegel. 2008. Cardiac Nursing


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45 y/o white female sudden 45 y/o white female sudden syncope while teachingsyncope while teaching

♥ CPR started, AED applied and delivered one shock

Admission EKGAdmission EKG12:2612:26

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EF 40EF 40-- 45%45%

45 y/o post cardiac arrest pre ICD45 y/o post cardiac arrest pre ICD

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♥ PMH: Father fatal MI at age 57♥ No smoking, alcohol, or illicit drug use♥ Wt: 60 kg♥ D-Dimer 2443, Potassium 3.3♥ DX- Aborted sudden cardiac death

etiology secondary to cardiomyopathyalong with hypokalemia

♥ Thyroid Stimulating Hormone– TSH = 0.15 µIU/mL (0.4–4.0) ��

♥ T3-FREE – FREE T-3 2.2 pg/ml (2.2-4.0)

♥ T4 FREE– FREE T4 1.16 ng/dl (0.80-1.50)

♥ THYROID PEROXIDASE AB– TPO AB <0.3 IU/mL (0.0-3.9)

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Discharge diagnosisDischarge diagnosis

♥ Cardiomyopathy with EF 40 – 45% presumably related to thyrotoxicosis

♥ ICD implanted

EKG 3 days laterEKG 3 days later

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EKG 2 years prior to eventEKG 2 years prior to event


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A Woman’s Heart Is Different

Heart Attack Signs & Symptoms for Women

♥ “Atypical” Chest Pain♥ Shortness of Breath/

Trouble Breathing♥ Tingling of Fingers♥ Extreme Fatigue♥ Heartburn / Nausea♥ Sweating♥ Dizziness♥ Feeling of Apprehension

or Impending Doom

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93 y/o female c/o jaw pain, pain in shoulders.93 y/o female c/o jaw pain, pain in shoulders.BP 75/50BP 75/50

Completely Occluded LAD StentCompletely Occluded LAD Stent–– took 2 took 2 hours to open. Looked like a stent when hours to open. Looked like a stent when

PlavixPlavix stoppedstopped

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Post opening LAD stentPost opening LAD stent

76 y/o female76 y/o female1 hour post stents to LAD, and 1 hour post stents to LAD, and DiagnoalDiagnoal 1. 1.

Nausea, pain in right armNausea, pain in right arm–– Past Past HxHx of shoulder painof shoulder pain15 minutes later: Chest heaviness15 minutes later: Chest heaviness

♥ Back to cath lab: Occluded D2 -- stent

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62 y/o female62 y/o femaleChest pain for 8 hours prior to coming to EDChest pain for 8 hours prior to coming to ED

100% occluded RCA100% occluded RCA

100 % occluded

RCA

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RCA post stentRCA post stent

♥ Troponin 3.73 CK 153

In SummaryIn Summary

Scary Coronary EventsScary Coronary Events

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ALL chest pain is ALL chest pain is cardiaccardiac until until proven otherwiseproven otherwise

♥ Ask Questions to get a good history!♥ No fibrinolytics for Broken Heart Syndrome

or Cocaine Induced AMI♥ Women have different symptoms than

males

Time is MuscleTime is Muscle

74 minutes Door to PCI Time!

scary coronary eventsnormal coronary anatomy – no cad severe hypokinesis to akinesis of the distal...

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