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CCU Case ConferenceCCU Case Conference

Chief ComplaintChief Complaint

45 yo Pakistani M with HTN, diet 45 yo Pakistani M with HTN, diet controlled hyperlipidemia, psoriasis controlled hyperlipidemia, psoriasis presents with 5/10 midsternal chest presents with 5/10 midsternal chest pain with nausea while driving home pain with nausea while driving home from work that lasted one hourfrom work that lasted one hour

History of Present IllnessHistory of Present Illness

Patient’s pain began suddenly at 4:30 Patient’s pain began suddenly at 4:30 pm and was not exacerbated with pm and was not exacerbated with exertion. He took acetaminophen exertion. He took acetaminophen which offered no relief.which offered no relief.

At 5:30 pm, the patient continued to At 5:30 pm, the patient continued to have pain which prompted him to have pain which prompted him to call the EMS.call the EMS.

Past Medical HistoryPast Medical History

PMH: HTN, borderline hyperlipidemia, PMH: HTN, borderline hyperlipidemia, psoriasispsoriasis

Meds: on HTN meds which he did now Meds: on HTN meds which he did now the names that he took irregularlythe names that he took irregularly

ROS: negativeROS: negative

What were his cardiac risk factors?What were his cardiac risk factors?

QuickTime™ and a decompressor

are needed to see this picture.



South Asians and CV riskSouth Asians and CV risk









Physical ExamPhysical ExamGen:Gen: Anxious, AOx3, NADAnxious, AOx3, NADVS:VS: 98.9 108/81 103 reg 114 98% RA98.9 108/81 103 reg 114 98% RA

65 in 202 lbs 65 in 202 lbs HEENT: HEENT: MMMMMMNeck:Neck: JVP around 8 cmJVP around 8 cmCV:CV: Tachy, RRR systolic murmur III/VI at Tachy, RRR systolic murmur III/VI at

LLSB, RV heaveLLSB, RV heaveLungs: Lungs: b/l crackles at basesb/l crackles at basesAbd:Abd: SoftSoftExt:Ext: Warm, 2+ pedal pulses, dry scaly skin Warm, 2+ pedal pulses, dry scaly skin

at shins b/lat shins b/l

Laboratory AssessmentLaboratory AssessmentTESTTEST REFERENCE REFERENCE

RANGERANGEON ON ADMISSIONADMISSION

CHEMISTRYCHEMISTRY

Sodium (mmol/liter)Sodium (mmol/liter) 135 – 145135 – 145 137137

Potassium (mmol/liter)Potassium (mmol/liter) 3.4 – 4.83.4 – 4.8 5.45.4

Chloride (mmol/liter)Chloride (mmol/liter) 100 – 108100 – 108 102102

Carbon dioxide (mmol/liter)Carbon dioxide (mmol/liter) 23.0 – 31.923.0 – 31.9 2222

Urea nitrogen (mg/dl)Urea nitrogen (mg/dl) 8 – 258 – 25 2020

Creatinine (mg/dl)Creatinine (mg/dl) 0.6 – 1.50.6 – 1.5 1.51.5

Glucose (mg/dl)Glucose (mg/dl) 70 - 11070 - 110 136136

Calcium (mg/dl)Calcium (mg/dl) 8.5 – 10.58.5 – 10.5 8.58.5

Laboratory AssessmentLaboratory AssessmentTESTTEST REFERENCE REFERENCE

RANGERANGEON ON

ADMISSIONADMISSION

HEMATOLOGYHEMATOLOGY

Hemoglobin (g/dl)Hemoglobin (g/dl) 13.5 – 17.513.5 – 17.5 13.913.9

Hematocrit (%)Hematocrit (%)41.0 – 53.041.0 – 53.0 41.341.3

White-cell count (per mmWhite-cell count (per mm33)) 4,500 – 11,0004,500 – 11,000 15.015.0

Differential Count (%)Differential Count (%)

NeutrophilsNeutrophils 40 – 7040 – 70 7474

BandsBands 2-82-8 00

LymphocytesLymphocytes 22 – 4422 – 44 1515

MonocytesMonocytes 4 – 114 – 11 1111

Platelet Count (per mmPlatelet Count (per mm33)) 150,000 – 150,000 – 300,000300,000 269269

Partial-thromboplastin time (sec)Partial-thromboplastin time (sec) 22.1 – 35.122.1 – 35.1 13.913.9

INRINR 11.3 – 13.311.3 – 13.3 1.11.1

Laboratory AssessmentLaboratory Assessment

Troponins 12Troponins 12

CKCK

CK MB 24CK MB 24

BNPBNP

Hospital CourseHospital Course

Overnight, the patient remained Overnight, the patient remained tachycardic, but his blood pressure tachycardic, but his blood pressure was stable. The patient, however, was stable. The patient, however, did have increasing oxygen did have increasing oxygen requirements.requirements.

He was started on nitroprusside to He was started on nitroprusside to maintain a systolic blood pressure < maintain a systolic blood pressure < 110 mmHg110 mmHg


On HD # 2, a intra-aortic balloon On HD # 2, a intra-aortic balloon pump was placed to improve the pump was placed to improve the patient’s cardiac output. Throughout patient’s cardiac output. Throughout the patient remained stable but the patient remained stable but continued to have worsening continued to have worsening pulmonary edemapulmonary edema

The following blood gases were The following blood gases were drawn to meaure a shunt fractiondrawn to meaure a shunt fraction


On HD # 3, the patient was On HD # 3, the patient was intubated due to worsening intubated due to worsening pulmonary edema and to perform a pulmonary edema and to perform a TEETEE


After much deliberation on HD # 5, After much deliberation on HD # 5, the patient went for surgical repair of the patient went for surgical repair of the VSDthe VSD

Post – operative coursePost – operative course

After the surgery, patient was After the surgery, patient was extubated and IABP was discontinued extubated and IABP was discontinued on POD #1. After sedation was on POD #1. After sedation was weaned, the patient continued to be weaned, the patient continued to be confused and have delirium.confused and have delirium.

In addition, the patient had In addition, the patient had worsening renal and hepatic failure worsening renal and hepatic failure over the next tthree days. over the next tthree days.

Post – operative coursePost – operative course

On POD #4, the patient became On POD #4, the patient became flaccid on his L side and had flaccid on his L side and had worsening of his cognitive function. worsening of his cognitive function. Stroke team was called and the Stroke team was called and the patient was taken for an MRI. patient was taken for an MRI.

Ventricular Septal RuptureVentricular Septal Rupture

IncidenceIncidence Before reperfusion therapy, septal rupture Before reperfusion therapy, septal rupture

complicated 1 to 3 percent of acute myocardial complicated 1 to 3 percent of acute myocardial infarction (AMI) infarction (AMI) 11

Reperfusion therapy decreases the incidence Reperfusion therapy decreases the incidence to 0.2 percent to 0.2 percent 22

Risk FactorsRisk Factors Before reperfusion era – hypertension, Before reperfusion era – hypertension,

advanced age, female sex, absence of angina advanced age, female sex, absence of angina preceding MIpreceding MI

Reperfusion era – advanced age, female sex, Reperfusion era – advanced age, female sex, absence of smokingabsence of smoking

1 Birnbaum, NEJM 2002

2 Crenshaw, Circulation 2000

The Evolution of an MIThe Evolution of an MI

TimeTime Morphological ChangesMorphological Changes0 to 30 0 to 30 minmin

Relaxation of myofibrils; glycogen loss; mitochondrial Relaxation of myofibrils; glycogen loss; mitochondrial swelling swelling

30 min to 30 min to 4 hrs4 hrs

Variable waviness of fibers at border Variable waviness of fibers at border

4 to 12 hrs4 to 12 hrs Early coagulation necrosis; edema; hemorrhage Early coagulation necrosis; edema; hemorrhage

12 to 24 12 to 24 hrshrs

Ongoing coagulation necrosis; myocyte Ongoing coagulation necrosis; myocyte hypereosinophilia; marginal contraction band necrosis; hypereosinophilia; marginal contraction band necrosis; early neutrophilic infiltrate early neutrophilic infiltrate

1 to 3 days1 to 3 days Coagulation necrosis, with loss of nuclei and striations; Coagulation necrosis, with loss of nuclei and striations; brisk interstitial infiltrate of neutrophils brisk interstitial infiltrate of neutrophils

3–7 days 3–7 days Beginning disintegration of dead myofibers, with dying Beginning disintegration of dead myofibers, with dying neutrophils; early phagocytosis of dead cells by neutrophils; early phagocytosis of dead cells by macrophages at infarct border macrophages at infarct border

7–10 days 7–10 days Well-developed phagocytosis of dead cells; early Well-developed phagocytosis of dead cells; early formation of fibrovascular granulation tissue at margins formation of fibrovascular granulation tissue at margins

10–14 10–14 days days

Well-established granulation tissue with new blood Well-established granulation tissue with new blood vessels and collagen deposition vessels and collagen deposition

2–8 wk 2–8 wk Increased collagen deposition, with decreased cellularity Increased collagen deposition, with decreased cellularity

>2 mo >2 mo Dense collagenous scar Dense collagenous scar

7 - 10 d

3 - 4 d

30 m - 4 h

10 - 14 d

2 -8 wk

Myocardial apoptosis associated with Myocardial apoptosis associated with the expression of proinflammatory the expression of proinflammatory cytokines during the course of cytokines during the course of myocardial infarction FREEmyocardial infarction FREE

Yoshikiyo Akasaka, Noriko Morimoto, Yoshikiyo Akasaka, Noriko Morimoto, Yukio Ishikawa, Kazuko Fujita, Kinji Ito, Yukio Ishikawa, Kazuko Fujita, Kinji Ito, Masayo Kimura-Matsumoto, Masayo Kimura-Matsumoto, Shigeki Ishiguro, Hiroshi Morita, Shigeki Ishiguro, Hiroshi Morita, Yoshiro Kobayashi and Toshiharu IshiiYoshiro Kobayashi and Toshiharu Ishii

Mod Pathol 19: 588-598; advance online Mod Pathol 19: 588-598; advance online publication, March 3, 2006publication, March 3, 2006

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