Clinic-Pathologic Clinic-Pathologic ConferenceConference

主講者主講者 :: 楊仰榮楊仰榮指導者指導者 :: 褚佩寰褚佩寰 ,, 韋建華韋建華

96-09-2196-09-21

Presenting complaintPresenting complaint

Nausea followed by respiratory failure and hypotension

Present illnessPresent illness

• The cough was accompanied by chills, sweats, malaise, lightheadedness, aching in the teeth, anorexia, and insomnia.

• Denied fever, wheezing, shortness of breath, crushing chest pain, dizziness, or urinary symptoms.

• The next afternoon, her family took her to the emergency department of another hospital.

Physical examinationPhysical examination

Appearance: uncomfortable. BP: 90/50 mm Hg, PR: 107/min, BT:36.7°C;RR:22 – 33/min, O2 Sat: 85 to 92% (ambient air)Neck: No JVD or bruitsChest :breath sounds were diminished bilaterally, with fine scattered crackles.Heart: a rapid rhythm; PMI: normal.The remainder of the physical examination was

normal.

CXR CXR

Result of Hematological laboratory Test. ppt

TreatmentTreatment

• Intravenous fluids, • ceftriaxone, azithromycin, and

methylprednisolone.• The patient was admitted to the other hospital 9

hours after arrival in the emergency department.

At Other hospitalAt Other hospital

• Hypoxemia, acidosis and hypercapnia.

• 4 hr after admission—sedated and intubated and initiated MV

• Suction--Pink secretions• reduced normal saline infusion rate, and

furosemide (80 mg) IV .• During the next 2 hours --worsening hypotension• IV dobutamine drip -- discontinued because

Increase HR without improvement in BP

• phenylephrine and norepinephrine, HR:125/min, > ECG:a 1-mm ST-segment elevation in lead aVL,

a 2-mm ST-segment depression in leads II, III, and aVF.

> Condition did not improve, and 22 hours after

her arrival at the other hospital, she was transferred to this hospital and admitted to the coronary care unit.

Past historyPast history

7 Months Earlier>h/o TIA >An inpatient evaluation by the neurology service

at this hospital showed that BMI:22.3, BP:163/72

mm Hg. >The results of a neurologic examination were

normal.

>The results of laboratory tests from that admission are shown .

Result of Hematologic laboratory Test.ppt

CT, CT angiography, MRI brain—-No stenosis or occlusion of the intracranial or cervical

arteries-No evidence of acute infarction, -Microangiopathic white-matter changesCXR, ECG: No abnormalities.

Echocardiography :EF: 68%, trace mitral regurgitation, and thickening and prolapse of the mitral leaflets.

24 hr Holter monitor :no evidence of arrhythmias. >The patient was discharged on the second hospital

day, with instructions to take aspirin and omeprazole.

• An exercise tolerance test with thallium performed 3 months later showed a normal exercise capacity (7 metabolic equivalents [MET];

• Stage 2 of 7 stages of graduated exercise on a standard Bruce protocol, with no evidence of ischemia.

• Because of persistently elevated blood pressure, she began to receive lisinopril 1 month later.

• Consultants in neurology and cardiology recommended the addition of a statin.

Past , Personal and Social historyPast , Personal and Social history

1. Graves' disease-- treated with radioactive iodine2. GERD, peptic ulcer disease,Diverticulitis3. Operation: several cesarean sections, a total

abdominal hysterectomy, and vocal-cord polyps. 4. Allergy: NKA5. Smoking: smoked 2-3 cigarettes per week for 50

years, but stopped after the transient ischemic attack.

6. Family history: Her mother had died of a myocardial infarction at age 75. She lived with her husband.

7. Travel history: She had not traveled recently.

Medication historyMedication history

• levothyroxine, fexofenadine, lisinopril,

omeprazole, and aspirin at home. • When she was transferred to this hospital, her

medications included vancomycin, ceftriaxone,

azithromycin, methylprednisolone, phenylephrine (200 µg per minute), norepinephrine (25 µg per minute), and intravenous heparin.

Physical examinationPhysical examination >The patient was intubated and sedated. >BP: 92/41 mm Hg, PR: 154/min, BT: 38.9°C, RR: 22/min > O2 sat :91%,FiO2 :1.0. > Heart: Normal S1 and S2, S3 gallop

Grade 2/6 holosystolic murmur that radiated from the apex to the axilla

>Lungs: Crackles were heard throughout both lungs. Result of Hematologic laboratory Test.ppt > ECG: showed sinus tachycardia , 146/min , a 2-mm ST-segment elevation in leads I and aVL and a

2-mm ST-segment depression in leads II, III, and aVF.

Problems:Problems:

• acute myocardial infarction with pulmonary edema

• 2 days before—Nausea and vomiting---onset of AMI

• Next 24hr—pulmonary edema & shock—extension of infarction

• Pneumonia and septic shock

DDX: cardiogenic shock due to MI:DDX: cardiogenic shock due to MI:

Mechanical Causes of Cardiogenic ShockExtensive Ischemia or infarctionEndocarditis

Mechanical Causes of Cardiogenic Mechanical Causes of Cardiogenic ShockShock

1)Ventricular septal rupture :

• 1 to 4% of MI.• Reperfusion by means of either thrombolytic

therapy or primary angioplasty has decreased the incidence of ventricular septal rupture.

• Occurs 3 to 7 days after myocardial infarction

• PE: a harsh holosystolic murmur, an S3 gallop, and a thrill, which was not present in this patient.

2)Rupture of the left ventricular free wall with tamponade

• occurs with similar frequency and within a similar time frame;

• PE: • JVD , PEA , and a pulsus paradoxus, none of

which were present in this patient.

3)Rupture of a papillary muscle 1% of patients, 2 - 7 days after MI.• PE: A murmur of MR in about 50% of patients, but soft

rather than harshRupture -- Posterior papillary >Anterior papillary muscle Posterior papillary muscle- -blood supply from a single vessel, either RCA or a

tributary, -rupture is usually associated with an inferior MIAnterior papillary muscle -2 sources, which are often an obtuse marginal

branch and the first diagonal branch of the LCA

-rupture --- associated with an anterior MI.

Extensive Ischemia or InfarctionExtensive Ischemia or Infarction

• Cardiogenic shock ---Infarction or ischemia of a large area of the myocardium(3 V-D or Left main)

• MR can occur when left ventricular

dysfunction due to ischemia involves the mitral-valve apparatus.

• This patient--S/S of septic shock• circulating cytokines--further decrease LV

function. • an extensive RV infarct and volume

depletion---Hypotension

EndocarditisEndocarditis

• Endocarditis-- patient had an abnormal myxomatous mitral valve but less likely----no history of an event that might have lead to entry of an organism likely to cause

endocarditis.

• In this patient with a 2-day-old MI, hypotension,

pulmonary edema, and a holosystolic murmur---rupture of the anterior papillary muscle and cardiogenic shock with concomitant septic shock.

ECG changes and elevated levels of cardiac enzymes indicated ischemic myocardial damage--- immediate cardiac catheterization.

Clinical DiagnosisClinical Diagnosis

• Acute myocardial infarction with cardiogenic shock and possible septic shock.

Pathological Discussion Pathological Discussion

Right-sided cardiac catheterization : >RA pressure of 12 mm Hg, >RV pressure of 41/13 mm Hg, >Pulmonary arterial pressure of 41/26/32 mm Hg,

> PCWP of 21 mm Hg (with mild V waves), >Cardiac output of 7.9 liters per minute, >Cardiac index of 4.9 liters per minute per square

meter of body-surface area, >Calculated systemic vascular resistance of 527

dyne·sec·cm–5. >These findings suggested a combination of

cardiogenic shock and septic shock.

Coronary arteriographyCoronary arteriography

• Because the degree of shock was out of proportion to the extent of coronary artery

disease, left ventriculography was performed.• LV ejection fraction-- 45%, with anterolateral

hypokinesis.• 3+(moderate-to-severe) mitral regurgitation.• AMI( anterolaterla) with MR due to dysfunction or

rupture of an ischemic papillary muscle. • IABP was immediately placed through the right

femoral artery.

percutaneous transluminal coronary angioplastypercutaneous transluminal coronary angioplasty

CXR after catheterizationCXR after catheterization

Transesophageal Echocardiogram.Transesophageal Echocardiogram.

Color Doppler ultrasonographyColor Doppler ultrasonography

> Referred to a cardiac surgeon. > patient was operated.>IABP inserted and monitor overnight, and the

serum creatinine level fell, the cardiac enzyme levels began a downward trend, and the need for

pressors decreased.

Ramus occlusion was causing global hypokinesis and the ST-segment changes in the inferior leads.

First bypassed the right coronary artery and then excised the anterior leaflet of the mitral valve.

Findings:The papillary muscle had ruptured near its

attachment to anterior lateral mitral-valve leaflet.

a 27-mm porcine valve was placed.• This leaflet-sparing valve replacement preserves

the geometry of the ventricle, which is important in a patient who has had a recent myocardial infarction and is in shock.

• After this procedure, the patient's heart rate slowed, and the ventricular walls moved normally.

postoperative coursepostoperative course >complications: delayed recovery of consciousness,

aspiration pneumonia, and ischemia of the right foot due to a popliteal arterial thrombus--resolved with anticoagulation therapy.

>Discharged to a rehabilitation facility on the 23rd day

> went home 8 days later.

>During the next month, she resumed exercising at home

>30 months after discharge,-- cardiac rehabilitation

program Medications: aspirin, warfarin, metoprolol, and

simvastatin

Discussion And Management

1.Assessment of the risk of1.Assessment of the risk of coronary artery coronary artery diseasedisease

• (risk of CVD >20% in next 10 yr. hypertension,• a family history of CVD, smoking, and TIA>The class 1 recommendations --- lifestyle

modifications, including smoking cessation, physical activity, diet, and weight control.

>Lipid control and statin therapy for high-risk category

>Depression increases the risk of a recurrent cardiac event among patients who have had a myocardial infarction.

2. stress testing-2. stress testing-

>To determine whether ischemia could be provoked This patient -- about 7 MET, equivalent to an oxygen

uptake of 3.5 ml per kilogram of body weight per minute (stage 2 according to a standard Bruce protocol).

> In elderly women, who tend to have poor exercise capacity, it is important to look not only at the end result of provokable ischemia, but also at the level of exercise they are able to attain.

> Women an exercise level of <5 MET- higher rates of death

> Women with exercise level of <5MET-- pharmacologic stress testing.

3.atypical presentations3.atypical presentations of coronary artery of coronary artery diseasedisease

• nausea and anorexia; • the absence of chest pain -- a delay in the

diagnosis. • Women >men: dyspnea, nausea and vomiting,

indigestion, fatigue, and sweating , arm and shoulder pain.

• Inferior MI women >men--higher incidence of GI

symptoms among women.

4.treatment of myocardial infarction4.treatment of myocardial infarction

and its timingand its timing

• Diagnosis of AMI in the absence of chest pain, especially when other risk factors are present, is critical if women are to survive myocardial infarction; in the era of reperfusion, every minute counts.

• Among other factors, the absence of chest pain and female sex are associated with delays in performing primary angioplasty (the so-called door-to-balloon time).

>If this patient had sought medical attention when her nausea began, and if her symptoms of ischemia had been recognized, reperfusion might have prevented rupture of the papillary muscle

Posteriorfarction CarePosteriorfarction Care

• This patient's postinfarction care will be very important. She should be screened for depression.

• Cardiac rehabilitation is underused in women. In one study, women were less than half as likely as men to be enrolled in a cardiac rehabilitation

program after myocardial infarction. • Women with myocardial infarction tend to be

older than men delay in treatment and referral to a cardiac rehabilitation program.

Anatomical(Final) Anatomical(Final) DiagnosisDiagnosis

• Acute myocardial infarction (3 to 5 days old) with rupture of

the anterolateral papillary muscle.