Nausea followed by respiratory failure and hypotension
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.
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 bruits
Chest :breath sounds were diminished bilaterally,
with fine scattered crackles.
Heart: a rapid rhythm; PMI: normal.
The remainder of the physical examination was normal.
Result of Hematological laboratory Test. ppt
ceftriaxone, azithromycin, and methylprednisolone.
The patient was admitted to the other hospital 9 hours after arrival in the emergency department .
At Other hospital
Hypoxemia, acidosis and hypercapnia.
4 hr after admission — sedated and intubated and initiated MV
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.
7 Months Earlier
>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 changes
CXR, 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 history
Graves' disease-- treated with radioactive iodine
GERD, peptic ulcer disease,Diverticulitis
Operation: several cesarean sections, a total abdominal hysterectomy, and vocal-cord polyps.
Smoking: smoked 2-3 cigarettes per week for 50 years, but stopped after the transient ischemic attack.
Family history: Her mother had died of a myocardial infarction at age 75. She lived with her husband.
Travel history: She had not traveled recently.
levothyroxine, fexofenadine, lisinopril, omeprazole, and aspirin at home.
When she was transferred to this hospital, her medications included vancomycin, ceftriaxone, azithromycin, methylprednisolone, phenylephrine (200 µ g per minute), norepinephrine (25 µ g per minute), and intravenous heparin.
>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, S 3 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 aV L and a 2-mm ST-segment depression in leads II, III, and aVF.
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:
Mechanical Causes of Cardiogenic Shock
Extensive Ischemia or infarction
Mechanical Causes of Cardiogenic Shock
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 S 3 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;
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 harsh
an extensive RV infarct and volume depletion---Hypotension
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.
Acute myocardial infarction with cardiogenic shock and possible septic shock.
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.
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 angioplasty
CXR after catheterization
Color 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.
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.
>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 of coronary artery disease
(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-
>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 presentations of coronary artery disease
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 infarction and 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
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.
Acute myocardial infarction (3 to 5 days old) with rupture of the anterolateral papillary muscle.