ST Elevation Myocardial Infarction (STEMI)

An acute ST-elevation myocardial infarction occurs due to occlusion of one or more coronary arteries, causing transmural myocardial ischemia which in turn results in myocardial injury or necrosis. MI in general can be classified from Type 1 to Type 5 MI based on the etiology and pathogenesis.

·         Type 1 MI is due to acute coronary atherothrombotic myocardial injury with plaque rupture. Most patients with STEMI and many with NSTEMI comprise this category.

·         Type 2 MI is the most common type of MI encountered in clinical settings in which is there is demand-supply mismatch resulting in myocardial ischemia. This demand supply mismatch can be due to multiple reasons including but not limited to presence of a fixed stable coronary obstruction, tachycardia, hypoxia or stress. Other potential etiologies include coronary vasospasm, coronary embolus, and spontaneous coronary artery dissection (SCAD).

·         Type 3 MI include patient with Sudden cardiac death who succumb before any troponin elevation comprise.

·         Types 4 and 5 MIs are related to coronary revascularization procedures like PCI or CABG.

The American College of Cardiology, American Heart Association, European Society of Cardiology, and the World Heart Federation committee established the following ECG criteria for ST-elevation myocardial infarction STEMI:

·         New ST-segment elevation at the J point in 2 contiguous leads with the cutoff point as greater than 0.1 mV in all leads other than V2 or V3

·         In leads V2-V3 the cutoff point is greater than 0.2 mV in men older than 40 years old and greater than 0.25 in men younger than 40 years old, or greater than 0.15 mV in women

Patients with a pre-existing left bundle branch block can be further evaluated using Sgarbossa's criteria:

·         ST-segment elevation of 1 mm or more that is concordant with (in the same direction as) the QRS complex

·         ST-segment depression of 1 mm or more in lead V1, V2, or V3

·         ST-segment elevation of 5 mm or more that is discordant with (in the opposite direction) the QRS complex

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Cardiomyopathies

 Cardiomyopathies are a heterogeneous group of diseases of the myocardium associated with mechanical and/or electric dysfunction that usually (but not invariably) exhibit inappropriate ventricular hypertrophy or dilatation and are due to a variety of causes that frequently are genetic. Cardiomyopathies either are confined to the heart or are part of generalized systemic disorders.

John F. Goodwin developed a classification based on structural and functional changes.

·         Congestive cardiomyopathy, now referred to as dilated cardiomyopathy (DCM),

·         Hypertrophic cardiomyopathy (HCM), and

·         Constrictive (now referred to as restrictive) cardio myopathy (RCM).

·         Arrhythmogenic right ventricular cardiomyopathy (arrhythmogenic cardiomyopathy),

Each of these categories was further subdivided by pathogenesis, such as secondary to a systemic disorder, an infection, inflammation, an inherited disorder, or idiopathic cardiomyopathies.

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Guideline-directed Medical Therapies for Heart Failure (GDMT)

 In patients with heart failure (HF), the goals of treatment are to improve their clinical condition, functional capacity, quality of life, and to prevent the events of hospital readmissions and mortality. GDMT includes the following drug therapies: renin-angiotensin-aldosterone system inhibitors (RAAS-I), with or without a neprilysin inhibitor, β-blockers, and mineralocorticoid-receptor-antagonists (MRA).

Recently, sodium-glucose cotransporter-2 inhibitors (SGLT2i) demonstrated efficacy as an important fourth pillar of GDMT. Together, this combination can add over six additional years of lifespan for HFrEF patients compared to the traditional approach of RAAS-I and β-blockers alone. However, studies highlight that many eligible HFrEF patients are not receiving one or more of the recommended medications, in the absence of contraindications or intolerance. Even among patients who are treated, less than half receive optimal doses of GDMT. Additionally, time to initiation and optimization of dosing may be exceedingly slow in the outpatient setting.

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Iron deficiency anemia

 

Iron deficiency develops in stages. In the first stage, iron requirement exceeds intake, causing progressive depletion of bone marrow iron stores. As stores decrease, absorption of dietary iron increases in compensation. During later stages, deficiency impairs RBC synthesis, ultimately causing anemia. Severe and prolonged iron deficiency also may cause dysfunction of iron-containing cellular enzymes.

Iron deficiency anemia is classically described as a microcytic anemia. The differential diagnosis includes thalassemia, sideroblastic anemias, some types of anemia of chronic disease, and lead poisoning. Serum ferritin is the preferred initial diagnostic test. Total iron-binding capacity, transferrin saturation, serum iron, and serum transferrin receptor levels may be helpful if the ferritin level is between 46 and 99 ng per mL (46 and 99 mcg per L); bone marrow biopsy may be necessary in these patients for a definitive diagnosis.

 

The diagnosis of IDA requires that a patient be anemic and show laboratory evidence of iron deficiency. Red blood cells in IDA are usually described as being microcytic (i.e., mean corpuscular volume less than 80 μm3 [80 fL]) and hypochromic, however the manifestation of iron deficiency occurs in several stages. Patients with a serum ferritin concentration less than 25 ng per mL (25 mcg per L) have a very high probability of being iron deficient. The most accurate initial diagnostic test for IDA is the serum ferritin measurement. Serum ferritin values greater than 100 ng per mL (100 mcg per L) indicate adequate iron stores and a low likelihood of IDA

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Tumor lysis syndrome

Tumor lysis syndrome is a clinical condition that can occur spontaneously or after the initiation of chemotherapy associated with the following metabolic disorders: hyperkalemia, hyperphosphatemia, hypocalcemia, and hyperuricemia leading to end-organ damage. It is most common in patients with solid tumors. Tumor lysis syndrome usually develops after the initiation of chemotherapy treatment. However, there are more cases of spontaneous development of tumor lysis syndrome with high-grade hematology-oncology malignancies.

Hallmarks of this condition

• Potassium >6.0 meq/L or a 25% increase from baseline
• Phosphorous >4.5 mg/dL or a 25% increase from baseline
• Calcium <7 mg/dL or a 25% decrease from baseline
• Uric acid >8 mg/dL or a 25% increase from baseline

Clinical tumor lysis syndrome:

• Creatinine greater than 1.5 times normal
• Cardiac arrhythmia/sudden death
• Seizure

Most of the symptoms seen in patients with tumor lysis syndrome are related to the release of intracellular chemical substances that cause impairment in the functions of target organs. This can lead to acute kidney injury (AKI), fatal arrhythmia, and even death.

In patients at low risk for developing TLS, management includes hydration and close monitoring of volume status and renal function. The use of urine alkalinization to promote elimination of urate is not recommended because it can induce calcium phosphate deposition and therefore aggravate TLS.
In patients at intermediate risk with uric acid levels lower than 8 mg/dl, a xanthine oxidase inhibitor such as allopurinol also should be started 2 days before chemotherapy, whereas rasburicase should be used in patients with uric acid levels higher than 8 mg/dl. 

Rasburicase should not be used in patients with glucose-6-phosphate dehydrogenase (G6PD) deficiency. For high-risk patients, a single dose of rasburicase (up to 0.2 mg/kg, although a lower dose is usually prescribed) is recommended, followed by close monitoring of uric acid levels. If uric acid normalizes, allopurinol treatment can be started. If urine output decreases despite adequate fluid administration, a loop diuretic should be added, and RRT will be required if oliguria persists.

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INGUINAL HERNIA

 

An inguinal hernia is a protrusion of abdominal or pelvic contents through a dilated internal inguinal ring or attenuated inguinal floor into the inguinal canal and usually, but not always, out of the external inguinal ring, causing a visible or easily palpable bulge.

Presents with visible or easily palpable swelling in the groin, often with discomfort during strenuous exercise or heavy lifting.

Complications are rare but include incarceration, bowel obstruction, and strangulation.

Diagnosis is usually clinical; imaging may be helpful where there is doubt about diagnosis, but also identifies many clinically insignificant apparent hernias.

Surgical repair remains the mainstay of therapy, although watchful waiting is reasonable in adults with minimally symptomatic or asymptomatic inguinal hernia.

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Model for End-Stage Liver Disease (MELD) score

 Model for End-Stage Liver Disease (MELD) score is a prognostic scoring system, based on laboratory parameters, used to predict 3-month mortality due to liver disease

MELD scores range from 6 to 40; the higher the score, the higher the 3-month mortality related to liver disease

The MELD score does not accurately predict survival in all patients with cirrhosis; conditions such as liver cancer, hepatopulmonary syndrome, and porto-pulmonary hypertension, are associated with a higher mortality rate than MELD score would reflect. Therefore, patients with these conditions may receive additional MELD points when listed for liver transplantation

Recommendations

• Calculate a MELD score every 3-6 months in all patients with cirrhosis to repeatedly assess their score
• Consider referral for liver transplantation in patients with MELD score of 10 or higher
• Consider using MELD score to assess mortality in patients with acute liver failure or acute variceal bleeding
• Calculate MELD scores for patients who have:
• cirrhosis and are undergoing surgery (abdominal, orthopedic, cardiac, etc.)
• cirrhosis and are being considered for TIPS
• alcoholic hepatitis and are being considered for steroids
• acute liver failure or acute variceal bleeding

Appropriate Use of the MELD

• The original MELD calculator was used to predict mortality in those undergoing placement of a transjugular intrahepatic portosystemic shunt (TIPS)
• The MELD score has been validated to predict short-term survival in patients with cirrhosis waiting for liver transplantation, but it also was found to be useful in predicting liver-related mortality in patients with alcoholic hepatitis, acute liver failure, acute variceal hemorrhage, or postsurgical procedures
• MELD is useful in determining when a patient should be evaluated for transplant; the benefit of liver transplantation outweighs the risk once MELD score is 15 or higher
• In patients with alcoholic hepatitis, MELD score of >20 identifies severe disease, when steroid treatment should be considered
• Patients listed for liver transplantation will have their MELD scores updated at regular intervals (from every 7 days if 25 or greater, to every 1-3 months

Understanding the MELD Score Calculation

• When inputting values, laboratory values of less than 1 are rounded to 1
• A score of 40 is set as the upper limit regardless of how high the inputted laboratory values may be.

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“Courvoisier's law”

In 1890, Ludwig Courvoisier described his observation that patients with painless jaundice and a palpable gallbladder often have a malignant obstruction of the common bile duct; this is known as “Courvoisier's law.” Painless jaundice and a palpable gallbladder are present in 50%–70% of patients with periampullary cancer or carcinoma of the head of pancreas. The gallbladder with stones is usually chronically fibrosed and so, incapable of enlargement.

 

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Asymptomatic microscopic hematuria

 The prevalence of asymptomatic microscopic hematuria in adults ranges from 0.19 to 21 percent. Patients with asymptomatic microscopic hematuria or with hematuria persisting after treatment of urinary tract infection also need to be evaluated. Because upper and lower urinary tract pathologies often coexist, patients should be evaluated using cytology plus intravenous urography, computed tomography, or ultrasonography. When urine cytology results are abnormal, cystoscopy should be performed to complete the investigation.

Microscopic hematuria generally is defined as one to 10 red blood cells per high-power field of urine sediment. The American Urological Association (AUA) defines clinically significant microscopic hematuria as three or more red blood cells per high-power field on microscopic evaluation of urinary sediment from two of three properly collected urinalysis specimens. May be associated with urologic malignancy in up to 10 percent of adults.

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Antiarrhythmic Medications

 Antiarrhythmic Medications - Vaughan-Williams Classification

 • Class I (Ia, Ib, Ic)

 • Class II

 • Class III

 • Class IV

 • Other anti-antiarrhythmic drugs: Adenosine, Digoxin, Ivabradine

Satyendra Dhar, MD 

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D-dimer & interpretation

D-dimer is the smallest fibrinolysis-specific degradation product found in the circulation. The D-dimer is very sensitive to intravascular thrombus and may be markedly elevated in disseminated intravascular coagulation, acute aortic dissection, and pulmonary embolus. Because of its exquisite sensitivity, negative tests are useful in the exclusion venous thromboembolism. Elevations occur in normal pregnancy, rising two- to fourfold by delivery. D-dimer also rises with age, limiting its use in those > 80 years old. There is a variable rise in D-dimer in active malignancy and indicates increased thrombosis risk in active disease. Elevated D-dimer following anticoagulation for a thrombotic event indicates increased risk of recurrent thrombosis. 

Satyendra Dhar MD

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Lactic acid & interpretation

 

Lactic acid was first found & described in sour milk by Karl Wilhelm Scheele in 1780. German physician–chemist Johann Joseph Scherer (1841–1869) demonstrated the occurrence of lactic acid in human blood under pathological conditions in 1843 & 1851.

Lactic acid is essentially a carbohydrate within cellular metabolism and its levels rise with increased metabolism during exercise and with catecholamine stimulation. Glucose-6-phosphate is converted anaerobically to pyruvate via the Embden-Meyerhof pathway. Pyruvate is in equilibrium with lactate with a ratio of about 25 lactate to 1 pyruvate molecules. Thus, lactate is the normal endpoint of the anaerobic breakdown of glucose in the tissues.

The causes of lactic acidosis can generally be divided into those associated with obviously impaired tissue oxygenation (type A) and those in which systemic impairment in oxygenation does not exist or is not readily apparent (type B). However, there is frequently overlap between type A and type B lactic acidosis. In sepsis, for example, there is both an increase in lactate production resulting from microcirculatory failure and also a decrease in lactate clearance that is not solely due to diminished oxygen delivery.

Satyendra Dhar MD, 

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