Oral Drugs used for Hypertensive Urgency

In this article, we will discuss the Oral Drugs used for Hypertensive Urgency. So, let’s get started.


Amlodipine (dose 5-10 mg)

  • Action starts within 45-60 min and remains for 24 hours
  • Side effects include hypotension and tachycardia

Clonidine (dose 0.1-0.2 mg every hour)

  • Action starts within 45-60 min and remains for 6-8 hours
  • Side effects include dry mouth and sedation

Captopril or enalapril (captopril dose 6.25-20 mg and enalapril dose 10-30 mg)

  • Action starts within 15-30 min and lasts for 4-6 hours
  • Side effects include acute renal failure, dry cough, angioneurotic edema and hyperkalemia

Labetolol (dose 100-300 mg)

  • Action starts within 30-60 min and lasts for 6-12 hours
  • Side effects include bronchospasm, nausea, vomiting, tingling of scalp

Carvedilol (dose 2.5-50 mg)

  • The half life period of carvedilol is between 7-10 hours
  • Side effects include burning in throat, dizziness, postural hypotension

Prazosin (dose 1-2 mg)

  • Onset of action 15-60 min and remains for 6 hours
  • Side effects include flushing and hypotension

Losartan (dose 25-100 mg)

  • Action starts within half and hour and lasts for 6-8 hours
  • Side effects include ARF, dry cough, angioneurotic edema and hyperkalemia

Immunophenotyping in Acute Leukemia

In this article, we will discuss the Immunophenotyping in Acute Leukemia. So, let’s get started.


The recent development of monoclonal antibodies as well as advances in flow cytometry has made immunophenotyping readily available. It is useful in:

  • Definite lineage (B cell versus T cell) and stages of differentiation of ALL and identifying characteristic features of AML
  • Aiding in lineage determination of acute leukemias that are morphologically undifferentiated
  • In differentiating acute leukemias from other non-hematological disorders
  • Recognising mixed lineage/biphenotypic acute leukemia (ALL with myeloid markers or AML with lymphoid markers)

Immunophenotyping in acute leukemias

  • Subtype
  • ALL
  • T-cell
  • B-cell
  • Pre-B
  • AML
  • M1, M2, M3
  • M4, M5
  • M6
  • M7
  • Flow cytometry
  • CD4 (helper)/CD8 (suppressor)
  • CD19(B4)/CD20(B1)/CD22(surface)
  • CD9
  • CD10
  • CD13 or CD33
  • CD11 or 13 or 14 or 15 or CD33
  • Glycoprotein, spectrin
  • CD41 (glycoprotein IIb/IIa)/CD43

Diagnosis of Cardiac Tamponade

In this article, we will discuss the Diagnosis of Cardiac Tamponade. So, let’s get started.

Diagnosis and Investigations

Cardiac tamponade should be suspected in a patient who appears to be in shock but has high jugular venous pressure and distended neck veins. This is especially true in setting of trauma. The physical signs of low cardiac output with silent heart, enlarged area of dullness further strengthen the diagnosis which is confirmed by demonstrating the fluid in the pericardial sac on echocardiography. The investigations that help in diagnosis are:

  • Chest X-ray may show enlarged globular heart (money-bag appearance) with oligaemic lungs
  • Fluoroscopy may show diminished cardiac pulsations with enlarged cardiac shadow
  • The electrocardiogram may show low voltage graph, sinus tachycardia and electric alternans (QRS alternans)
  • The echocardiogram shows, significant anterior and posterior echo-free space, right ventricular and right atrial cavities are reduced in diameter and there is diastolic inward motion (collapse of RV and RA free wall due to high pericardial pressure), enlarged inferior vena cava with absence of respiratory variations.
  • Doppler study: The characteristic and diagnostic feature on Doppler study is the exaggerated respiratory variations in tricuspid and pulmonary valve inflow velocity. Venous flow is prominently systolic with exaggerated respiratory variations in inferior vena cava (IVC) and hepatic vein flow (diminished forward flow during expiration)
  • CT or MRI: Cardiac CT or MRI may be necessary to diagnose loculated effusion responsible for cardiac tamponade
  • CVP monitoring helps in the diagnosis, differential diagnosis and serves as a guide to fluid therapy. CVP is raised in pericardial effusion with shock, hence, differentiates it from hypovolemic shock where CVP is low
  • Other investigations are done to find out the cause such as biochemical, microbiological (culture for DNA of M.tuberculosis by PCR) and cytological examination (RBC, WBCs) of pericardial fluid. Fluid may be transudate, exudate or bloody depending on the cause.

Clinical Features and Pathogenesis of Cardiogenic Shock

In this article, we will discuss the Clinical Features and Pathogenesis of Cardiogenic Shock. So, let’s get started.

Clinical Features and Pathogenesis

Irrespective of the cause of cardiogenic shock, it is characterized by a vicious circle of severe myocardial (systolic and diastolic) dysfunction. Systolic dysfunction results in fall in cardiac output, BP and thereby coronary perfusion pressure falls. Hypotension, oliguria, confusion or altered mental state, tachypnea, tachycardia and cold, clammy extremities are the manifestations of low output state or acute circulatory failure. Diastolic dysfunction on the other side of cycle causes a rise in CVP, left ventricular end-diastolic pressure, rise in PCWP, pulmonary congestion and edema, leading to hypoxia which further worsens the myocardial ischemia. Breathlessness, orthopnea, PND, cyanosis, cough, hemoptysis, hypoxia, perspiration and inspiratory crackles at the bases of the lungs, S3 and S4 gallops are features of acute pulmonary edema.

A systemic inflammatory response syndrome (SIRS) may accompany large infarction and shock. Inflammatory cytokines and excess nitric oxide may contribute to genesis of cardiogenic shock. Severe acidosis (lactic acidosis) reduces the efficacy of catecholamines and provoke arrhythmias. A Swan-Ganz catheter can be used to measure the pulmonary artery wedge pressure which is >18 mmHg.

Untreated or refractory shock leads to multiple organ dysfunction, e.g. heart, brain, lungs, kidney and liver.

Older patients mostly females, prior MI, diabetes and extensive anterior MI (EF<30%) are at increased risk of cardiogenic shock.

Difference between clinical features of Acute and Chronic Hepatic Encephalopathy

In this article, we will discuss the Difference between clinical features of Acute and Chronic Hepatic Encephalopathy. So, let’s get started.

  • Acute hepatic encephalopathy
  • Acute onset
  • Acute fulminant hepatitis is the common cause
  • No precipitating factors
  • Ascites and portal hypertension absent
  • Liver span is reduced
  • Prognosis is bad
  • Chronic hepatic encephalopathy
  • Slow chronic onset
  • Chronic hepatitis or cirrhosis is the commonest cause
  • It is precipitated by certain factors
  • Ascites and portal hypertension present
  • Liver span is normal or increased
  • Prognosis is better
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