Learning Critical Care Medicine

"The difficulty lies, not in new ideas  but escaping old ones,  which ramifies,  for those brought up with them,  as most of us has been,  into every corner of our minds" - John Maynard Keynes  Hyponatremia is defined as serum sodium concentration less than 135 mmol/L. Biochemical severity of hyponatremia has been described as mild (S. Na of 130-135 mmol/L), moderate (125- 129 mmol/L) and Severe/ profound (125 mmol/L). Clinical severity of hyponatremia is recognized based on urgency of treatment. Severe symptoms are the result of cerebral edema and increased intracranial pressure with risk herniation. It manifests as vomiting, seizures, obtundation and cardiorespiratory distress.                                Moderately severe symptoms of hyponatremia are due to mild cerebral edema but no risk of herniation. Clinically it presents as headache, nausea and confusion. Hyponatremia is classified as acute and chronic depending upon time profile of existence.

Pathophysiology of sepsis explains that after fluid resuscitation with 20-30 ml/kg ( which is the pressure volume of intravascular space), it is unlikely that septic shock will respond to additional fluid resuscitation. There may be transient response, as only five percent of the crystalloid will remain in the intravascular space, and rest of the fluid will accumulate in third space, giving rise to further organ damage. Fluid resuscitation further exacerbates the deranged physiology including vasodilatation. Multiple Clinical trials have suggested that positive fluid balance independently causes increased morbidity and mortality. Vasopressors should not be delayed after initial fluid resuscitation with 20-30ml/kg. Thereafter further fluid boluses may be given based on dynamic parameters of fluid responsiveness.

“Central venous pressure measurement is not a surrogate of intravascular volume or ventricular preload for fluid resuscitation. For this, fluid responsiveness has to be assessed.” This discussion is for physiological purpose only. Invasive pressure monitoring of central venous pressure, is measurement of intramural pressure (Pim) of the vessel.                                                                                              Flow across a vessel is a function of intramural pressure gradient and resistance to the flow.                                     Force driving flow (F) = ∆P/ R                                                       According to Poiseuille equation resistance is inversely proportional to fourth power of radius.                                                                                ( ⁿ = viscosity of fluid, L= length of tube, r= radius of tube) Radius of a distensible tube depends on transmural pressure (Ptm),

BASIC LIFE SUPPORT (BLS) : Compression rate is modified to a range of 100 to 120/min. (Should not exceed 120/min ).  Compression depth for adults is modified to at least 2 inches (5 cm). (Should not exceed 2.4 inches (6 cm). To allow full chest wall recoil after each compression, rescuers must avoid leaning on the chest between compressions.  Criteria for minimizing interruptions is clarified with a goal of chest compression fraction as high as possible, with a target of at least 60%.  For patients with ongoing CPR and an advanced airway in place, a simplified ventilation rate of 1 breath every 6 seconds (10 breaths per minute) is recommended. For witnessed OHCA with a shockable rhythm , it may be reasonable to delay positive-pressure ventilation (PPV) by using a strategy of up to 3 cycles of 200 continuous compressions with passive oxygen insufflation and airway adjuncts. ADVANCE CARDIAC LIFE SUPPORT (ACLS) :     Vasopressin has been removed from the

"It does not matter how slowly you go, as long as you do not stop"                                             - Confucious Since the introduction of central venous catheterization by Forssman in 1929, this invasive procedure evolved to be very helpful in management of both inpatient and outpatients. Central venous catheters are used for indication as varied as hemodynamic monitoring, vasopressors administration, renal replacement therapy, administration of chemotherapeutic agents and total parenteral nutrition. But central venous catheters have also evolved to be an important source of healthcare related infection, translating to increased morbidity, mortality and financial burden. Intravenous catheter related blood stream infection is the third leading cause of device related infection, after catheter associated urinary tract infection (CAUTI) and ventilator associated pneumonia (VAP). Intravascular catheter related blood stream infection is one of the ‘ne

"There is only one corner of universe, you can be certain of improving, and that is your own self"                                              - Aldous Huxley Guideline for Management of Spontaneous Intracerebral Hemorrhage: ACC/AHA 2015- Salient points: In patient on oral anticoagulation, coagulopathy should be rapidly corrected.  Patients on vitamin K antagonist (warfarin), should be given vitamin K (5-10 mg intravenous) and fresh frozen plasma or prothrombin complex concentrate (PCC). PCC corrects INR more rapidly, requires less volume and associated with fewer complication compared to fresh frozen plasma. Therefore PCC may be preferred.  Although rFVIIa may correct INR, clotting may not be restored in vivo, as it does replace all clotting factors. Therefore it is not recommended for vitamin K antagonist reversal in ICH. For newer oral anticoagulant (NOAC) like debigatron, rivaroxaban and apixaban, activated charcoal can be useful if given within 2 hou

"Variability is the law of life,  And as no two faces are same, s o no two bodies are alike, And no two individuals react alike and behave alike, Under the abnormal  conditions, which we know as disease."                                                                       - William Olser Lactic acidosis is caused by accumulation of lactate and protons in the body. It is often associated with poor clinical outcomes. The impact of lactic acidosis is determined by its severity, duration and the causative pathophysiology.  Sustained hyperlactatemia in hospitalized patients with diverse disorders is associated with a  large increase in mortality, regardless of status  with respect to shock or hypotension.  Hyperlactatemia is not the same as lactic acidosis. Under physiological pH lactic acid is 99 percent dissociated into lactate and [H + ]. As per steward’s strong ion difference (SID) concept, acid base balance is determined by the independent effect of CO 2 , concen

Causes of lactic acidosis: ●Type A lactic acidosis: caused by impaired tissue oxygen delivery, as in- •anaerobic muscle activity- physical exercise, generalises tonic conic convulsions; •impaired tissue perfusion- global (shock- hypovolemic, cardiac ir sepsis) or regional (mesenteric ischaemia); •impaired tissue oxygen delivery or utilization- carbon monoxide poisoning, severe anemia, hypoximia. ●Type B lactic acidosis: not associated with any evidence of impaired oxygen delivery. It may be due to various mechanism- •Type B1: Associated with disease states- diabetes, hematological malignancies, AIDS, chronic alcoholism, thiamine deficiency; Diabetic patients may develop lactic acidosis of various etiology. This type of lactic acidosis is due to decrease activity of pyruvate dehydrogenase. Increased lactate production by neoplastic cells give rise to lactic acidosis in leukemia and lymphoma. In chronic alcoholics lactic acidosis develops because of hepatic dysfunction and redu

"Heard melodies are sweet, those unheard are sweeter"                       - John Keats Pyroglutamic acid (5-oxoproline) is an intermediate metabolite of gamma glutamyl cycle. Gamma glutamyl cycle is responsible for glutathione synthesis and degradation. Glutathione (gamma glutamyl cysteinyl glycine-GSH) is an antioxidant substance, involved in many biological function, including inactivation of free radicals. Glutathione is synthesized by glutamate, glycine and cysteine. Glutamate and cysteine is converted to gamma glutamyl cysteine, by gamma glutamyl cysteine synthetase (GCS), which then reacts with glycine, in the presence of glutathione synthetase, to produce glutathione. Glutathione is degraded by gamma glutamyl transpeptidase (GGT) and gamma glutamyl cyclotransferase to pyroglutamic acid (5-oxoproline). Pyroglutamic acid (5-oxoproline) is catalyzed by 5-oxoprolinase to glutamate, which enters into gamma glutamyl cycle. Glutathione synthesis is kept

  "Life is struggle, not against sin,    not against money or power,    but against hydrogen ion"                              - H.L. Mencken D lactic acid is a stereo-isomer of L lactic acid. L lactic acid is the principle isomer produced by human and is responsible for usual lactic acidosis. D lactate is produced in small amount in humans, by colonic bacteria, as metabolic product of carbohydrate. D lactic acid is not metabolized by lactate dehydrogenase (which converts L lactate to pyruvate), therefore D lactate is slowly eliminated from body in urine and faeces.  D lactate accumulates in three clinical settings- 1. Short bowel syndrome, 2. Propylene glycol toxicity, 3. Diabetes ketoacidosis. In short bowel syndrome, overgrowth of colonic gram positive anaerobes, like lactobacili, produce D lactate. Increased delivery of glucose and other carbohydrates to colon after resection of small bowel, leads to overproduction of D lactate by the colonic micr