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 Normal coagulation pathway represents a balance between the pro coagulant pathway that is responsible for clot formation and the mechanisms that inhibit the same beyond the injury site. Imbalance of the coagulation system may occur in the perioperative period or during critical illness, which may be secondary to numerous factors leading to a tendency of either thrombosis or bleeding.

The plasma coagulation system in mammalian blood consists of a cascade of enzyme activation events in which serine proteases activate the proteins (proenzymes and procofactors) in the next step of the cascade via limited proteolysis. The ultimate outcome is the polymerization of fibrin and the activation of platelets, leading to a blood clot. This process is protective, as it prevents excessive blood loss following injury (normal hemostasis). Unfortunately, the blood clotting system can also lead to unwanted blood clots inside blood vessels (pathologic thrombosis), which is a leading cause of disability and death in the developed world. There are two main mechanisms for triggering the blood clotting, termed the tissue factor pathway and the contact pathway. Only one of these pathways (the tissue factor pathway) functions in normal hemostasis. Both pathways, however, contribute to thrombosis. 

The blood coagulation cascade culminates with the conversion of fibrinogen to fibrin, essentially transmitting the proteolytic injury signal into a fibrin clot capable of occluding the inciting tissue defect. Fibrinogen is the most abundant coagulation protein in plasma, consistent with its mechanical rather than signaling role.


 A gut diverticulum (singular) is an outpouching of the wall of the gut to form a sac. Diverticula (plural) may occur at any level from esophagus to colon. A true diverticulum includes all three layers of the gut; the lining mucosa, the muscularis, and the outer serosa. False diverticula are missing the muscularis and are therefore very thin walled. Colonic diverticula are typically false.


 There are 3 types of artificial pacemakers:

  • Implantable pulse generators with endocardial or myocardial electrodes
  • External, miniaturized, patient portable, battery-powered, pulse generators with exteriorized electrodes for temporary transvenous endocardial or transthoracic myocardial pacing
  • Console battery or AC-powered cardioverters or monitors with high-current external transcutaneous or low-current endocardial or myocardial circuits for temporary pacing in asynchronous or demand modes, with manual or triggered initiation of pacing

Following conditions are included in the ACC/AHA/HRS guidelines for the pacemaker insertion

  • Sinus Node Dysfunction

  1. Documented symptomatic sinus bradycardia including frequent sinus pauses which produce symptoms and symptomatic sinus bradycardia that results from required drug therapy for medical condition
  2. Symptomatic chronotropic incompetence (failure to achieve 85% of age-predicted maximal heart rate during formal or informal stress test or inability to mount age appropriate heart rate during activities of daily living)

  • Acquired Atrioventricular (AV) Block

  1. Complete third-degree AV block with or without symptoms.
  2. Symptomatic second degree AV block, Mobitz type I and II
  3. Exercise-induced second or third degree AV block in the absence of myocardial infarction
  4. Mobitz II with widened QRS complex

  • Chronic Bifascicular Block

  1. Advanced second-degree AV block or intermittent third-degree AV block
  2. Alternating bundle-branch block
  3. Type II second-degree AV block.

  • After Acute Phase of Myocardial Infarction

  1. Permanent ventricular pacing for persistent second degree AV block in the His-Purkinje system with alternating bundle branch block or third degree AV block within or below the His-Purkinje system after the ST-segment elevation MI (STEMI)
  2. Permanent ventricular pacing for a transient advanced second or third-degree infranodal AV block and associated bundle branch block
  3. Permanent ventricular pacing for persistent and symptomatic second or third degree AV block

  • Neurocardiogenic Syncope and Hypersensitive Carotid Sinus Syndrome

  1. Recurrent syncope caused by spontaneously occurring carotid sinus stimulation and carotid sinus pressure that induces ventricular asystole of more than 3 seconds

  • Post Cardiac Transplantation

  1. For persistent inappropriate or symptomatic bradycardia not expected to resolve and for other class I indications of permanent pacing.

  • Hypertrophic Cardiomyopathy (HCM)

  1. Patients with HCM having Sinus node dysfunction and AV block

  • Pacing to Prevent Tachycardia

  1. For sustained pause dependent VT, with or without QT prolongation

  • Cardiac Resynchronization Therapy (CRT) in Patients with Severe Systolic Heart Failure

  1. Patients with left ventricular ejection fraction (LVEF) of less than or equal to 35%, sinus rhythm, LBBB (left bundle branch block), New York Heart Association (NYHA) Class II, III or IV symptoms while on optimal medical therapy with a QRS duration of greater than or equal to 150 ms, CRT with or without ICD is indicated

  • Congenital Heart Disease

  1. For advanced second or third-degree AV block associated with symptomatic bradycardia, ventricular dysfunction, or low cardiac output; also for advanced second or third-degree AV block which is not expected to resolve or persists for 7 days or longer after cardiac surgery
  2. For sinus node dysfunction with a correlation of symptoms during age inappropriate bradycardia
  3. Congenital third-degree AV block with a wide QRS escape rhythm, complex ventricular ectopy or ventricular dysfunction
  4. Congenital third-degree AV block in an infant with a ventricular rate of less than or equal to 55 bpm or with congenital heart disease with a ventricular rate of less than or equal to 70 bpm


 Sodium-glucose co-transporter 2 (SGLT2) inhibitors are a new class of glucose-lowering drugs. They work by blocking the low-affinity, high-capacity SGLT2 protein located in the proximal convoluted tubule of the nephron. The SGLT2 protein is responsible for the resorption of approximately 90% of filtered glucose while the remainder is reabsorbed by SGLT1 proteins found on the distal part of the proximal convoluted tubule. SGLT2 inhibition results in glycosuria (and natriuresis as the protein is a co-transporter), thereby lowering plasma glucose concentrations. This mechanism is unique compared with all other glucose-lowering agents as it does not interfere with endogenous insulin or incretin pathways.

In recent cardiovascular outcome trials, SGLT2 inhibitors are associated with 30%–35% lower risk of hospitalization for heart failure. Other glucose-lowering agents appear to be more potent than SGLT2 inhibitors, but fail to reduce cardiovascular risk, particularly with regard to heart failure outcomes. Moreover, although the glucose-lowering efficacy of SGLT2-inhibitor therapy declines at lower estimated glomerular filtration rates, its cardiovascular benefits are remarkably preserved, even in patients with renal impairment. This implies differing mechanisms of action in glycemic control and cardiovascular risk reduction. 


Color coding plays a vital role in the safe and efficient operation of medical devices. By providing clear visual cues for identification, it helps prevent errors, enhances efficiency and promotes patient safety.
Outlined below are some key reasons why it is essential:
  • Enhanced safety: Color coding helps healthcare professionals quickly and accurately identify different components, reducing the risk of errors such as misconnections or incorrect usage. This is particularly critical in high-stress environments such as emergency rooms or operating theaters.
  • Standardization: By adhering to standardized color schemes, manufacturers can ensure consistency across different medical devices and systems. This facilitates easier training for healthcare staff and promotes interoperability between various equipment from different manufacturers.
  • Efficiency: Rapid identification of components through color coding saves valuable time during medical procedures, allowing healthcare providers to focus more on patient care and less on sorting through equipment.
  • Accessibility: For individuals with visual impairments or color blindness, alternative methods such as tactile markings or embossed symbols can complement color coding to ensure inclusivity and accessibility in healthcare settings.
  • Prevention of contamination: Clear differentiation between components reduces the likelihood of cross-contamination, particularly in settings where multiple patients are treated using the same equipment.
  • Regulatory compliance: Adherence to color-coding standards, such as those outlined in ISO 80369, ensures compliance with regulatory requirements and demonstrates a commitment to patient safety and quality standards.


 Hypermagnesemia occurs primarily in patients with acute or chronic kidney disease. In these individuals, some conditions, including proton pump inhibitors, malnourishment, and alcoholism, can increase the risk of hypermagnesemia. Hypothyroidism and especially cortico-adrenal insufficiency, are other recognized causes.

Hyperparathyroidism and alterations in calcium metabolism involving hypercalcemia and/or hypo-calciuria can lead to hypermagnesemia through an increased calcium-induced magnesium absorption in the tubule. Patients with familial hypocalciuric hypercalcemia (FHH), a rare autosomal dominant condition, can manifest hypermagnesemia.

Lithium-based psychotropic drugs can also lead to hypermagnesemia by reducing excretion. Patients with milk-alkali syndrome due to the ingestion of large amounts of calcium and absorbable alkali are more susceptible to develop hypermagnesemia. Magnesium levels can increase in hemolysis patients. Red blood cells contain three times as much magnesium as compared to plasma. The rupture of these cells pours magnesium into the plasma. However, symptomatic hypermagnesemia occurs only in the case of aggressive hemolysis. Tumor lysis syndrome, rhabdomyolysis, and acidosis (e.g., decompensated diabetes with ketoacidosis) can also induce hypermagnesemia through extracellular shifts.

Summary:

  • Mild hypermagnesemia (less than 7 mg/dL) - Asymptomatic or pauci-symptomatic: weakness, nausea, dizziness, and confusion
  • Moderate hypermagnesemia (7 to 12 mg/dL) - Decreased reflexes, worsening of the confusional state and sleepiness, bladder paralysis, flushing, headache, and constipation. A slight reduction in blood pressure, bradycardia, and blurred vision caused by diminished accommodation and convergence are usually present.
  • Severe hypermagnesemia (greater than 12 mg/dL) - Muscle flaccid paralysis, decreased breathing rate, more evident hypotension and bradycardia, prolongation of the P-R interval, atrioventricular block, and lethargy are common. Coma and cardiorespiratory arrest can occur for higher values (over 15 mg/dL).


Ionized calcium is the physiologically active form. Ionized calcium acts as an intracellular 2nd messenger; it is involved in skeletal muscle contraction, excitation-contraction coupling in cardiac and smooth muscle, and activation of protein kinases and enzyme phosphorylation. Calcium is also involved in the action of other intracellular messengers, such as cAMP (cyclic adenosine monophosphate) and inositol 1,4,5-triphosphate, and thus mediates the cellular response to numerous hormones, including epinephrine, glucagon, vasopressin (antidiuretic hormone), secretin, and cholecystokinin.

Despite its important intracellular roles, about 99% of body calcium is in bone, mainly as hydroxyapatite crystals. About 1% of bone calcium is freely exchangeable with the extracellular fluid and, therefore, is available for buffering changes in calcium balance.

Normal total serum calcium concentration ranges from 8.8 to 10.4 mg/dL. About 40% of the total blood calcium is bound to plasma proteins, primarily albumin. The remaining 60% includes ionized calcium plus calcium complexed with phosphate and citrate. Total calcium (ie, protein-bound, complexed, and ionized calcium) is usually what is determined by clinical laboratory measurement.

However, ideally, ionized (or free) calcium should be estimated or measured because it is the physiologically active form of calcium in plasma and because its blood level does not always correlate with total serum calcium.

Ionized calcium is generally assumed to be about 50% of the total serum calcium.

Ionized calcium can be estimated, based on total serum calcium and serum albumin levels. Direct determination of ionized calcium, because of its technical difficulty, is usually restricted to patients in whom significant alteration of protein binding of serum calcium is suspected.

Normal ionized serum calcium concentration range varies somewhat between laboratories, but is typically 4.7 to 5.2 mg/dL.

 The regulation of both calcium and phosphate balance is greatly influenced by concentrations of circulating PTH, vitamin D, and, to a lesser extent, calcitonin. Calcium and phosphate concentrations are also linked by their ability to chemically react to form calcium phosphate. The product of concentrations of calcium and phosphate (in mg/dL) is estimated to be < 60 mg2/dL2 (< 4.8 mmol2/L2) normally; when the product exceeds 70 mg2/dL2 (5.6 mmol2/L2), precipitation of calcium phosphate crystals in soft tissue is much more likely. Calcification of vascular tissue accelerates arteriosclerotic vascular disease and may occur when the calcium and phosphate product is even lower (> 55 mg2/dL2 [4.4 mmol2/L2]), especially in patients with chronic kidney disease.


 Abdominal Aortic Aneurysms

  • Abdominal aortic aneurysms are much more common than thoracic aortic aneurysms.
  • Age is an important risk factor, and the incidence of abdominal aortic aneurysm rises rapidly after the age of 55 years in men and 70 in women.
  • The prevalence of abdominal aortic aneurysms is ≈5% among men ≥65 years of age screened by ultrasound.
  • Smoking is the risk factor most strongly associated with abdominal aortic aneurysms, followed by age, hypertension, hyperlipidemia, and atherosclerosis. Sex and genetics also influence aneurysm formation.
  • Men are 10 times more likely than women to have an abdominal aortic aneurysm of 4 cm or greater.
  • Those with a family history of abdominal aortic aneurysm have an increased risk of 30% and their aneurysms tend to occur at a younger age and carry a greater risk of rupture than do sporadic aneurysms.

 

Thoracic Aortic Aneurysms

  • Thoracic aneurysms may involve one or more aortic segments (aortic root, ascending aorta, arch, or descending aorta) and are classified accordingly.
  • Sixty percent of thoracic aortic aneurysms involve the aortic root and/or ascending aorta, 40% involve the descending aorta, 10% involve the arch, and 10% involve the thoracoabdominal aorta (with some involving >1 segment).
  • The etiology, natural history, and treatment of thoracic aneurysms differ for each of these segments.


 

PULMONARY NODULE

Evaluation is guided by nodule size & assessment of probability of malignancy. In addition is based on the yield of available diagnostic testing, patient comorbidities, & patient preferences. Focal pulmonary lesions that are > 3 cm in diameter are called lung masses & should be considered malignant until proven otherwise.

Pulmonary nodules are categorized as small solid (<8 mm), larger solid (≥8 mm), and subsolid.

Subsolid nodules are divided into ground-glass nodules (no solid component) and part-solid (both ground-glass and solid components).

The probability of malignancy is less than 1% for all nodules smaller than 6 mm and 1% to 2% for nodules 6 mm to 8 mm.

Nodules that are 6 mm to 8 mm can be followed with a repeat chest CT in 6 to 12 months, depending on the presence of patient risk factors and imaging characteristics associated with lung malignancy, clinical judgment about the probability of malignancy, and patient preferences.

The treatment of an individual with a solid pulmonary nodule 8 mm or larger is based on the estimated probability of malignancy; the presence of patient comorbidities, such as chronic obstructive pulmonary disease and coronary artery disease; and patient preferences. Management options include surveillance imaging, defined as monitoring for nodule growth with chest CT imaging, positron emission tomography-CT imaging, nonsurgical biopsy with bronchoscopy or transthoracic needle biopsy, and surgical resection.

Part-solid pulmonary nodules are managed according to the size of the solid component.

Larger solid components are associated with a higher risk of malignancy.

Ground-glass pulmonary nodules have a probability of malignancy of 10% to 50% when they persist beyond 3 months and are larger than 10 mm in diameter.

A malignant nodule that is entirely ground glass in appearance is typically slow growing.

Current bronchoscopy and transthoracic needle biopsy methods yield a sensitivity of 70% to 90% for a diagnosis of lung cancer.


The most common cause of hyperparathyroidism is Parathyroid adenoma. Another cause is hyperplasia of the parathyroid glands.

Parathyroid hormone (PTH) increases serum calcium by

·         Enhancing distal tubular calcium reabsorption

·         Rapidly mobilizing calcium and phosphate from bone (bone resorption)

·         Increasing intestinal absorption of calcium by stimulating conversion of vitamin D to its most active form, calcitriol

Hyperparathyroidism is characterized as:

·         Primary: Excessive secretion of PTH due to a disorder of the parathyroid glands

·         Secondary: Hypocalcemia due to non-parathyroid disorders leads to chronic PTH hypersecretion

·         Tertiary: Autonomous secretion of PTH unrelated to serum calcium concentration in patients with long-standing secondary hyperparathyroidism

Primary hyperparathyroidism: excessive secretion of PTH by one or more parathyroid glands. Incidence increases with age and is higher in postmenopausal women. Primary hyperparathyroidism causes hypercalcemia, hypophosphatemia, and excessive bone resorption (leading to osteoporosis).

Secondary hyperparathyroidism occurs most commonly in advanced chronic kidney disease when decreased formation of active vitamin D in the kidneys and other factors lead to hypocalcemia and chronic stimulation of PTH secretion. Hyperphosphatemia that develops in response to chronic kidney disease also contributes. Other less common causes of secondary hyperparathyroidism include

·         Decreased calcium intake

·         Poor calcium absorption in the intestine due to vitamin D deficiency

·         Excessive renal calcium loss due to loop diuretic use

·         Inhibition of bone resorption due to bisphosphonate use

Tertiary hyperparathyroidism results when PTH secretion becomes autonomous of serum calcium concentration and generally occurs in patients with long-standing secondary hyperparathyroidism, as in patients with ESRD of several years’ duration.

Indications of surgery:

·         Serum calcium 1 mg/dL greater than the upper limits of normal

·         Calciuria > 400 mg/day

·         Creatinine clearance < 60 mL/minute

·         Peak bone density at the hip, lumbar spine, or radius 2.5 SD below controls (T score = −2.5)

·         Age < 50 years

·         The possibility of poor adherence with follow-up

Secondary hyperparathyroidism in patients with renal failure can result in a number of symptoms, including

·         Osteitis fibrosa cystica with arthritis, bone pain, and pathologic fractures

·         Spontaneous tendon rupture

·         Proximal muscle weakness

·         Extra-skeletal calcifications, including soft tissue and vascular calcification

·         Pruritis


Total O2 content is expressed by the following equation:

O2 content (CaO2) = (Hgb x 1.34 x SaO2) + (0.0031 x PaO2)

where Hgb is hemoglobin concentration and SaO2 is hemoglobin saturation at the given PO2. 

The principal form of oxygen transport in blood is as hemoglobin-bound.

Each gram of hemoglobin can maximally bind 1.34 mL of oxygen.

The oxygen-carrying capacity of the blood is calculated as = [Hb] x 1.34.

In a healthy person, with a hemoglobin concentration of 15 g / dL blood, the oxygen carrying capacity is 20.1 mL O2 / dL blood.

 

Oxygen transport is dependent on both respiratory and circulatory function.

Total O2 delivery (DO2) to tissues is the product of arterial O2 content and cardiac output (CO).

DO2 = CaO2 x CO

Note that arterial O2 content is dependent on PaO2 as well as hemoglobin concentration. As a result, deficiencies in O2 delivery may be due to a low PaO2, a low hemoglobin concentration, or an inadequate cardiac output.

 

The Fick equation of O2 consumption

VO2 = CO x (CaO2 – CvO2)


Oxy-hemoglobin Dissociation Curve

With a normal O2 consumption of approximately 250 ml/min and cardiac output of 5000 ml/min the normal arteriovenous difference is calculated to be about 5 ml O2/dl blood. The normal extraction ratio is approximately 25%, thus the body normally consumes only ~25% of the O2 carried on hemoglobin. When O2 demand exceeds supply, the extraction fraction exceeds 25%, and conversely, if O2 supply exceeds demand, the extraction fraction falls below 25%.

When DO2 (oxygen delivery) is moderately reduced, VO2 usually remains normal because of increased O2 extraction (meaning mixed venous O2 saturation decreases). With further reductions in the DO2, a critical point is reached beyond which VO2 becomes directly proportional to DO2. This state of supply-dependent O2 is typically associated with progressive lactic acidosis caused by cellular hypoxia.


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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