Mean Arterial Pressure (MAP)

Average arterial pressure throughout one cardiac cycle, systole, and diastole. 

Surrogate indicator of blood flow and believed to be a better indicator of tissue perfusion.

To perfuse vital organs requires the maintenance of a minimum MAP of 60 mmHg. 

MAP = [Cardiac Output (CO) x Systemic Vascular Resistance (SVR)] + Central Venous Pressure (CVP)

MAP = (CO × SVR) + CVP

Because CVP is usually at or near 0 mmHg, this relationship is often simplified to:

MAP ≈ CO × SVR.

Cardiac output (CO) = Heart Rate (HR) X Stroke Volume (SV).

Stroke Volume is by ventricular inotropy and preload. 

Preload is affected by blood volume and the compliance of veins. 

Increasing the blood volume increases the preload, increasing the stroke volume and therefore increasing cardiac output. 

Afterload also affects the stroke volume in that an increase in afterload will decrease stroke volume. 

Heart rate is affected by the chronotropy, dromotropy, and lusitropy of the myocardium. 

Systemic vascular resistance is determined primarily by the radius of the blood vessels. 

Decreasing the radius of the vessels increases vascular resistance. 

Increasing the radius of the vessels would have the opposite effect. 

Blood viscosity can also affect systemic vascular resistance. 

An increase in hematocrit will increase blood viscosity and increase systemic vascular resistance. 

Viscosity, however, is considered only to play a minor role in systemic vascular resistance.

Common formula:

MAP = Diastolic blood pressure + 1/3 (Systolic Blood pressure – Diastolic Blood Pressure)

          = DBP + 1/3(SBP – DBP) or 

MAP = DBP + 1/3(Pulse Pressure)

MAP = [Systolic Blood Pressure + (2 x Diastolic Blood Pressure)]

                                                      3

Example, if blood pressure is 82 mm Hg/50 mm Hg,

MAP = SBP + 2 (DBP) = 82 +2 (50) = 182 = 60.67 mmHg; or

                3                              3              3

MAP = 1/3 (SBP – DBP) + DBP = 1/3 (82-50) + 50 = 10.67 + 50 = 60.67 mmHg

In sepsis, vasopressors are often titrated based on the MAP. 

In the guidelines of the Surviving Sepsis Campaign, it is recommended that MAP be maintained ≥ 65 mm Hg.

Chronotropy = Heart Rate

Dromotropy = Speed of electrical conduction in the Heart

Lusitropy = Rate of myocardial relaxation

Inotropy = Contractility

Mean Arterial Pressure (MAP) = 70-100 mmHg

Cardiac Index (CI) = Cardiac Output (CO)/ Body Surface Area (BSA) 

                               = 2.5-4 L/min/m2.

Stroke volume (SV) = Cardiac output / Heart Rate 

                                 = 60-120 mL/beat.

Systemic vascular resistance (SVR) = (MAP – Mean Right Atrial Pressure) x 80 / CO 

                                                          = 800-1200 dynes x sec/cm3.

Pulmonary Vascular Resistance = (Mean Pulmonary Artery Pressure – Mean Pulmonary Capillary Wedge Pressure) X 80 / Cardiac Output 

                                                 =125-250 dynes X sec/cm3.

Pulse Pressure (PP)

Pulse Pressure (PP) = Systolic Blood Pressure – Diastolic Blood Pressure

Normal pulse pressure, approximately 40 mmHg.

Change in pulse pressure (Delta Pp) = Volume change (Delta-V) = Stroke volume (SV)

                                                                 Arterial compliance (C)     Arterial compliance (C)

                                                                         

                                                            = Approximately 80 mL = Approximately 40 mm Hg

                                                                       2 mL/mm Hg

Arterial compliance (C) = Delta V/Delta P

Because the aorta is the most compliant portion of the human arterial system, the pulse pressure is the lowest. Compliance progressively decreases until it reaches a minimum in the femoral and saphenous arteries, and then it begins to increase again. 

Narrowed PP (Low) < 25% of the SBP.

Widened PP (High) > 100 % of SBP.

Widened (High) Pulse Pressure (PP)

> 100 % of SBP

Indicative of a noncompliant stiff aorta with a reduced ability to distend and recoil.

With age there is a decrease in compliance of the aorta & small arteries.

In majority, SBP increase while DBP remain near normal. 

In aortic regurgitation (AR), backward, or regurgitant flow, increase SBP and decrease DBP, and therefore increased PP.

Heart valve conditions (Aortic regurgitation, Aortic sclerosis)

Reduced blood viscosity (Severe Iron deficiency anemia)

Increased systolic pressure (Hyperthyroidism), 

Less compliant arteries (Arteriosclerosis)

Narrow (Low) Pulse Pressures (PP)

< 25% of the SBP

Decreased pumping (Heart failure), 

Decreased Stroke Volume (Aortic Stenosis)

Decreased Blood Volume (Blood loss), 

Decreased Filling Time (Cardiac Tamponade/Pericarditis). 

Dysautonomia/postural orthostatic tachycardia syndrome (POTS)

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Rheumatoid Lung Disease

• RA-associated interstitial lung disease (RA-ILD).
• Pleural disease (pleural thickening/effusions).
• Airway disease (Both upper & lower airway).
• Rheumatoid nodules
• Drug-induced lung toxicity (i.e., Methotrexate-induced lung injury)
• Fibro-bullous disease
• Thoracic cage immobility
• Venous thromboembolic disease
• Vasculitis
• Pneumonia.

RHEUMATOID EFFUSION:

• WCC <5000/mm3
• Fluid glucose <60 mg/Dl
• Pleural fluid to serum glucose ratio < 0.5
• pH < 7.3
• High pleural LDH level (ie, > 700 IU/L)
• Cytology: Slender or elongated multinucleated macrophages, round giant multinucleated macrophages, and necrotic background debris.

Pulmonary function testing in ILD (PFT):

• Reduced VC, lung volumes, & DLCO.
• Oxygen desaturation during exercise.
• Restrictive abnormalities common (poor muscle strength or kyphosis due to osteoporosis rather than ILD).

 

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Albuminuria

• Indicator of kidney damage and / or a biomarker of systemic diseases dates back to 1969, when elevated albumin levels were first demonstrated in the urine of patients with newly diagnosed diabetes.

• Urine dipstick is a relatively insensitive marker for albuminuria, not becoming positive until albumin excretion exceeds 300-500 mg/day. 
• Normal rate of albumin excretion is < 30 mg/day (20 mcg/min).
• Persistent albumin excretion between 30-300 mg/day (20 to 200 mcg/min) is called moderately increased albuminuria (formerly called "microalbuminuria").
• Excretion > 300 mg/day (200 mcg/min) represents overt or dipstick positive proteinuria (severely increased albuminuria [formerly called "macroalbuminuria"].

• Albuminuria reflects functional and / or structural changes in the glomerular filtration membrane that allow increased leakage of albumin into primary urine in amounts exceeding the reabsorption capacity of the proximal nephron tubules. 
• Albuminuria considered as an indicator of early damage (dysfunction) of the vascular endothelium (including the glomerular vessels), which leads to increased permeability of the vascular wall. 

• Relationship between albuminuria and cardiovascular risk has been shown in studies of the general population. 
• It is linear and risk is independent of eGFR. 
• Associated with arterial stiffness assessed by the pulse wave velocity measurement

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Lactate Dehydrogenase.

• Cytoplasmic enzymes present in tissues throughout the body.
• Oxidoreductase, enzyme of the anaerobic metabolic pathway.
• Heart, muscle, kidney, lung, and RBC’s have the highest concentration.
• Upon tissue damage, the cells release LDH in the bloodstream.
• Drugs that can increase LDH include alcohol, aspirin, fluorides, narcotics, anesthetics, clofibrate, mithramycin, and procainamide.
• Cancer cells employ LDH to increase their aerobic metabolism (glycolysis, ATP production, & lactate production): Warburg effect.
• CSF LDH increases in bacterial meningitis (normal in viral meningitis).
• Cancer cells undergo LDH mediated energy production to fulfill the demand for fast cellular growth (marker of metastases, prognosis, survival rates., and radiosensitivity).
• LDH serves as a general indicator of acute and chronic diseases.
• LDH helps in distinguishing exudate from transudate effusions.
• Isozymes, named LDH-1 through LDH-5, have differential expression in different tissues.

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Bile acids

 

Role of Bile acids

• Bile acids play a key role in the absorption of lipids in the small intestine. 
• Contribute to cholesterol metabolism by promoting the excretion of cholesterol. 
• Denature dietary proteins, thereby accelerating their breakdown by pancreatic proteases. 
• Direct and indirect antimicrobial effects. In this capacity, recent evidence suggests bile acids are mediators of high-fat diet-induced changes in the gut microbiota. 
• Act as signaling molecules outside of the gastrointestinal tract.

The primary bile acids—cholic acid and cheno-deoxycholic acid—are synthesized from cholesterol in the liver.

The maximal rate of bile acid synthesis is on the order of 4 to 6 g/day.

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Horseshoe Kidney

Horseshoe kidneys are often asymptomatic with incidence of approximately 1 in 500 in the normal population with a male preponderance of 2:1.

The isthmus connecting the two renal masses may be positioned in the midline or laterally resulting in an asymmetric horseshoe kidney, 70% of which are left dominant.

The isthmus consists of renal parenchyma in about 80% of cases with the remainder being composed of a fibrous band.

In more than 90% of cases, fusion occurs at the lower pole, although fusion may occur at the upper pole in a small minority of cases.

Higher incidence of UPJ obstructions, nephrolithiasis, and reflux compared to the general population. Increased frequency of some common renal cancers including transitional cell tumors (three to four times more common), Wilms tumor (twice as frequently), and an extremely large increase in very rare tumors such as carcinoid (62 to 82 times).

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Polycystic kidney disease (ADPKD)

Autosomal Dominant, M = F, by 60 yrs-50% need renal replacement therapy

Multisystem & progressive disease with cysts formation

Kidney enlargement with other organ involvement (liver∼ 80%, pancreas 7-36%, spleen)

Intracranial aneurysms in ∼6% of pts without family history & ∼20% with a family history (rupture in 65-75%, usually before age 50)

Cardiac Valve abnormalities in 25-30%

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Urinary Bladder and Micturition

• First sensation of bladder filling at 100–150ml in an adult.
• Feeling of need to pee at 200 - 350 ml of urine
• Can comfortably hold between 300 - 450 ml
• Wall pressure of 5 - 15 mm Hg creates a sensation of bladder fullness while 30 mm Hg & beyond is painful.
• Most people pee 6 or 7 times/ 24 hours (4 -10 times daily is healthy).
• Normal 24-hour Urine output is 800 - 2000 ml/day (at normal fluid intake of about 2 liters/day).

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Calot’s Triangle (CT)

Calot's triangle is a small (potential) triangular space at the porta hepatis of surgical importance as it is dissected during cholecystectomy. Its contents, the cystic artery and cystic duct must be identified before ligation and division to avoid intraoperative injury.

Borders

• Medial – common hepatic duct.
• Inferior – cystic duct.
• Superior – inferior surface of the liver.
  

The above differ from the original description of Calot’s triangle in 1891 – where the cystic artery is given as the superior border of the triangle. The modern definition gives a more consistent border (the cystic artery has considerable variation in its anatomical course and origin).

Contents

• Right hepatic artery
• Cystic artery
• Cystic lymph node (of Lund)
• Connective tissue
  
  
  
• Lymphatics
• Occasionally accessory hepatic ducts and arteries

Significance

• Cystic artery arises from Right Hepatic Artery in the Calot's triangle in 75%
• Cystic artery origin & course vary in 25% of population.
  
  
  

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ACTH stimulation test

IV/IM admin of cosyntropin (250 μg), with collection of serum & measurement of cortisol at baseline & 30–60 min post stimulation.

Supra-physiological dose stimulates the pituitary & releases cortisol from the adrenal cortex, as long as the adrenal cortex has a functional reserve.

Factors affecting ACTH stim test interpretation:

• Falsely negative or normal in mild disease or disease of recent onset.
• Most common- false-positive test is seen in recent use of corticosteroids
• Exogenous steroids lead to both baselines &adrenal responsiveness to cosyntropin.
• Propofol impairs adrenal steroidogenesis
• Midazolam, morphine, and fentanyl blunt the HPA axis, thereby interfering with corticosteroid metabolism.
• Metyrapone, etomidate, ketoconazole, megesterol, & mitotate interfere with cosyntropin function.
• Rifampin & phenytoin may increase cortisol metabolism.

In females, response to ACTH may be affected OCs which increase CBG levels.

• Salivary cortisol response can be useful as their measurement is a surrogate for serum free cortisol & are not affected by OCs
• Opioid receptors are present in the pituitary gland & hypothalamus, & opioids may impact HPA function.
• Nenke et al studied 17 pts treated with long-term opioids. Five of the 17 (29%) were found to have evidence of AI, with cortisol levels of <5 μg/dL.

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Diabetes and hemoglobin A1c

 

In patients ≥65 years of age treated with medication for type 2 diabetes, hemoglobin A1c values of 7%–8% have shown the greatest reduction in mortality in multiple studies. The specific hemoglobin A1c target between 7% and 8% should be based on shared decision-making and the overall condition of the patient at that specific age, with goals in the lower 7% range for those with good to excellent functional status. It is suggested that lower hemoglobin A1c values are associated with frequent hypoglycemia, which presents a greater risk than a higher hemoglobin A1c value alone. Hemoglobin A1c values over 9% are associated with greater mortality. Thus, while the risk of complications increases linearly with hemoglobin A1c, mortality has a U-shaped curve. Management of blood pressure and treatment with statins improves mortality in these patients as well and is important in addressing overall cardiovascular risk.

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Xanthogranulomatous pyelonephritis

 

Xanthogranulomatous pyelonephritis is an uncommon, severe, subacute, or chronic suppurative process characterized by destruction and replacement of the renal parenchyma by granulomatous tissue containing histocytes and foamy cells. It is most often associated with chronic obstruction and stones with ongoing infection. It is also referred to as a pseudotumor due to an enlarged kidney resembling a tumor and the ability of local invasion and destruction.

The etiology remains unknown. However, most of the cases result from chronic urinary obstruction and infection. The organisms most commonly associated with XGP are Escherichia coli, Proteus mirabilis, Pseudomonas, Enterococcus faecalis, and Klebsiella, etc. Urinary obstruction occurs as a result of calculus, most commonly, staghorn calculus (in almost 80% of patients), which serves as a nidus for infection resulting in the destruction of the renal parenchyma.

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