Presentation on theme: "CLIs OMS I Fall 2014 Block 2. MOSBY’S Anion gap (pages 66-67) A venous blood evaluation of patients with acid-base disorders Attempts to identify cause."— Presentation transcript:
Anion gap (pages 66-67) A venous blood evaluation of patients with acid-base disorders Attempts to identify cause of the disorder and also to monitor ongoing therapies for acid- base abnormality Test explanation: Difference between cations and anions in extracellular space (sodium + potassium) – (chloride + bicarbonate) Normal: 12 (+/- 4) Test should be adjusted downwards if potassium is eliminated from test Normal: 16 (+/- 4) Bicarb is actually venous CO2 not arterial bicarb, because test is venous sample Determines cause of metabolic acidosis, most acidotic states result in increased AG The build up of ketoacids and lactic acid will cause increased AG Albumin is one of the leading factors in increasing AG Nephrotic syndrome ( decrease in anions) or increased calcium or magnesium will cause decreased AG Increased bicarb causes low AG Hypoproteinemia and increased immunoglobulins can lower AG Gives a complex metabolic picture along with ABG Interfering factors: Decreasing factors: hyperlipidemia, acetazolamide, lithium, polymyxin B, spironolactone, and sulindac Increasing factors: carbenicillin, carbonic anhydrase inhibitors (acetaloamide), diuretics, ethanol, methanol, penicillin, and salicylate
Anion Gap – Increased and Decreased Values Increased Levels: Lactic acidosis, DKA, alcoholic ketoacidosis, alcohol intoxication, starvation (b/c of increased ketoacids), renal failure (b/c non- excretion of organic anions decreases bicarb), diarrhea (loss of bicarb from GI triact), hypoaldosteronism ( b/c of decreased H+/Na+ pump activity in distal renal tubule) Decreased levels: Excess alkali ingestion, multiple myeloma, chronic vomiting or gastric suction (b/c of loss of gastric acid), hyperaldosteronism, hypoproteinemia ( b/c loss of anionic proteins increases bicarb), lithium toxicity
Arterial blood gases Monitor patients on ventilators, monitor critically ill nonventilator patients, establish preoperative baseline parameters, and regulate electrolyte therapy pH –log[H+] Acids normally found in blood: carbonic, dietary, lactic and ketoacids Elevated indicates alkalosis Decreased indicates acidosis Normal pH: 7.35-7.45 (slightly larger range in infants and children) pH (Venous): 7.31-7.41 - It is more acidic b/c it contains more CO2
Blood gases PCO2 Measure of partial pressure of carbon dioxide in the blood Measure of ventilation (faster and deeper breathing removes more CO2) PCO2 is a major medullary drive for respiration. 10% free floating in plasma, 90% carried by RBCs Respiratory component of acid-base determination Co2 and pH are inversely proportional Normal PCO2 = 35-45 mmHg (again infants and v. young children wider range) PCO2 (venous) = 40-50 mmHg This is a measure of partial pressure, don’t confuse with HCO3- concentration.
Blood gases HCO3- (or CO2 content) Concentration Measure of the metabolic component of the acid-base equilibrium Regulated by the kidney Directly proportional to pH (CO2 would be an indirect measure of bicarbonate) In alkalosis kidneys excrete more into the urine to lower pH (compensating) Adult Normal HCO3-: 21-28 mEq/mL (infants lower) PO2 Pressure of oxygen dissolved in plasma Indirect measure of O2 content Determines effectiveness of oxygen therapy Determines the force of oxygen to diffuse across the pulmonary alveoli membrane Low if O2 diffusion difficulties (eg Pneumonia, shock lung, congestive failure) Low if ventilation/profusion rations are off (under ventilated or over perfused alveoli) Normal PO2 = 80-100 mmHg (newborns less) PO2 (venous) = 40-50 mmHg
Blood gases Oxygen saturation Percentage of hemoglobin saturated with oxygen As PO2 decreases so does saturation of hemoglobin (think about the sigmoidal shape of the disassociation curve >75% stat, things are going very badly for the patient) Normal Adult/Child O2 saturation = 95%-100% Oxygen content The amount of oxygen in the blood Nearly all of it is bound to hemoglobin Arterial: 15-22 vol% Venous: 11-16 vol % Base excess/deficit Amount of anions in the blood, bicarbonate being the largest. Also hemoglobin, proteins, phosphates. Normal Base Excess = 0 +/- 2 mEq/L Negative base excess indicates metabolic acidosis (eg lactic acidosis) positive alkalosis (either metabolic or compensation to prolonged respiratory acidosis) Alveolar to Arterial O2 difference Normally should be <10 mmHg
How to interpret ABG levels 1. Evaluation the pH If the pH is < 7.4 acidosis is present If the pH is > 7.4 alkalosis is present 2. Next look at the PCO2 (careful: text same, order different from book) A. If the PCO2 is high with acidosis = Respiratory acidosis (primary problem is with decreased breathing eg drugs or lung disease) B. If the PCO2 is low with acidosis = Metabolic acidosis (with increased ventilation to blow off of CO2) C. If PCO2 is high with alkalosis = Metabolic alkalosis (with compensatory retention of CO2, down ventilation) D. If PCO2 is low with alkalosis = Respiratory alkalosis (Primary problem is hyperventilation) 3. Next look at the bicarbonate ion (HCO3-) Respiratory acidosis you would expect to see high HCO3- [kidneys compensating with increased reabsorption] Metabolic acidosis you would expect to see a low HCO3- [lack of bicarb is part of primary problem Ex: diabetes, renal failure] Metabolic alkalosis you would expect to see a high HCO3- [excess bicarb is part of primary problem Ex: prolonged vomiting] Respiratory alkalosis you would expect to see a low HCO3- [kidneys decrease reabsorption to compensate]
Cholesterol Normal Findings: Adult: <200 mg/dL Child: 120-200 mg/dL Newborn: 53-135 mg/dL -Needed for production of steroids, sex hormones, bile acids, and cellular membranes -The main lipid associated with arteriosclerotic disease -Metabolized by the liver -75% bound inside LDL and 25% is in HDL - Main component of LDL (minimal in HDL and VLDL) - Testing is typically part of a lipid profile (by itself is not an accurate predictor of heart disease) - Individual cholesterol levels can vary daily by 15% -Positional changes affect levels (15% decrease seen in lateral recumbent position, often seen in hospitalized patients) -Repeat tests should be done for abnormal values and an average will be established -Used to predict risk of CHD within the Framingham Coronary Prediction algorithm (determines overall risk of ischemic event)
Cholesterol Increased levels: liver disease, pregnancy, oorophorectomy, postmenopausal status, familial hyperlipidemias or hypercholesterolemias, hypothyroidism, uncontrolled diabetes mellitus, nephrotic syndrome, xanthomatosis, hypertension, atherosclerosis, biliary cirrhosis, stress Drugs that increase levels: adrenocorticotropic hormone, anabolic steroids, beta-adrenergic blocking agents, corticosteroids, cyclosporine, epinephrine, oral contraceptives, phenytoin, sulfonamides, thiazide diuretics, and vit D
Creatinine kinase Adult/elderly (values higher after exercise): 55-170 units/L (males); 30-135 units/L (females) Newborn: 68-580 units/L Isoenzymes: CK-MM: 100%, CK-MB: 0%, CK-BB: 0% This test is used to support the diagnosis of myocardial muscle injury…it can also be used to indicate neurologic or skeletal muscle diseases. CK is predominantly found in heart muscle, skeletal muscle, and brain…CK levels elevate when muscles or nerve cells are damaged: Rise within 6 hrs. after damage Levels peak at 18 hours (if damage is not persistent) Return to normal in 2-3 days Interfering Factors: IM injections, strenuous exercise, early pregnancy, muscle mass Drugs that cause increased CK levels: alcohol, amphotericin B, ampicillin, anesthetics, anticoagulants, aspirin, colchicine, dexamethasone, lithium, lidocaine, morphine, statins.
Creatinine kinase Electrophoresis is used to detect the 3 CK isoenzymes: CK-BB (CK1): Found predominantly in the brain and lung CK-MB (CK2): specific for myocardial cells. Rise 3-6 hrs. post-infarction, levels peak at 12-24hrs., return to normal in 12-48 hrs. Do not usually rise with transient chest pain cause by angina, PE, or CHF. Will see a rise in patients with shock, malignant hyperthermia, myopathies, or myocarditis. CK-MB levels used to determine the appropriateness of thrombolytic therapy (MI) CK-MM (CK3): makes up almost all of the circulatory total CK enzymes in healthy people. Increases in CK-MM suggest skeletal muscle damage. *See Chart p. 201—levels of Troponin, CK-MB, and Myoglobin post-MI*
Creatine kinase, pp. CK is the main cardiac enzyme used to detect MI…others used include: Lactic dehydrogenase (LDH), and aspartate amino transferase (AST) *See Chart p. 201—levels of Troponin, CK-MB, and Myoglobin post-MI* AVOID IM injections in patients with cardiac disease (they cause elevated CK levels) Interfering Factors: IM injections, strenuous exercise, early pregnancy, muscle mass Drugs that cause increased CK levels: alcohol, amphotericin B, ampicillin, anesthetics, anticoagulants, aspirin, colchicine, dexamethasone, lithium, lidocaine, morphine, statins.
D-dimer Normal Findings: <0.4 mcg/mL ELISA and ELFA test, (Enzyme-linked fluorescent immunoassay is faster and more reliable) D-dimer is used to identify intravascular clotting by assessing both thrombin and plasmin activity. (Disseminated intravascular coagulation). D-dimer is a fibrin degradation fragment that is made through lysis of cross-linked (d-dimerized) fibrin. The D-dimer assay provides a highly specific measurement of the amount of fibrin degradation that occurs…normal plasma does not have detectable amounts of d-dimer fragments.
D-dimer D-dimer may be used in combination with the Fibrin Degradation Products assay for high sensitivity and specificity of disseminated intravascular coagulation (DIC). Levels of D-dimer will increase during thrombolytic therapy of fibrin clots and can be used to determine the duration of anticoagulant therapy in patients with DVT. High D-dimer levels are associated with PE, DVT, sickle cell anemia, and thrombosis of malignancy.
Factor V-Leiden Normal: Negative FVL The test is used to diagnose factor V-Leiden thrombophilia Factor V is an important factor in reaction 4 (common pathway) of normal hemostasis. The term “factor V-Leiden” refers to an abnormal form of factor V in which there is a specific glutamine to arginine substitution at nucleotide 1619 in the gene of factor V. FVL is inactivated 10 times slower than regular factor V due to a mutation in the site where protein C normally binds to deactivate and breakdown factor V. Result: increased thombin generation and a mild hypercoagulable state. FVL is the most common hereditary blood coagulation disorder in the US.(5% of Causcasian, 1.2% of Black Americans). Only about 10% of patients with FVL experience a thrombotic event. Testing for FVL is sometimes preceded by a screening coagulation test called the activated protein C (APC) resistance test, used to identify the resistance of factor V to activated protein C.
Factor V-Leiden Individuals who are candidates for FVL testing include those who have: Experienced a thrombotic event without any predisposing factors A strong family history of thrombotic events Experienced a thrombotic event before 30 years of age Experienced DVT during pregnancy or while on birth control pills Had venous thrombosis at usual sites Experienced an arterial clot
Lipoproteins Lipoproteins Should be collected after a 12-14 hour fast. Measured and classified by their density. Interfering Factors: smoking and alcohol ingestion decrease HDL, binge eating alter lipoproteins, HDL values are age and sex- dependent, HDL values (similar to cholesterol) decrease for 3 months post-MI, elevated HDL in hypothyroid, high triglyceride levels make LDL calculations inaccurate. General Categories: Chylomicrons-carry TAGs from the intestine à liver, skeletal muscle, adipose tissue VLDLs- carry newly synthesized TAGs from liver adipose tissue. VLDLs are the predominant carriers of triglycerides. To a lesser degree, VLDLs are also associated with increased risk of CAD because they can be converted to LDL by lipoprotein lipase in skeletal muscle. IDLs- intermediates between VLDLs and LDLs, not detectable in blood LDLs- carry cholesterol from liver cells of the body. “bad cholesterol” HDLs- collects cholesterol from the body’s tissues and brings it back to the liver, protective effect against heart disease. Out of the 5 subclasses of HDL, only 2b is cardioprotective
Lipoproteins Risk for Coronary Heart Disease Based on Ratio of Cholesterol to HDL High levels of LDLs are atherogenic…target levels vary according to risk profile of patient (see p. 359). LDL= total cholesterol- ((TGs/5)- HDL). SGGE divides LDL into 7 classes based on particle size. IIIa and IIIb are the most commonly elevated forms, IVa and IVb are associated with aggressive arterial plaques (nearly all patients with IVa and IVb levels greater than 10% of total LDL have a cardiovascular events within months!) LDL patterns have been identified to assess risk of CAD: (LDLs can be lowered with diet, exercise, and statins) LDL Pattern A: mostly large LDL particles, no increased risk for coronary artery disease (CAD) LDL Pattern B: mostly small LDL particles associated with increased risk for CAD Intermediate pattern: small and large LDL molecules, carries an intermediate risk.
Lipoproteins Lipoproteins- accurate predictor of heart disease -Proteins in the blood whose main purpose is to transport cholesterol, triglycerides, and other insoluble fats -Used as markers to indicate the levels of lipids Risk for Heart DiseaseMaleFemale High60 mg/dL70 mg/dL Moderate45 mg/dL55 mg/dL Low25 mg/dL35 mg/dL Risk of CHDMaleFemale ½ the average3.43.3 Average (3:1)5.04.4 2x average (moderate)10.07.0 3x average (high)24.011.0
Prothrombin time Adequacy of extrinsic system and common pathway Activation of factor X in the presence of factor V and phospholipid and calcium Stimulates platelet aggregation and converts fibrinogen to fibrin in clot stabilization Tests: Factors I (fibrinogen), II (prothrombin), V, VII, and X
PT Hepatocellular liver disease (cirrhosis, hepatitis, neoplastic invasive processes) Factors I, II, V, VII, IX, X Obstructive biliary disease bile necessary for fat absorption decreases A,D,E and K are all fat soluble. II, VII, IX, X all dependent on vitamin K, differentiate from liver disease because it responds to vitamin K Coumarin ingestion (warfarin) interfere with vitamin K associated factors; effects long lasting, can be fixed by vitamin K. Monitors warfarin tx.
PT and INR Evaluate extrinsic and common pathway Fibrinogen, prothrombin, V, VII, X Decreased levels: hepatocellular disease affect factors I, II, V, VII, IX, and X Obstructive biliary disease causes fat malabsorption A, D, E, and K affected Coumarin (warfarin) ingestion INR is a stardardized ratio to correct for laboratory, environmental variations in clotting time, unrelated to sample quality. Warfarin interferes with vitamin K may be enhanced by aspirin, quinidine, sulfa, and indomethacin Barbituates, chloral hydrate and oral contraceptives cause increased coumarin drug binding decreasing the effects Alcohol can prolong Diet high in fat or leafy vegetables may shorten OT Diarrhea or malabsorption can prolong
Troponins Normal Findings: Cardiac Troponin T: <0.2 ng/mL Cardiac Troponin I: <0.03 ng/mL This test is performed on patients experiencing chest pain to determine if the pain is caused by cardiac ischemia. It is a specific indicator of cardiac muscle injury. Cardiac troponins are biochemical markers for cardiac disease and can actually be used in patients with unstable angina to determine the likelihood of a cardiac event. Their sensitivity and specificity are similar to that of CK-MB (but troponins are even more sensitive)—Cardiac troponin levels become elevated as early as 3 hrs. post-myocardial injury and stay elevated for 7-14 days (7-10 days for troponin I, 10-14 days for troponin T) ELISA method w/monoclonal Abs—fast, can be done bedside.
Troponins If reinfarction is suspected, troponins may not be as helpful because levels could still be elevated from the first ischemic event. [Stay elevated longer than CK-MB] Cardiac troponins are useful for the following situations: Evaluation of patient with unstable angina Detection of reperfusion associated with coronary recanalization Estimation of MI size Detection of perioperative MI Evaluation of severity of PE Congestive heart failure Interfering factors: Troponin T levels are falsely elevated in dialysis patient.
Oximetry >95% is normal Monitors arterial oxygen saturation in patients at risk for hypoxemia. Surgery, cardiac stress testing, mechanical ventilation, heavy sedation, lung function testing or trauma Non-invasive measures how many hemoglobin have oxygen attached to them Fetal oxygen saturation monitoring: if heart is in distress but saturation is fine you can avoid c-section, placed on cheek between 30 and 70% Interfering factors: Falsely elevated in carboxyhemoglobin poisoning Severe anemia Nail polish (can put monitor on pt’s ear)
Radiology, Ch 1 Be familiar with the different kind of views and when you might use Lateral, versus AP, versus PA Eg, PA and AP have similar appearances, but difference in magnification of the heart AP is the standard portable technique w/ the pt sitting or supine The density of the object determines how much of the x-ray beam will be absorbed or attenuated. As the density of an object increases, fewer x-rays pass through it. Table 1.1-Basic radiograph film densities or appearances Radiographic films, photographic films and the currently used phosphor plates for digital radiography all respond in a similar manner to light and x-rays
Radiology, Ch 1 Computed radiography (CR) or digital radiography (DR) is the process of producing a digital radiographic image; instead of film, a special phosphor plate is exposed to the x-ray beam. The intensity of the emitted light depends on local radiation exposure Contrast media: The use of intravascular pharmaceuticals to differentiate between normal and abnormal tissues, to define vascular anatomy, and to improve visualization of some organs (use chemically bound iodine) Generally, there is a difference in uptake between normal and abnormal tissues; the whiter the contrast media appears is referred to as enhancement There are complications using high-osmolar contrast agents in infants and individuals w/ compromised renal function Vomiting, pain at injection site, respiratory sx, urticarial, generalized burning sensation Low osmolar contrast agents reduces these, but not for pts w/ nephropathies; alternatives should be sought for pts w/ DM, vascular dz or renal dysfx
Radiology, Ch 1 Uses for iodinated compounds: angiography, myelography, arthrography, CT Angiography: injection of iodinated contrast media directly into a vein or artery via a needle/catheter Arthrography: injection of contrast media or air into a joint; less important since the invention of CT and MRI Air can improve contrast Myelography: placement of contrast media in the spinal subarachnoid space, especially by LP; useful for dx of dz near the spinal canal/cord Also generally less useful since the invention of CT/MRI Barium is used for contrast in the GI tract (introduced by swallowing, an intestinal tube, or an enema); called a double-contrast study Safer, better tolerated, sensitive, specific; lower concentration, not volume can be used for bowel visualization in CT Barium studies are contraindicated if there is any potential for extravasation of the barium into the mediastinum or peritoneum Use water-soluble contrast agents in this case Standard iodinized compounds are NOT used in MRI Use gadolinium; other medals like iron oxide Gadolinium does NOT produce an MR signal but causes changes in local magnetic fields by inducing TI shortening in tissues where it has localized Useful for imaging tumors, infx, cerebral vascular accidents Lesions will be whiter than the surrounding tissues Gadolinium is low-risk for rxns, but can cause a severe connective tissue disorder called nephrogenic sclerosing fibrosis; usually only happens in pts on dialysis or creatinine clearance e< 30 mg/DL
Radiology, Ch1 CT-sectional anatomy imaging in the sagittal, coronal, axial planes (Fig 1.7) Looks at “slices of bread” as opposed to the “whole loaf”) CT images are produced by a combination of x-rays, computers and detectors Pts generally don’t have problems w/ breath holding since images only take a few seconds Average scan takes 10-20 minutes See figs 1.9-10 As in a radiography, the amount of X-ray beam that passes through each slice is inversely proportional to the density of the tissues X-rays strike detectors, and the detectors convert incident x-rays to an electron stream; this stream is digitized into CT units or “Hounsfield” units Density principles are the same as radiography; one major difference is that a radiograph displays the entire anatomic structure, whereas a CT image visualizes “slices” Can be accomplished w/ or w/o contrast-contrast will highlight pathologic tissues Contrast not needed for intracerebral hemorrhage, suspected fracture, or fracture fragment within a joint Contrast used for evaluating liver, kidney, and brain for suspected neoplasms Table 1.2-indications for CT imaging Helical-/Spiral CT; patient continuously moves through the gantry (see Fig 1.11)
Radiology, Ch 1 Multislice/Dynamic CT-multiple contiguous rows of detectors w/ only one rotation around the X-ray tube around the pt; large volumes can be scanned at one time Especially beneficial in CT angiography, dynamic CT Table 1.3-advantages and disadvantages of multislice CT Dual Source: 2 different x-ray energies that originate from a single tube; use multiple detectors and helical scanning Gray value in CT images dependent on density, thickness, and energy of x-rays (same object could have different gray values depending on if you used hih versus low energy) Dual energy applications: direct removal of bone for angiographic imagine, plaque characterization, lung perfusion, identifying tendons, ligaments, assessment of tissue composition Radiation dose is a concern using dual-source scanners
Radiology, CH 1 MRI-essentially the imaging of photons; displays anatomy in the axial, sagittal and coronal plane; slice thickness varies between 1 and 10 mm Although the magnetic fields are generally believed to be harmless, caution should be used in the first trimester (teratogenic, possible acoustic damage) Can be a problem for pts w/ claustrophobia Table 1.4 and 1.5 Hydrogen protons absorb the broadcast radio wave energy and resonate; as the protons decay back to normal state and relax, they continue to resonate and broadcast radio waves that can be detected by a radio wave receiver set to the same frequency as the broadcast radio waves and the H+ spin frequency Bottom line: there are many H+ atoms/protons in fat-> the image will be very bright; bone will be black Radio wave signal intensity is determined by the number of H+ atoms and the T1/T2 relaxation times T1-if listening early during decay after radio signal discontinued T2- listening late; water will be a lighter gray and fat appears gray Table 1.6 T1 used for anatomic information; T2 used for pathology because pathology has + water/hydrogen and will light up well T1 has better resolution; T2 has better contrast To differentiate between CT and MR; look at the fat; subcutaneous fat will be black on CT and white on MRI; bones will have a gray medullary canal and white cortex on radiographs and CT images; on TI MR all of the bone medullary cavities will be white and bone cortex will be black
Radiology, Ch 1 MRA-non-interventional study to image vessels w/o needles, catheters, contrast media (though gadolinium could be used) Flowing blood will be black, but special imagine techniques can light it up 3D images of vasculature Imaging arteries/veins in head and neck, abdomen, chest, and extremities F-MRI Assesses brain/cardiac function as oxygenated/deoxygenated blood cause variations Identifies areas that are active/inactive as working areas of the brain consume more oxygen; changes in hemoglobin oxygenation= BOLD method; Images are T2-weighted Good for cognitive tests
Radiology Ch 1 Functional Cardiac MRI- measures left ventricular volume and ejection fraction Delayed contrast enhancement can distinguish infarct from normal myocardium (bright signal=regions of infarct/scar) Diffusion-Weighted MRI Sensitive to cell injuries of multiple etiologies Used in the diagnosis of ischemic stroke, can reliably detect hypoxic ischemia within minutes of symptom onset Susceptibility-weighted MRI-sensitive to venous blood hemorrhage and iron storage; useful for assessing TBI, stroke, hemorrhage, MS, tumors Magnetic Resonance Spectroscopy-metabolite concentrations in the body; protons from water are suppressed so that NAA, choline, creatinine etc can be detected. Used to evaluate lesions to determine cancer, since cancer has shown and elevation of choline and a reduction in NAA. Also used for stroke imaging and inflammatory dz
Radiology Ch 1 Ultrasonography-Table 1.7 and 1.8 Safe, painless, inexpensive, well-tolerated Produces sectional images in multiple planes (like CT and MRI) Solid organs usually have a homogenous echo pattern; fluid filled organs have fewer “internal echoes” Digitizes sound waves, converting images to black, white and gray
Radiology 101:Pages 25-32 Reading frontal chest x-ray Designed to look at lungs, not trauma to the ribs etc. R marker should be on your left side Glance over the image for any obvious abnormality always look at your four corners Anterior posterior and posteroanterior Start at top and make sure trachea is midline Move to heart, transverse diameter of cardiac silhouette should not be more than 50% transverse diameter of thoracic cage Greater the distance between and object and film, the greater the magnification
Radiology 101: Frontal chest X-ray (continued) Right heart convex, left cardiac border at the top should be concave Left ventricle makes up left heart SVC makes straight right border In enlargement left superior border becomes convex Left enlargement cardiac apex moves down and out Right enlarges right border is more protuberant Left and right pulmonary arteries form hilar shadows, left should be more cephalad Aorta forms knob Aortopulmonary window between knob and pulmonary artery shadow; should be concave or suspect mass or adenopathy
Radiology 101:Pages 25-32 Frontal chest X-ray (continued) Mediastinum shadow is caused by great vessels and vascular pedicle Pedicle extends from thoracic inlet to base of heart; right border is SVC left is aortic knob Divide lungs into horizontal thirds Domed diaphragm with right side higher than left Lateral costophrenic angles should be sharp and acute Look at lower cervical spine and ribs Ribs we see are posterior arcs anterior ribs are angled downward
Radiology 101: Lateral radiograph Right ventricle is anterior border Left ventricle is inferior-posterior cardiac border Left atrium forms superior-posterior cardiac border IVC can be seen as it enters from abdomen If left ventricle is 2 cm or more posterior to IVC then it is enlarged Evaluating hila left is posterior to line drawn down from tracheal air column and one third the size of the right Silhouette sign when two objects of similar density are in direct juxtaposition interface or borders are lost
DrugUsesSide effectsContraindicationsTherapeutic considerations Aspirin (ASA) MOA-Inhibits synthesis of prostaglandin by cyclooxygenase; inhibits platelets aggregation; has antipyretic (anti- fever) and analgesic activity. Metabolized by the liver. Prophylaxis against transient ischemic attack, MI, acute coronary syndrome, prevent reocclusion, arthritis, mild pain or fever GI bleeding, acute renal insufficiency, thrombocytopenia, Reye dz, asthma, tinnitus, dyspepsia, occult bleeding, prolonged bleeding, rash NSAID induced sensitivity, chickenpox of flu like symptoms, G6PD deficiency Bleeding like hemophilia, von Willebrand thrombocytopenia Inhibit both Cox 1 and 2 Use cautiously with GI bleeds impaired renal function, vit K deficiency, purpura, hepatic impairment
DrugUsesSide effectsContraindicationsTherapeutic considerations Atenolol MOA: Blocks response to beta- adrenergic stimulation; cardio selective for beta 1 receptors at low doses with little to NO effect on beta two (safer in asthmatics) Limited metabolization in liver. Beta-blocker (B1 specific) HTN, angina, thyroid storm, HFAV block, bradyarrythmia, sedation, decreased libido, mask hypoglycemia, depression, dyspnea, wheezing Bronchial asthma, COPD, cardiogenic shock, decompensated heart failure, 2 nd and 3 rd degree AV block, severe sinus bradycardia Beta one selective adrenergic antagonists
DrugUsesSide effectsContraindicationsTherapeutic considerations Atorvastatin Pg 330 MOA: HMG-COA reductase inhibitor, inhibits rate-limiting step in cholesterol biosynthesis by competitively inhibiting HMG- COA reductase Class: Inhibitor of cholesterol synthesis (Statin) Mech: inhibits HMG-CoA reductase Indications: Hypercholesterolemia Familial hypercholesterolemia Coronary atherosclerosis Prophylaxis for coronary aterosclerosis Myopathy-increased risk Rhabdomyolysis Hepatotoxicity Abdominal pain (constipation, diarrhea, nausea) Headache Active liver disease Pregnancy and lactation Up to 60% dec. in LDL 10% HDL increase 40% Triglyceride dec. Drug of choice for lowering LDL, one of the most potent Metabolism by P450 3A4 Combo with bile acid sequestrant yields lower LDL Co-admin with Niacin-> inc. risk of myopathy Co-admin with gemfibrozil can induce rhabdomyolysis
DrugClinical appAdverse affectsContraindicationsTherapeutic considerations Atropine MOA: Antimuscarinic; inhibits action of acetylcholine at parasympathetic sites in smooth muscle, CNS, and secretory glands. Increases cardiac output and dries secretions. Metabolized: Liver Anticholinergic Agent, Anticholinesterase overdose, bradycardia, excessive salivation and mucus production during surgery “No See, No Pee, No Spit, No Sh*t” Blurry vision, xerostomia (dry mouth), constipation, urinary hesitancy, increased IOP, loss of taste, hypotension, confusion, coma, ataxia, insomnia, headache, Actions of PNS inhibited Narrow Angle glaucomamarginal nicotinic effect; more effective at reversal of exogenous rather than endogenous cholinergic activity
DrugUsesSide effectsContraindicationsTherapeutic considerations Clopidogrel (Plavix) MOA: Inhibitor of adenosine (ADP)- induced pathway for platelet aggregation. Metabolized in liver by CYP450 enzymes. ACS, recent MI, stroke, peripheral artery disease, CAD, cardioembolic stroke 1-10% URI, chest pain, headache, flu like syndrome, arthralgias, pain, dizziness, diarrhea, depression, rhinitis, rash, UTI <1% neutropenia, acute liver failure, TTP, hypotension, hepatitis, myalgia, eczema Active bleeding disorderNeeds loading dose. Less side effects tha ticlopidne
DrugClinical appAdverse affectsContraindicationsTherapeutic considerations Eptifibatide (integrelin)- antiplatelet agent MOA: blocks binding of fibrinogen & von willebrand factor of glycoprotein IIB/IIIA receptor on platelet surface. Acute coronary syndrome, percutaneous coronary intervention Major bleeding, intracerebral hemorrhage, hypotension, bleeding History of bleeding, recent major surgery, recent stroke, intracranial hemorrhage, uncontrolled hypertension Don’t give with second, second anti GIIb-IIIa agent, minimize arterial and venous puncture, synthetic peptide as parenteral
DrugClinical appAdverse affectsContraindicationsTherapeutic considerations Heparin- Anticoagulant MOA: Low dose: inactivates factor Xa and inhibits conversion of prothrombin to thrombin High dose: inactivates factor IX, X, XI, & XII and thrombin and inhibits conversion of fibrinogen to fibrin Also inhibits activation of factor VIII Prevent embolism, thrombosis, prevent systemic embolism with MI, unstable angina, open heart surgery, DIC, maintain patency IV cath Hemorrhage, heparin induced thrombocytopenia, hypersensitivity, prolonged clotting time, mucosal ulceration, hematoma Heparin induced thrombocytopenia, active major bleeding, bleeding tendencies, open ulcerative wounds, conditions that increase capillary permeability, severe HTN, bacterial endocarditis Unfractionated causes thrombocytopenia more than LMW, antihistamines, cardiac glycosides, nicotine and tetracycline affect ability Cephalosporins, penicillins, oral anticoagulants, platelet inhibitors may increase affects Don’t use ginger, garlic, ginkgo
DrugClinical appAdverse affectsContraindicationsTherapeutic considerations Metoprolol (Lopressor) – Beta Blockers, Beta 1 selective MOA: Blocks response to beta-adrenergic stimulation; cardio selective for beta 1 receptors at low doses with little to NO effect on beta two (safer in asthmatics) [B2 are in bronchiole smooth muscle, blocking causes bronchoconstriction] Metabolized in liver by CYP2D6. AMI, CHF, HTN, Angina, Hyperthyroidism, Acute Tachy, Side Effects: 1-10% Dizziness, headache, tiredness, depression, diarrhea, pruritus, dyspepsia, heart failure, wheezing, nausea Asthma or COPD, cardiogenic shock, Decompensated cardiac failure, 2nd & 3rd degree AV Beta 1 selective adrenergic antagonists
DrugClinical appAdverse affectsContraindicationsTherapeutic considerations Ramipril (Altace) – ACE Inhibitor “End in pril” MOA: Competitively inhibits angiotensin- converting enzymes, resulting in decreased plasma angiotensin II concentrations; BP may be reduced in part through decreased vasoconstriction increased renin, activity, and decreased aldosterone secretion; increases renal blood flow Hypertension, heart failure, diabetic nephropathy, myocardial infarction > 10% Cough (if cough switch to an ARB), hypotension, 1-10% headache, angina, dizziness, N/V, postural hypotension, syncope, vertigo, <1% angioedema Hx of angioedema, bilateral renal artery stenosis [They depend on RAA axis for renal perfusion], renal failure, pregnacny 3 patterns of metabolism: 1) active drug --> active metabolite 2)prodrug -- >active drug 3) active drug and excreted unchanged. Cough and angioedema are caused by bradykinin action: potentially life- threatening. Delay progression of cardiac contractile dysfunction in heart failure and after MI, and delay progression of diabetic nephropathy
DrugClinical appAdverse effectsContraindicationsTherapeutic considerations Simvastatin (Zocor) – Lipid Lowering Agent, Statin MOA: HMG-COA reductase inhibitor, inhibits rate- limiting step in cholesterol biosynthesis by competitively inhibiting HMG-COA reductase Hypercholesteremia, familial, coronary atherosclerosis, prophylaxis for coronary atherosclerosis Myopathy, rhaddomyolysis, hepatotoxicity, dermatomyositis, abdominal pain, constipation, diarrhea, nausea, headache Active liver disease pregnancy and lactation Lowering LDL metabolized by P450, 3A4 inhibitors increase risk of myopathy, combo with bile acid sequestrant or cholesterol absorption inhibitor additive decrease in LDL, combo with niacin maybe used in high LDL and low HDL increases risk of myopathy, gemfibrozil decreases statin clearance induce rhabdo
DrugClinical appAdverse affectsContraindicationsTherapeutic considerations Tissue plasminogen activator (t-PA) (Alteplase, Activase) – Thrombolytics MOA: Recombinant human tissue-type plasminogen activator (t- pa); produces local fibrinolysis. Promotes thrombolysis by converting plasminogen to plasmin which degrades fibrin and fibrinogen. AMI = acute MI, PE, Acute Ischemic Stroke pulmonary edema, arterial embolism, bleeding, DVT, hypotension, intracranial hemorrhage, stroke, fever, chills, N/V, sepsis, shock Internal bleeding, intracranial/spinal trauma, surgery, masses, recent stroke, uncontrolled hypertension Binds to newly formed thrombi with high affinity, causing fibrinolysis at the site of a thrombus Can generate a systemic lytic state and cause unwanted bleeding
DrugClinical appAdverse effectsContraindicationsTherapeutic considerations triamterene/ Hydrocholorothiazide (Maxide,Dyazide) – Thiazide Combos, HTN Triamterene – Direct effect on renal distal tubule to inhibit Na reabsorption. Inhibits Na/K- ATPase, decreases Ca and MG and hydrogen excretion =Postassium sparing diuretic HCTZ- inhibits Na reabsorption in distal renal tubules; results in increased excretion of Na and water also K and H ions. -is a sulfa drug HTN, adjunct in edema states associated with HF, cirrhosis, renal dysfunction, corticosteroid and estrogen Arrhythmia, stevens-johnson, pancreatitis, hepatotoxicity, SLE, hypotension, alkalosis, vasculitis, photosensitivity, electrolyte abnormalities, impotence, restlessness, blurrred vision, headache, hyperglycemia, hyperuricemia Anuria, hypersensitivity to sulfonamides, co administration with agents that prolong QT First line in treating HTN, diminish hypercalcuria in patients at risk for nephrolithiasis, decreases glucose tolerance may unmask diabetes, don’t use with antiarrhythmic
DrugClinical appAdverse affectsContraindicationsTherapeutic considerations Warfarin (Coumadin) – Anticoagulants MOA: Interferes with hepatic synthesis of vitamin K dependent clotting factors II, VII, IX, & X as well as proteins C and S. Venous Thrombosis, DVT, Afib, Cardiac Valve Replacement, Post MI 1-10% Intraocular Hemorrhage, UNK Freq – abd pain, rash, pruritus, tissue necrosis, headache, lethargy, anemia, hemorrhage, fever, purple toe syndrome, Pregnancy, Hemorrhage, Bleeding tendency, uncontrolled Hypertension Monitor with PT/INR. Many drug-drug interactions, never give to pregnant woman, can cause skin necrosis, receive fresh frozen plasma if hemorrhaging occurs