Complete Acute ECG Solution Guide: Updated Latest 2026| 100% A+ Guide.

Complete Acute ECG Solution Guide: Updated Latest 2026| 100% A+ Guide. ECG. HEART BLOCKS: FIRST DEGREE: ◆ Elongated PR interval of 0.20. Regular rhythm. ◆ Causes: Digitalis, drugs, CAD, vagal tone. SECOND DEGREE: Mobitz I ◆ Progressively prolong the PR interval until one QRS is dropped. ◆ Atrial is regular. No missing Ps. SECOND DEGREE: Morbitz II ◆ PR interval normal or prolonged. With some missing QRS. ◆ QRS wide. ◆ Atrial regular. ◆ THIRD DEGREE BLOCK: ◆ P waves not associated with QRS. Rhythm independent. ◆ No atrial impulse conducted through ventricles. ◆Causes of blocks: ● Vagal (1st degree and 2nd degree), Degenerative, Autoimmune, infectious, acute ischemia/infarction, surgical (ablation or valve surgery), drugs. WAP: Multifocal Atrial Tachycardia. ● Sinus and ectopic P wave, all of different shapes, because they originate in different locations thus the different P shapes. ● Atrial Flutter Atria beats fast but regular. Originates from a single focus in atria, all P waves have the same shape. Irregular ventricular rhythm. Decreased cardiac output. Atrial Fibrillation: Paroxysmal, persistent, or permanent. ● Rapid, irregular, disorganized rhythm. ● Absent P waves ● Irregular - irregular (both atria and ventricular). ● Decreased cardiac output and risk of thrombosis. ● Causes: PIRATES. ○ Pulmonary, Ischemic, Rheumatic valve (mitral), Anemia, Thyroid, HTN, Sleep apnea.○ ○ SLOW A FIB → ○CHAD Scores.Left BBB Right BBB Wide QRS 120msec (3 small boxes). Wide QRS. ST seg’ is the opposite direction to the QRS. I, V1, V5, V6. Slurred “S” in I, aVL, V5, and V6. ● Mostly I and aVL. Tip: LOOK AT V1: - Is QRS DOWN? - Abnormally large ST and T wave up? = LEFT BBBB ● BOTH HAVE BUNNY EARS. ● ONLY LEFT BBB HAS QRS DOWNWARDS (REVERSED) IN V-1.ELECTRICAL AXIS. ELECTRICAL AXIS is the sum total of all the vectors generated in the action potential in the individual myocardial myocytes. Different pathologies of the heart can change direction of the electrical vectors. Left axis deviation: -30 to -90. → left ventricle. Normal axis: -30 (aVL) and +90 (III). → Left atrium, left ventricle areas. Right axis deviation: +90 (III) to +180 (I). → right ventricle. Extreme axis: -/+180 to -90. → Right atrium.Acronyming: “ISALP” → Inferior, Septal, Anterior, Lateral, Posterior. I II, III, aVF Right Coronary Artery (RCA) S V1, V2 Left Anterior Descending (LAD) A V3, V4 LAD L I, aVL, V5, V6 Circumflex P V8, V9 RCAAnterior Wall MI → V2 and V3 are the absolute worst QRSs. Antero-Lateral Acute MI: Antero: V2-V4 and Lateral I, aVL, V5 and V6.Inferior Lateral MI Inferior-PosteriorPOSTERIOR MI → Unique presentation on ECG. ST elevation on V7, V8, V9. DEPRESSION, not elevation, on V1 to V4. If “inferior” MI also present, will see elevation on II, III, and avF (see below). PERICARDITIS. PR segment depression, concave elevated ST segment. T wave inversion after ST normalizes.TORSADES Diarrhea = Hypokalemia and hypomagnesaemia QT prolonging meds Haldol, biaxin taken with CYP 450 inhibitors fluoxetine and cimetidine. Side effect: Amio, methadone, lithium, chloroquine, erythromycin, amphetamine, pseudoephedrine. LVH Hypothermia Subarachnoid hemorrhage Hypothyroidism.HYPERTENSION MANAGEMENT: Predisposing Factors ● Over age 60 ● Male gender, or women postmenopausal ● Cardiovascular disease hx ● Smoking ● High cholesterol diet ● DM, obesity, hyperlipidemia ● Alcohol intake ● Sedentary lifestyle. Secondary (5%) HTN: Has a demonstrable underlying cause such as ABCDE. ● A: accuracy, apnea, aldosteronism. ● B: Bruits, bad kidney ● C: catecholamines, coarctation, cushing’s syndrome. ● D: Drugs (NSAIDS, stimulants), Diet ● E: Erythropoietin in COPD and RF, endocrine (preg, thyroid, parathy, pheochromocytoma, acromegaly).Med Action Example Notes Diuretic Drops: - Blood Vol’ - CO - PVR. Thiazides Drugs of choice in elderly - Drops Na+ and K+. - Hyperlipidaemia. - Hyperuricemia (c/i with gout). - Hyperglycemia: Not safe in DM. - Not safe in renal and hepatic insufficiency. Beta blockers 1. Blocks B1 in the heart. Drops CO 2. Blocks B2 in kidney. 3. Inhibits Renin release in kidney. Atenolol Metoprolol Carvedilol - Drug of choice for coronary heart disease. - Adverse: lethargy, impotency, bradycardia. - Not safe in asthma and DM. - Adverse effect in lipid profile. Ca Blockers Vasodilation Reduce PVR Amlodipine Felodipine Lercanidipine Nicardipine Drug of choice for asthma co-exist. Adverse: flushing, HA, pedal edema. Alpha Blockers A-1 blockers Vasodilators Reduce PVR Doxazosin Prazosin Terazosin Beneficial for high lipid and insulin sensitivity. Drug of choice for co-existing hyperlipidemia, DM, and BPH. Adverse: Postural HTN. ACE Inhibitor ACE I X ACE II Lisinopril Enalapril Ramipril Fosinopril Drug of choice in HT + DM. Adverse: dry cough and angioedema. ARBs Block angiotensin II receptors Losartan Valsartan Telmisartan Drug of choice in coexisting DM. Dry cough, angioedema.DRUGS IN SPECIAL CONDITIONS - Pregnancy: nifedipine, labetalol, hydralazine, beta blocker, methyldopa, prazosin. - Coronary Heart Disease: beta blocker, ACE, Ca+ blocker. - Congestive Heart Failure: ACE, beta blocker. HEART FAILURE - ACE & ARB - BB - Loop Diuretic - Aldosterone blocker. Post MI - BB - ACE-I - Aldosterone Blocker → ARB → Sartan. High Risk of CAD - BB → test question “HTN + CAD” best tx? = BB for control”. - ACE-I - CCB - Thiazide ACE - I and ARB → Prevents Neuropathy. CKD → ACE and ARB. Recurrent stroke: ACE. Follow up: - Initially, see pt as much as needed to stabilize BP. - Then, every 4-6 months for 1st year. - Or, more often if pt needs motivation - Monitor BP, Weight, RL, U/A, Lipids, EKG - Encourage diet/exercise.HYPERTENSIVE EMERGENCY: Systolic 220 or Diastolic 120. Wrose to least → HTN Emergency Accelerated HTN HTN Urgency Notes Known as “crisis” Recent significant increase in BP baseline. BP is potential damage, but not yet. Clinical finding Organ damage present → Renal, CNS, CV. Papill-edema: Malignant HTN. Means swollen optic nerve in eyes. Target organ damage. 1 vascular damage on a fundoscopic exam → 2“flame-shaped” hemorrhages or soft exudates 3 No papilledema. No rgan damage Treatment BP control over days or weeksCASE PRACTICES (slide 29). 1. A 56 yo CM with no significant PMH presents to the ER with headache,found to have BP 210/110mmHg and papilledema. MALIGNANT HYPERTENSION 2. An 82 yo male with h/o HTN, chronic renal insufficiency presents for a routine physical, found to have BP of 230/130mmHg. ACCELERATED HYPERTENSION → because there is no papilledema is not “malignant”. Because of renal issue, it’s more than “urgency” so accelerated. 3. A 76 yo female is brought to the ER by the family due to altered mental status. BP is 240/110 mmHg with no focal neuro findings. HYPERTENSIVE EMERGENCY “CRISIS”. PATHOPHYSIOLOGY OF BP. BP = PVR x CO Where CO is (SV x HR). RAAS plays an important role in initiating and perpetuating BP rise by causing vasoconstriction and fluid retention. CENTRAL NERVOUS SYSTEM BP EFFECTS During normal circumstances: if BP rises, cerebral arterioles vasoconstrict and cerebral blood flow remains constant. During HTN emergency: BP rises and overwhelms arteriolar control over vasoconstriction and autoregulation of CBF. ◆ Results in transudate leak across capillaries. ◆ Continued arteriolar damage. ◆ Fibrinoid necrosis causes normal autoregulatory mechanisms to fail, leading to clinically apparent papilledema → sign of malignant hypertension. End stage damage: focal neuro deficits, seizures, stupur, coma, papilledema, hemorrhages, exudates, closed-angle glaucoma. CARDIOVASCULAR SYSTEM BP EFFECTS Increased BP → increased cardiac workload → cardiac failure (pulmonary edema or myocardial ischemia and/or myocardial infarction). JVD, RENAL SYSTEM Increased BP → arteriosclerosis, fibrinoid necrosis, overall impairment of renal protective autoregulation mechanisms. Worsening renal function, hematuria, RBC cast formation, proteinuria.DIFFERENTIAL DIAGNOSIS: ● Steroid use ● Recreational drugs ● Pheochromocytoma ● Acute vasculitis ● Serotonin syndrome CNS pathology ● Coarctation of the aorta. INITIAL STEPS OF TREATMENT ● Initial considerations: Place a patient who is not in distress in a quiet room and reevaluate after an initial interview. In one study, 27% of patients with an initial DBP 130 mm Hg had their DBP fall below critical levels after relaxation without specific treatment. ● Consider the context of the elevated BP (eg, severe pain) ● Screen for end-organ damage- Patients with end-organ damage usually require admission and rapid lowering of BP using iv meds.Suggested meds depend on the end-organ system damaged. ● Patients without evidence of end-organ effects may be discharged with follow–up. ○ It is a misconception that a patient should not be discharged from the ER with elevated BP → TEST QUESTION. ○ Giving oral meds such as nifedipine to rapidly lower BP may be dangerous as the BP may have been elevated for some time and there may be organ hypoperfusion. ○ Acute control has not improved long term mortality and morbidity rates. ● Once the diagnosis of hypertension is made, and end-organ damage confirmed, the BP should be lowered by about 25% of the mean arterial pressure (MAP).RAPID BP REDUCTION ● Acute myocardial ischemia ○ IV nitroglycerine, Beta blocker, ACE inhibitor. ● CHF with pulmonary edema. ○ IV Nitro, furosemide, beta blockers. ● Acute aortic dissection ○ IV nitro, beta blockers, IV trimethaphan. *BRAIN → Avoid Nitroprusside and Hydralazine in STROKEs.* ● Hypertensive encephalopathy or subarachnoid hemorrhage. ○ IV Cardene (not nitro like the PPT says!), Labetalol, or Nimodipine. ○ Test question: IV Nicardipine (Cardine) to lower by 20-25%. ● Intracranial Hemorrhage ○ Agents of choice: Esmolol, Labetalol. ● Subarachnoid Hemorrhage ○ Nimodipine: decreases vasospasm. ○ Agents of choice: Esmolol, Labetalol. ● Ischemic Stroke ○ BP can make an ischemic stroke into a hemorrhagic one. ○ Unless organ damage occurs, do not lower BP that is less than 220 sys or 120 diastolic. For thrombolysis 185/110 systolic max. ○ MEDS: Labetalol, Cardene (NOT Nitro like PPT says). ● MAO-Tyramine ○ IV phentolamine. AORTIC DISSECTION ● Immediately reduce to 100-120 systolic, or lower levels that allow perfusion. ● Drugs: Labetalol + beta blocker like propranolol agents of choice. ACUTE LEFT VENTRICULAR FAILURE ● IV nitroglycerin, nitroprusside. ● Drop BP until signs of heart failure alleviated. FOLLOW UP ● Systolic 140-159 / 90 - 99 = within 2 months. ● 160-179 / 100-109 = within 1 months. → most adults. ● 180-209 / 11/119 = within 1 week. ● 210/120 = Evaluate immediately.Normal: 120/80 Pre-HTN → 120-139/80-89 Stage 1 → 140-159/90-99 Stage 2 → 160/100. ATRIAL FIBRILLATION CLASSIFICATION ● PAROXYSMAL = 1 WEEK, CONVERTS TO NSR. ○ WHETHER SPONTANEOUS OR WITH INTERVENTION. ● Persistent = Lasts 1 week. ● Long standing = 1 year, but there is still the possibility of restoring to sinus. ● Permanent = Cannot be converted to sinus. ● Rapid Ventricular Response = Ventricular rate 100. Causes: HTN, CAD, Cardiomyopathy, Valve disorder, hyperthyroidism, binge alcohol. Pulmonary embolism, CHD, COPD, Myocarditis, pericarditis.ELECTRICAL CARDIOVERSION → FOR THE UNSTABLE PATIENT. ● Afib + RVR + symptomatic = Unstable Synchronized cardioversion ○ hemodynamically, hypotension, angina, decompensated heart failure, altered mental status. ● Sedate patient and place setting on direct synchronization then shock. ○ Initial shock setting of 100J, 200J, 300J, 360J; until sinus rhythm returns. ○ Make sure you perform direct cardioversion with R wave synchronization to prevent an “R on T” phenomenon which can lead to V fib. ○ Perform a 2D ECHO or TEE prior, to rule out left atrial thrombus. ● Restoration of normal sinus rhythm takes precedence over need for protection from thromboembolic risk → This is in life threatening, symptomatic, afib (irregular HR of 160+). ○ If Afib presents more than 48hrs, and cardioversion can wait, anticoagulation should be attempted before cardioverting. ● Initial rate control agents: Diltiazem or Metoprolol (Not dig or Amio). ● If PT cannot take rate-control drugs = AV node ablation. THE STABLE PATIENT ● Goal is ventricular rate control (100 bpm) and anticoagulation ● Resting HR goal should be 60-85 bpm in symptomatic patient ● Roughly 50% of patients with new onset AF will spontaneously convert to NSR spontaneously within 48 hours of onset Rate control or Rhythm control? ● AFFIRM trial and RACE trial ● No survival advantage in terms of stroke prevention rhythm control over rate control rate control. ● Rate control agents ○ Calcium Channel Blockers ○ Beta blockers (caution in patients with reactive airway disease). ○ Digoxin ○ Amiodarone (for patients intolerant or unresponsive to other agents).DRUGS (DOC = Diltiazem and Metoprolol, NOT Amio). Start P.O at same time as IV. ● Diltiazem: Calcium blocker. ○ loading dose 10mg IV first, 20mg IV max. ○ 10mg IV Q6H. P.O: 30mg, Q6H. → may do long acting as well. ● Metoprolol: Beta blocker. ○ Loading: 5mg IV push, three times max. ○ P.O: 25 mg BID, may go up to 100mg BID as needed. ● Digoxin: Inotropic agent. ○ 0.5mg loading dose IV, then 0.25mg IV Q6H. ○ Maintenance: 0.125mg P.O, Daily. ○ NOT FOR RENAL PATIENTS → renal excreted. ○ Least effective, but preferred if heart failure is present too. ● Amiodarone: ● HOSPITAL DRIP: 150mg IV push, 1mg/min IV 6 hrs then 0.5 mg/min for 18 hrs. ● 100-200mg P.O Daily. ● PT must be on anticoagulation! ● Preferred agent in WPW. CHA2DS2-VASc 0 = None or Aspirin. → with Zero anticoagulation is not required. 1 = Moderate risk = Aspirin, warfarin, Pradaxa, Xarelto, Eliquis. 2 = Moderate to High risk = Warfarin, Pradaza, Xarelto.ANTICOAGULATION ● First Line = Warfarin (Vit K antagonist). ● Pradaxa (Dabigatran) = Thrombin inhibitor. ○ 150mg BID, without need for coagulation monitoring. ○ The risk of stroke is lower with Pradaxa, than with Warfarin. ○ The risk of MI was numerically greater with Pradaxa. ○ Risk of bleeding is lower with Pradaxa. ○ 80% renal clearance. ■ Renal function must be assessed before starting Pradaxa. ● Creatinine clearance ○ 30mL/min = 150mg BID (normal dose). ○ 15-30mL/min = 75mg BID (reduced dosing). ○ 15mL/min = No recommendation dosing. ○ Stop prior to invasive procedure due to risk of bleeding. ■ At least 1-2 days. Ideally 3-5 days. ■ If surgery cannot be delayed = D/C Pradaxa, give FFP, and RBC prior to SX, and consider Platelet transfusion in cases of Thrombocytopenia. ■ With dialysis, 60% of the drug goes out in 2-3 hours. ■ No reversal agent. ● Xarelto - Rivaroxaban: Xa inhibitor. ○ Once daily, with the largest meal (evening), no coagulation monitoring. ○ ⅓ renal excretion, ⅔ CYP enzyme (liver). ■ No reversal agent. ■ Dialysis does not help due to protein-bound affinity. ○ For surgery: ■ Stop at least 24 hrs prior. ■ If 24 hrs, decide if risk of bleeding is worth the urgency of the sx. ■ Wait 18 hrs post any dose before removing catheters, ■ Do not restart until 6 hrs after catheter removals.● Eliquis -Apixaban: Xa inhibitor. ○ Dosage: Oral, BID, 5mg or 2.5mg. ○ Drug interactions: ■ Decrease 5mg dose to 2.5mg if taking: ● Ketoconazole, itraconazole, ritonavir, clarithromycin. ● These are “strong dual inhibitors of CYP-3A4 and P-gp” which intensify Eliquis effects. ■ If already taking 2.5 mg dose, then avoid those meds completely. ■ Do not give with: Rifampin (TB drug), carbamazepine (seizure drug), phenytoin, and St. John’s wort. ○ Clearance: 27% direct renal excretion. Rest is biliary and GI excretion. ○ D/C 48 hrs prior to invasive sx, in which bleeding is likely. ○ D/C 24 hrs prior to simple sx, where bleeding is easily controlled. MEDICATION TO AVOID WITH ANTICOAGULATION TYPE PRADAXA DVT, PE, Extended XARELTO DVT, PE, Extended Hip and Knee prophylaxis. ELIQUIS DVT, PE, Extended Hip and Knee prophylaxis. Rifampin Quinidine Rifampin Carbamazepine Phenytoin St. John’s Wart Rifampin Carbamazepine Phenytoin St. John’s wart. Reduce dose with: - Multaq - Ketoconazole - Verapamil Avoid: - Multaq - Ketoconazole, Troco’ - Verapamil - Conivaptan (vasop’) - Erythromycin - cimetidine - Itonavir, Indavir, Ritonavir - Amiodorone, Diltiazem, Verapamil. Reduce to 2.5mg with: - Ketoconazole - Itraconazole - Biaxan If on 2.5, then stop completely.ACUTE CORONARY SYNDROME - Murmurs ChartUnstable Angina *1st time is ALWAYS unstable* Non STEMI STEMI Chest pain / SOB Anginal symptoms at rest Angina + more symptoms No thrombus Thrombus and tissue damage, partial occlusion Complete occlusion NO specific ECG ST depression T wave inversion ST elevation New LBBB No Cardiac Enzymes Elevated enzymes Elevated enzymes No necrosis Necrosis exist Necrosis exists No Q wave Develops Q wave later on Develops Q wave later on NON - STEMI ● Early PCI criteria: 4-24 hours ○ Increased cardiac biomarkers (troponin, CK-MB) ○ New ST segment depression ○ Signs or symptoms of congestive heart failure (rales on examination, hypoxia with pulmonary edema on chest x-ray) ○ Hemodynamic instability ○ Sustained ventricular tachycardia or ventricular fibrillation ○ Recent coronary intervention within 6 months ○ Prior coronary artery bypass grafting ○ High TIMI risk score ○ Reduced left ventricular systolic function (EF 40%). ○ Recurrent angina at rest or with low level activity ○ High risk findings from non-invasive testing. ● Anticoagulation ○ Lovenox or Fondaparinux ○ Unfractionated Heparin. ● Chest pain + no markers + no ECG changes = Angina only. ● (Angina) + (↑↑biomarker) + (no ECG CHANGE or ST depression) = NSTEMI. ● (Angina) + (ST elev’) + (↑markers (or no markers initially!)) = STEMI.Three Factors of O2 demand: 1. LV wall stress 2. Contractility 3. Heart rate DIABETES ● MAGNIFIES THE EFFECTS OF OTHER RISK FACTORS ● MED WITH TYPE 2 = HAVE 2-4 MORE FOLDS CHANGE OF CAD ● WOMEN WITH TYPE 2 = 3-5 FOLDS CHANCE OF CAD! ALCOHOL ● Binges increases risks of CAD ● While 1-2 drinks daily is associated with reduced change of CAD. HOMOCYSTEINE ● High levels of LIPOPROTEINS in your plasma are associated with CAD ● High homocysteine makes the person prone to endothelial injury → inflammation → atherogenesis → ischemic injury (MI/ unstable angina). STRESS TESTING ● ECG, before, during and after exertion ● Most sensitive to detect stenosis of 70% or greater. ● Criteria to stop testing ○ Chest pain ○ Severe SOB, Dizziness, Severe Fatigue, ST segment depression .2 MV . Drop Sys BP 10mmHg.DIFFERENTIAL DIAGNOSIS = AnginaDIAGNOSIS: Angina Cardiac stress testing: Stenosis of more than 70%. CTA: Computed Tomographic Angiography. → Gold Standard. Coronary Calcium Scoring Angiography: Gold Standard. MANAGEMENT 1. Nitrates: vasodilation, which decrease LV-ED volume and pressure. a. Decrease myocardial wall tension and O2 demand b. Release NO. c. There is short (during episode) or long acting (prophylaxis). 2. Phosphodiesterase Inhibitors: Cause pulmonary vasodilation and penile smooth muscle relaxation. a. Sildenafil 24hrs b. Vardenafil and tadalafil 48 hrs c. Enhances nitric oxide production, enabling bronchial dilation in severe COPD. 3. Beta Blockers a. Decrease HR, arterial pressure, and myocardial contractility. b. Reduce mortality and re-infarction rates c. Initiate early when there are no contraindications. d. Do not give with HX of Asthma. 4. Calcium Channel Blocker a. Coronary vasodilators (such as Nicardipine / Cardene drip!) b. Reduce myocardial O2 demand, contractility, and arterial pressure. c. Choose BB and nitrates fail, adverse reactions to BB or asthma exist, choose in Prinzmetal angina, and if signs of PAD. d. Amlodipine and nifedipine are vasodilators. e. Diltiazem and verapamil decrease HR (good for AFib rate control). ANTIPLATELET THERAPY ● Aspirin ● Plavix ○ Blocks receptor mediated platelet aggregation. ○ Combo with ASA ○ Pre stent and 1 yr post stent placement.Variant “Prinzmetal” Angina ● Variant angina, or Prinzmetal angina. ● Characterized by chest pain at rest due to coronary arteries spasms. ● Transient ischemic electrocardiographic changes in the ST segment. ○ But coronary arteries are NORMAL on ANGIO. ● Prompt response to nitrates. ● Usually middle age women. PERICARDITIS ● PERICARDIAL FRICTION RUB IN THREE PHASES OF CARDIAC CYCLE. ○ ATRIAL SYSTOLE ○ VENTRICULAR SYSTOLE ○ VENTRICULAR DIASTOLE ○ It can be distinguished from a pleural rub by the fact that it will still be heard when the patient holds their breath. ● Clinical findings: ○ BIPHASIC ‘TO AND FRO’ RUB ○ Leukocytosis ○ Lymphocytosis ○ Pericardial effusions. ○ ECG MIMICS A STEMI. DIFFUSE CONCAVE ST SEGMENT ELEVATION AND PT DEPRESSIONS. ● Symptoms: ○ Sharp central chest pain ■ EXACERBATED BY MOVEMENT, RESPIRATION, AND LYING DOWN. ■ RELIEVED BY SITTING FORWARD ■ MAY BE REFERRED TO NECK OR SHOULDER ○ FEVER. ● Idiopathic: Viral, bacterial, TB, post MI, trauma, post cardiac sx, neoplastic, uremia, inflammatory or autoimmune disease, wall irradiation, drug induced. ○ Post MI 1-3 days: transmural Necrosis causing adjacent pericarditis. ○ Post MI 1 week: Autoimmune by Dressler Syndrome.PERICARDITIS ON ECG ● Changes are diffuse because pericarditis involves large surfaces rather than specific coronary artery anatomy. ● ST elevation, mostly V5 and V6 (70%). → similar to a “Lateral” MI. ○ ST elevation is “concave” or “saddle”. ○ ST depression in aVR and V1 in 64%. ● PR elevation (see below ECG). MYOCARDITIS ● Asymptomatic ● Fatigue, dyspnea ● Chest pain, palpitations, tachycardia, friction rub ● S3, soft heart sounds AORTIC DISSECTION → TEE and CT chest STAT. ● SEVERE CENTRAL CHEST PAIN → TEST QUESTION HAS “RIPPING PAIN & LOWER LIMB ISCHEMIA”. ● Signs of cardiogenic shock ● Neurological symptoms ● Hypoperfusion = Renal failure, Lower limb ischemia, visceral ischemia. ● Risks: HTN and Marfan’s Syndrome.PULMONARY EMBOLISM ● SYMPTOMS: cough, dyspnea (not otherwise explained), chest pain, haemoptysis, DVT, fever. ● Signs: tachypnea, tachycardia, shocked, pale, sweaty, pleural rub, crepts, febrile, hypotension, peripheral shutdown, raised JVD, gallop, split S2. ST ELEVATION - ACUTE MINEW L-BBB QRS 12, PROMINENT R IN V1-V3, T INVERSION IN V5-V6. 53 Y/O WITH COMPLAINT OF CRUSHING PAIN. INTERPRETATION: INFERIOR MI→ ST ELEVATION IN II, III, AND AVF.ANTERO-SEPTAL INFARCT : ST ELEVATION IN V1, V2, AND V3. MARKERS → both Troponin and CK predict mortality. ● Troponin doesn't rise until 4-8 hrs after the injury ○ Remains elevated for 2 weeks +. ○ Elevated with other conditions too. ● CK-MB ○ Rises 4-6 hours after ○ Peaks at 24 hrs, remains 36-48hrs. ○ False positive with exercise, trauma, muscle dz. ACUTE CORONARY SYNDROME KEY QUESTIONS ● ST-elevation? ● Rise in troponin? Low Risk Intermediate High Risk Pain 10 min No ECG change No marker 70 y/o. Angina ST or T change in ECG Elevated Troponin DM, renal dysfunction. PCI within 6 months CABG history Recurrent Angina ST change 2MM. Deep T wave inversion HF signs Hem’ instability Arrhythmias (VT/VF) ASA, clopidogrel, ticlopidine, beta blocker, nitrates. Coronary angiography Intervention Urgent Coronary angio.STEMI MEDICAL TREATMENT ● ARRANGE EMERGENCY AMBULANCE ● ASPIRIN 300MG. ● NTG S/L. 0.3-1 MG.----REPEAT ● OXYGEN 2-4 L/M ● IV DIAMORPHINE 2.5-5MG+ METOCLOPRAMIDE 10 MG. ○ NOT IM ~~~RISK OF BLEEDING WITH THROMBOLYSIS. ● BETA-BLOCKER (IF NO C/I ) ○ FOR ONGOING CHEST PAIN, HTN, TACHYCARDIA. ○ NOT IN ASTHMATICS. ● IF PRIMARY PCI AVAILABLE GIVE GP11b/111a INHIBITOR. ○ ALTERNATIVELY GIVE THROMBOLYSIS. ● ACE INHIBITORS ○ LISINOPRIL 2.5MG. ○ STANT IN NORMOTENSIVE PTS WITHIN 24 HRS. ○ ESPECIALLY IN EVIDENCE OF LV DYSFUNCTION AND HF SIGNS. THROMBOLYSIS ● ST ELEVATION 2 MM IN 2 OR MORE chest LEADS. ● ST ELEVATION 1 MM IN 2 OR MORE LIMB LEADS. ● Posterior infarction ● NEW LBBB ● CONTRAINDICATIONS: ○ HEMORRHAGIC STROKE OR STROKE OF UNKNOWN ORIGIN AT ANY TIME ○ ISCHEMIC STROKE IN PRECEDING 6 MONTHS ○ CNS DAMAGE OR NEOPLASM ○ RECENT MAJOR TRAUMA/SURGERY/HEAD INJURY/ WITHIN PRECEDING 3 WEEKS ○ GI BLEEDING WITHIN LAST MONTH ○ KNOWN BLEEDING DISORDER ○ AORTIC DISSECTIONTHROMBOLYTIC AGENTS ● STREPTOKINASE ○ Initiated within 12 hrs ○ 1.5 million units over 1 HR ○ May repeat only within 4 days of 1st administration. ● Alteplase ○ Accelerated (within 6 hrs of symptom) ■ Plasminogen activator ■ Initiated within 6H of symptoms onset. ■ 15mg IV push (if 65K, then 15mg push only). ● then 50mg over 30min. ● Then 35 over 60min. ● Total 100mg over 90min. ○ Non-accelerated within 6-12 hrs of symptoms) ■ 10mg IV injection ■ 50mg over 60 min ■ 4 infusions of 10mg over 30min each. ■ Total dose 100mg over 3 hrs. Non - STEMI ● LMWH or Enoxaparin 1mg/kg ● Heparin 5000-U IV bolus, then infusion at 0.25unit/kg/hr ○ Ptt Q6H ○ Stop when pain free (~24hrs). ● Nitrates for pain ● Record ECG while in pain. ● Check markers 2-3 days ● Address modifiable risk factors.HEART FAILURE TOPICS ● Systolic Heart Failure ○ Reduced EF ○ Primary cause CAD or MI ○ Secondary Dilated Cardiomyopathy(50% idiopathic) ○ Viral (Coxsackie virus, influenza B, HIV, enteroviruses) ○ Chemotherapy (Cytoxan) ○ Pregnancy ○ Parasitic (Chaga’s disease) ○ ETOH ○ Stress-induced (Takotsubo), broken heart syndrome ○ Acute HF, lethal ventricular arrhythmias, ventricular rupture ● Diastolic Heart Failure ○ Hypertensive heart disease ○ Aging of the heart ○ Restrictive cardiomyopathy ○ Amyloidosis, Sarcoid Disease ○ Valvular heart disease ○ Mitral and aortic stenosis ○ Tachyarrhythmias ○ Constrictive pericarditisRight Left Hepatomegaly Dyspnea splenomegaly Coarse rails JVD / PND wheezing Displaced PMI cough Abdominal fullness Murmur of mitral regurg Easy fatigue S3 and S4 DRUG TREATMENT - HEART FAILURE ● Diuretics ○ in patients with fluid retention. ● ACE inhibitors or ARBs in all patients unless contraindicated. ● bB-blockers ○ in all stable patients unless contraindicated. ● Bisoprolol, metroprolol succinate and Carvedilol ● Digoxin → NOT FIRST LINE. ○ (no data to show improved survival) ● IF PREVIOUS DON’T WORK ○ Spironolactone (aldosterone antagonist) ○ Nitrates & hydralazine. ○ Calcium channel blockers Afib (diltiazem or verapamil if LV func 40) ○ ● Nitroprusside (Nipride) ○ indicated when there is a need for combined preload and afterload reduction ○ Acute aortic and Mitrial regurgitation ● Nesiritide: Natrecor (Natriuretic Peptide): venous, arterial and modest coronary vasodilatory properties that reduce preload and afterload. ○ Has no direct inotropic effects● Intravenous Inotropic agents for pheripheral hypoperfusion ○ Dobutamine ○ Milrinone ○ Dopamine ● OTHER SLIDE SAYS THE FOLLOWING: * NOTE NO DIGOXIN IN HERE* ○ Antiplatelet therapy ■ ASA, Plavix ○ ACE/ARB ○ Beta Blocker ○ Coumadin in HF with Afib unless contraindicated. INR goal 2-3 ○ Indicated in HF with evidence of systemic or pulmonary emboli, stroke or TIA VALVULAR DISEASEENDOCRINOLOGY● Hypothalamus Pituitary Adrenal Axis. ○ Hypothalamus → Corticotropin RH (CRH) → Anterior Pituitary → Adrenal Corticotropin Hormone (ACTH) → Adrenal Cortex → Cortisol. ○ When is hypothalamus stimulated to release CRH? Hypoglycemic state. ○ Negative feedback mechanism = if we have enough CORTISOL, the hypothalamus doesn’t release more CRH… and so on. ● Hypothalamus Pituitary Thyroid Axis. ○ Hypothalamus → TRH → Pituitary → TSH → Thyroid → T3 & T4. ○ For T3 and T4 we have to have IODINE. ○ Negative feedback mechanism = shuts off the loop when we have T3 and T4.● Prolactin = Milk release from mammary glands. ○ Stimulated by: ■ Noepi ■ TRH → test question! ● How are “hypothyroidism and prolactin related”? During hypothyroidism, T3 and T4 are low, so TRH gets released to elevate TSH. ○ TRH increases T3/T4 but also Prolactic. ○ Hypothyroidism PT = elevated TSH and elevated prolactin. ■ Dopamine antagonist (inhibitors). ● Block Dopamine = Increase Prolactin. ● Dopamine Agonist = Decrease Prolactin. ● ■ SSRIs. ● ADH: vasoconstrict and reabsorbs water. ○ Released in hypotension and hypovolemia. ○ Once volume rises too much, ANP (heart) rises, and tells hypothalamus to stop ADH release. ■ ANP blocks ADH! ● Growth Hormone ○ Insulin like growth factor. ○ Stimulates liver to release IFI. ○ We have more of it before the age of 21. ○ Hypoglycemia → GH rises. ○ Hyperglycemia → GH decreases ● Insulin = regulates plasma glucose. ○ Secreted from the beta cells of islets of the pancreas ■ Compare: Amylin comes from alpha cells of pancreas. ■ Amylin suppresses glucagon = lower BG. ○ Circulates in plasma unbound ○ Binds to specific receptor tyrosine kinase to the plasma membrane and increases its activity to phosphorylate numerous regulatory enzymes and other protein substrates. ○ Binds at insulin receptor sites on cell membranes allowing glucose to enter cells (enter the muscle).○ Acts on the liver to increase storage of glucose as glycogen. ○ Promotes protein synthesis on muscle cells ○ Reduces circulation of free fatty acids and promotes storage of triglycerides in adipose tissue. ● Glucagon = Hormone, raises BG. ○ Stored in alpha cells in the islet of pancreas. ○ Target cells: Hepatic cells. ○ Antagonizes insulin effect on hepatocytes cells of the liver. ○ Enhances glycogenolysis = Glycogen breaks into glucose = raise BG. ○ Promotes oxidation of fats = formation of ketone bodies. Amylin = Lowers glucose = like INSULIN. ● Secreted from beta cells of islets of the pancreas . ● Co secreted with insulin in response to caloric intake. ● Alpha cells of the pancreas and hypothalamus ● Suppresses glucagon secretion from the alpha cells in the islets in the pancreas ● Slows gastric emptying which slows glucose absorption from the small intestines to the circulation. ● Stimulates satiety centers in the brain to limit food consumption.Somatostatin. ● Secreted from the delta cells of the pancreas, hypothalamus and the D cells of the gastric gland. ● Works on the islets cells of the pancreas, somatotroph cells in the anterior pituitary gland and the G cells of the gastric gland ● Stimulates the release of growth hormone, insulin, vasoactive peptides and thyroid stimulating hormone. Ghrelin = stimulates appetite = increases glucose. ● Released from the epsilon cells of the pancreas, endocrine cells of the stomach and the hypothalamus. ● Target cells: Beta cells of the islets of the pancreas and somatotroph cells of the anterior pituitary gland. ● Inhibits the secretion of insulin from the beta cells of the pancreas via paracrine interaction between delta cells of the islets of the pancreas via paracrine interaction between delta and beta cells of the islets of the pancreas. ● Stimulates appetite and growth hormone secretion. _____________________________________________________________________________________Endocrine Part I PPT ● Slide 3: ○ 55-year-old female presents to your clinic for a physical. She reports that she just moved to the area and needs the physical for work. She reports feels fine, no current complaints. She reports a medical history significant for borderline HTN, and BMI of 30. She has a family history significant for HTN, Diabetes and obesity. She reports that on her last physical she was told to start a low-calorie diet and implement an exercise regimen, but she admits that she has not been able to do so because of her job and family responsibilities. On evaluation today her blood pressure is 145/95. On her examination you observe acanthosis nigricans at the neck, rest of her exam is within normal limits. You obtain a fasting plasma glucose test which comes back at 150. ■ Acanthosis nigricans = black line behind the neck, most predominant in DM2. ■ Fasting glucose 150 = elevated, should be below 126. ● Diabetes ○ Insulin production fails, or insulin resistance ○ Type I = absolute absence of insulin ○ Type II = there is some insulin production, but not enough. ○ Chronic hyperglycemia. ○ Normal person = insulin puts extra glucose into the muscle cells. Not sitting outside of the cell (which damages them). ○ Symptoms: ■ Thirst ■ Polyuria ■ Blurred vision ■ Weight loss → HIV, cancer PTs, and type 1 DM. ■ Type I = Ketoacidosis, high anion gap acidosis. ■ Type II = non-ketosis. ■ Some pts have NO symptoms. ● Type I → less common than Type II. ○ Autoimmune ○ Pancreas beta cell destruction = no insulin production at all. ○ Presentation = hyperglycemia and metabolic acidosis.● Type II ○ Insulin resistance ○ Most prevalent ○ Prolonged asymptomatic phase! Hormone Function Glucagon Simulates breakdown of glycogen for glucose release Somatostatin Inhibits secretion of insulin and glucagon Einephrine and norepinephrine Regulates glucose metabolism from storage depots. Promotes glycogenolysis, promotes lipolysis and release of free fatty acids Cortisol - Your ICU PTs usually have high BP because of high cortisol. Released in response to hypoglycemia or heavy exercise. Promotes gluconeogenesis. Inhibits protein synthesis. Promotes release of free fatty acids Growth hormone Stimulates cell growth and division, stimulates protein synthesis. Increases the rate of fat usage by the cell Thyroxine Regulates meta of lipids, proteins, & Carb. Stimulates cells to use Carb as energy source● In general, for the CV system, having a DX of diabetes will have the SAME negative effect as having had 1 MI or having CVD!. ○ Reduce their CV risks if they already have DM: ■ Keep LDL below 100, per (guideline). ● Optimal is less than 70. ■ Manage HTN ● Systolic 130, and diastolic 85. ● DM + kidney dysfunction/insufficiency: ○ systolic goal is 120 and diastolic goal is 75. Test Normal Impaired Fasting / tolerance Diabetes Fasting Plasma Glucose mg/dL → EDUCATION! 126 Hemoglobin A1C 5.6 5.75-6.4 6.5 2-hour glucose tolerance test (75g load) 200● Prediabetic = exercise, diet changes, but no medications. ○ Quiz questions! Education with pre-diabetic pts! ● If fasting is 126, order a second test and if still + then diagnose. ● Treatment: Index Goal HbA1c 7.0% (→ ideally 6.0) Pre-Prandial Capillary Glucose 80-130 mg/dL Peak PostPrandial glucose 180 Blood Pressure ADA 130/80 JNC 140/90 LDL → test question. 100 mg/dL → Test Question. HDL Men 40 mg/dL Women 50 mg/dL Triglycerides 150 mg/dL ● Metabolic Syndrome: 3-4 = official dx of meta’ syndrome. ○ Waist circumference /= 40 inches in men and /= 35 in women ○ BP /= 130/85 ○ Triglycerides /= 150 → High CV RISK! ○ FBG /= 100 ○ HDL 40 in men and 50 in women●● Start screen: ○ Every 3 yrs beginning at age 45, unless they meet any of the above mentioned. ○ BMI /= 25. ● Criteria for Dx of DM A1C /= 6.5% The test should be performed in a laboratory using a method that is certified by the national Glycohemoglobin and Standardized to the DCCT assay. Fasting plasma glucose /= 126 mg/dl (7.0 mmol/L). Fasting is defined as no caloric intake for at least 8 h. Two-hour plasma Glucose /= 200mg/dl (11.1 mmol/L) during a Oral Glucose Tolerance Test. The test should be performed by using a glucose load containing the equivalent of 75 g anhydrous glucose dissolved in H2O. In a patient with classic symptoms of hyperglycemia or hyperglycemia crisis, a random plasma glucose /= 200 mg/dl. In the absence of unequivocal hyperglycemia tests should be confirmed by repeat testing.● Components of Diabetic Evaluations. ○ 1. Medical HX ■ Age and characteristic of DM ■ Eating patterns, physical activity, nutrition wt history, growth and development in adolescent ■ Diabetic education hx ■ Review tx and response via HA1C. ○ 2. Medical HX 2 ■ Current treatment of DM: medication, meal plan, activity ■ DKA frequency. If too often, why? ■ Hypoglycemic episodes, awareness ■ Any severe hypoglycemia frequency? Cause? ○ 3. Medical HX 3 ■ DM complications ● Microvascular: retinopathy, nephropathy, neuropathy. ● Macrovascular: CHD, CVD, PAD ● Dental disease. ○ Physical Examination 1. ■ HTN, wt, BMI. ■ BP determination, orthostatic measurements ■ Fundoscopic examination ■ Thyroid examination → they don’t metabolize glucose the same way as a normal person. ■ Skin exam → Acanthosis Nigricans and insulin injection sites. ○ Physical Exam 2. ■ Foot exam ■ Inspection ■ Palpation of dorsalis pedis and posterior tibial pulses → PAD detection. ■ Presence of patellar and achilles reflexes ■ Determination of proprioception, vibration (tuning fork). ● Use their big toe, they close their eyes, put their toe down, and find if they have intact prioception or no due to PAD. Could indicate imbalance state of PAD.○ Laboratory Evaluation: ■ A1C ■ Fast lipid profile, total cholesterol, LDL, HDl ■ Liver function ■ Urine ● Albumin excretion ■ Kidney ● GFR ● Creatinine ■ TSH ● Type 1 especially in woman, and women over 50 ● High risk for hypothyroidism. ● Acceptable levels for those with DM diagnosis ○ Before meals and overnight = 70-140. ○ 1 hr after meal = no higher than 180. ■ If 1 HR after meals is higher than 180, you need to increase their glucose control. ○ Two hours after meal = no higher than 150-160. ● Interventions ○ Primary prevention = delay development, especially with familial HX. ○ Secondary = already have DM, but improves glycemic control or delays complications. ○ Tertiary = already have DM, already has complication, managing complications. ○ Type 1 DM can experience hypoglycemia if they start working out without measuring their levels. ■ Ingest carb if glucose 100. ■ Delay exercise if 250. To prevent ketosis formation. ■ Type 2 don’t have these issues, but hold exercise if 250 and ketones are present. ● BP Treatment for DM. ○ Target 130/80. ○ 1st line = ACE or ARB, renal protection. ○ Thiazide diuretic added if GFR 30, normal is 90-120. ○ Loop diuretic if GFR 30. ○ If renal insufficiency + increased proteinuria = target BP is 120/75.● Monitoring ○ Ophthalmological exam annual. ○ HA1C every 3-6 months. ○ Urine screen for microalbuminuria. ■ If + means going into ESRD due to DM. ● Slide 42: Case study ○ 18-year-old female brought into the ED by her boyfriend with reports of acute onset confusion, and nausea and vomiting that has been present for two days. He reports she had been battling a “stomach bug” for the past weeks, she has been weak and tired, and sleeping most of the day. He also notes that she had been urinating several times during the day and night and had had 3 yeast infections in the past 2 months. He because worried because she did not recognize him or acted like she was not familiar. On exam you note a slender white female lying in the bed with her eyes closed. She awakens to name call and answers orientation question appropriately. ■ VS 98.1, 120, 130/75. Respirations are deep and rapid at 26 bpm. Upon standing her HR goes up to 160. ■ Oral mucosa is dry, neck veins are flat, chest clear. CV S1, S2 no murmurs, no rubs, no gallops, Abdomen is soft, +BS, mild diffuse tenderness, but no guarding or rebound. Neuro no focal deficits. ■ Laboratory Studies ● Na 133, K 5.3, CL 95, Co2 9, BUN 35, Creat 1.3, glucose 475. Arterial blood gas Ph 7.12, Pco2 24, Po2 95, ● UA drug and preg screen –, 3+ glucose 3+ketones. ■ Abdominal films: nonspecific gas patterns ○ Class discussion: ■ Kussmaul Respirations: deep, rapid breathing pattern. It is typically an indication that the body or organs have become too acidic. ■ Why BP rise when standing up? Dehydration. ■ Minute 1:23:31 on recording: ● Exam question: K+ is elevated in DKA because the dehydration will make K+ leave the cell into the bloodstream. The 5.3 is there “now” but once you correct the DKA, it will correct itself. ● Intricately, during DKAm they are in potassium depletion.● Most of the time they need K+ replacement. ■ There should not be glucose or proteins in the urine. ■ Acidotic = 7.12 ● Blood CO2 9 = equivalent to Bicarb = 9 HCO3. ● Bicarb 9 = Metabolic Acidosis. ● Metabolic equal = Bicarb and CO2 going in same direction. ● ● Type I management ○ Optimal control: 0.5 - 0.8 Units /Kg /day. ○ Initial dose 0.4 (or 0.5) Units/Kg/day. ○ Long acting gets divided by 1 = 50% of daily dose. ■ 50% basal → Usually BOD (twice a day). ■ 50% in short acting ■ Example: ● A person needs 100 units a day. ● 50 basal (long) and 50 short acting. ● 25 in AM and 25 PM (your 50% basal).○ NPH insulin regimen. ■ ⅔ in the AM and ⅓ in the PM ■ Example: PT needs 90 units total. ● So 60 units will be long acting in the AM and 30 short acting. ● Of the ⅓ PM, half is long acting and ½ is short acting. ● Dawn phenomenon: ○ Overnight tissue becomes desensitized to insulin and therefore causes a raise in BG.. 3am BG high, 7am BG high. ○ Increase evening dose or bring the night dose to 10 PM. ● Somogyi effect: ○ Nocturnal hypoglycemia leads to a surge of counter regulatory hormones leading to rise in blood sugar. ■ 3am BG low, 7am BG high. ○ Decrease night time insulin, or give snacks.● Insulin ○ ABD absorbs insulin better than other injection sites. ○ CYP1A2 metabolism. ○ Excreted in the urine. ○ Standard is 100 Units/mL. ○ Alcohol causes hypoglycemia. ○ Drug interactions: Beta blockers masks the effects of hypoglycemia. ○ Pregnant women can only use human insulin. ■ Because it doesn’t cross the placenta ■ Insulin aspart, glargine, glulisine are Category C. ○ Hypothyroidism = Delays insulin, requiring less insulin. ○ Hyperthyroidism: increased metabolic state = Increases renal inulin clearance = higher glucose = requires more insulin. ○ Lispro (Humalog) and Novolog are rapid acting. ● Serious complication ○ Ketoacidosis ○ Dehydration ○ Infection ○ Hypoglycemia from insulin overdos● DKA: ○ Diagnosis = Anion gap 12, Hyperglycemia, Ketones. ■ *Gluc 250 or more, anion, and ketones = DKA!* ■ (HHS is higher gluc’, usually 500). ■ Anion gap formula = Na - (CL + HCO3) ● Normal 10-12. ● Greater 12 = you have more ions in the plasma than normal. ■ Osmolality 275-295. ○ Presentation: ■ Polyuria, polydipsia, WT loss, N/V, mental status change, ABD pain, dehydration, kussmaul respiration, coma, vasodilation, hypothermia. ■ Most common precipitant: INFECTION. ○ Labs: hyperkalemia (false one), leukocytosis, hyperosmolality, hyponatremia (falsely low), azotemia, elevated amylase. ■ Corrected Na level check: ● Formula = 1.6 x (Glucose - 100) / 100. ● Example: PT has Na of 128 and glucose of 600. ● 1.6 x (500) / 100 = 8. ● 128 + 8 = 138 → that’s their REAL sodium. ○ Acidosis: ■ H+ goes into the cells and K+ goes out. ■ Replace potassium as you are correcting the DKA. ■ K+ is “falsely” elevated. ■ If the PT gets admitted in DKA and has low K+, do not give insulin until K+ is corrected. Otherwise you will give insulin, the insulin will drive potassium back into cells, and will lower K+ even more. ○ First thing you need to give them: FLUIDS!! ■ Every hemodynamically unstable PT gets 0.9NS.● Fluid replacement: Over 12 - 24 hrs. ■ 1st: Isotonic if in hypovolemic shock. ● Until hemodynamically stable, and urine output normal. ● 0.9 NS first 1-3 liters. ● Over 30min-1 hr. ■ 2nd: 0.45 NS 250-500mL / hr ● if normal or elevated Na. ● If Na is low = continue 0.9 Na. ● Use the “corrected Na” to decide. ● BP must be stable for Na replacements or hypotonic saline. ● Cannot give 0.9Na with Na 150. ■ 3rd: Add dextrose when serum glucose is 200. Or 250? Check that. ● Do not “drop” the glucose fast, slow process. ■ Electrolytes = K+ is usually high. ● If K 5.5, do not add KCL to fluids. ● 4.5 - 4 = add 20mEq ● 3.9 - 3 = add 40mEq ● 3 = add 60 mEq ● If K 3, do not give insulin until K+ is corrected. ○ Bicarbonate = Should not be replaced in DKA. ■ Exceptions. ● pH 7 and stop once 7.1. ● Bicard 10 ● Acidosis already induced cardiac or respiratory arrest. ● Severe hyperkalemia. ○ Insulin Tx ■ Bolus 0.12units/Kg IV ■ Regular insulin continuous ■ If glucose doesn’t fall by 50-70 mg/dL in 1 hr, double the dose. ■ If it drops by more than 100 in 1 hr, decrease drip by 50%. ■ Give 1 Sub Q dose 30 min before stopping drip.○ BG close monitoring ■ Q1H glucose checks ■ Add D5 if glucose 250 ■ Maintain BG 150-200 until anion gap closes. ■ If anion gap is not closed = DKA still exists regardless of glucose level. ■ To start subQ: ● Anion gap closes ● Bicard 18. ● PT is able to eat ● Mental status improves. ■ To stop insulin drip: ● Lispro or aspart given SC 2x the hourly IV rate. ● Long acting sc = 0.2-0.3 U/Kg ● HHS: Hyperglycemia of 600 glucose, No ketones, no acidosis, no anion gap.Type II DM - Recording lecture 2:17:02. ● Was previously called non-insulin-dependent diabetes mellitus (NIDDM) or adult-onset diabetes. ● Type 2 diabetes may account for about 90% to 95% of all diagnosed cases of diabetes. ● It usually begins as insulin resistance, a disorder in which the cells do not use insulin properly. As the need for insulin rises, the pancreas gradually loses its ability to produce insulin. → becomes the same as Type I eventually. ● Type 2 diabetes is associated with older age, obesity, family history of diabetes, history of gestational diabetes, impaired glucose metabolism, physical inactivity, and race/ethnicity. ● African Americans, Hispanic/Latino Americans, American Indians, and some Asian Americans and Native Hawaiians or Other Pacific Islanders are at particularly high risk for type 2 diabetes. → Note: Not asians for type 2. ● Type 2 diabetes is increasingly being diagnosed in children and adolescents.Type II Diabetes: Insulin resistance. ● Insufficient production of endogenous insulin. ○ Sulfonylureas: cause an increase in insulin production. ● Tissue insensitivity to insulin ○ Thiazolidinediones: Improve insulin sensitivity. ● Impaired response of beta cells ○ Meglitinides: Increase secretion of insulin. ● Excessive production of glucose by the liver. ○ Metformin: improves hepatic response to elevated BG and decreases glucose production, and decreases GI absorption. ○ Alpha-Glucosidase inhibitors: inhibit absorption of CHO in GI. ■ Cause lots of flatulence → they take it before eating a meal. ■ Causes hepatotoxicity so be careful.Complications of Type II ● HHNK ○ 400 BG, Osmolality 315, CVD, HTN, Renal Failure, P ● BG 400 ● They come in with severe cellular dehydration ○ They all get NS. Some come in with shock. ○ Start 1000 L per hr, may need more. ■ Low corrected sodium = start 0.9% NS. ■ Normal corrected sodium = 0.45% NS. ■ High corrected sodium = start them on 0.45% NS. ● Do not let the BG drop below 150-200.Secondary DM: ● Secondary causes of DM include: ○ Acromegaly ○ Cushing syndrome ○ Thyrotoxicosis ○ Pheochromocytoma ○ Chronic pancreatitis ○ Cancer. ● Drug induced hyperglycemia: ○ Atypical Antipsychotics - Alter receptor binding characteristics, leading to increased insulin resistance. ○ *****Beta-blockers***** - Inhibit insulin secretion. ■ Block “betta” cells in the heart, but also in pancreas. ○ Calcium Channel Blockers ■ Inhibits secretion of insulin by interfering with cytosolic calcium release. ○ ****Corticosteroids**** ■ Cause peripheral insulin resistance and gluconeogenesis. ○ Fluoroquinolones - Inhibits insulin secretion by blocking ATP sensitive potassium channels. ■ Cipro for chronic TB especially. ○ Niacin - They cause increased insulin resistance due to increased free fatty acid mobilization. ○ Phenothiazines - Inhibit insulin secretion. ○ Protease Inhibitors - Inhibit the conversion of proinsulin to insulin. ○ Thiazide Diuretics - Inhibit insulin secretion due to hypokalemia. They also cause increased insulin resistance due to increased free fatty acid mobilization. ● Cerebral Edema ○ Complication of DKA and HHS. ○ Most common in children but seen in adults. ○ Risk increases with rapid correction of free H2O and rapid decline in BG. ○ Sentinel sign: ■ Failure of Na to rise during treatment is a sign of excessive hydration. → you can tell if you’re giving fluids, and the Na drops.○ Management: ■ Mannitol .5-1 g/kg IV over 20 minutes repeat in 30 min- 1 hour if no response. ■ Hypertonic saline may be alternative 5-10 ml/kg over 30min. ■ Reduce the rate of fluid administered by 1/3 . ■ HOB elevated ■ Intubation for airway protection and impending resp failure ■ CT brain to eval for thrombus or hem (CT should not delay treatment). Thyroid disorders ● Case Scenario: ○ 36 years old comes for general check up, has hx of fibromyalgia, requested to have thyroid check up because her mother was recently dx with HYPOthyroidism. Complains of hair loss - and has taken supplements for that. Thyroid gland is not enlarged and the physical exam is normal. ○ Blood work: T3/T4 are elevated and TSH is low. ○ TX for now: ■ Shows Hyperthyroidism blood work, but the physical exam does not show that, so you re-check them. The reason is that BIOTIN vitamin (the supplement she is taking for hair loss) causes thyroid studies to be off. ■ TX: STOP Biotin, then redraw blood work. ● Thyroid Hormone: ○ Increase basal metabolic rate ○ Affect protein synthesis ○ Increase the sensitivity of tissue to catecholamines. ○ TRH, TSH, T3, T4 ■ TSH stimulates release of T4 (inactive). ■ T4 is converted to T3 (active form) by LIVER. ○ Iodine: necessary for that conversion. For use of thyroid hormones. ○ 5-deiodinase ○ Thyroid binding Globin ○ 99% of T3 and T4 bounded.Hyperthyroidism Hypothyroidism High metabolic state → Increased catecholamine. Dx / Labs: ● TSH is the first LAB always. ● Low TSH + Elev T3 = Hyperthyro. ○ T4 may or may not be elv’. Dx/ Labs: ● TSH elevated, normal or low T3/T4. ● TSH 10 = Clinical Hypothyroidism. Primary: ● Thyroid gland originated. ● TSH low, T3 & T4 high. ○ TRH low. Secondary: ● Amiodorone induced. ● Pituitary originary. ● TSH high, T3 & T4 high. ○ TRH low. Tertiary: ● Hypothalamus originated. ● Everything is high, even TRH! Symptoms: Hot Fine straight hair Bulging eyes Facial blushing Enlarged thyroid gland Tachycardia, HTN (sys), clubbing Breast enlargement Weight loss Muscle wasting Edema Amenorrhea Diarrhea Tremors. Symptoms: Cold Facial and eyelid edema Dull blank expression Fatigue, lethargy. Thick tongue, slow speech. Anorexia Brittle nails, hair, receding hairline, hair loss. Menstrual disturbances Muscle aches, weakness. Constipation Dry skin Depression, apathy. Late: hypothermia, brady, wt gain, dec’ LOC, thick skin, cardiac complications.Graves Disease: ● Autoimmune disease. ● Antibody attack the thyroid and cause hyperplasia. ● Lymphocytes invade thyroid and cause goiter. ● Extho-thalamus develops because thyroid and extraocular muscles share common antigen. ● Lid retraction, periorbital edema, conjunctival edema and proptosis, thyroid dermopathy over the lateral shins . ● Radioactive scan→ Inject IODINE. ○ High uptake = graves. ○ Low uptake = thyroiditis. ○ Scan identifies Graves vs Autoimmune vs Exogenous intake of T3. ● Elevated ANA → autoimmune. ● TSH low, T3 high, and T4 may or may not be elevated. Hashimotos: ● Lymphocytic infiltration of thyroid. Myxedema Coma: ● Severe hypothyroidism with AMS. ● Medical emergency. ● TX: ○ Rewarm (Slowly) ○ Synthroid ○ Glucocorticoids. ● Labs/symptoms: ○ Brady, hypotension ○ Hypoventilation. ○ Seizures, coma. ○ Hyponatremia, ele’ Cr ○ Hypoxia, hypercapnia ○ Eleva’ CSF, ○ Neutropenia with left shift ○ Elev TSH, low T4 ■ Central low TSH. TX: ● Antithyroid med ○ PTU, Tapazole. ○ PTU for pregnant women. ○ ADR: agranulocytosis: Monitor CBC, blood counts. ● Radioactive iodine. ● Sx removal ○ Always give antithyroid drugs prior to sx, to avoid thyroid storm. ● Beta blockers. ○ Propranolol ○ Esmolol. Tx: ● Levothyroxine (T4) ● Liothyronine (T3) ● Liotrix (a 4:1 mixture of T4 and T3). ● First thing in AM, nothing in the stomach. Especially: ○ Questran ○ Carafate ○ Aluminum antacids ○ Calcium carbonate. ● Estrogen increases T3/T4. ● Lithium - causes hypothyroidism, you might have to take them off.Thyroiditis = PAINFUL inflammation of the thyroid glad. ● Sub-acute = gives you the picture of hyperthyroidism = elevated T3 & T4. ● It ends up being hypothyroidism. ○ Low TSH and high T3/T4 = hyperthyroidism picture. ○ But when you do the radioactive scan, the thyroid is inflamed, and it doesn’t work, the thyroid gland will NOT take in the iodine. ○ Scan results = NO iodine reuptake = HYPO-thyroidism. ● TX: ASA (painful inflammation !!), steroids, propranolol. Nodules ● Hot = concentrate the radionuclide, always benign. ○ Dark circles in study images. ○ Active iodine tissue ○ Graves disease.● Cold = mostly benign, can be malignant. 90% of all palpable ones are cold nodules. ○ White circles in images. ○ Fine needle biopsy helps decide cancer or no cancer.Thyroid Storm = Hypermetabolism. ● Causes: ○ Graves disease. ○ hypermetabolism/physiological stress states: ■ Infections, stroke, DKA, thyroid surgery, discontinuation of antithyroid therapy, radioactive iodine treatment, pregnancy, excessive thyroid hormone replacement, MI and other cardiac emergencies. ● Treatment: ○ PTU or Tapazole orally or via NGT q 6 hours. 2 hours after the first dose give 1-2 gtts of saturated solution of K iodide or 0.5 of iopanoic acid repeat for 11 hours. ○ Propranolol initial treatment of choice for HR ■ Verapamil for HF if they have asthma. ○ Glucocorticoids for GRAVES. ○ ASA worsens thyroid storms, Lithium for iodine allergy pts.Hypothyroidism = High TSH ! Primary hypothyroidism ● Hashimoto’s thyroiditis is an immune-mediated disorder where TSH receptors are damaged. ● Subacute thyroiditis is inflammation of thyroid ● Congenital hypothyroidism Secondary hypothyroidism ● Pituitary or hypothalamic failure ● Cushing’s syndrome ● Lagtrogenic ● Overtreatment with antithyroid drugs ● Radioactive iodine, or radiation therapy Concomitant diseases (diseases that can be the cause of hypothyroidism). ● Recent acute myocardial infarction ● Coronary artery disease ○ Hypercholesterolemia and Hypertriglyceridemia ○ ST and T wave changes, QT prolongation, low amplitude QRS, Brady ○ Anginal chest pain, diastolic hypertension ● Women with osteoporosis require careful monitoring ● Infertility and menstrual irregularity may improve with thyroid hormone replacement. ● Hypothyroid evaluation should be part of depression workup. ○ Hypothyroidism = can cause severe depression. ● Pericardial effusions.Slide 19: ● 33 Y/O female presents with menstrual irregularity with long periods of amenorrhea and milky discharge from her breast. Upon further questioning, she reports headache, and changes in vision. She has no medical problems and is taking no medications. On physical examination she is noted to have galactorrhea and diminished peripheral vision bilaterally. The remainder of her exam is normal. Pregnancy test done is negative, serum prolactin levels are extremely elevated. ● What is the most common etiology? ○ Pituitary adenoma = prolactinoma. Pituitary adenoma ● Headache, Visual disturbances, Field defect, Blurred, Double ophthalmoplegia, Vertigo, Decreased libido, Gynecomastia. ● Presses on the optic chiasm. ● TX: ○ asymptomatic = Bromocriptine (dopamine agonist). ○ Symptomatic = sx is optimal. ●Pituitary apoplexy = bleeding into pituitary ● Results in hypo-pituitary function. ● Signs: visual loss, HA, N/V, double vision, stiff neck ● Sx emergency! Acromegaly ● Excess in growth hormone in adults ● Testing: ○ IGF1 level ○ Stimulate the release of growth hormone ■ Give 100 grams of Glucose ● Low glucose = increase growth hormone. ● High glucose = causes low growth hormoneAdrenal Glands ● Sits on top of the kidneys ● Adrenal cortex ○ Largest section. 90% ○ Secretes glucocorticoids and mineralocorticoids hormones . ○ Stimulated by ACTH. ○ Glucocorticoid hormones functions: ■ carbohydrate metabolism ■ Anti-inflammatory, growth-suppressing effects ■ awareness and sleep habits ■ Most potent naturally occurring glucocorticoid is cortisol. ○ Most potent mineralocorticoid = aldosterone (RAAS) . ● Adrenal medulla ○ Innervated by the para and sympathetic systems. ○ Secrete norepinephrine and epinephrine. → fight + flight response. ○ Secretes catecholamines → epi, dopamine.Adrenal Insufficiency. Cortisol = gluconeogenesis + glyconeolysis elevated glucose. Aldosterone = Na++ retention, WATER RETENTION, and K+ loss. → HYPOKALEMIA. Adrenal insufficiency (ADDISON DISEASE)= loss of cortisol and aldosterone (both). Adrenal Cortex Disorders ● Hyperaldosteronism ● Primary hyperaldosteronism (Conn disease) ○ Tumor on adrenal gland ● Secondary hyperaldosteronism ○ Renal artery stenosis = low perfusion, Renin, angiotensin, and aldosterone system activated, Na retention, and BP increase. ● HYPERALDOSTERONE Labs: ○ Hypernatremia, high fluid expansion, hypertension. ○ Hypokalemia Adrenal Medulla ● tumors derived from the chromaffin cells of the adrenal medulla ○ #1 Pheochromocytomas. ● Secrete catecholamines on a continuous or episodic basis. ○ Epi, Norepi, Dopamine.Slime 49: 30 year old man C/O increasing weakness and fatigue of two years duration. He is depressed and has episodes of dizziness. He is not eating and is losing weight. His wife notes that he is more irritable: ● Which adrenal dysfunction do you think the patient has? ○ Little cortisol (addison's disease). ● How will you work him up to confirm or deny your suspicion? ○ Refer to endo, draw cortisol levels for now. ○ Hyperpigmentation also happens from too much ACTH. Addison’s: Adrenal Insufficiency. ● Lack of adrenal hormones: Cortisol and aldosterone. ● Causes: ○ Autoimmune, TB, cancer tumor, hemorrhage, HIV, Surgical removal or Radiation of adrenal gland, Amyloidosis Sarcoidosis , Bilateral adrenal hem as a result of sepsis, HIT, trauma, Autoimmune destruction (most common cause in the US), Histoplasmosis infection, Adrenoleukodystrophy : X-Linked recessive disorder. ● Drugs Causes: ○ Ketoconazole, Fluconazole, Rifampin, Phenytoin, Barbiturates, Megestrol Acetate, Aminoglutethimide, etomidate (post op PTs), metyrapone, suramin, mitotane. ● Labs: ○ Low cortisol, low aldosterone, high ACTH, elev’ ESR, metabolic acidosis. ■ Draw cortisol first thing in the AM, as it is highest then. ○ Order: BMP (Na + K), CBC, blood cultures, cortisol level. ○ Chest x-ray, CT adrenal gland, MRI adrenal glands. ○ IF ACTH IS NOT HIGH THEN SKIN PIGMENTATION IS NOT SEEN! ○ If chronic adrenal insufficiency is secondary to pituitary failure (atrophy, necrosis, tumor), Mineralocorticoid production (controlled by the renin-angiotensin system) persists and hyperkalemia is not present. ■ If chronic = no hyperkalemia. ● Clinical presentation: ○ Hypoglycemia, weakness, hypotension, tachycardia, hyperkalemia (low aldosterone), hyperpigmentation. ○ Irregular shaped melanocytes patches, especially around mucosa. ○ Reasoning: decreased gluconeogenesis, hypoglycemia, low epinephrine, low aldosterone, high ACTH (if it’s primary insufficiency).Dx: Addison ● Two part process ○ Primary adrenocortical deficiency ○ Identification of specific cause ● Eval medical hx. ○ Physical examination, selected laboratory test. ● Rapid onset if: ○ Adrenal hemorrhage, infection, sudden discontinuation of exogenous hormonal replacement. ● Dx: Low Plasma Cortisol level at 0800. ■ especially if accompanied by simultaneous elevation in the plasma ACTH level. ■ High ACTH levels with low cortisol indicates adrenal hypofunction ● Rapid ACTH or cosyntropin stimulation test. ○ Helps determine if deficit is from adrenal gland or pituitary origin. ■ If you give ACTH and the adrenal gland is working, you will get cortisol response, so the problem is SECONDARY (pituitary), because the primary (Adrenal) is working properly. ■ If you give you ACTH and no Cortisol or aldosterone result = problem with adrenal gland = primary. ○ Test: ■ 1. Baseline cortisol and Aldosterone levels. ■ 2. Cosyntropin 0.25 mg given intravenously. ■ 3. 30-60 minutes normal adrenal function = elevated aldosterone and cortisol. ● Diagnosis if: depending on CORTISOL response from giving ACTH. ○ Cortisol values do not increase 7ug/dL after cosyntropin ad ○ Serum cortisol do not increase at least 20ug/dL within 30-60 minutes ○ Failure of aldosterone to increase by at least 4ng/dL hypofunction mineralocorticoid. ○ Random serum cortisol 25 .Water-House-Fredrichsen syndrome? → RUN with these PTs. They die quickly! ● Medical emergency → given ABX prior to lumbar puncture. ● Hemorrhage of the adrenal gland due to meningococcal infection . ○ Adrenal gland failure due to bleeding into the adrenal glands ● Severe bacterial infection: Neisseria meningitidis. Scenario by Dr. Morton: THIS IS WHAT YOU NEED TO UNDERSTAND. ● Pt comes in with adrenal insufficiency: Low Sodium, low gluc, potassium is high. ○ You give ACTH and nothing happens = Primary adrenal insufficiency. ■ Primary: not producing glucocorticoid or mineralocorticoids. ● Give BOTH → Glucocorticoids (steroids like solumedrol) and mineralocorticoids (fludrocortisone). ○ You give ACTH and they do make cortical + aldosterone. ■ Secondary: Pituitary apoplexy or tumor → MRI ! Addisonian Crisis → rapid withdrawals from STEROIDs! TX: ● Hydrocortisone 100-300 IV, fluids, vasopressors, tx underlying cause.Slide 73: A 35 Y/O female experiences anterior pituitary hemorrhagic necrosis (Sheehan Syndrome) After postpartum hemorrhage. She feels light-headed, dizzy, and weak. Which of the following hormones is most likely responsible. ● Sheeham syndrome = pituitary apoplexy = no ACTH secretion = no CORTISOL. ● Probably gluc is low, BP low because no Aldosterone, due to no ACTH = no mineral or glucocorticoids at all. ● TX: ○ Hydrocortisone (glucocorticoid) and Fludrocortisone (mineralocorticoids). ○ Tx all infections. Cushing’s Disease and Syndrome ● Disease = pituitary = excess ACTH. ● Syndrome