INTERNAL MEDICINE EOR EXAM REVIEW CRITICAL CARE
Acute adrenal insufficiency
MC cause of primary adrenal insufficiency is Addison dz Adrenal crisis occurs in the following situations:
1) stress
2) sudden withdrawal of adrenocortical hormone in pt with chronic insufficiency or chronic use of corticosteroids = MC cause of secondary insufficiency
3) following bilateral adrenalectomy or removal of a functioning adrenal tumor that had suppressed the other adrenal
4) following sudden destruction of the pituitary gland (necrosis) 5) when thyroid hormone is given to pt with hypoadrenalism
6) following injury to both adrenals by trauma, hemorrhage, anticoag therapy, thrombosis, infection following admin of etomidate – used for IV anesthesia induction or intubation
s/s: h/a, lassitude, n/v, abd pain, diarrhea, confusion, coma, fever >40.6, low BP sometimes: cyanosis, dehydration, skin hyperpigmentation, sparse axillary hair hypoglycemia with lessening required need for insulin in Type I DM pts Lab: eosinophil count high, Low Na and high K, Hypoglycemia, >’d Ca
Dx made by: cosyntropin stimulation test (normal cortisol level is >20 mcg/dL) and plasma ACTH (>200 pg/mL)
Tr: 2 phases
1) acute phase: draw blood to determine cortisol level and treat with hydrocortisone 100-300 mg IV and saline immediately without waiting for the results. Following, give hydrocortisone phosphate or hydrocortisone sodium succinate 100 mg IV immediately and continue IV infusions 50-100 mg q 6 hrs for 1st day. Give the same amt every 8 hrs on the 2nd day, then adjust dose based on clinical picture.
2) Convalescent phase: hydrocortisone PO 10-20 mg q6hrs, and reduce to maintenance level as needed (typically given q12hrs 10-20 mg am and 5-10mg pm + fludrocortisone acetate .05-.2mg PO daily.
After rapid treatment and crisis has passed, assess for possible cause and permanent treatment options Thyroid storm Extreme thyrotoxicosis triggered by:
1) stressful illness 2) thyroid sx
3) RAI administration
s/s: marked delirium, severe tachycardia, vomiting, diarrhea, dehydration, very high fever mortality high
tr: thiourea drug (eg methimazole 15-25 mg PO qhrs) or propylthiouracil 150-250mg PO q6hrs) + Ipodate sodium 500 mg/day PO 1 hr after thiourea
+ iodine (Lugol solution 10 drops 3x’s/day PO or sodium iodine ig IV slowly) given 1 hr later + propranolol 0.5-2mgIV q4hrs or 20-120 mg PO q6rs
+ hydrocortisone is usually given in doses of 50 mg orally q6hr (reduce rapidly as pt improves) Diabetic
Ketoacidosis/acute hypoglycemia
Can be initial manifestation of type I DM, or d/t >’d insulin requirement in type 1DM during infection, trauma, MI, or sx; may occur in Type 2DM with severe stress (sepsis, trauma)
Mortality greater in elderly than <40 Poor compliance = MC cause
s/s: precedes with polyuria, polydipsia, fatigue, n/v, mild hypothermia, hypotension and tachycardia, cholecystitis or pancreatitis -> mental stupor -> coma
PE: stuporous pt w/ rapid deep breathing and a “fruity” breath odor of acetone = strong suggestion of dx Labs: moderately severe:
Glucose 350-900 mg/dL
Serum ketones at a dilution of 1:8 or greater
Hyperkalemia 5-8 mEq/L – occurs despite total body K depletion b/c shift of K from intra to extracellular spaces d/t systemic acidosis
Slight hyponatremia 130 mEq/L – d/t vomiting and polyuria Hyperphosphatemia 6-7 mg/dL
Elevated blood urea nitrogen and serum creatinine Acidosis severe ranging from 6.9-7.2
Serum bicarb 5-15 mEq/L
PCO2 is low related to hyperventilation Fluid depletion
Hyperosmolar coma – occurs when osmolality exceeds 320-330 Mild = pH 7.25-7.3 – alert – treat in ER
Mod = pH 7.0-7.24 – either alert or a little drowsy – admission to ICU Severe = <7.0 – stuporose – admission to ICU
Treatment:
1) gastric intubation to prevent vomiting/aspiration 2) indwelling cath
3) Swan-Ganz cath to motior hypovolemia in pts with preexisting cardiac or renal insuff. 4) Blood glucose and electrolytes recorded every hour, pH q2hrs
5) No opioids and sedatives
6) Fluid replacement – 0.9%saline = fluid of choice 1L/hr for 1st 1-2 hrs; after 2L, infuse 300-400 mL/h – not to exceed 5L in 8 hrs; if glucose falls, change to 5%glucose-containing solution
7) Insulin replacement – after fluid replacement has started, give regular insulin IV bolus 0.1 unit/kg, followed with 0.1 IV unit/kg/h continuously infused – corrects acidosis; if glucose doesn’t fall in 1st hour, then another bolus 0.1 should be given
8) Potassium – once acidosis is fixed, then K flows back into cells and hypokalemia can result – substitute with KCl 10-30 mEq/h in 2nd or 3rd hour after of therapy; if K is <3.5, delay insulin until level is >3.5. EKG monitoring necessary
9) Sodium Bicarb – severe cases when pH <7.0 – 1 or 2 ampules to 1L of .45% saline rapidly – given only until pH reaches 7.1 = fatal arrhythmia
10) Phosphate - only in severe hypophosphatemia < 1 mg/dL
Hyperchloremic acidosis – usually resolves by itself after 12-24 hrs after initiation of treatment Acute glaucoma Only occurs with closure of preexisting narrow anterior chamber angle
Predisposing factors: age, farsightedness, inheritance (Asians and inuits)
Primary - Usually precipitated by pupillary dilation – dark rooms, times of stress, sympathomimetic agents Secondary causes: ant uveitis, dislocation of lens, or topiramate.
s/s: extreme pain, blurred vision, halos around lights, nausea, abd pain possible, eye is red, cornea cloudy, pupil moderately dilated and nonreactive to light
IOP >50 mm Hg Tr: primary:
Reduction of IOP – single 500 mg IV acetazolamide followed by 250 mg PO 4x’s/day
Osmotic diuretics – glycerin PO and urea or mannitol IV 1-2 g/kg – may be necessary if there is no response to acetazolamide
Laser therapy to peripheral iris or ant chamber paracentesis
After IOP has <’d, topical 4% pilocarpine, 1 drop q15min FOR 1 HR AND THEN 4X’S/day - to reverse underlying angle closure
Definitive tr = laser peripheral iridectomy or surgical peripheral iridectomy.
Prophylactic laser peripheral iridotomy to unaffected eye should be done, unless it has already been done Secondary: systemic acetazolamide
Pulmonary embolism
Can be d/t air, amniotic fluid, fat, foreign bodies, parasitic eggs, septic emboli (infectious endocarditis), tumor cells.
MC = thrombus, which can arise anywhere in venous system. MC = DVT in lower leg that propagate proximally to the popliteal and ileofemoral veings
50-60% of DVT will develop into a PE
leads to right ventricular failure, hypoxemia through right to left shunting, <’d cardiac output, and surfactant depletion
reflex bronchoconstriction promotes wheezing and >’d work of breathing s/s: difficult to dx
dyspnea and pain on inspiration, tachypnea, chest pain with breathing, 30% hemoptysis, coughing labs: ECG NORMAL, arterial blood gases – hypoxia with normal chest radiograph in absence of preexisting lung dz is highly suspicious for PE; D-Dimer elevation; Toponin I, Troponin T and plasma beta-natriuretic peptide (BNP) elevation
imaging: CXR – to r/o other lung dz
CT – helical CT pulmonary angiography for initial dx study for suspected PE V/Q scan – not as specific
Venous ultrasound – to assess proximal DVT Pulmonary angiography = reference standard for dx Tr:
Anticoag – not definitive, but more preventative – Heparin + 6 mo of Warfarin
Thrombolytic tr – Streptokinase, urokinase, and recombinant tissue plasminogen activator (rt-PA, alteplase) – contraindicated in those with uncontrolled HTN and surgery/trauma in last 6 wks
Possible IVC filter for recurrent and high risk pts
Surgical extraction for high risk pts who can’t tolerate thrombolytic therapy Well’s criteria for Risk of DVT:
CLINICAL FEATURE POINTS
Active cancer (treatment within 6 months, or palliation) 1 Paralysis, paresis, or immobilization of lower extremity 1 Bedridden for more than 3 days because of surgery (within 4 weeks) 1
Localized tenderness along distribution of deep veins 1
Entire leg swollen 1
Unilateral calf swelling of greater than 3 cm (below tibial tuberosity) 1
Unilateral pitting edema 1
Collateral superficial veins 1
Alternative diagnosis as likely as or more likely than DVT −2 Total points:
Risk score interpretation (probability of DVT): 3 points: high risk (75%); 1 to 2 points: moderate risk (17%);<1 point: low risk (3%).
Wells criteria for PE:
CLINICAL FEATURE POINTS
Clinical symptoms of DVT 3
Other diagnosis less likely than PE 3
Heart rate greater than 100 beats per minute [corrected] 1.5 Immobilization or surgery within past 4 weeks 1.5
Previous DVT or PE 1.5
Hemoptysis 1
Malignancy 1
Risk score interpretation (probability of DVT): >6 points: high risk (78.4%); 2 to 6 points: moderate risk (27.8%); <2 points: low risk (3.4%)
Acute Respiratory Distress/failure
Acute hypoxemic respiratory failure following a systemic or pulmonary insult w/o evidence of heart failure. d/t pro-inflammatory cytokines relased from stimulated inflammatory cells causing lung injury; causes < surfactant production, leading to pulmonary edema, alveolar collapse, and hypoxemia
Risk factors: sepsis, aspiration of gastric contents, shock, infection, lung contusion, nonthoracic trauma, toxic inhalation, near-drowning, and multiple blood transfusions
s/s: profound dyspnea (12-48 hrs after event), labored breathing, tachypnea, intercostal retractions, and crackles.
labs: CXR shows bilateral widespread pulmonary infiltrates. Patchy and diffuse -> confluent, sparing costophrenic angles.
Can cause multiple organ failure, particularly kidneys, liver, gut, CNS, and CV systems.
Tr: ID and treat underlying precipitating and secondary conditions. Hypoxemia tr with intubation and positive pressure ventilation. Lowest level of PEEP and supplemental O2 required to maintain PaO2 above 55mgHg or SaO2 >60%, not to exceed 60% FiO2.
Hemodynamic monitoring and fluid management for pts with acute lung injury
Pneumothorax Accumulation of air in pleural space, classified as spontaneous (primary or secondary) or traumatic: Traumatic: penetrating or blunt trauma
Iatrogenic: following procedures – thoracocentesis, pleural biopsy, subclavian or internal jugular vein catheter placement, percutaneous lung biopsy, bronchoscopy with transbronchial biopsy, and + poressure mechanical vent
s/s: acute onset of unilateral chest pain and dyspnea, minimal physical exam findings in mild cases; unilateral chest expansion, <’d tactile fremitus, hyperresonance, diminished breath sounds, mediastinal shift, cyanosis and hypotension in tension pneumo
presence of pleural air on CXR
Angina pectoris Stable Angina Unstable Angina
Signs & symptoms
-Gradual onset chest pain due to myocardial ischemia that occurs predictably and reproducibly on exertion -May also have SOB
-Relieved by rest or NG -Usually lasts 2-5 minutes -Diffuse discomfort Management
-Goal is to relieve symptoms and prevent future cardiac events
-Nitrates and β-blockers are initial DOCs -CCB for refractory symptoms
-Exercise -Daily aspirin
-CV risk reduction: BP control, smoking cessation, statins, weight reduction, glycemic control -Periodic reevaluation with EKGs
-Revascularization therapy an option for select candidates
Signs & symptoms
-Chest pain refractory to NG treatment or chest pain at rest or nocturnally
-May be associated with SOB, nausea, diaphoresis Management
-Treat like other ACS: admission, MOANS, serial troponins, EKGs
-Stabilize
-Antiplatelet therapy and possible reperfusion for select patients
- β-blockers -Statins
-ACEI with DM, HF, LV EF < 40%, or HTN -CV risk reduction
MI Signs & symptoms
-Sudden onset chest pain, nausea,
vomiting, diaphoresis, SOB
-Jaw, neck, scapular, throat, or arm pain -DOE
-Chest pain > 30 min not responsive to NG -Hypovolemia -HTN or hypotension -Tachy or bradycardia -S3 or S4 -Signs of CHF -Systolic murmurs -Friction rub if day 2 or later
-Remember that women, the elderly, and diabetics may have atypical presentations
Workup
-Obtain 12 lead within 10 min of arrival and repeat every 10 minutes if initial EKG is not diagnostic (1st EKG is negative 40% of the time)
-Look for early peaked T waves, ST elevation, Q waves, J point elevation -NSTEMI does not have EKG changes because the infarction is in an
electrically silent area
-Emergent cardiac consult for patients with cardiogenic shock, left heart failure, or sustained ventricular tachyarrhythmia -Electrolytes, coagulation studies, H/H -Serial troponins: specific cardiac damage marker, including damage from defibrillation, arrhythmias, cardiac procedures, CHF, vasospasms, etc; elevation begins within 1 hour and remains ↑ for 5-14 days
-CK: found in skeletal muscle throughout the body; shows up in 1-6 hours and lasts up to 1.5 days
-CK-MB: cardiac specific CK; shows up in 2 hours and declines after 24-72 hours Emergent Management (any ACS)
Additional STEMI Treatment
-Antiplatelet and anticoagulant therapy for all patients (in addition to aspirin)
-Emergent stent if < 3 hours from symptom onset -Alternative is lytic therapy if not contraindicated, symptoms < 12 hours, and PCI unavailable within 90-120 minutes
-CABG rarely performed during acute MI Additional NSTEMI Treatment
-Antiplatelet therapy for all patients (in addition to aspirin)
-Anticoagulant therapy for all patients
-Invasive intervention based on presence of high risk factors (recurrent angina at rest, elevated troponin, ST depression, high risk stress test result, EF < 40%, hemodynamic instability, sustained VT, recent PCI, prior CABG)
Treatment of Cocaine-Related ACS -Benzos every 15 minutes PRN -DON’T give β-blockers Prognosis
-33% are fatal
-Complications: CHF, RV infarction, ventricular rupture, arrhythmias, mural embolus, stroke, pericarditis, postinfarction angina
-Morphine, oxygen (only if sats < 90% or resp distress), aspirin, NG
-Treat HF if present with NG, furosemide
-Give β-blocker if HF is not present in order to reduce myocardial oxygen demand
-Begin 80 mg atorvastatin for pts not already on
of death, recurrent MI, or need for urgent revascularization using TIMI score (Skyscape)
Cardiac arrest Abrupt cessation of cardiac mechanical function, which may be reversible by a prompt intervention but will lead to death (sudden cardiac death) in its absence; complete cessation of heartbeat
Mechanism: Ventricular fibrillation, ventricular tachycardia, asystole, bradycardia, pulseless electrical activity, mechanical factors
Structural causes: Coronary heart dz, coronary abnormalities, chronic atherosclerotic lesions, thrombosis, MI (acute or healed), Myocardial hypertrophy; hypertrophic cardiomyopathy (obstructive, nonobstructive), dilated cardiomyopathy, inflammatory and infiltrative disorders (myocarditis, noninfectious inflammatory dz, infiltrative dz), valvular heart dz,electrophysiologic abnormalities, WPW syndrome, conducting dz
Function contributing factors: coronary blood flow alterations, transient ischemia, reperfusion after
ischemia, low cardiac output states, HF (chronic, acute, shock), systemic metabolic abnormalities (electrolyte imbalance, hypoxemia, acidosis, neurologic distrubances), toxic responses (cocaine, digitalis, drug
interactions)
s/s: Usually, the first sign of sudden cardiac arrest (SCA) is loss of consciousness (fainting). At the same time, no heartbeat (or pulse) can be felt.
Some people may have a racing heartbeat or feel dizzy or light-headed just before they faint. Within an hour before SCA, some people have chest pain, shortness of breath, nausea (feeling sick to the stomach), or vomiting.
Dx: EKG, Echo, cardiac MRI, cardiac cath, electrophysiology, CMP (electrolyte abnormalities), BNP, troponin, CPK-MB
Tr: CABG, PCI, ICD, angioplasty Cardiac
arrhythmias and blocks
Bradyarrhythmias
-Either a delay in impulse formation or conduction Etiologies -Hypoxia -↑ ICP -Hypothermia -Hypothyroid -Hyperkalemia -Sarcoidosis or amyloidosis
-Degenerative disease of conduction system -Ischemia
-Lyme
-Rheumatic heart disease
-Drugs: CCBs, β-blockers, digoxin
Signs & symptoms -Syncope or presyncope -Dyspnea from CHF -Angina pectoris -Hypotension Differential
-Regular rate sinus brady, complete heart block,
2:1 AV block, sinus arrest with escape rhythm, “regularized” slow a-fib
-Irregular rate sick sinus syndrome,
2° AV block (Wenckebach or Mobitz type II), slow a-fib
Management
-Treat underlying cause -Meds
-Pacemaker or transcutaneous pacing -Emergent: atropine
-Either a result of abnormal impulse
formation or abnormal propagation (reentry) -Risk factors for SVT: hyperthyroid, HTN, mitral valve disease, COPD, post cardiac surgery
-Risk factors for VT: prior MI, ischemia, long QT syndrome, antiarrhythmics, TCAs, hypoMg, hypo or hyperK
Signs & symptoms -Syncope or presyncope -Palpitations
-Diaphoresis -Chest pain Differential
-Narrow complex afib, multifocal atrial tachycardia, aflutter, atrial tachycardia, sinus tachycardia, WPW, junctional tachycardia, AVNRT
-Wide complex torsades, polymorphic VT, AF with aberrant conduction, VT, SVT
Workup
-Labs to exclude underlying exacerbating conditions: BMP, Mg, digoxin levels, TSH
Management
-Cardioversion for any tachyarrhythmias if there is hemodynamic instability; add amiodarone if VT is involved
-Transcutaneous pacing for torsades
-If stable SVT, can try vagal maneuvers, adenosine, beta blockers, CCBs, or digoxin
-For stable VT, lidocaine is DOC
-Atrial fibrillation or flutter: control ventricular response with CCB, beta blockers, or digoxin, and consider anticoagulation with warfarin; can electrically or chemically cardiovert but afib may recur
-VT: beta blockers if asymptomatic and nonsustained, ICD placement if more severe due to risk of death
-Torsades: IV magnesium and phenytoin AV Blocks Signs and symptoms Management
First degree
-Asymptomatic -Treat reversible causes such as ischemia, increased -EKG showing lengthened PR interval vagal tone, or meds; pacemaker usually not -Determine site of block using EKG recommended
findings, atropine, exercise, or vagal maneuvers
-Treat reversible causes such as ischemia, increased vagal tone, or meds
-Pacemaker usually not recommended Second
degree Wenckebac h Mobitz I
-Typically asymptomatic -Treat reversible causes; pacemaker if there is -EKG shows progressive PR symptomatic bradycardia
prolongation for several beats prior to nonconducted P wave
-Beats classically occur in ratios of 3:2, 4:3, or 5:4 -Can be a result of inferior MI
-Treat reversible causes such as ischemia, increased vagal tone, or meds
-Pacemaker if there is symptomatic bradycardia
Mobitz type II
-May be asymptomatic or have signs of -Treat reversible causes; most pts will required pace hypoperfusion or HF
-PR interval remains unchanged prior to a nonconducted P wave
-Treat reversible causes such as ischemia, increased vagal tone, or meds
-Most patients will require a pacemaker Third
degree
-May have dizziness, presyncope, syncope, v-tach, v-fib, worsening HF, or angina -P waves don’t correlate to QRS
-Escape rhythm takes over for QRS (junctional or ventricular)
1st degree EKG:
Mobitz type II:
3rd degree:
Cardiac failure Most often a result of ischemic heart disease (systolic HF) myocardial remodeling -Other causes: bad valves, HTN (diastolic HF), myocarditis, pericarditis, alcoholism (R HF), substance abuse, COPD or other lung disease (R HF)
-Usually associated with low cardiac output but can be high Acute/flash pulmonary edema with acute MI, severe illness, PE, HTN, end stage valvular disease Beware acute HF with massive MI, tachyarrhythmias, or endocarditis with valve rupture: severe SOB, cool skin,
diaphoresis, AMS, pallor, cyanosis Decompensated HF with new or worsening sx, new murmur, pt is “cold and wet”, CHF “decision rule” predicts 30 day mortality, avoid β-blockers
Signs & symptoms -R CHF ascites, + hepatojugular reflex, weight gain, JVD, hepatomegaly, edema, abdominal distension, mostly clear lungs with dullness at the bases, ↑ JVP with hepatojugular reflux, tricuspid regurg, peripheral edema
-L CHF (mostly heart and lung sx) dyspnea, cough, S3 or S4, crackles, wheezes, dullness at bases, frothy or pink sputum, pulse alternans (alternating strong-weak pulse), palpitations, fatigue,
diaphoresis, displaced PMI, mitral regurg, pulmonary edema, orthopnea, PND But research shows there are no hard and fast physical exam differentiations for R vs L CHF; all of these s/s can overlap!
Workup
-Referral for echo -EKG for LVH -Stress test
-CXR for pulmonary edema (Kerley B lines)
-Labs: BNP, CBC, CMP, fasting glucose, lipids -Cardiovascular MRI can help distinguish ischemic heart disease from cardiomyopathy
Other Management
-Salt restriction, daily weights -Avoid NSAIDs, CCBs
-ATP III recommends giving aspirin to reduce prothrombotic state -Exercise training program for stable NYHA class II to III -Devices: AICD, intra-aortic pump, LVAD
Drugs with proven mortality benefit
-Note that there is only evidence for systolic HF for these drugs; use with diastolic CHF is not yet substantiated -ACEI or ARB
-Hydralazine + isosorbide dinitrate: most beneficial for black man as an add on therapy to those already on β-blocker and ACEI that are still symptomatic
-β-blockers
-Aldosterone antagonists Prognosis
-Diet and prescription noncompliance are a major cause of hospital readmission for CHF Main causes of death are arrhythmia and progressive pump failure
Hypertensive crisis Hypertensive urgency = stable or no end organ damage, no raised ICP -May have SOB, headache, BPs usually > 220/110
-Tx is to lower BP in clinic slowly over several hours (≤160/100) with labetalol, clonidine, captopril -Close follow-up
Hypertensive emergency = rapidly progressing end organ damage -Papilledema if malignant
-Chest pain, AMS, weakness, MI, acute CHF, renal failure, ICH, eclampsia, aortic dissection -Don’t lower BP by more than 25% original value
Monitoring HTN:
-Annual urine microalbumin -Annual BMP
-Annual lipids
-Baseline EKG, look for LVH
Pharm for HTN single agents only lower by 10-20 mm Hg, may need a 2nd agents
Thiazides: HCTZ, chlorthalidone -DOC for HTN but can’t use once CrCl < 30 -Ca sparing = good for osteoporosis pts -Need to check BMP before and after starting
-Chlorthalidone has the most evidence but my preceptor thinks it causes a lot of hypokalemia
Loops: furosemide K-sparing: spironolactone, eplerenone
Not very potent ACEi’s: benazepril, enalapril,
lisinopril
-Cough
-Can cause renal failure = need to monitor BMP 1 week and 1 month after starting and periodically after that, STOP if serum Cr ↑ by 30% -Ok to use in patients with no renal function left
-Pregnancy D ARBs: irbesartan, losartan,
olmesartan, valsartan
-Same AEs as ACEIs and also pregnancy D CCB’s: dihydropyridine (nifedipine,
amlodipine)
and non-dihydropyridine (verapamil and diltiazem)
-Useful in the elderly
-FDA warning about amlodipine, verapamil, and diltiazem use with simvastatin
-Contraindicated in heart failure Other direct vasodilators: hydralazine, minoxidil
α-blockers -Clonidine: only for refractory HTN due to risk of falls -Methyldopa: DOC for HTN in pregnancy
β-Blockers -Questionable role in the treatment of essential HTN unless patient also has CHF or MI
-Need strict β-1 blockers for asthma/COPD patients so that bronchial relaxation is not blocked (atenolol or metoprolol)
-Propranolol and labetalol block at multiple sites -Can mask signs of hypoglycemia
-Contraindications: heart block Acute
Gastrointestinal bleed
Upper GI bleed causes: coffee ground or red hematemesis -> bleeding proximal to the ligament of Treitz. Frank blood -> mod to severe bleeding that may be ongoing; coffee ground -> limited bleeding
Lower GI bleed: melena (black tarry) proximal to the ligament of Treitz; Hematochezia (red or maroon blood in stool) -> lower GI bleed or massive upper GI bleed that’s associated with orthostatic hypotension
Potential sources of GI bleed: varices or portal hypertensive gastropathy w/ liver dz or alcohol abuse Aorto-enteric fistula
Angiodysplasia PUD w/ H pyolori
Medication hx – aspirin or NSAID use, antiplatelet agents, iron, bismuth Esophageal ulcer
Mallory-weiss tear Variceal hemorrhage Malignancy
PE: mild to mod hypovolemia (resting tachy), stool color, abd pain, rebound tenderness and involuntary guarding can indicate perforation
Lab: CBC (hemoglobin loss with normocytic/chromic RBC’s), CMP, ALT/AST, Alk Phos, PTT/PT, INR, EKG, cardiac enzymes with MI risk pts with chest pain/dyspnea; elevated BUN/CR ratio (higher ratio = upper GI) Dx studies: upper endoscopy, angiography for upper GI, colonscopy for Lower GI bleed
Triage: all pts w/ hemodynamic instability -> admit to ICU for resuscitation and close monitoring
Oxygen, fluid resuscitation (500mL normal saline or lactate Ringer over 30 minutes), type and crossed, and transfused for pts <7 g/dL hemoglobin (with the exception of variceal bleeding, only transfuse to <10 g/dL) Meds: PPI, prokinetics (erythromycin or metoclopramide) for upper GI bleed to clear visualization for endoscope, Somatostatin for variceal bleeding (Octreaotide 20-50 mcg bolus + 25-50 mcg/hr; ABX for pts with cirrhosis
SEIZURES History & Physical Focal seizures:
w/o impairment of consciousness aka “simple partial” seizures - focal motor symptoms (convulsive jerking)
- somatosensory symptoms (eg, paresthesias or tingling) that spread (or “march”) to different parts of the limb or body
- special sensory symptoms (eg, light flashes or buzzing) indicate involvement of visual, auditory, olfactory, or gustatory regions of the brain
- there may be autonomic symptoms or signs (eg, abnormal epigastric sensations, sweating, flushing, pupillary dilation).
- The sole manifestations of some seizures are phenomena such as dysphasia, dysmnesic symptoms (eg, déjà vu), affective disturbances, illusions, or structured hallucinations, but such symptoms are usually accompanied by impairment of consciousness.
With impairment of consciousness – aka “complex partial” seizures
- Impaired consciousness or responsiveness may be preceded, accompanied, or followed by the various symptoms mentioned above, AND automatisms may occur.
Absence seizures
- impairment of consciousness, sometimes w/ mild clonic, tonic, or atonic components (ie, reduction or loss of postural tone), autonomic components (eg, enuresis), or accompanying automatisms
- Onset and termination of attacks are abrupt
- If attacks occur during conversation, the patient may miss a few words or may break off in midsentence for a few seconds.
- The impairment of external awareness is so brief that the patient is unaware of it - Absence (“petit mal”) seizures almost always begin in childhood and frequently cease by
the age of 20 years or are then replaced by other forms of generalized seizure. Atypical absence seizures
- More marked changes in tone or attacks may have more gradual onset and termination than in typical absence seizures
- Commonly occur in patients w/ multiple seizure types, may be accompanied by developmental delay or mental retardation
Myoclonic seizures
- Myoclonic seizures consist of single or multiple myoclonic jerks. Tonic-clonic (“grand mal”) seizures
- Tonic phase - sudden loss of consciousness, the patient becomes rigid and falls to the ground, and respiration is arrested; usually lasts for < 1 min
- followed by a clonic phase - jerking of the body musculature that may last for 2 or 3 minutes
- followed by a stage of flaccid coma
- During the seizure, the tongue or lips may be bitten, urinary or fecal incontinence may occur, and the patient may be injured. Immediately after the seizure, the patient may recover consciousness, drift into sleep, have a further convulsion without recovery of consciousness between the attacks (status epilepticus), or after recovering consciousness have a further convulsion (serial seizures).
- In other cases, patients will behave in an abnormal fashion in the immediate postictal period, without subsequent awareness or memory of events (postepileptic automatism). - Headache, disorientation, confusion, drowsiness, nausea, soreness of the muscles, or some
combination of these symptoms commonly occurs postictally. Tonic, clonic, or atonic seizures
- Loss of consciousness may occur with either the tonic or clonic accompaniments described above, especially in children. Atonic seizures (epileptic drop attacks) have also been described.
Symptoms & Signs
- Nonspecific changes such as HA, mood alterations, lethargy, myoclonic jerking alert some patients to an impending seizure hours before it occurs
- External precipitants o Lack of sleep o Missed meals o Emotional stress o Menstruation o Alcohol ingestion o Use of certain drugs
o Fever and nonspecific infections
- In a few patients, seizures are provoked by specific stimuli – flashing lights, flickering TV set (photosensitive epilepsy), music, or reading
Physical exam
- Exam b/w seizures shows no abnormality in patients with idiopathic epilepsy - In immediate postictal period, extensor plantar responses may be seen
- Presence of lateralized or focal signs suggest that seizures may have a focal origin - In symptomatic epilepsy, findings on exam will reflect underlying cause
Diagnostic studies - MRI is indicated for patients with focal neurologic symptoms or signs, focal seizures, or electroencephalographic findings of a focal disturbance
- some clinicians routinely order MRI for all patients with new-onset seizure disorders - studies should be performed in patients with clinical evidence of a progressive disorder
and in those with new onset of seizures after the age of 20 years because of the possibility of an underlying neoplasm.
- Initial investigations should include CBC, serum glucose, electrolytes, creatinine, calcium, magnesium, and liver function tests to exclude various causes of seizures and to provide a baseline for subsequent monitoring of long-term effects of treatment
- A lumbar puncture may be necessary when any sign of infection is present or in the evaluation of new-onset seizures in the acute setting.
- Electroencephalography may support the clinical diagnosis of epilepsy (by demonstrating paroxysmal abnormalities containing spikes or sharp waves), provide a guide to prognosis, and help classify the seizure disorder.
Diagnosis DDx of focal seizures - TIA - Panic attacks DDx of generalized seizures - Syncope - Cardiac disease - Brainstem ischemia
Clinical
therapeutics Monotherapy - Monotherapy is preferable to the use of several drugs because fewer toxic effects, less likelihood of drug interactions, and better compliance.
- The drug of choice should be slowly increased until seizures are controlled or until clinic of toxicity develop.
- If seizures are not adequately controlled at the maximum to dosage, a second AED is slowly introduced. After the second drug attains therapeutic levels, the first drug is gradually withdrawn.
- Monotherapy adequately control onset epilepsy in about two-thirds of the patients. Polytherapy
- Polytherapy with a combination of two AEDs (usually one traditional and one newer AED) may necessary only if monotherapy with two or more first-line AEDs been unsuccessful.
- When using two AEDs, select those with different mechanism of action. - Avoid using more than two AEDs simultaneously.
After two appropriate AEDs fail to control seizures, monotherapy with a third AED or polytherapy is successful in only 4% of the patients.
STATUS EPILEPTICUS
History & Physical - A brief history and physical examination should be directed toward discovery of the cause of the seizures and to any injury that may have resulted
- Any of the causes of seizures may result in status epilepticus Clinical
Therapeutics Initial Supportive Care 1. Maintain airway with cervical spine precautions.
2. Deliver oxygen by nasal cannula.
3. Monitor ECG and blood pressure.
4. Maintain normal temperature. Pharmacologic Therapy
1. Establish IV, administer thiamine 100 mg IV
2. Administer 1 amp of D50 IV in an adult unless obviously hyperglycemic.
3. Administer IV lorazepam or diazepam initially (midazolam 0.2 mg/kg)
o Lorazepam is considered the initial agent of choice d/t it’s longer duration of action (12-24 h); more effective than phenytoin or phenobarbital
4. If seizures persist, give fosphenytoin or phenytoin.
o Phenytoin should not be mixed with any glucose-containing IV fluid and should not be given IM due to erratic absorption. The drug is contraindicated in the presence of second- or third-degree atrioventricular block
5. If seizures persist, give phenobarbital, paraldehyde.
6. If still no response, obtain emergency neurosurgery and anesthesiology consultations. Scientific concepts Definition: The traditional definition of status epilepticus (SE) is a prolonged seizure, or cluster of
seizures, without a return to baseline, lasting longer than 30 minutes. A revised operational definition, proposed to lower morbidity and mortality, is any seizure lasting more than five minutes.
SHOCK History & Physical History
- Check for unsuspected trauma, unsuspected/known pregnancy, new meds, allergies, overdose, or depression
- Look for potential drug interactions such as sildenafil & nitroglycerin - Obtain travel hx (SARS)
- Tampon-use hx (toxic shock syndrome) - CP & dyspnea ACS or PE
- Fever or hypothermia sepsis Essentials of diagnosis
- Hypotension, tachycardia, oliguria, altered mental status, metabolic acidosis d/t elevated lactic acid
- Peripheral hypoperfusion and impaired oxygen delivery Hypovolemic shock (20-30% volume loss)
- Oliguria, AMS, cool extremities, jugular venous pressure is low, narrow pulse pressure Cardiogenic shock
- L-sided heart failure: pulmonary edema - R-sided heart failure: peripheral edema, JVD Distributive shock
- Hyperdynamic heart sounds - Warm extremities initially
Diagnostic studies Labs
- CBC, coagulation studies, electrolytes, BUN, creatinine, arterial blood gas, and serum lactate - In septic shock, obtain pan cultures.
- Obtain urinalysis in all patients and perform urine pregnancy testing in all women of child-bearing age.
- Type and crossmatch the patients for packed RBCs. - In cardiogenic shock, obtain cardiac enzymes. Imaging
- A chest radiograph and ECG are valuable initial examinations with further testing dictated by clinical suspicion
- Bedside U/S can have a key role with evaluation of pericardial fluid and hemoperitoneum but complex imaging studies should wait until the patient is resuscitated.
Diagnosis
Clinical
therapeutics - - ABCs Establish multiple short-length, large-bore peripheral IV access - Cardiac monitor
- Identify if reversible condition
o Traumatic blood loss – CXR, US
o Nontraumatic blood loss – check for abd mass (AAA), GI bleed o Dysrhythmia
o Tension pneumothorax o Cardiac tamponade
o Massive pulmonary embolism o Overt anaphylaxis
o Spinal cord injury o Problem w/ SVR Hypovolemic shock
- Crystalloid infusion of NS or lactated ringer’s solution of 20 cc/kg as general resuscitation measures
Hemorrhagic shock
factors) should be given if not responding to crystalloid infusion of 40 cc/kg Cardiogenic shock
- Supportive measures oxygen, aspirin, heparin, fluid challenges (250cc) if no overt pulmonary edema
- Vasopressors – dopamine, norepinephrine, dobutamine - For STEMI – revascularization by PCI or emergent CABG Anaphylactic shock
- Early intubation
- β-agonist aerosol - albuterol nebulizer - epinephrine
- H1 & H2 histamine receptor blockade - Steroids
Septic shock
- Aggressive volume resuscitation - Early antibiotic use
- Supportive care Neurogenic shock
- Evaluation of other potential causes of shock - Fluid challenge of 20 cc/kg x 2
- If volume replacement is unsuccessful, vasopressors w/ α activity Obstructive shock
- Tension pneumothorax – immediate needle decompression followed by chest tube thoracostomy
- Pericardial tamponade – pericardiocentesis
- Massive PE – BP should be augmented w/ appropriate vasopressor (norepinephrine); thrombolytics if no contraindications
Scientific concepts
COMA
History & Physical - Pupillary enlargement w/ loss of light reaction & loss of vertical & adduction movements of the eyes = lesion in upper brainstem
- Preservation of pupillary light reactivity & of eye movements = widespread structural lesions or metabolic suppression of cerebral hemispheres
- Fever – systemic infection, bacterial meningitis, encephalitis, heat stroke, neuroleptic malignant syndrome, malignant hyperthermia d/t anesthetics or anticholinergic drug intoxication
- Hypothermia – characteristic of coma from alcohol or barbiturate intoxication, internal hemorrhage, MI, sepsis, profound hypothyroidism, or Addisonian crisis
Diagnostic studies - Chemical-toxicologic analysis of blood and urine - Cranial CT or MRI
- EEG
- CSF examination
functions; CT scan and cellular content of the CSF are normal a. Intoxications: alcohol, sedative drugs, opiates, etc.
b. Metabolic disturbances: anoxia, hyponatremia, hypernatremia, hypercalcemia, diabetic acidosis, nonketotic hyperosmolar hyperglycemia, hypoglycemia, uremia, hepatic coma, hypercarbia, addisonian crisis, hypo- and hyperthyroid states, profound nutritional deficiency c. Severe systemic infections: pneumonia, septicemia, typhoid fever, malaria, Waterhouse-Friderichsen syndrome
d. Shock from any cause
e. Postseizure states, status epilepticus, subclinical epilepsy f. Hypertensive encephalopathy, eclampsia
g. Severe hyperthermia, hypothermia h. Concussion
i. Acute hydrocephalus
2. Diseases that cause meningeal irritation with or without fever, and with an excess of WBCs or RBCs in the CSF, usually without focal or lateralizing cerebral or brainstem signs; CT or MRI shows no mass lesion
a. Subarachnoid hemorrhage from ruptured aneurysm, arteriovenous malformation, trauma
b. Acute bacterial meningitis c. Viral encephalitis
d. Miscellaneous: fat embolism, cholesterol embolism, carcinomatous and lymphomatous meningitis, etc.
3. Diseases that cause focal brainstem or lateralizing cerebral signs, with or without changes in the CSF; CT and MRI are abnormal
a. Hemispheral hemorrhage (basal ganglionic, thalamic) or infarction (large middle cerebral artery territory) with secondary brainstem compression
b. Brainstem infarction due to basilar artery thrombosis or embolism c. Brain abscess, subdural empyema
d. Epidural and subdural hemorrhage, brain contusion e. Brain tumor with surrounding edema
f. Cerebellar and pontine hemorrhage and infarction g. Widespread traumatic brain injury
h. Metabolic coma (see above) with preexisting focal damage
i. Miscellaneous: Cortical vein thrombosis, herpes simplex encephalitis, multiple cerebral emboli due to bacterial endocarditis, acute hemorrhagic leukoencephalitis, acute disseminated (postinfectious) encephalomyelitis, thrombotic thrombocytopenic purpura, cerebral vasculitis, gliomatosis cerebri, pituitary apoplexy, intravascular lymphoma, etc.
Clinical
therapeutics - - ABCs IV access
- Hypotension, hypoglycemia, hypercalcemia, hypoxia, hypercapnia, and hyperthermia should be corrected rapidly.
- naloxone and dextrose are administered if narcotic overdose or hypoglycemia are possibilities
- thiamine is given along with glucose to avoid provoking Wernicke's disease in malnourished patients
- In cases of suspected basilar thrombosis with brainstem ischemia, IV heparin or a thrombolytic agent is often utilized, after cerebral hemorrhage has been excluded by a neuroimaging study.
- Physostigmine may awaken patients with anticholinergic-type drug overdose but should be used only with careful monitoring
Scientific concepts Definition – deep sleeplike state from which the patient cannot be aroused Principal causes of coma
- (1) lesions that damage the RAS (reticular activating system) in the upper midbrain or its projections
- (2) destruction of large portions of both cerebral hemispheres
- (3) suppression of reticulocerebral function by drugs, toxins, or metabolic derangements such as hypoglycemia, anoxia, uremia, and hepatic failure.
CARDIAC TAMPONADE
History & Physical - tachycardia, decreased cardiac output, and hypotension, although hypertension occasionally is present.
- Dyspnea & cough
Characteristic features of tamponade – Tachycardia
– Tachypnea
– Narrow pulse pressure – Preserved systolic pressure
Diagnostic studies - primary diagnostic imaging modality for cardiac tamponade is transthoracic Doppler echocardiography
- Electrocardiographic features of tamponade include low voltage and electrical alternan - A paradoxical pulse is the most helpful clinical test for cardiac tamponade
Clinical
therapeutics - The presence of cardiac tamponade should be considered a medical emergency, warranting admission to an intensive care unit with prompt consultation of a cardiovascular diseases specialist to perform an urgent pericardiocentesis. If the patient becomes pulseless, pericardiocentesis should be performed immediately, even by inexperienced practitioners. - Removal of the pericardial fluid with pericardiocentesis is the definitive treatment for
cardiac tamponade.
Scientific concepts - The rate of fluid accumulation is very important; if slow, the pericardium stretches over time and large volumes (up to several liters) may collect before causing hemodynamic difficulty
- if the fluid accumulates quickly, the noncompliant pericardium does not stretch and tamponade can be caused by as little as 150 to 200 mL. As pericardial pressure increases, transmural ventricular pressures decrease despite increased intracavitary pressures.
PERICARDIAL EFFUSION
History & Physical • Pain in acute inflammatory pericarditis; neoplastic and uremic effusions are often painless • Dyspnea and cough
• Other symptoms reflect primary disease
• Pericardial friction rub may be present (even with large effusions)
• Pulsus paradoxus (> 10 mm Hg decline in systolic pressure during inspiration) is common • Elevation of central venous pressure, edema, or ascites in chronic processes
• Hypotension, paradoxical pulse and an elevated jugular venous pressure all important signs Diagnostic studies • ECG
– Often reveals nonspecific T wave changes and reduced QRS voltage – Electrical alternans is pathognomonic
• Chest radiograph: normal or enlarged cardiac silhouette with a globular configuration • Echocardiography is primary mode of diagnosis
• Diagnostic pericardiocentesis or biopsy is often indicated for microbiologic and cytologic studies
• Yield of diagnostic pericardial tap is low
Clinical therapeutics • Small effusions can be followed clinically and by echocardiogram • Urgent pericardiocentesis is required for tamponade
• Partial pericardiectomy may be required for recurrent effusion in neoplastic disease and uremia, either by video-assisted thoracic surgery (VATS) or thoracotomy
Scientific concepts - Can develop from any form of pericarditis
- Slow development of large effusions may produce no hemodynamic effects - Rapid appearance of smaller effusions can cause cardiac tamponade (elevated
intrapericardial pressure that restricts venous return and ventricular filling), leading to shock and death
Cardiology
INTERNAL MED EOR EXAM STUDY GUIDE: CHF
Scientific Concepts SYMPTOM COMPLEX, NOT DX
Condition from any functional or structural cardiac disorder that impairs the ability of the heart to fill or pump a sufficient amount of blood through the body. (or a combo of both)
Systolic- depressed ejection fraction (this is more common dysfunction, dilation)
Diastolic- preserved ejection fraction. Not enough blood volume. Passive stiffness
Causes:
o CAD (with or without MI)
o Ischemic Cardiomyopathy (CMO)- Most Common ( – ischemic event that caused an exacerbation acutely o Non-Ischemic CMO (rare- sarcoid/amyloid)
Stages of Heart Failure
CHF Prognosis Risk increases with diastolic dysfunction and worsening prognosis (because the pulmonary system is getting worse- affecting everything behind it)
Improving with use of ACEI and Beta blockers CHF History and Physical Symps
o Dyspnea (at rest and exertional) o Orthopnea
o Paroxysmal Nocturnal Dyspnea (PND)
o Chronic cough (non-productive) –vascular congestion o Nocturia
o Fatigue
o With RV Failure: RUQ Pain, Nausea, Loss of appetite, Peripheral edema, Ascites
PE
o Vitals: can be normal, may have Tachycardia, Hypotension , Decreased pulse pressure, Diaphoresis, Cool extremities o WEIGHT! Follow very closely
o JVD
o Thyromegaly
o Carotid pulse- Aortic Stenosis (AS)
o Lungs: Crackles, Wheezes, Rhonchi, Pleural effusions o LV lift or sustained pulsation
o Diminished first sound: annulus around the valves change, not getting closing snap
o S3 gallop o Murmurs
o RV failure: hepatomegaly CHF Lab Eval and Workup CBC – Anemia
BMP- Renal insufficiency (BUN and Cr increased, but still making urine)/Renal Failure Electrolytes (K, Mg), Decreased Na,
Hypokalemia in Afib
Thyroid
BNP (BRAIN NATRIURETIC PEPTIDE)
o Major source is the cardiac ventricles
o direct proportion to ventricular volume expansion and pressure overload.
CHF Workup: EKG Hypertrophy
MI
Non-specific
*Compare priors
CHF Workup: CXR Cardiomegaly – silhouette should not be more than one half the size of the chest
Pulmonary venous hypertension
Perivascular edema (haziness of vessel outlines)
Interstitial edema
Pleural effusions (transudate)
CHF Treatment Underlying
o Valvular disease
o MI : Stent, Angioplasty, CABG o HTN
o Arrhythmias o Alcohol
o Drugs: CA++ channel blockers o Pericardial disease
Diuretics
o Most effective for symptoms o Careful for excessive use o Electrolyte abnormalities (K+ ) o Thiazide diuretics
HCTZ 25mg Daily
Metolazone 2.5-5 mg Daily Chlorthalidone 50 mg Daily
Works on distal loop, prevention of absorbtion of Na+
Worsening HF (adding more diuretics – want to assess by symptomology)
o Furosemide (Lasix) 20-40 mg Daily, titrate o Bumetinide (Bumex) 0.5-2 mg Daily o Torsemide
o BID preferred o Watch electrolytes
K+ sparing drugs (aldosterone antagonists)
o Spironolactone (Aldactone) 25-50 mg Daily o Triamterene
o Amiloride
o Eplerenone (Inspra)
o Along with ACE and diuretics, reduction in mortality and improve symps
ACEI
o Prevents hospitalizations o Increased exercise tolerance o Decreases symptoms
o Enalapril, Ramipril, Benazepril, Avoid if Renal artery stenosis
o ACEI First line tx in pts with EF < 40%
o Used in combo with diuretics: Potential side effects are hypotension and hyponatremia.
o Cough, angioedema, hypotension
o Not to be used with ACEI
o Chronic Failure: Candesartan or valsartan can benefit as alone or in addition to diuretic
o Losartan (Cozaar®)
Beta Blockers (Carvedilol, Metoprolol)
o Decreased HR allows more time for the heart to fill. o Clinical effects: improve long term symps; reduce
hospitalizations, sudden death; improve survival; reduce remodling/progression
Caution: Could worsen LV function
Detrimental to use a pure beta blocker for HF
Digoxin/Digitalis
o Only oral positive inotrope
o Used in conjunction with patients with atrial fibrillation o Enhances sympathetic tone which delays AV conduction o Can be given with other meds
o Amiodarone (CORDARONE) o Quinidine o Propafenone (RYTHMOL) o Verapamil Vasodilators/Nitrates o Reduction of AV afterload
o Need an agent or a combination of agents to improve both factors
o NTG, Sodium Nitroprusside, Isosorbide 20-80 mg TID, NTG paste
o Hydralazine
Potent arterial vasodilator Markedly increased CO
Stand alone does not perform well to improve symptoms or exercise tolerance
Combination of nitrate and hydralazine has greater hemodynamic effects (BiDil: Hydralazine + Isosorbide)
Frequently limited by side effects GI, HA,Hypotension
Dobutamine/Milrinone: positive inotropes, role is limited to pts with hypoperfusion and deteriorating kidney function, or pts awaiting transplant. Continuous therapy increases mortality.
CHF Tx: CCB’s May accelerate progression of HF
Exception is Amlodipine (NORVASC)
General rule is to avoid use unless treating HTN associated angina Anticoagulation LV failure and reduced EF can give risk of intra-cardiac thrombus
formation and systemic embolus
Antiarrhythmic Therapy Moderate to severe failure can have increased incidence of arrhythmia
Tx: Implantable Defibrillators Reduction of sudden death from heart failure related arrhythmia (EF <30%, risk of sudden cardiac death increases significantly)
INDICATED IN CLASS III HF for primary prevention of sudden death
Non-Pharm Tx Diet, exercise management
o Reduction in weight, sodium intake o Exercise training to reverse deconditioning
Biventricular Pacing For use in widened QRS complex situations
Can improve EF and exercise tolerance
Reduction in death and hospitalizations Cardiac Transplantation Last ends of care
INTERNAL MED EOR STUDY GUIDE: HYPERTENSION JNC7 Classification
Diagnosis Serial blood pressure measurements on at least 3 separate occasions
Major exceptions to single elevated BP measurement
o Unequivocal evidence of life-threatening end-organ damage (hypertensive emergency)
o BP is >220/125 mm Hg, but life-threatening end-organ damage is absent (hypertensive urgency)
Patient Evaluation 1. Assess CV risk factors and comorbidities 2. Reveal identifiable causes of HTN
3. Assess presence of target organ damage and CVD Risk Factors and
Comorbidities
Identifiable Causes HTN
Target Organ Damage and CVD
Scientific Concepts: Primary Essential HTN
**95% of hypertensive patients, onset between ages 25 and 50 Genetic and Environmental Factors
Sympathetic NS hyperactivity: Younger persons with tachycardia and elevated CO
RAAS: High Renin Activity, Caucasian and younger
Elevated intracellular sodium and calcium levels Exacerbating factors
Obesity, Sleep apnea, Increased salt, ETOH, Cigarettes, Polycythemia, NSAID’s, Low potassium intake
History and Physical Symptoms
o Asymptomatic : “Silent killer”
o Nonspecific: HA, Blurred vision, Dizziness, Facial flushing o Severe Symps: N/V, Irregular HR, Tinnitus, Dyspnea
PE
o BMI
o Verify contralat arm o Funduscopic exam o Palpate peripheral pulses o Bruits (carotid, renal, femoral) o Thyroid gland enlargement or masses o Cardiac (LVH)
o Kidney enlargement
o Abdominal masses and AAA pulsation o BLE edema and pulses
o Neurological assessment (cerebrovascular dz) Diagnostic Studies Labs
UA
FBG or HgA1c, K+, creatinine, GFR, Ca++
Fasting lipid panel
Hematocrit Target organ damage
Labs, radiologic studies, EKG- but echo better Complications of
Longstanding Hypertension
CV: LVH, CAD, CHF, Afib
Cerebrovascular Disease: Stroke, hemorrhage, encephalopathy
Renal: Nephrosclerosis, accelerates DM Nephropathy
Aortic Dissection: HTN contributing factor Hypertensive
Emergencies
Require substantial reduction of BP within 1 hour to avoid risk of serious morbidity or death
Includes:
o Hypertensive encephalopathy (HA, irritability, confusion, AMS) o Hypertensive nephropathy (hematuria, proteinuria, progressive
kidney dysfunction)
o Intracranial hemorrhage, aortic dissection, preeclampsia-eclampsia, pulmonary edema, unstable angina, MI
Malignant Hypertension
o Elevated BP results in target organ damage (CNS, CV, renal system) o Characterized by encephalopathy or nephropathy with accompanying
papilledema (must be present)
o Progressive kidney disease results if treatment not provided o Same treatment as other hypertensive emergencies, table 11-12
CMDT. Depends on organ affected, includes: Nicardipine, Ntg + Labetalol or Esmelol, Fenoldopam, Clevidipine, Labetalol
Health Maintenance& Treatment Goals
Primary focus is reaching SBP goal, most reach DBP goal once SBP goal is reached
Treating to <140/90 is associated with decrease in CVD complications
Goal is <130/80 for patients with HTN and DM or renal dz
Lifestyle: sodium recommended 1500 mg, no more than 2300 mg/day or 1 TSP
F/U monthly intervals for adjustment of medications until BP goal is reached and assess for adverse reactions
More frequent visits for stage 2 HTN or if complicating comorbid conditions
Labs: Serum potassium and creatinine 1-2 times/year and other labs as indicated
BP to goal and stable: 3 to 6 months intervals Clinical Therapeutics Multidrug treatment
o 2 drugs at lower doses avoid adverse effects that may occur with higher doses of single agent
Thiazide Diuretics Chlorthaizide, Chlorthalidone, HCTZ, Polythiazide, Indapamide, Metolazone
Initial therapy for most patients with HTN
Enhance the antihypertensive effects of multi-drug regimens (ACEI, BB)
Adverse: Decrease K, Mg, Ca, Na; Increase uric acid, glucose, lipid
Hypotension, HA, weakness, muscle cramps, photosensitivity, rash, ED ACE Inhibitors Benazepril, Captopril, Enalapril, Fosinopril, Lisinopril, Moexipril, Perindopril,
Quinapril, Ramipril, Trandolapril
More effective in Caucasians and younger patients
Less effective in African Americans and older patients
Benefits
o Slow progression of loss of kidney function (diabetic nephropathy and CKD)
o Reduce LVH and indicated for CHF
Adverse Effects
o Increase K, uric acid; elevated BUN/Cr
o Hypotension,** cough **angioedema (severe rxn) o If cough, switch to ARB
Blockers Valsartan
Benefits
o Less side effects than ACEI (cough and angioedema)
o Effectiveness and enhanced interaction with diuretics is similar to ACEIs
o Prevention of stroke,
o Possibly diminish progression of Alzheimer’s
ADE’s similar to ACEI Calcium Channel
Blockers
Benefits: Effective in treating arrhythmias
Adverse reactions: HA, peripheral edema, bradycardia, heartburn, constipation
Beta Blockers Atenolol, Betaxolol, Bisoprolol, Metoprolol, Nadolol, Propranolol, Timolol
Cardioselective – primarily beta-1 receptors (heart)
Nonselective – beta-1 and beta-2 (lungs, blood vessels, tissues
Benefits
o Cardioprotective
o Useful in patients with angina, prior MI, stable CHF o Treatment for migraines and anxiety
Adverse reactions
o Worsen chronic lung disorders
o Possibly worsen heart failure and peripheral vascular disease o Abrupt withdrawal may trigger angina or MI in patients with heart
disease
o Dizziness, fatigue, insomnia, depression, erectile dysfunction, Raynaud’s, increase TG
Treatment: Compelling Indications
INTERNAL MED EOR EXAM STUDY GUIDE: HEART MURMURS
Aortic Stenosis Harsh systolic ejection murmur heard best at right upper sternal border (RUSB)
o Mid to late peak
o Reduced intensity of second heart sound o Radiates to carotids
o Pulses-parvus et tardus (slow and late) o Narrow pulse pressure
o Begins after S1, ends before A2 Aortic Insufficiency (aka High pitched diastolic decrescendo murmur
regurgitation) o Louder along left sternal border in third to fourth intercostal space
Widened pulse pressure
Water hammer/Corrigan pulse
Optimum auscultation: diaphragm, pt leaning forward, breath held in expiration
Austin Flint: Aortic Regurg may be associated with low pitched mid-diastolic murmur at apex
Mitral Stenosis Opening snap following A2
Low pitched diastolic rumble heard best at apex, Lt Lat position, using bell
Left sided after expiration
Mitral Regurgitation Holosystolic murmur heard best at left sternal border and radiates to axilla
Loudest over PMI
Begins with S1 and ends at or after A2 Mitral Valve Prolapse Mid systolic click with late systolic murmur
Ausculatory findings accentuated in the standing position or valsalva Pulmonic Insufficiency diastolic decrescendo murmur
Pulmonary Stenosis systolic murmur with S2 split
Tricuspid Regurgitation pansystolic murmur, right heart failure
Best heard at third to fifth ICS along left sternal border
Can be hard to hear, blowing, coarse or musical
Begins with S1 and fills systole
Louder during inspiration
Tricuspid Stenosis Rumble often follows audible opening snap
Heard at third to fifth ICS along lefts sternal border out to apex.
Murmur increases with inspiration
Murmurs in Stable Angina Occasionally a gallop rhythm and apical systolic murmur due to transient mitral regurg from papillary muscle dysfunction
**Here is a youtube video with a mnemonic to remember the diastolic vs systolic murmurs ** http://www.youtube.com/watch?v=sL0vHiXLZ-4
INTERNAL MED EOR EXAM STUDY GUIDE: VALVULAR HEART DISEASE Definitions
Stenosis- abnormal narrowing
Regurgitation- backward flowing of blood Aortic Stenosis (AS)
Congenital: Unicuspid or bicuspid valves, younger population Rheumatic
Untreated Strep pharyngitis- usually between 5-15y
Fusion of the leaflets, also effects mitral valve Degenerative calcific (most cases > 70y)
Lipid accumulation, inflammation and calcification AS pathophysiology
Bulky calcification > obstruction of the outflow tract leads to hypertrophy of the left ventricle > eventually leads to less compliance > diastolic dysfunction (elevated LVEDP)
AS symptoms
3 cardinal symptoms: Angina, Syncope, Dyspnea AS treatment
Surgical aortic valve replacement (gold standard) Mechanical vs bioprosthetic
Transcatheter aortic valve replacement (TAVR) Palliative percutaneous aortic balloon valvuloplasty Medical therapy
Aortic Insufficiency
Regurgitation of aortic valve into left ventricle
Multiple etiologies- endocarditis, iatrogenic, bicuspid vs acute in setting of aortic dissection Prognosis determined by symptoms and LV size/function
AI clinical manifestations
Diagnosed with auscultation/echocardiogram AI treatment options
Medical therapy to help slow progression of symptoms ACEi, Diuretics
Surgical valve replacement if evidence of LV systolic dysfunction with or without symptoms Mitral Stenosis
Thickening and immobility of mitral valve leaflets (fusion or shortening of chordae tendonae)> increased pressure in left atrium > increased pressure in pulmonary vasculature > elevated pressures in right heart
Etiology: Rheumatic fever (majority), Congenital MS clinical manifestations
Dyspnea
Pulmonary hypertension- can progress to right heart failure Hemoptysis
Embolic events (mostly with Afib) Atrial fibrillation
PE: Evidence of right heart failure- JVD, lower extremity edema, hepatomegaly MS management
Medical management: Diuretics, Beta blockers, +/- Anticoagulants (if Afib), Statins Mitral balloon valvuloplasty (PMBV)
Surgical valve replacement Mitral Regurgitation (MR)
Etiologies: Mitral valve prolapse, Rheumatic , Flail leaflet, Endocarditis MR manifestations
Exercise intolerance, Dyspnea on exertion, Easy fatigability MR treatment
Medical therapy- ACEi/ARB, beta blockers, diuretics
SURGERY if severe MR with LV impairment and/or pulmonary hypertension or new onset atrial fibrillation (with or without symptoms)
Mitral Valve Repair (ring annuloplasty) may be superior to replacement Mitral Valve Prolapse
female predominance
Causes: myxomatous degenerative changes, connective tissue disorders, ruptured chord or papillary muscles, enlarged annulus or trauma
Non-specific symptoms- chest pain, dizziness, dyspnea, lightheadedness, exercise intolerance, anxiety disorders
Pulmonic Insufficiency
Causes: Dilation of pulmonic ring, Abnormality of leaflets, Congenital Pulmonary stenosis
Congenital is MC Tricuspid Regurgitation
Causes: Abnormality of valve leaflets , Endocarditis, Dilation of right ventricle Treatment: diuretics, surgery
