Internal Medicine EOR Topics

Premature atrial contractions (PACs)

Early beat originating from an ectopic pacemaker site in the atria, early beat interrupts the regularity of sinus rhythm, increase automacity of pacemaker cells

• Same ectopic site= regular irregular rhythm

• Different ectopic site= irregular, regular rhythm

• Risks: caffeine, nicotine, cocaine, amphetamines, thyroid disease, post-MI, stress/anxiety, hypoxia, CHF, Pulm dz

• Tx: Infrequent: no treatment, Frequent: underlying cause

Multifocal atrial tachycardia and wandering atrial pacemaker (WAP)

Occurs when the pacemaker site shifts back and forth b/t sinus node and ectopic atrial sites; P-waves vary in size, shape or direction across the rhythm strip as the pacemaker “wanders” b/t multiple sites

• 3 different P-wave morphologies AND MAT: HR>100 OR WAP: HR<100

Atrial flutter

Originates in ectopic pacemaker site in the atria discharging atria impulses at a rate of 250-400 bpm; ventricular contraction rate typically regular and ranges from 75-150 bpm, blood pools and the atria cannot drain

• rapid atrial impulses create a V-shaped waveform with a sawtooth pattern

• TX:

  • Unstable: Cardioversion (synchronized electric shock)

  • Stable: Rate control (B-blocker or CCB) or Rhythm control (amiodarone or cardioversion with med failure), catheter ablation (PREFERRED LONG TERM MANAGEMENT)

• Anticoagulation (decrease stroke incidence)

  • Onset <48 hrs can convert rhythm

  • Onset >48 hrs begin anticoag or schedule TEE for clot evaluation before cardiovert

  • Long term anticoag with a DOAC

Atrial fibrillation (A-fib)

MC arrhythmia requiring treatment and can be secondary to many medical conditions; atria contracts 300-500 contractions in a minute

• atrial pathology: increase atrial pressure, atrial dilation (disrupts underlying conduction path)

• Atrial rate >300 bpm, irregular rhythm, variable ventricular rate, absence of P-waves, irregularly regular, varying R-R interval

• Risks: enveloping blood clots, stroke, 60 and older

• S/S: dizziness, palpitations, fatigue, mild dyspnea, chest pain

• Tx: rate control, rhythm control, stroke prevention (anticoagulation)

  • Unstable: Cardioversion (synchronized cardioversion)→ TEE or anticoag first

    • DO a CHADS-VAS risk score (stroke risk >2 in men, >3 in women)

  • Stable: 1ST LINE- Rate control and anticoag for long term maintenance

    • Rate: Beta blocker (metoprolol, atenolol), CCBs (diltiazemn, verapamil), amiodarone

    • Anticoag: DOAC (apixaban, rivaroxaban)

Heart block

Rhythms where there is a delay or block in the conduction of impulses from the atria to the ventricles, 3 classes

1. First degree AV block: all conducted just delayed

2. Second Degree AV block

A. Mobitz I: Progressive PR interval with a dropped beat

B: Mobitz II: Fixed PR interval with a dropped beat

3. Third degree AV block: non conducted, firing completely on their own

Second degree heart block Mobitz Type I (Wenckebach)

Initial impulse leaves the sinus node and travels through the AV node, is conducted through the ventricles but each successive impulse has increasing difficulty passing through the AV node until finally an impulse does conduct to the ventricles

• PR intervals longer and longer until dropped QRS

Second Degree Heart block Mobitz Type II

More than one P-wave to each QRS complex

• PR is normal or prolonged but will be consistent

• Can progress suddenly to 3rd degree

• TX: PERMANENT PACING if it does not resolve

Third degree heart block

Impulses fail from atria to ventricles, complete heart block, beat totally separate of eachother

• TX: permanent pacemaker

Junctional escape rhythm

Junctional arrhythmia the heart rate is low at 40-60 bpm, SA node fails to initiate impulse so a secondary pacemaker within AV junction takes over

• P-waves typically absent/buried

• Bradycardia

Premature ventricular contractions (PVCs)

Early ectopic impulse that originates in ventricular tissue either in the right or left ventricle, premature wide morphology

• QRS complex is wide and morphology is different b/c of underlying rhythm

• Pause follows the PVC, usually compensatory

• Risks: MC in those w/ heart disease

• Tx: not indicated if asymptomatic

Supraventricular arrhythmias

Originate ABOVE the cardiac ventricles

• narrow QRS complex, less serious because ventricle activity is preserved

• S/S

  • Fast heart rate: palpitations, chest pain, nausea, diaphoresis

  • Slow heart rate: dizziness, syncope

Supraventricular Tachycardia (SVT)

Often occurs in patients without structural heart disease, episodes start and end abruptly (seconds to hours)

• Rate 140-240 bpm, regular rhythm (not sinus)

• Loss of normal contour, P-wave differs in contour from sinus beats and is often buried in the T-wave (no sinus), Normal QRS complex

• S/S: palpitations and anxiety

• Tx: depends on pt stability

  • Unstable (hypotension, AMS, HF): cardioversion (synchronized electric shock)

  • Stable (least to most invasive)

    • Vagal maneuvers (carotid massage, Valsalva)

    • Bolus of adenosine IV →If that doesn’t work do another bolus of adenosine→ If ineffective do another bolus of adenosine

Ventricular Tachycardia (V-Tach)

Originates from an ectopic site in the ventricles discharging impulses at a rate of 140-250 beats per minute (complication of MI or cardiomyopathy)

• 3 or more premature beats

• Tombstone appearance

• Tx

  • Unstable: cardioversion (w/pulse)→ if recurs give amiodarone and shock again

  • Stable: amiodarone, if unsuccessful sedate patient and perform cardioversion as indicated

  • Long term: B-blocker or CCB

Ventricular fibrillation

No regularity, no complexes or waves present are able to be analyzed (no pulse), death is imminent unless rhythm is treated immediately

1. Defibrilate at highest energy level (unsuccessful do IV lines and intubate)→ Administer epinephrine and perform 5 cycles of CPR→ Continue drug therapy, CPR and defibrillation attempts

• Once pt is revived, tx the underlying cause

Right bundle branch block

QRS >120 ms elongated, in lead V1 or V2 an rSR or rSR (rabbit ears pattern is typical, wide or slurred S-waves in leads I and/or V6, T-wave inversion

• Often incidental finding and benign in pts w/o heart disease

• Dx: ECG, ECHO

• TX: underlying cause, evaluate for pacemaker

Left bundle branch block

Prolonged QRS duration >120 ms with normal morphology; dominant S-wave in V1 and tall R waves in V6, often associated with underlying heart conditions like HTN or CAD

• Risks: more significant cardiac issues (ischemic heart disease, cardiomyopathy, valvular heart disease)

• S/S: fatigue, SOB, palpatations, chest pain/discomfort, syncope/presyncope

• Dx: ECG, ECHO, evaluate for extensive heart disease

• Tx: underlying cause, pacemaker, cardiac resynchronization therapy (CRT)

QT Prolongation

Delayed ventricular repolarization , longer reset of the heart after each beat

1. Congenital Long QT Syndrome: 1 in 2500 live births, long QT interval (usually >470 msec), ventricular arrhythmia, typically polymorphic ventricular tachycardia in presence of congenital deafness

2. Acquired long QT Syndrome: usually second to the use of antiarrythmic agents, certain abx, electrolyte abnormalities, myocardial ischemia, or bradycardia

• S/S: asymptomatic; palpatations, syncope (can be misdiagnosed for seizures), cardiac arrest

• DX: Personal and family history, ECG, exercise ECG for long QT, genetic testing (cardiac arrest)

• Tx: Long QT- Beta blockers, Inherited Syndrome- cardiac arrest due to genetics, implantable cardioverter-defibrilator

  • refer to cardiology

Dilated cardiomyopathy

LV or bi-ventricular chamber thinning and enlargement and systolic dysfunction, high end-diastolic and high end-systolic volumes; diminished cardiac output, interstitial and endocardial fibrosis, enlargement of the remaining heart chambers

• Risks: viral, bacterial, chemo, ethanol, cocaine, uremia, thyroid hormone, pregnancy, HEAVY EXPOSURE, SMOKER

• S/S: HF- progressive DOE, orthopnea, peripheral edema,JVD, PND, edema, abd pain, nausea, congestive cough, fatigue, weakness, rales

• Acute presentation is often misdiagnosed as a viral URI in young adults

• DX: Hx is important, ECG ± a Holter monitor, ECHO (LV dial, thin ventricular walls, decrease EF), Cardiac cath

• TX: Underlying cause

  • ANRI or ACE/ARB

  • B- Blocker

  • Aldosterone agonist

  • SGLT2I w/ loop diuretic

• Sx: LVAD, cardiac resynchronization (CRT), automatic implantable cardioverter-defibrillator, heart transplant

Hypertrophic cardiomyopathy

Genetic disease of heart muscle (myocardium)- frequently autosomal dominant, mutation in sarcomere (muscle gene), unexplained LV hypertrophy w/o dilation for the ventricles or a cardiovascular disease that could cause the degree of hypertrophy seen; LV is small and hypercontractile with increase wall stress

RISKS: STUDENT ATHLETES, males, 3rd decade, structural abnormalities of septum , subendocardial ischemia

1. Obstructive: midsystolic obstruction of flow through the LV outflow tract as a result of systolic anterior motion of the mitral valve toward the septum (SAM)

2. Non-obstructive

• S/S: most patients asymptomatic until sudden death from V-tach or V-fib, fatigue, dyspnea, angina, palpatations, presyncope/syncope

• PE: double apical impulse, S2 split, systolic ejection murmur

• ECHO: LVH with no dilated LV

• ECG: left axis deviation and abnormal Q waves

• TX: BETA BLOCKER

• Sx: surgical septal myectomy or alcohol septal ablation

Restrictive cardiomyopathy

Deposits in tissue causing stiffness (does not relax), non-dilated, non-hypertrophied ventricles w/ impaired LV filling; diastolic dysfunction, LV wall thickness may be increased by infiltrative disease, bi-atrial enlargement often severe

• Risks: primary idiopathic (most cases), amyloidosis, sarcoidosis, hemosiderosis, genetics, Loeffler Eosinophilic Endocardial Disease

• S/S: symptoms of HFpEF, orthostatic HoTN, syncope, orthopnea, fatigue

• PE: R sided heart failure, cardiac cachexia, loud S3 murmur, systolic murmur, apical impulse, JVD

  • Amyloidosis: periorbital purpura, macroglossia, easy bruising

• DX: ECHO (front line- biatrial enlargement and diastolic dysfunction), BX for amyloidosis, Lab (eosinophilia), ECG (90% abnormal- nonspecific ST-T wave changes, low voltage QRS)

  • Cardiac cath or Bx is the best

• TX

  • Medication: Beta blocker or non-DHP CCB (verapamil, diltiazem)

  • Tx underlying disorder ex. Chemo for amyloidosis

  • Pacemaker implantation

Coronary artery disease (CAD)

Blood vessels become narrowed or blocked by a buildup of fatty plaque

• Risks: atherosclerosis, smoking, poor diet, high cholesterol, diabetes, HTN, family history

• S/S: angina, SOB, fatigue, “silent”

• Tx: lifestyle changes, treat underlying

Acute coronary syndrome

Spectrum of clinical symptoms that include

• Unstable angina, acute myocardial infarction (N-STEMI, STEMI)

• Acute myocardial injury and evidence of ischemia and elevated troponin with one of the following

  • Ischemic symptoms (chest pain, dyspnea)

  • Development of pathological Q waves on ECG

  • ECG changes indicative of ischemia (ST segment elevation or depression)

  • Imaging evidence of new loss of viable myocardium

  • Identification of coronary thrombus by angiography or autopsy

STEMI

Occlusive coronary thrombus at site of pre-existing atherosclerotic plaque; ST elevation denotes an acute coronary occlusion and warrants immediate reperfusion

• COCAINE considered in young individuals w/o risk factors

• Stress cardiomyopathy can mimic a STEMI

S/S: worsening angina, occur at rest, MC in early morning, more severe than angina and builds up to maximum intensity, nitroglycerin has little to no affect on the pain, cold sweats, diaphoresis, weakness, apprehension, pre/syncope, N/V, dyspnea, cough, wheezing, can be Brady or tachy, decreased cardiac output, RA hypertension, Kussmaul sign, soft heart (LV dys), atrial gallop (S4), mitral regurg, pericardial friction rub, cyanosis/decreased body temp

Dx: cardiac enzymes, ECG, CXR

Management of a STEMI

• Medication

  • Aspirin immediately through the door

  • Anticoag- heparin, use bivalrudin if undergoing PCI

  • Nitro/morphine for s/s

  • ACE

  • Beta-blocker

  • DAPT for reperfusion (Aspirin, prasugrel/ticagrelor)

  • All pts on antithrombitic tx need prophylactic GI tx with PPI (rabeprazole, esomeprazole)

• Reperfusion Tx (PCI-preffered, or fibrinolytic)

  • Primary PCI: usually a stent (drug-eluding, bare metal if unable)- give glycoprotein with heparin for pts undergoing PCI

    • After PCI stenting DAPT w/ ASA and P2Y12 inhibitor for 1 yr

  • Fibrinolysis: recombinant DNA products (tPA, reteplase), require heparin

    • Be careful of previous hemorrhagic stroke, ischemic stroke, intracranial neoplasms, head trauma, internal bleeding

    • DAPT with ASA and clopidogrel

Killip Classification in pts that experience MI to evaluate for heart failure

• Class I: No evidence of HF

• Class II: mild-moderate HF (S3 gallop, rales, increased JVP)

• Class III: pulmonary edema

• Class IV: cardiogenic shock BP <90 mmHg and hypoperfusion

N-STEMI

• S/S of ACS with positive biomarkers and ECG without ST elevation

• TX: Medium/high risk hospitalize the pt with limited activity

  • Medication

    • Aspirin upon arrival and then lifelong

    • Add ticagrelor or prasugrel to aspirin

    • Anticoagulation: Heparin

    • Nitrates PRN for chest pain

    • Beta-blocker (CCB 3rd line)

    • Statins

  • Home meds: Aspirin, Statin (atorvastatin), Beta blocker (metoprolol), Nitrate PRN, (DAPT only if stent)

  • Evaluate with GRACE and TIMI scores to determine need for PCI (most will not need)

    • Bivalrudin (anticoagulation) for pts going to PCI

    • Glycoprotein IIB/IIIA for pts undergoing PCI- tirofiban

Unstable angina

Angina pectoris or equivalent ischemic discomfort with at least one of three features:

1. Occurs at rest or minimal exertion and prolonged

2. Severe and new onset

3. Recent acceleration- crescendo pattern

• Signal rapidly worsening heart disease and high risk for MI

• On ACS spectrum work up as MI, admit to chest pain observation unit

• Management is per non-ST elevation MI (STEMI)

Stable angina

Manifestation of stable CAD due to atherosclerotic heart disease, coronary vasospasm may occur on lesion site or “normal” vessel; can also be caused by congenital abnormalities, embolism, arteritis, dissection, severe hypertrophy, severe aortic stenosis/regurgitation, in response to increased demands (anemia or hyperthyoidism)

• Risks: CAD, stress, exertion, meals, excitement, morning hours, cold exposure

• S/S: Helps to remain upright (preload pain), tight squeeze, pressing burn, Levine sign, substernal pain L of mid sternum, radiates to L shoulder and upper arm

• PE: significant increase in BP/or hypotension, arrhythmia, gallop rhythm, diaphoresis/pallor

• DX: supported if nitroglycerin permits increased exertion tolerance or prevents angina entirely, Labs to evaluate for ACS

  • ECG: usually normal, angina episode can show down sloping of ST-segment, may have occasional T wave flattening or inversion

• Tx: Identify trigger, Nitro before activity, long—acting nitrate if that doesn’t work, Beta-blocker (1st line) + Aspirin if not CI

Vasoplastic angina (Prinzmetal (variant) angina)

Ischemia from vasoconstriction, chest pain w/o normal precipitating factors

• ST elevation rather than depression

• Risks: women under 50 yo, early morning, AWAKENS pt, arrhythmia, conduction deficit

• DX: vasoconstrictor challenge (NOT a good idea)

• TX

  • ST-segment elevation= coronary arteriography- CCB and nitrates for prophylaxis

  • Lesion= med therapy or revascularization

  • No lesion= endothelial disruption

Heart failure

Heart cannot pump blood to the body at a rate commensurate with its needs, or can only do so at the cost off high filling pressure

• Systolic HF (HFrEF): heart failure with reduced ejection fracture ,<40%, loss of contractility, excess preload or afterload (pump failure), HR too slow or too rapid (MCC OF ISCHEMIC CARDIOMYOPATHY)

• Diastolic HF (HFpEF): LV or RV filling is abnormal, impaired myocardial relaxation or chamber noncompliance/stiffness (EF IS preserved)→ HFpEF>50%

• R Sided HF: fluid retention predominant, congestion of the peripheral tissues (MC due to LHF)

• L sided HF: dyspnea predominant, impaired gas exchange and pulmonary edema

• RISKS: ischemic cardiomyopathy, HTN, valvular disease, pericardial disease, chronic arrhythmias and cardiomyopathies

Heart failure signs and symptoms

• Left HF: exertional dyspnea, orthopedic, PND, Pulm edema, chronic productive cough (transudate), tachycardia, fatigue, exercise intolerance

• Right HF: fluid distention (JVD, edema, hepatic congestion, ascites), loss of appetite, nausea, gut edema, impaired GI perfusion, abdominal discomfort (ascites)

• Acute: SOB at rest or w/ exertion, orthopnea, PND, RUQ discomfort

• Chronic: fatigue, peripheral edema, anorexia, abdominal distention

Primary hypertension

HTN without an identifiable secondary cause

• RF: genetics, age, diet, sedentary lifestyle, obesity, stress

• Tx: Stage 1 HTN with CVD, CKD, diabetes, Prevent risk >7.5%

  • BP >130/80 mmHg after 3-6 mo of lifestyle change

  • Stage 2 HTN (>140/90 mmHg): start 2 drugs (single pill combo preferred)

    • ACE/ARB+CCB (MC)

Secondary Hypertension

Appears suddenly and caused by an underlying medical condition; kidney disease, thyroid problems, adrenal gland tumors, me

• Tx: Stage 1 HTN with CVD, CKD, diabetes, Prevent risk >7.5%

  • BP >130/80 mmHg after 3-6 mo of lifestyle change

  • Stage 2 HTN (>140/90 mmHg): start 2 drugs (single pill combo preferred)

    • ACE/ARB+CCB (MC)

Hypertensive urgency (severe asymptomatic hypertension)

Chronic uncontrolled HTN or medication nonadherence, slow vascular adaptation, NO ORGAN DAMAGE

• >180 or >120 without organ damage

• Risk: non-compliance with meds, abrupt withdrawal of B-blocker or clonidine, pain/anxiety/stress

• Dx: BP measurement and evaluation for organ damage

• Tx: Outpatient or observation unit

  • Usually always a PO med- ACE/ARB, CCB (DHP), BB

  • Med adherence, diet, and at home BP monitoring

Hypertensive emergency

Sudden rise in systemic vascular resistance, endothelial injury, fibrinoid necrosis of arterioles, ischemia, organ dysfunction

• usually >180, >120 WITH ORGAN DAMAGE

• Risks: med non-adherence, renal disease, drugs, post-op, aortic dissection

• S/S: organ damage, headaches, confusion, HF, aortic dissection, acute kidney injury, retinal hemorrhages, stroke symptoms

• DX: confirm BP, Labs, Imaging (for signs of organ damage)

• TX: Need ICU and continuous monitoring

  • IV Meds (sodium nitroprusside, B-Blocker, CCB), NO ACE

Orthostatic hypotension

Exaggerated increase in blood pressure upon standing, reflects autonomic dysregulation or abnormal vascular response

• Risks: impaired baroreflex buffering, arterial stiffness, increase norepinephrine release, older adults w/ HTN, DM

• S/S: may be asymptomatic, light-headedness, headache, palpatations, chest discomfort

• Dx: measure orthostatic BP, 24 ambulatory BP, R/O other causes

• TX: Identify and tx underlying cause, BP control, lifestyle control

Vasovagal hypotension

Vasovagal reflex is due to a nervous system-cause vasodilation, bradycardia, dilation of arteries, decrease in blood pressure due to stress, a sudden unexpected pain, fear, blood drawing, unpleasant sight, sounds or smells or Valsalva maneuvers (prolonged standing, bearing down)

• S/S: Prodrome (hallmark)- nausea, diaphoresis, tachycardia, pallor, better with lying down or removing trigger

• Dx: Hx, ECG (r/o cardiac causes), Tilt table test (+ in Vasovagal)

  • Tilt Test: exaggerated drop in BP, light headed/dizzy, presyncope/syncope

• Tx: First line: avoid stimuli , avoid injury during episode, counter pressure and education

  • Second line: Meds- Minodrine (1st line), B-blockers or SSRIs

Dyslipidemia

Abnormal levels of lipids (fats) in the blood that are divided on the basis of density

• Risks: Primary (genetic)- familial hypercholesterolemia, Secondary- sedentary lifestyle, T2DM, excessive alcohol, poor diet, CKD, B-blockers, atypical antipsychotics

• S/S: >1000 triglycerides- eruptive xanthomas, High LDL- tendinous xanthomas, lipidemia retinalis

• Dx: Labs (lipid panel/profile)→ start screening at 20 and do once a year

• Tx: Lifestyle changes, statins if lifestyle measure don’t improve

  • Ezetimbe (Zetia), PCSK9-I (Repatha, Praluent), Omega 3 fatty acids, Bempedoic acid (nexletol)

Cardiogenic shock

Heart is not filling enough, blood pump problems decrease in CO leads to oliguria, hepatic failure, anaerobic metabolism, lactic acidosis, hypoxia→ further impairs cardiac function

• RF: age, female, large anterior wall MI, previous MI, previous CHF, DM

• S/S: HoTN, tachy/bradycardia, cool/clammy skin, oliguric, AMS, LV failure (tachypnea, rales, frothy sputum), valvular dysfunction and septal defect, JVD and abdominal jugular reflex

• Dx: Hx, ECG(consistent with MI), CHR- CHF, 2D TEE, cardiac enzymes, coag parameters, serum lactate, BNP to predict HF after MI

• Tx: medical therapy (Dobutamine OR Dopamine + Norepi) until permanent coronary patency (reperfusion modalities)

  • stabilize pt- ET tube, IV, O2, pulse ox

  • consult cardio or thoracic surgery and admit to ICU

Hypovolemic shock

Loss of circulating volume (external- dehydration, blood loss: internal- loss of vascular integrity)

• 15%: well compensated, little to no change

• 15-30%: low BP, oliguria, hypoxemia

• 30-40%: impaired compensation, severe shock

• 40-50%: refractory, death or severe organ damage

• Tx: restore volume- judicious fluid replacement, optimize O2, vasoconstrictor is BP is still low with fluids

Obstructive shock

Mechanical or physical obstruction to cardiac flow; decreased CO→ body initially compensate with vasoconstriction to increase BP→ pressure will cause back flow/obstruction

• RF: cardiac tamponade, large PE, tension pneumothorax, air embolism

• Tx: urgent eval and management of underlying cause

Acute rheumatic carditis

Inflammation of heart tissues that occurs as a serious complication of acute rheumatic fever after an untreated strep infection

• S/S: new heart murmur (MC mitral), SOB, chest discomfort, tachycardia, fatigue

• Tx: Abx to tx strep infection, anti-inflammatory drugs

Infective endocarditis

Microbial infection of valvular or endocardial surface of the heart (bacterial or fungal); commonly involves heart valves, produces lesion-vegetation

• Risks: Males, age >60 yo, IV drug use (R sided tricuspid), poor dentition, 20% on prosthetic valves, underlying heart condition, impaired immune system, HIV, hx of bacteremia, indwelling intravascular device, chronic hemodialysis (indwelling catheter)

  • Staph aureus (MC, severe s/s), strep viridians, enterococcus

• S/S: Fever, chills, sweats, anorexia, weight loss, malaise, cough

• PE: murmur, temp, emboli, splenomegaly, clubbing

  • Petechiae: microbleeding in peripheral capillaries

  • Splinter Hemorrhages: bleeding/lines under the nails

  • OSLER NODES: “OUCH”- painful violaceous nodules on finger, toes, and feet

  • JANEWAY LESIONS: painless, erythematous macules on palms or soles

  • ROTH SPOTS: retinal hemorrhages w/ pale center

• Dx: TEE, blood cultures (prior to abx)

• Tx: Empiric Vanc+Cef

Myocarditis

Inflammatory disease of the cardiac muscle; infectious, cardio toxins, hypersensitivity reactions, systemic disorders

1. Primary: acute viral or post-viral immune response

2. Secondary: non-viral pathogens, medications (cocaine), chemicals, physical agents; injury can be fulminant, subclinical (subacute), or chronic

*Chronic injury subgroups can benefit from immunosuppression

COVID19: viral infection, possibly after the vaccination, younger males (CORTICOSTEROIDS)

Viruses: Coxsackie C, cytomegalovirus, Hep C, Echovirus, Herpes 6, EBV, Flu, COVID, some childhood

S/S: Days→ weeks; acute febrile illness or respiratory infection

• Dyspnea, pleural/pericardial chest pain, arrhythmia

PE: Tachycardia, gallop rhythm, heart failure, pericardial friction rub

*CAN MIMIC AN MI W/ ST CHANGES AND BIOMARKERS

Dx: Bx dependent

Tx: Abx, colchicine, NSAIDs→ may need cardiac transplant or long term LV assist device

Pericardial effusion

Accumulation of fluid in the pericardial sac→ gradual= stretch and accommodate OR quickly= cardiac tamponade (1st affected= right atrium and ventricle)

• Transudate= L heart failure, overhydration, hypoproteinemia

• Exudate= renal failure, malignancies, infection

S/S: underlying cause, dull chest pain, dyspnea, muffled heart sounds, poorly palpated apical pulse, pulsus paradoxus

Dx: ECHO (fluid around the heart), CXR (enlarged flask shaped cardiac silhouette)

Tx: Underlying, NSAIDs, Large/cardiac tamponade= pericardiocentesis

Pericarditis

Less than 2 weeks, inflammation of the pericardium

• Risks: idiopathic, infection, surgery, CT disease, radiation, pericardial injury. myxedema, Infectious→ Viral: coxsackie, echo, influenza, EBV, varicella, hepatitis, mumps, HIV, COVID→ Bacterial: rare (TB), Males <50 yo, Uremic, neoplastic, post MI (Dressler syndrome), radiation, CT disease, drug induced

• S/S: chest pain (significant, continuous, sharp), dyspnea, fever, pericardial friction rub, TB: TB symptoms, Bacteria: inflammatory, toxic, critically ill (septic), Uremic: w/ or w/o symptoms, absent fever, Neoplastic: Often painless, increase risk of pericardial effusion

• Dx: Clinical based on criteria

• Tx: Tx underlying, NSAIDs, colchicine

Aortic stenosis

Mid-systolic (ejection) murmur due to stenosis of the aortic semilunar valve; degenerative/calcific or congenital uni/bicuspid valve

• Risks: age, males, smoker, Hx of HTN, aortic SCLEROSIS, concentric LV hypertrophy (pressure overload)

• S/S: associated with severe AS (non-severe is asymptomatic), dyspnea on exertion, presyncope/syncope, exertional angina- SAD (syncope, angina, dyspnea, w/ diminished carotid pulse)

• PE: systolic murmur, ± an ejection click, palpable LV thrill/heave, delayed/diminished carotid pulse

• DX: TTE (ECHO)

  • ECG: LVH

  • CXR: cardiomegaly, calcification of the aortic valve

• TX: Sx in pts with symptomatic severe ALWAYS, Sx in asymptomatic severe as indicated

  • SAVR (open heart): bio prosthetic or mechanical

    • Mechanical valve= permanent Warfarin tx

    • On-X= Warfarin+ ASA

    • INR target 2-3, average 2.5

  • TAVR (MC transfemoral): always a bio prosthetic valve

*Ross procedure: younger pt with bicuspid valve

Aortic regurgitation

Early diastolic murmur due to insufficiency of the aortic valve

• Risks: bicuspid valves, ineffective endocarditis, HTN, secondary to aortic root disease

  • Chronic AR: eccentric hypertrophy (dilation, grow outward for more space)

  • Acute AR: most likely from aortic dissection or endocarditis

• S/S

  • Chronic: asymptomatic, exertional dyspnea, fatigue, PND, pulmonary edema

  • Acute: LV failure→ pulmonary edema, develops rapidly

• PE: (widened pulse pressure and other weird stuff)

  • Widened pulse pressure, Watter/Hammer Corigan pulse, Quincke pulse (nail bed), Duroziez sign (sys and dia built over femoral artery), de Musset (head bob), Hill sign (BP in leg >40 mmHg higher than in arm), prominent and laterally displaces apical impulse

• DX: TTE confirmatory, EKG= mod/severe LVH, CXR= cardiomegaly ± dilated aorta

• Tx: Afterload reduction if hypertensive (ACE/ARB)

  • Acute AR: Sx replacement even if infection (SAVR tx of choice, repair possibly for younger pts)

  • Chronic AR: prognosis is poor when s/s start

Coarctation of the aorta

Localized narrowing of the aortic arch just distal to the origin of the left subclavian artery; thought to be related to accessory ductal material that contracts soon after birth

• Risks: secondary HTN, cerebral berry aneurysms, age

• S/S: if no cardiac failure in infancy, usually no s/s until LV failure, strong arterial pulses in the neck, HTN in arms, femoral pulses are weak

  • Associated w/ Turner Syndrome (X-linked)- may have webbed neck

• DX: ECHO/Doppler, cardiac cath done if stent is needed

• TX: peak gradient >20 mmHg or collateral blood vessels consider endovascular stent (if correct anatomy) or resection of coarctation site, balloon dilation

  • Long term f/u with cardiologist

Rheumatic heart disease

Permanent, chronic heart condition caused by the scarring and deformation of one or more heart valves→ typically the Mitral or the aortic valve

• S/S: “Silent”→ may cause severe damage 10-30 years after the infection, SOB, fatigue and muscle weakness, chest pain or discomfort, heart palpitations, swelling (edema)

• Dx: Hx, auscultation, ECHO, strep titers

• Tx: secondary abx prophylaxis, symptom management, surgical intervention if necessary

Mitral regurgitation

Insufficiency of the mitral valve and leaking during systolic

1. Primary MR: abnormality of 1 or more components of the valve

• Mitral valve prolapse (MC), rheumatic heart disease, endocarditis, congenital

2. Secondary MR: alterations in the left heart geometry and function

• Ventricular (CAD< cardiomyopathy), atrial (A-fib, HFpEF)

S/S: (SEVERE if ERO>40 cm²)

• Chronic MR: asymptomatic, exertional dyspnea, fatigue, A-fib (dilation of aorta)

• Acute MR: pulmonary edema

DX: ECHO

TX: Repair (preferred)- primary wait until indicated, secondary wait until severe s/s, acute emergency Sx

Mitral valve prolapse

Valve leaflets balloon upward as the ventricle contracts (regurg); midsystolic clicks ± regurgitant systolic murmur

• Risks: Pectus excavatum, scoliosis, connective tissue disease, 10% OF HEALTHY WOMEN

• S/S: usually asymptomatic, chest pain, dyspnea, fatigue, palpatations, hyperandrenergic syndrome (controversial)

• Dx: ECHO

• TX: Mitral valve repair, refer to cardiology

Mitral stenosis

Calcification, congenital, iatrogenic, rheumatic heart disease; A-fib is common, LA enlargement due to increased LA pressure

• S/S: A-fib, chest pain, pregnancy worsens s/s, Pulm HTN, diastolic

  • Mild/moderate: >1.5 cm, asymptomatic, symptomatic with extreme exertion

  • Severe: <1.5cm, decrease exercise tolerance and increase exertional dyspnea

• Dx: ECHO

• Tx: A-fib (control heart rate), valvular A-fib tx with WARFARIN (NO DOAC W/ VALVULAR A-FIB)

  • Tx of choice- percutaneous balloon valvuloplasty (repair)→ replacement if stenosis and regurg at the same time

  • MAZE at same time for A-fib

  • INR target 2.5-3.5

Pulmonic regurgitation

RV tolerated volume load better than pressure load, tends to tolerate low pressure PR for longer

• High pressure causes: Pulm HTN

• Low pressure causes: dilated Pulm, annulus, congenital bicuspid/dysplastic valve, plaque from carcinoid dz

• S/S: most asymptomatic, if marked S/S of RH volume overload

• PE: palpable RV lift possible, Graham Steel murmur (high pressure PR), low pressure PR can be absent

• Tx: Treatment of the primary cause

  • HTN: tx HTN

  • Carcinoid heart dz: PVR with bioprosthetic

  • SX: if valve is damaged (usually bioprosthetic)

Pulmonic stenosis

Most often congenital and associated other cardiac lesions

1. Domed valve (MC)

• fused or absent commissures with thickened PV leaflet

2. Dysplastic valve (Noonan Syndrome)

• irregular with prominent leaflet thickening→ small valve annulus and decreased mobility

*MC is valvular stenosis of the pulmonic valve itself

*Severe PS→ RV hypertrophy

• S/S (Mild <36mmHg, Mod 36-64 mmHg, Severe >64 mmHg)

  • Mild: asymptmatic

  • Mod/Severe: dyspnea on exertion, syncope, chest pain, RV failure

• PE: palpable parasite renal lift due to RVH, cyanosis

• DX: ECHO

• TX: Intervention in symptomatic pts and severe PS

  • Percutaneous balloon valvuloplasty= TX of choice in domed valves

  • Pulmonary valve replacement= dysplastic valve or Noonan syndrome (bioprosthetic)

Tricuspid regurgitation

• Secondary/functional TR (MC): often whenever RV dilation

  • Pulm HTN, pulmonary valve stenosis or regurgitation, cardiomyopathy, MI

• Primary TR (least common cause)

  • Valve injury from pacemaker, endocarditis, congenital

• S/S: identical to RV failure; fatigue, weakness, SOB, increased JVP, peripheral edema, hepatomegaly, ascites, S3 common

• PE: ± RV heave on palpation, uni or bilateral pleural effusions common in Pulm HTN

• DX: ECHO

• TX: Mild- diuretics, fluid overload

  • SX- annual dilation at the end of diastole exceeds 4.0 cm and patient is symptomatic- Repair over replacement if possible

Tricuspid stenosis

MCC worldwide- rheumatic fever

MCC US-carcinoid syndrome and stenosis of prior TV replacement or repair

*Frequently accompanies by tricuspid regurgitation

• S/S:fatigue, dyspnea, JVD, hepatomegaly, ascites, peripheral edema

  • SEVERE: pressure ½ time is >190 ms and valve area is <1 cm

• Tx: Diuretics, and a valve replacement (MC)

  • Percutaneous balloon valvotomy if severe

Aortic aneurysm

Localized dilation or out pouching of abdominal aorta, can be apart of aging, 90% are below renal artery (healthy is 2 cm)

• RF: Aneurysm present when diameter exceeds 3 cm, Rarely rupture until >5 cm, Male to female ration 4:1, occurs in 2% of men over 55 yo, Involve the aortic bifurcation and often the common iliac arteries

• Dx: US (screen), CT for emergent surgical planning

• Tx: Emergent surgical consult

Aortic dissection

Spontaneous initimal tear develops, blood dissects into the media of the aorta and blood flows into the lining and not the lumen, HTN is a key finding, often confused for an MI

If there is an absence of HTN, abnormalities of smooth muscle, elastic tissue, or collagen are present

• Type A: arch proximal to the left subclavian artery

• Type B: proximal descending thoracic aorta beyond the left subclavian artery

• S/S: severe sudden onset of chest pain, radiates down back-anterior chest-and neck, HTN, syncope or paralysis of lower extremities, new murmur, peripheral pulses diminished

• Dx: EKG (to eliminate MI confusion)- can show LVH might be clear, CT Chest and Abdomen (TEST OF CHOICE): line (dissection)

• Tx: Bring down BP: Beta blockers (labetelol or Esmolol), CCB if doesn’t work (nicardipine or nitroprusside IV)

• Sx

  • Type A: URGENT Sx repair

  • Type B: early thoracic stent repair if signs of malperfusion

• Uncomplicated: BP control, urgent Sx not required, monitor with yearly CT

Acute arterial insufficiency

Usually occurs acutely as a result of thrombosis or embolism (MCC- emboli from heart)

• emboli from A-fib/flutter, mitral stenosis, transmural infarction

• 10x more likely in lower extremity than upper (most common superficial femoral artery)

• Acute occlusion= severe ischemia (no collateral circulation)

• Must catch within 4-6 hours to minimize the risks of limb loss

AV malformation

Abnormal tangled web of blood vessels where high-pressure arteries that connect to low pressure veins that completely skip the capillary bed→ this increased the risk of a rupture and life threatening internal bleeding and steals oxygenated blood from healthy tissues

• Dx: CT (emergency), MRI (non-emergency), digital subtraction angiography

• Tx: endovascular embolization, microsurgical resection, stereotactic radio surgery

Atherosclerosis

1. Stage 1: endothelial dysfunction leads to formation of a fatty streak

2. Stage 2: LDL enters the intima and becomes oxidized, attracts macrophages

3. Stage 3: plaque matures to fibrous cap, vessel of lumen narrows

• Plaques can remain stable or progressive or narrowing of arteries or can rupture

  • Risks for rupture: high lipid content, high concentration of macropahage, thin fibrous cap (signs of young, immature plaques)

• Can be asymptomatic; angina, arrhythmia, MI, possible sudden death

Coronary Heart Disease

• Risks:

  • Nonmodifiable: age (Men >45, women >55), family hx, Males, Race (Hispanic, south asain, Indian)

  • Modifiable: Hyperlipidemia (hypercholesterolemia), HTN, smoking, DM, obesity, sedentary, diet/alc, psychosocial, METABOLIC SYNDROME

• S/S: Always in a state of inflammation (high-sensitivity CRP inflammatory marker)

  • Atherosclerosis: CHD results from endothelial cell dysfunction, dyslipidemia and inflammation

Deep vein thrombosis

Blood clot (thrombus) that forms in venous system, deep veins, or R side of the heart

• Can lead to PE or underlying cardiac dysfunction of stasis

• Virchow’s Triad: venous stasis, endothelial injury, hypercoagulability

• Risks: atrial dilations, catheters, pacemaker, ICD

• DX: Venous Doppler, ECHO (atrial/vent thrombi), CT Pulm angio (PE), D-dimer

• Tx: Anticoag (heparin then DOAC/Warfarin, IVC if no meds), thrombolysis or surgical thrombectomy (massive unstable)

Peripheral artery disease (PAD)

Most commonly atherosclerotic disease of the arteries that perfuse the limbs an occlusion can reduce or completely obstruct blood flow to distal tissues (arterial insufficiency) it’s chronic or acute→ occlusion of 50% of arterial lumen (75% of vessel diameter), produces significant reduction in blood flow→ Decreases blood flow causes tissue hypoxia and ischemia (severe: tissue necrosis w/ gangrene)

• Dx: First- Ankle-Brachial Ratio/Index (ABI/AAI)- normal is 1.0-1.1, <0.9 is PAD, <0.5 is critical PAD, Second- USN: arterial duplex scanning, Third- CTA/MRA: precise location and extent of vascular occlusion with contrast (Gold standard test)

• Tx: Reduce cardiovascular risk (smoking cessation, lipid/BP control, weight loss, antiplatelet), Exercise program (daily walking and tracking point of claudication)

  • Meds (after initial lifestyle changes)

    • Aspirin

    • High dose statin (atorvastatin)

    • ± Rivaroxaban (DOAC)

    • ± Cliostazol (symptom relief of claudication)

• SEVERE: vascular reconstruction or angioplasty and stenting, arterial grafts, thromboendarectomy (repairing diseased arteries), amputation in the case of gangrene

• F/U 3-6 months with stable disease and consult vascular surgery

Superficial venous thrombophlebitis

Red, painful in duration along a superficial veins, MC @ the site of an IV Line

• Risks: Pregnancy, trauma, varicose veins, systemic hyper-coagulable states, IV lines

  • Monitor site for SEPTIC phlebitis (erythema, fever, fatigue, leukocytosis)

• Dx: Hx and PE

• Tx: Symptomatic: analgesics (Tylenol) and warm compresses

  • Septic thrombophlebitis: remove lines/catheters, IV abx (VANC and CEFTRIAXONE)

Varicose veins

Dilated tortuous superficial veins in the legs due to high venous pressure

• Risks: prolonged standing, pregnancy, heavy lifting, hereditary

• S/S: dull aching heaviness of legs, worse w/ standing, itching over the ankles or large varicosities

  • older patients bleed with minimal trauma

• Dx: Hx and PE

• Tx:

  • Non-surgical: medical grade compression stockings

  • Scleortherapy: sclerosing agents to veins

  • Surgical: thermal ablation or vein stripping

Giant cell arteritis (GCA)/ Temporal arteritis

Chronic-inflammatory disease involving large and medium sized arteries, can be widespread causing stenosis and aneurysm of affected vessels

• Risks: Age (almost never before 50, usually 70-79), MC in women, caucasians (Scandinavian), Polymyalgia Rheumatica

• S/S: fever, fatigue, weight-loss, headache (scalp tenderness), jaw claudication, ocular involvement (amaruosis fugax)

• Dx: Labs- increased ESR, CRP, TEMPORAL ARTERY BIOPSY

• Tx: 1 mo prednisone (do steroid taper)

Granulomatosis with polyangitis (Wegner’s granulomatosis)

Rare, chronic autoimmune disease that cause inflammation of small to medium blood vessels (vasculitis)→ causes clusters of inflammatory cells called granulomas

• S/S: Upper respiratory (sinus, saddle nose deformity), lungs, kidneys, fevers/night sweats/joint pain

• Dx: ANCA blood test, X-ray/CT for noduels, bx

• Tx: Prednisone +Rituximab

Polyarteritis Nodosa

Rare, systemic AI disease with necrotizing inflammation of medium and small muscular arteries that causes microaneurysms

• S/S: typically spares the lungs, painful red subcutaneous nodules, deep skin ulcers, livedo reticularis (purple lace like web discoloration), damage to peripheral nerves, difficult to control high blood pressure

• Dx: tissue bx, angiography

• Tx: IV glucocorticoids, Aziathoprine (maintenance)

IgA Vasculitis (Henoch-Schonlein Purpura)

Immune complex mediated small vessel vasculitis; IgA deposits on the inside walls of capillaries, venules and arterioles

• S/S: palpable purpura, arthralgia, GI distress, Kidney involvement/nephritis

• Dx: skin biopsy, urine analysis and serum creatine

• Tx: self limiting

Chronic venous insufficiency

Inadequate venous return over a long period of time

• Risks: prior DVT, leg trauma/surgery, obesity

• S/S: progressive pitting edema, itching-dull-aching after standing, taut shiny skin at ankle, brownish discoloration of the skin, ulcerations above the ankles, frequent cellulitis

• Dx: Hx and PE

• Tx: prevention of primary causes, graduated compression stockings, meticulous wound care in cellulitis

Acute respiratory distress syndrome

onset of respiratory distress, progressive respiratory failure within 7 days of known clinical insult, new bilateral radiographic pulmonary opacities not explained by pleural effusion, atelectasis, or nodules/heart failure or volume overload→ alveoli cannot expand or exchange oxygen

• impaired oxygenation of paO2/fiO2 <300 mmHg w/ peep 5 cm of H2O or more

• Risks: ICU patients, age, organ dysfunction, chronic medical illness, lung injury, pneumonia (MC), severe sepsis, aspiration

• S/S: profound dyspnea, labored breathing, tachypnea, intercostal retractions, crackles, marked hypoxemia that is refractory to supplemental O2

• Dx: Chest x-ray (new bilateral radiographic opacities), diffuse or patchy bilateral infiltrates, air bronchograms, possible PE

• Tx: treat underlying cause, decrease tidal volume ventilation, use low setting PEEP vent, prone position, monitor airway pressures, conservative fluid management (dieresis), HOB at 30 degrees, pressure ulcer prevention

Acute respiratory failure

respiratory dysfunction causing impairment of ventilation severe enough to threaten vital organs (consequence of a disease)

• ABGs criteria: PO2 <60 mmHg, PCO2 >55 mmHg

• Risks: lung parenchyma infections, lung parenchyma disorders, pleural/chest wall/airway disorders

• S/S: of the underlying cause, hypoxemia (cyanosis, confusion, tachypnea, lethargy), hypercapnia (dyspnea, headache, hyperemia, asterixis)

• Dx: ABG (use criteria)

• Tx: adequate oxygenation, possible mechanical ventilation, general supportive care

Asthma

airway inflammation resulting in reversible bronchoconstriction (obstruction); airway edema and inflammation, airway hyperactivity and remodeling→ IgE mast cell response

• Risks: Black pts, low socioeconomic status, obesity, genetic (atopic patients), childhood males

  • Triggers: allergens, exercise, URIs, rhinosinusitis, PND, aspiration, GERD, change in weather

• S/S: can be asymptomatic b/t exacerbations→ dyspnea, wheezing, coughing, severe disease can be nocturnal, hyperresonance to percussion (excess air), possible accessory muscle use 

• Dx: Hx and PE confirmed with PFTs, bronchodilator challenge, bronchial provocation testing

• Tx

  • Intermittent- low dose ICS-formoterol PRN

  • Mild persistent- low dose ICS-formoterol PRN (can add SABA)

  • Moderate persistent- low dose ICS-formoterol maintenance with reliever therapy

  • Severe persistent- medium dose ICS-formoterol maintenance with reliever therapy

Bronchiectasis

manifestation of disease→ Obstructive Pulmonary disease; manifestation of dilation and destruction of larger bronchi caused by chronic inflammation or infection (diffuse or focal)

• Risks: CF, immune defects, recurrent infection, TB and HIV, sometimes idiopathic 

• S/S: chronic cough with copious purulent sputum, hemoptysis, Pleuritic chest pain, dyspnea (75%), Persistent crackles at lung base, clubbing

• Dx: Hx, Chest X-Ray (dilated airways), High Resolution CT (gold standard), Culture (P. aeruginosa, S. Pneumonia and S. aureus, H. flu (CF))

• Tx: Abx, inhaled bronchodilators

• Complications: hemoptysis, cor pulmonale, secondary visceral abscess at distant sites

COPD

small airway disease with parenchymal obstruction; obstructive pulmonary disease that is non/partially reversible

1. Emphysema: “pink puffer”, permanent abnormal distention of air spaces distal to the terminal bronchiole with destruction of alveolar septa and attachments to bronchial walls, lung hyperinflammation, air flow limit and trapping, barrel chest, absent breath sounds

2. Chronic bronchitis: “blue bloater”, chronic productive cough for at least 3 months for 2 years, cyanotic, crackles/rhonchi/wheezing

Can be mixed

• Risks: smokers (MC), low birth weight, low socioeconomic status, air pollution, family hx, allergies

• Dx: based on pt history

• Tx: smoking cessation, pulmonary rehab, vaccinations, bronchodilators, ICS, supplemental O2 if needed

Idiopathic pulmonary fibrosis

Chronic, progressive, and irreversible lung disease characterized by the scarring (fibrosis) of lung tissue without an identifiable cause→ over time the normal lung tissue will be replace by a thick, stiff scare tissue that prevents alveoli from transferring O2

• S/S: progressive dyspnea, persistent dry cough, digital clubbing, constitutional symptoms

• Dx: CT, PFTs

• Tx: antifibrotic drugs, supportive care, lung transplant

Acute bronchitis

infectious disorder; inflammation (self-limited) of the large airways of the lung that extends to the tertiary bronchi; leads to inflammation and thickening of bronchial and tracheal mucosa; can be obstructive with bronchial hyperresponsiveness

• MC from a viral infection (No abx needed), Can be bacterial

  • Influenza A and B, parainfluenza, RSV, COVID, adenovirus, rhinovirus

• Risks: adults, winter season, exposure to virus/bacteria

• S/S: cough of recent onset, extended period of cough >7 days, coughs that start nonproductive and progress to productive coughs, URI, wheezing, dyspnea

  • PE: cough, wheeze, rhonchi, URI symptoms, can vary at time of exam

• Dx: Clinical and r/o pneumonia

• Tx: supportive care

Acute epiglottis

life-threatening airway emergency caused by inflammation and swelling of the epiglottis and surrounding supra epiglottic tissues- rapidly obstruct airway

• Risks: Children 2-6, unvaccinated/immunocompromised pts

• Etiology: H Fly type B, Strep, Staph including MRSA

• S/S: (4D,S: Dysphagia, drooling, dysphonia, dyspnea, stridor)

• Dx: SECURE AIRWAY, Lateral neck X-Ray (thumbprint sign)

• Tx: Intubation, IV antibiotics (ceftriaxone), IV corticosteroids

• Hib vaccine for prevention

Mnemonic: Tripod child with thumbprint sign 

Empyema

Collection of pus in the pleural cavity

• Risks: bacterial pneumonia, thoracic sx or trauma, aspiration, esophageal perforation

• S/S: high fever, chills/nightsweats, pleuritic pain, progressive SOB,

• Dx: CT with contrast, US, thoracentesis

• Tx: medical drainage vs sx options

Influenza

nfectious disorder, viral respiratory infection caused by the influenza viruses and other viral respiratory pathogens; trick immune system through antigenic drift and antigenic shifts

• Risks: fall/winter, young children, old age, pregnancy, impaired respiratory function

• S/S: Rhinitis, cough, sore throat, increase fever with chills, severe myalgia, anorexia/malaise, ocular symptoms

• Dx: Rapid influenza diagnostic tests→ can also use PCR

• Tx: Supportive care, antivirals if critically ill

Bacterial pneumonia

• Risks: Strep pneumoniae, H flu, klebsiella pneumoniae, staph aureus, psuedomonas, Atypical- Mycoplasma, legionella, chlamydia

• S/S: acute onset high fever, productive cough with purulent sputum, pleuritic chest pain

• Dx: CXR- lobar consolidation in typical, interstitial infiltrate in atypical, blood cultures and sputum gram stain

• Tx

  • Outpatient: Amoxicillin OR Doxy OR Azithromycin

  • Inpatient: Respiratory fluoroquinolone OR Ceftriaxone+Macrolide

Viral pneumonia

• Influenza is the MCC of viral CAP; others include RSV, parainfluenza, adenovirus, COVID

• S/S: acute/subacute onset of fever, cough, dyspnea, ± sputum production, sweats, chills, rigors, chest discomfort, pleurisy, myalgias, fatigue

• Elderly patients: present atypically (falls, AMS, lethargy)

• PE: increase temp, tachypnea (besides Legionarre’s), O2 desat, inspiratory disease, inspiratory crackles, (+) special tests, dullness to percussion

• Dx: Chest XRAY, isolate with sputum culture, Pneumonia severity index (PSI)

  • 90 or less= tx at home

  • 90 more more= hospital

• Tx: supportive, can give antivirals for influenza within 48 hrs of symptom onset

HIV-related Pneumonia

Directly related to CD4 T-lymphocyte count; Pneumocystis jirovecii pneumonia (PCP) under 200 cells/microliter (if under 200 can do prophylaxis with Bactrim)

• S/S: subacute dyspnea on exertion, non-productive cough, fevers, exertion hypoxemia

• Dx: markedly elevated LDH, CXR- bilateral diffuse ground glass perihilar infiltrates

• Tx: Bactrim and can add systemic corticosteroids

Histoplasma capsulatum

• Risks: Ohio and Mississippi River valleys, bat dropping or bird roosts, caves

• S/S: palatal/oral ulcers, hepatosplenomegaly

• Dx: urinary antigen , CXR- hilar lymphadenopathy and granulomas

• Tx: Itraconazole/Amphotericin B

Blastomyces dermatitidis

• Risks: Great Lakes and ohio river valleys, decaying wood, organic soil

• S/S: verrucous skin lesions and osteomyelitis

• Dx: smashed broad based budding yeast on smear