CVPR Exam: Aorta Diseases & Vascular System

• CVPR Summative Exam #1 will consist of 50 questions all on CV topics with ~30 CV topics covered.
• Each topic will provide 1-3 questions.
• Every question will be based on a PA objective like HYN, Correlations, Supplemental resources, PANCE Prep Pearls, Up To Date, and Books (Lilly, Costanzo).
• The exam will not cover any histology, pathology, or intracellular mechanisms.
• The blueprint will be posted by Friday April 10th at 5 PM.

Diseases of the Aorta Objectives

• Risk factors, causes, clinical presentation, differential diagnosis, tests, complications, and management, and any pharmacotherapy should be compared among: abdominal aortic aneurysm, thoracic aortic aneurysm, abdominal aortic rupture, coarctation of the aorta, and peripheral artery disease.
• The ankle-brachial index study results needs to be interpreted.
• Understand the clinical significance and treatment of claudication.
• The risk factors, common causes, clinical presentation, differential diagnosis, diagnostic tests, complications, management, and pharmacotherapy needs to be compared among peripheral arterial disease, venous insufficiency, renovascular disease, atheroembolic disease, cholesterol emboli, and arterial embolus/thrombosis.

Peripheral Arterial Disease (PAD)

• Risk factor is smoking.
• Characterized by narrowing or occlusion of peripheral arteries due to atherosclerotic plaque.
• Spectrum of supply/demand mismatch includes:
  • Stage I: Asymptomatic
  • Stage II: Pain on exertion
  • Stage III: Resting pain
  • Stage IV: Tissue death(necrosis), ulcers, or gangrene

PAD Diagnostics

• The diagnostics used are ankle brachial index, duplex ultrasonography, CT angiography and invasive angiography.

Clinical Manifestations of PAD

• Clinical manifestations include claudication (buttocks, hip, thigh, calf, foot), atypical extremity pain, diminished pulses, swelling and pain.
• Other symptoms are: Leg/foot being cool to the touch, discoloration (pallor or erythematous), no hair, shiny, taut skin.
• Can also present with deep well-demarcated ulcers, with sores, necrosis, and foot pallor with elevation of lower extremity.

Treatment of PAD

• Treatment includes smoking cessation, supervised exercise and Vasodilators.
• Medical options are anti-platelet meds (clopidogrel) and statins.
• Surgical Interventions to open blocked arteries can be considered, including bypass, ballooning, and stenting.
• Amputation can be needed

Venous Insufficiency (Venous Stasis)

• The pathophysiology of this disorder stems from blood pooling in the lower extremities, which leads to increased venous pressure, causing vein dilation, skin changes, and skin ulceration.
• Causes include incompetent valves, inadequate muscle pump, venous thrombosis, and non-thrombotic venous obstruction.
• Risk factors: Advancing age, female sex, FH of venous disease, prolonged standing, increased BMI, smoking, LE trauma, prior lower extremity VTE, and increased parity.

Venous Insufficiency Clinical Features

• Symptoms include leg pain, aching, heaviness, tightness, skin dryness or itching, and swelling.
• Signs include telangiectasias, reticular veins, varicose veins, edema, skin changes, lipodermasclerosis, venous ulcerations, and pigmentations and dermatitis.

PAD vs. Venous Insufficiency Changes

• Peripheral Arterial Disease: diminished pulses, swelling, painful, Leg/foot cool to touch, discolored, no hair, shiny and taut skin, deep well-demarcated ulcers, with sores, necrosis
• Venous Insufficiency: Palpable pulses, swelling, achy, leg is warm, discolored, still has hair, itchy and hardened flaky skin, hemosiderin staining on anterior shins, visible varicose veins, shallow and irregular-edged ulcers.

Pericardial Disease

• This comparison includes risk factors, pathophysiology, common causes, clinical presentation, differential diagnosis, diagnostic tests, complications, and management, and any pharmacotherapy between pericarditis, pericardial effusion, pericardial tamponade, and chronic constrictive pericarditis.

Acute Pericarditis

• The most common pericardial disorder where an immune mediated process causes inflammation of the pericardium, and it can be acute or chronic.

Etiology of Pericarditis

• The number one cause is viral(coxsackie virus).
• Other causes are: bacterial, uremic, post-MI(w/in 1-3 days), autoimmune disease, spread of pneumonia to pericardium and surgical complication.
• Rare causes include fungal, toxoplasmosis and tuberculosis.

Clinical Features/Diagnosis of Pericarditis

• Diagnosis is based on 2 of 4 criteria, 1) Characteristic chest pain, 2) Pericardial friction rub, 3) Typical EKG findings, and 4) New or worsening pericardial effusion

Symptoms

• Fever, sharp and acute pleuritic chest pain, improves when sitting up or leaning forward, worsens when laying flat, and recent URI symptoms

May Also See

• Fever, leukocytosis and elevated ESR/CRP

Treatment/Complications of Pericarditis

• NSAIDS with Ibuprofen or indomethacin.
• Treat symptomatically.
• Can also treat with steroids, colchicine, aspirin and underlying disorder.
• Can cause recurrent or chronic pericarditis and in very rare cases, pericardial tamponade.

Pericardial Effusion

• Fluid accumulation in the pericardium.
• Etiology is: Cancer mets to pericardium, uremia, pericarditis, ventricular free wall rupture and trauma.

Cardiac Tamponade

• Rapid accumulation of fluid that causes a decrease in cardiac output
• High pericardial pressures cause a restriction of chambers, resulting in the pericardium not being able to expand causing elevated pressures.
• Acute Effusions is when a small amount of fluid causes tamponade
• Chronic Effusions is when large amounts of fluid causes tamponade.

Clinical Presentation of Cardiac Tamponade

• Symptoms are pulsus paradoxus and dyspnea.
• Becks Triad includes distant heart sounds, elevated JVP, and hypotension.
• A CXR would show a water bottle sign.
• EKG Findings include sinus Tachycardia, low voltage on EKG, Electrical Alternans (pathognomonic) and Cardiac arrest (PEA) which causes death.

Pulsus Paradoxus

• It is manifested in a drop in SBP of >10 mm Hg with inspiration.

Treatment of Cardiac Tamponade

• Emergent pericardiocentesis and treating underlying cause
• Untreated Cardiac Arrest (PEA) leads to Death

Chronic Constrictive Pericarditis

• Pathophysiology involves thickening/rigidity of pericardium.
• Results in backward and forward flow problems which lead to low cardiac output
• Causes are: Acute pericarditis leading to chronic, radiation to the chest, and heart surgery

Symptoms

• Fatigue, dyspnea, and signs of right heart failure such as elevated Jugular Venous Pressure, peripheral lower extremity edema, liver congestion, "Pericardial knock" and Kussmaul's sign.
• Another indication is pulmonary edema which is a possible Left Heart Failure sign.
• Symptoms and physiology are very similar to restrictive cardiomyopathy.

Kussmauls Sign

• Most common causes are: Constrictive pericarditis, Right side heart failure, Right ventricular infarction, and restrictive cardiomyopathy

Diagnosis of Chronic Constrictive Pericarditis

• To diagnose use Echocardiogram to find Increased pericardial thickness, abnormal ventricular filling during early diastole, with variation in ventricular filling with inspiration, and look for moderate biatrial enlargement.
• Cardiac CT/MRI to find Pericardial thickening (>2mm), calcification, and assess the Normal Cardiac silhouette.
• Use CXR to see if the area is showing Normal or slightly increased.
• Looking for signs of Pericardial calcifications
• Finally use Pericardiocentesis with fluid analysis.

Heart Failure

• Heart failure is a clinical syndrome stemming from structural or functional impairment of ventricular filling or ejection.
• Diagnosis is clinical, characterized by a constellation of symptoms, lab values, and imaging findings.
• Remodeling from a prior insult, fibrosis, and cell death.
• If untreated, heart failure is progressive
• Increased LV end diastolic pressure (LVEDP) and decreased CO are hallmarks of heart failure.

Pathophysiology of Heart Failure

• Low CO leads to decreased blood flow and activation of RAAS, sympathetic nervous system, and antidiuretic hormone.
• Decreased blood flow will lead to vasoconstriction, increased afterload, increased water/sodium retention, and increased total body water.
• The end result is congestion.

Diastolic Heart Failure

• This also known as HFpEF (Heart Failure Preserved Ejection Fraction)
• Age >65, Restrictive or hypertrophic cardiomyopathy, HTN
• Symptoms of dyspnea on exertion, orthopnea, paroxysmal Nocturnal Dyspnea, cough with frothy white
• Will hear the S4 heart sound
• CXR will show Pulmonary congestion
• ECG with LVH
• Echocardiogram with Normal EF (>50%) with Abnormal LV indices
• Elevated BNP and Elevated ANP

Systolic Heart Failure

• This is also known as HFrEF (Heart Failure Reduced Ejection Fraction)
• Age
• Comorbidities are dilated cardiomyopathy, valvular heart disease, myocardial infarction.
• You will hear Displaced PMI and S3 and Valvular sounds
• CXR with cardiomegaly, pulmonary edema and pleural Effusions with curly B lines.
• Echocardiogram with Decreased EF (
• There are elevated BNP and Elevated ANP

Causes of Right Sided Heart Failure

• Can be caused by Left sided heart failure, pulmonary HTN (COPD, Interstitial Lung Disease, HIV, Drug Use), and Valvular Disease (Pulmonary, Tricuspid)

Symptoms of Right Sided Heart Failure

• Presents with Peripheral edema, Hepatomegaly, Splenomegaly, and Jugular venous distention Ascites

Treatment of Right Heart Failure

• Try to treat the underlying problem and use ACE-Inhibitors
• This will Decrease afterload and prevent aldosterone mediated salt and water retention

Cardiomyopathies

• These are diseases that affect the structural components of the myocardium.
• These lead to cardiac dysfunction.
• Primary categories are dilated, hypertrophic, and restrictive.
• A frequent end result is heart failure.

Hypertrophy and Cardiac Muscle Remodeling

• Eccentric: sarcomeres added in series
• Concentric: sarcomeres added in parallel

Concentric Cardiomyopathy

• 2 types include obstructive where there is a disordered septal hypertrophy that is secondary to genetic defects within the sarcomeres.
• Non-Obstructive shows concentric hypertrophy of the ventricle due to high afterload like HTN and Aortic stenosis.

Obstructive Hypertrophic Cardiomyopathy (HCM) Presentation

• Is genetic HOCM or the patient has Fredrich's ataxia
• Presentation of syncope, dyspnea, angina, mitral regurgitation, S4 gallop, Harsh Crescendo- decrescendo murmur
• A sudden cardiac death, especially in young athletes
• Check for CXR which will show cardiomegaly and dilated L atrium
• Echo is asymmetrical LVH preferentially involving the septum
• Can maintain ventricular filling to prevent obstruction by keeping preload high, and want to avoid dehydration.
• Beta Blocker and Calcium Channel Blockers can be used.
• Need to stop athletic endeavors

Non-Obstructive Hypertrophic Cardiomyopathy

• Is caused by Hypertension, Aortic Stenosis, Athletic Heart and Other valvular disease.
• Look for Syncope, Dyspnea, Angina or a S4 Gallop
• Diagnosis uses CXR to see cardiomegaly and enlarged L atrium
• Echo will show symmetrical LVH and diastolic dysfunction
• Treat the underlying disorder and manage diastolic heart failure like ACEI/ARBS, Beta Blockers, Diuretics

Eccentric LVH

• Chronic Increase end diastolic volume(preload) can cause dilated ventricle that starts to wall thinning as a direct result which leads to floppiness.
• Causes are Aortic/Mitral regurgitation, Ischemic heart disease, genetics or Myocarditis

Dilated Cardiomyopathy

• dilation of all 4 chambers that causes systolic dysfunction.
• Causes might be Idiopathic, genetic, ETOH, Thiamine Deficiency (wet beriberi), Chagas Disease, Chemo (Anthracyclines), Pregnancy, Hemochromatosis/Sarcoid, Iron poisoning, Thyrotoxicosis, Stress (Takotsubo) or Duchenne Muscular Dystrophy
• Sx are Dyspnea, Fatigue, Orthopnea, JVD, Lower extremity edema and Rales
• Use Transthoracic Echo for diagnosis that will lead to heart transplant or treat underlying cause

Cardiac Restrictive Disease

• Infiltrative diseases cause abnormal stiffness
• Leads to diastolic dysfunction
• Infiltrative causes like Amyloid, Sarcoid or Hyper- eosinophilic can lead to disease

Restrictive Cardiomyopathy (Take Homes)

• A disease known for Something taking place of normal heart muscle that creates Infiltrative Disorders like Amyloid, Sarcoid, Hyper- eosinophilic.
• Presentation of dyspnea on exertion, Weakness, Exercise intolerance, Peripheral edema, Ascites, or S4 Gallop which will lead to a diagnosis of cardiomegaly
• CXR is required for diagnosis of cardiomegaly
• Treatment needed to Treat underlying disease

Infective Endocarditis

• A 28-year-old heroin user presents to the emergency department with complaint of 4 days of fevers, chills, nausea, and night sweats, with T: 39.0, HR: 113, RR: 22, and Cardiac exam that is significant for a holosystolic murmur
• Differential diagnosis is infection, endocarditis, bacteremia, pneumonia, and a new heart murmur.
• Get 3 positive blood cultures growing Staph Aureus and his transthoracic echocardiogram demonstrated a vegetation one the tricuspid heart valve then treat with IV Vancomycin for infective endocarditis .
• Can lead to such complications
• Vascular: Major arterial emboli and Janeway lesions (painless)
• Immunologic: Osler nodes and Roth spots
• In conclusion to help diagnose use “Modified Duke Criteria"

Types of IE & Treatments (Take Homes)

• Common organisms are Staphylococcus aureus (31%), Streptococcus viridans (17%), Coagulase-negative staphylococci (11%), Enterococcus (11%), and Streptococcus bovis (7%).
• To help treat that bacteria use IV antibiotics tailored to the isolated bacteria like Vancomycin to target bacteria over a 6 week span that will help with the following conditions: Symptomatic heart failure and valvular dysfunction, Left sided IE caused by fungal infections or highly resistant organisms, Persistent infection despite 1 week of appropriate antibiotics

Right vs Left Sided Endocarditis

• Right sided infective endocarditis has most commonly a tricuspid valve and infective agent is Staph. aureus, but for a left side Mitral valve is impacted and infective agent is Strep.viridans.
• It has potential complications relating to morbidity with 31% of peripheral embolizations that can lead to a stroke at 17% as reported in a study done at 48% who had cardiac surgery
• In Conclusion Morality ranges at 20% in house and 40% at the 1 year mark.

Libman-Sacks Endocarditis

• Is non-bacterial endocarditis composed of small to medium-sized vegetations
• It manifests sterile platelet thrombi on heart valves and the thrombi are very fragile
• Is associated with lupus is found in most patients until a complication develops.
• If Complications manifest with is Embolization that has a long term affect it depends but typically you’ll find patients with Lupus and ant-phospholipid syndrome
• To help with future patients with this disease you will need to use anti-coagulates to reduce such risk.