UWorld 4 Flashcards
2 primary presentations of Chagas
Megacolon/megaesophagus and cardiac disease
What causes Chagas?
The protozoan Trypanosoma Cruzi. Endemic to Latin America. Look out for an immigrant with CHF symptoms or megacolon/megaesophagus. Megacolon/megaesophagus is secondary to destruction of the nerves controlling GI smooth muscle
Autonomic neuropathy in setting of orthostatic hypotension
Look out for this as a difficult to spot culprit leading to ortho hypo. Examples of conditions that an cause an autonomic neuropathy could be diabetes and Parkinson’s. Also Amyloid, Uremia, Hepatic diseases, vitamin deficiencies, Chagas, HIV, autoimmune diseases (like any of them), Lyme, Botulism, GBS, porphyria, etc.
Amiodarone-induced interstitial pneumonitis presentation
Progressive dyspnea, nonproductive cough, bilateral inspiratory crackles. CXR shows localized or diffuse reticular or ground-glass opacities (can be migratory). PFTs reveal restrictive pattern with reduced diffusion capacity for CO (DLCO).
Pulm side effects of amiodarone are interstitial pneumonitis (within MONTHS of therapy), organizing pneumonia, ARDS, diffuse alveolar hemorrhage, pulm nodules, and solitary masses.
Look out for a person who has been started on an “antiarrhytmic” months ago.
GERD typical presentation
Retrosternal burning that is worse when lying down (recumbent, supine) and is not associated with exertion. Classically, patients report symptoms 30-60 minutes after eating and describe relief with antacids.
Look out for chronic cough due to reflux of gastric secretions into lungs, and hoarseness from reflux-induced laryngitis.
Tx is with H2 blockers (ranitidine) or PPIs.
When is S4 heard?
TEN-nes-see. It is at the end of diastole just before S1. In adults, S4 indicates a stiff LV which occurs in setting of restrictive cardiomyopathy or LVH from prolonged HTN. S4 corresponds to atrial contraction and is believed to result from the sound of blood striking a stiffened LV.
The prolonged HTN is the most important thing to take away here.
Etiologies of PAD
1) Atherosclerosis due to risk factors (diabetes, hyperlipidemia, HTN, smoking, age over 70)
2) Thromboangiitis obliterans (Buerger’s Disease)
Clinical presentation of PAD
Asymptomatic (20-50%)
Physical Exam findings
1) Low or absent pulses below the level of stenosis
2) Occasional bruits over stenotic lesions
3) Poor wound healing in areas of diminished perfusion
4) Cool extremity with prolonged venous filling time
5) Shiny, atrophied skin with nail changes
6) Foot pallor with leg elevation (Buerger’s test)
Specific pain patterns
1) Butt and hip pain (aortoiliac disease) - Bilateral diminished or absent groin pulses, occasional bruits over iliac and femoral arteries, muscle atrophy and slow wound healing in legs. Leriche’s Syndrome - Triad of ED, butt and hip pain, and absent femoral pulses on exam.
2) Thigh pain (aortoiliac or common femoral disease) - normal groin pulses but decreases distal pulses
3) Calf pain (most common) - increasing pain with exertion and decreased with rest. Upper 2/3 of calf (superficial femoral artery disease). Lower 1/3 of calf is popliteal artery disease.
4) Foot pain (tibial or peroneal artery disease)
Tx for PAD
Most useful intervention to improve functional capacity and reduce claudication in PAD patients is a supervised graded exercise program.
Antiplatelet agents (aspirin, clopidogrel) do not consistently reduce claudication symptoms but are STILL indicated to reduce risk of MI, stroke, and CV mortality. Other measures for treating PAD including stopping smoking, aggressive diabetes control (A1C below 7), and BP control.
Also, high intensity statin (atorvastatin 40-80mg or rosuvastatin 20-40mg) is recommended for reducing CV risk in patients up to age 75 with clinically significant atherosclerotic CV Disease. ASCVD includes ACS, MI, stable or unstable angina, coronary or other arterial revascularization, stroke/TIA or PAD*.
Moderate intensity statin therapy may be considered in patients above 75.
Statin therapy is also rec’d for all patients 40-75 with diabetes, LDL baseline of at least 190 or ASCVD risk of at least 7.5%.
When is S3 heard?
Ken-tuc-KY. Low frequency diastolic sound heard just after S2. Believed to result when inflow from LA strikes blood that is already in LV, causing reverberation of blood between LV walls.
Extra sound can be normal in younger people and well-trained athletes, but later in life appearance is often associated with LV failure. When CHF signs are also present the most appropriate therapy is IV diuretics.
Stress testing in patients considered low risk for CAD
Men under 40 and women under 50 with atypical chest pain and no significant cardiac risk factors (non smoker, no FHx of premature CAD)
Stress testing in low risk patients has no benefit. A positive result is likely a false positive and will lead to more testing. Keep in mind that a negative result in a high risk patient is also likely to be false.
Stress testing is really only good for risk stratification in intermediate risk individuals.
MI leading to MR. What happens to LVEDP?
It goes up. Acute MR leads to excessive volume of blood leaking back into LA. During diastole, there is initial rapid passive filling of the LV, which is further augmented by LA contraction at end diastole. Acute MR (or acute AR) leads to excessive diastolic volume overload which in turns causes elevated LVEDP/filling pressure.
The elevated LV filling pressure is reflected back in LA and pulmonary circulation and is responsible for the signs and symptoms of acute pulmonary edema and CHF
Sudden onset of chest pain, ST elevations, holosystolic murmur at apex, and bibasilar crackles
Think inferior wall MI (leads II, III, aVF) with papillary muscle displacement leading to acute MR and pulm edema.
chronic MR heart changes
1) LA size and/or compliance are increased in chronic MR as the LA dilates gradually over time to accommodate excessive LA volume and pressure. A normal LA is not compliant, and the sudden increase in LA volume with acute MR causes an abrupt increase in LA pressures, leading to acute pulm edema. No real change in acute MR.
2) LV compliance is increased in patients with chronic LV volume overload (chronic MR or AR) but doesnt change much in acute MR. Patients with acute MI may have decreased LV compliance due to impaired myocardial contractility in ischemic or infarcted myocardium
Management of patients with acute aortic dissection
1) Pain relief with morphine
2) IV beta blockers for a target systolic BP of 100-120. Also decreases HR and LV contractility to reduce aortic wall stress.
3) Transfer to ICU
4) Initiate additional vasodilator (sodium nitroprusside) if systolic BP remains high
5) Surgery for acute ascending (type A) aortic dissections and complicated descending aortic dissections.
This is a surgical emergency (type A) with mortality rates of 1-2% per hour following symptom onset.
Avoid thrombolytics and anticoagulation due to risks of bleeding and propagation of dissection into pericardial space (hemopericardium). Though, IV heparin is appropriate sometimes in patients with ACS or pulm embolism)
Beck’s triad
Indicates cardiac tamponade. Hypotension, distended neck veins, and muffled heart sounds. Pulsus paradoxus is also common. Ab exam may also show hepatojugular reflux.
Cardiac tamponade effects on the heart
Restricts venous return to the heart and lowers right and left ventricular filling. Net result is decreased preload, stroke volume and CO.
Also decreases RV compliance and shifts IV septum towards LV cavity to further reduce LV filling.
Lung exam usually shows clear lungs due to decreased ventricular filling (preload) rather than volume overload.
Why does inspiration worsen cardiac tamponade?
By lowering intrathoracic pressure and increasing venous return to RV.
Under normal conditions, the RV is able to accomodate this increased venous return by expanding the RV free wall.
Cardiac tamponade decreases RV compliance and shifts IV septum towards LV cavity to further reduce LV filling.
This mechanism is also responsible for pulsus paradoxus.
Usual causes of LV outflow obstruction
Critical AS or Hypertrophic Obstructive Cardiomyopathy (HOCM)
Pulm Embolism CXR
May show atelectasis, infiltrates, pleural effusions, Westermark’s sign (peripheral hyperlucency due to oligemia), Hamptom’s hump (peripheral wedge of lung opacity due to pulm infarction)
The overall sensitivity and specificity of these findings are really low. CXRs can be totally normal and are not useful for PE diagnosis, though they are good for ruling out other causes of CP and dyspnea like pneumonia, pneumothorax, aortic dissection, and pericardial effusion
Cardiac myxoma
Tumor characteristics - 80% are in LA
Clinical
1) Constitutional symptoms (fever, weight loss, Raynaud). These symptoms come from overproduction of IL-6
2) CV complications - valvular issues (mitral), HF due to anatomic obstruction, myocardial invasion causing arrhythmia, heart block, or pericardial effusion
3) Embolization (L sided weakness for example, stroke, TIA, splenic infarct)
4) Lung invasion causing respiratory symptoms mimicking bronchogenic carcinoma
Dx and management
1) Echo (TEE most sensitive but TTE is usually fine)
2) Prompt surgical resection
You might hear the early diastolic sound (tumor plop)
ECG for AFib
Absent P waves replaced by tiny chaotic fibrillatory waves, irregularly irregular RR intervals and narrow QRS complexes
What is the most common side for ectopic foci in AFib
The pulmonary veins. Cardiac tissue extends into the pulm veins and normally functions like a sphincter to reduce reflux of blood into the PVs during atrial systole.
The tissue has different electrical properties than the surrounding atrial myocytes and is prone to ectopic electrical foci and/or aberrent conduction which can initiate AF
Origination of AF in the PVs is useful in patients who cannot achieve rate and/or rhythm control with standard medical therapy. In these patients, the myocardial tissue surrounding the PVs can be disrupted by catheter-based radiofrequency ablation, thereby electrically disconnecting the PVs from the LA.
Most common cause of Atrial flutter
Reentrant circuit around the tricuspid annulus, with slowing of the impulse through a region known as the cavotricuspid isthmus. Look for sawtooth flutter waves.
What causes AVNRT?
Results from reentrant circuit formed by 2 separate conducting pathways within the AV node.
What causes AVRT?
Reentrant circuit involving an accessory Atrioventricular bypass tract
Late presentation of aortic coarctation
Presentation
1) ASx HTN most common
2) CP, claudication, HA, epistaxis, HF, aortic dissection in severe cases
Exam
1) Brachial-femoral delay (palpate pulses simultaneously)
2) Upper extremity HTN, lower extremity hypotension
3) Continuous cardiac murmur from large collaterals
Dx
1) ECG - LVH
2) CXR - Notching of 3-8 ribs from enlarged intercostal arteries. 3 sign from aortic indentation.
3) Echo - diagnostic confirmation
Tx
1) Balloon angio plus or minus stent
Associated conditions
1) Bicuspid aortic valve
2) Ventricular septal defect
3) Turner Syndrome
3 physical exam features of severe AS
1) Diminished and delayed carotid pulse (pulsus parvus and tardus) due to blood flow obstruction
2) Mid to late peaking systolic murmur from turbulence due to the stenosis
3) Presence of soft and single second heart sound (S2)!!! Thickening and calcification of the aortic leaflets leads to reduced mobility and causes a soft S2, as S2 is due mainly to sudden aortic valve closure (A2). In addition, as a result of the reduced mobility, A2 is delayed and occurs simultaneously with pulmonic valve closure (P2) leading to a single S2 (not split)
Opening snap
Mitral Stenosis. Loud first heart sound.
Atheroembolism
AKA cholesterol embolism
It is a complication of cardiac cath and other vascular procedures. It is characterized by cutaneous findings (blue toe syndrome, livedo reticularis), cerebral or intestinal ischemia, AKI, and Hollenhorst plaques (retina - bright yellow refractile plaques in retinal artery. these indicate proximal source like internal carotid)
Clinical manifestations can be immediate or delayed (more than 30 days after inciting event).
It is caused by disruption of athero plaque causing cholesterol crystals and debris are showered into circulation.
Tx is supportive and includes statin therapy for risk factor reduction and prevention of recurrent cholesterol embolism
Tx of choice for Dressler
First of all, Dressler is a pericarditis that can occur weeks after MI. Malaise and sometimes fever are typical. ESR is often high.
NSAIDs. Avoid anticoagulation to prevent development of a hemorrhagic pericardial effusion.
Steroids can be used if refractory or NSAIDs are contraindicated.
WHO classification of pHTN (PAH)
1) Group 1 (PAH) - Due to idiopathic PAH
2) Group 2 - Due to L heart disease
3) Group 3 - Due to chronic lung disease (COPD, ILD, chronic hypoxemia)
4) Group 4 - Due to tromboembolic occlusion of the pulmonary vasculature
5) Group 5 - Due to hematologic disorders (myeloproliferative disorders), systemic conditions (sarcoid), metabolic disorders (glycogen storage diseases), or miscellaneous causes
Symptoms of pHTN
1) Dyspnea, fatigue/weakness
2) Exertional angina
3) Syncope
4) Abdominal distention/pain
Signs of pHTN
1) L parasternal lift or prominent RV heave
2) JVD
3) Loud P2 in 2nd heart sound
4) Pansystolic murmur of tricuspid regurgitation (systolic murmur at sternal border, increased with inspiration)
5) R-sided 3rd heart sign (S3)
6) Ascites and/or peripheral edema
7) Hepatomegaly
8) Cool extremities
Pulmonary Hypertension definition and management
Mean pulmonary arterial pressure of at least 25 at rest (normal is 20 and less)
Management of pHTN due to LV systolic dysfunction should include loop diuretics and ACEIs (or ARBs) often with B blockers and in some cases aldosterone antagonists.
Oxygen and/or bronchodilator therapy is indicated for PH due to hypoxemia from chronic lung disease
Endothelin receptor antagonists (bosentan), PDE5 inhibitors (sildenafil) and/or prostanoids (epoprostenol) are indicated for symptomatic idiopathic pHTN
Long term anticoagulation is indicated for patients with pHTN due to thromboembolic occlusion of pulmonary vasculature.
Graded exercises improves long-term outcomes in all pHTN patients, but patients must first be stabilized first.
Mitral stenosis increases risk for what?
Stenotic mitral valve causes increase in LA pressure which in turn gets transmitted to the pulmonary vascular bed. This causes pulm congestion which results in symptoms like exertional dyspnea, nocturnal cough, and hemoptysis. Hemoptysis in particular should raise suspicion for MS.
Patients with MS also are at high risk for AFib*** due to LA dilatation.
EKG findings in complete heart block
1) There is complete failure of atrial impulses (p waves) to capture the ventricles (QRS)
2) Unless an escape rhythm is initiated, ventricular asystole (suncope/death) will occur
3) The p waves have no relation to QRS complexes (complete AV dissociation)
4) Ventricular rate is always slower than the atrial rate and is usually less than 50.
Management of complete heart block
Patients with symptomatic third degree AV block should be managed with temporary pacemaker insertion while undergoing further evaluation to identify and correct reversible causes.
A permanent pacemaker is indicated if no reversible causes of heart block are found.
Reversible causes of complete heart block
1) Myocardial Ischemia
2) Increased vagal tone (during sleep or due to pain)
3) Metabolic disturbances (hyperK)
4) AV nodal blocking agents (B blockers, CCBs like verapamil, digoxin, adenosine)
How does adenosine work?
Blocks L-type calcium channels. This decreases conduction velocity in AV node.
Most common causes of constrictive pericarditis?
In developing countries and endemic areas (Africa, India, China), TB is number 1.
In USA, most common causes are idiopathic or viral (over 40%), radiation therapy (30), cardiac surgery (10) and connective tissue disorders.
Tx of hypertrophic cardiomyopathy
Negative inotropic agents (B blockers, verapamil, disopyramide) are recommended for the pharm management of symptomatic (syncope, heart failure, angina) patients with hypertrophic cardiomyopathy.
B blockers are preferred for initial therapy and verapamil or diso can be used as add on in patients with persistent symptoms.
They prolong diastole and decrease myocardial contractility which reduced the LVOT obstruction and improves symptoms of angina.
Risk factors for exertional heat stroke
1) Strenuous activity during hot and humid weather
2) Dehydration
3) Poor acclimatization
4) Lack of physical fitness
5) Obesity
6) Meds - anticholinergic, antihistamines, phenothiazines, tricyclics
Clinical manifestations of exertional heat stroke
1) Core temp above 40C (104F) immediately after collapse
AND
2) CNS dysfunction - AMS, confusion, irritability, seizure
3) Additional organ or tissue damage - renal/hepatic failure, DIC, ARDS
Management of exertional heat stroke
1) Rapid cooling - ice water immersion preferred; can consider high flow cool water dousing, ice/wet towel rotation, evaporative cooling
2) Fluid resuscitation
3) Lyte correction
4) Management of end organ complications
5) No role for antipyretic therapy
Nonexertional heat stroke
“Classic” heat stroke. It has similar features and complications as exertional heat stroke. Occurs in absence of strenuous activity and typically affects elderly patients with significant underlying comorbidities that limit their ability to escape or cope with excessive heat.
Management of nonexertional heat stroke emphasizes evaporative cooling (spraying lukewarm water while fans blow air on skin) rather than ice water immersion which is associated with increased mortality in classic heat stroke.
What does valsalva maneuver do?
Reduces venous return (during strain; increased during relaxation)
Which murmurs get louder with valsalva?
HCM and MVP
Which murmurs get softer with valsalva?
All except HCM and MVP
What does standing do?
Reduces venous return
Which murmurs get louder with standing?
HCM and MVP
Which murmurs get softer with standing?
All except HCM and MVP
What does squatting do?
1) Increases venous return
2) Increases afterload
3) Increases regurgitant fraction
What murmurs get louder with squatting?
AR, MR, VSD
What murmurs get softer with squatting?
HCM and MVP
What does handgrip do?
1) Increases afterload
2) Increases BP
3) Increases regurgitant fraction
What murmurs get louder with handgrip?
AR, MR, VSD
What murmurs get softer with handgrip?
HCM and AS
IVC obstruction
Presents with swelling and edema in lower extremities due to an increase in venous pressure below the liver. JVP is reduced or normal.
SVC Syndrome
Caused by external or internal compression of SVC. This leads to elevated upper body venous pressure, with facial swelling and distended veins in the neck and/or chest wall. Ascites and lower extremity edema are typically not present.
NE-induced vasospasm
NE has alpha 1 agonist properties which cause vasoconstriction. This is useful when trying to increase the BP of hypotensive patients. But, in some patients with decreased blood flow, vasoconstriction can result in ischemia and necrosis of distal fingers and toes.
A similar phenomenon can occur in intestines resulting in mesenteric ischemia or kidney causing renal failure
Diagnosis is suggested by symmetric duskiness and coolness of all fingertips
Costochondritis
Pain syndrome characterized by tenderness of the costochondral or costosternal junctions. Pain is sharp, focal, lasts for hours, and worsens with inspiration and movement. Reproducible tenderness with palpation suggests MSK etiology.
