UWorld 3 Flashcards
Acute pain, parasthesia, pallor and pulselessness of lower legs in patient with AFib
Acute arterial occlusion of lower extremity likely due to thromboembolism in setting of AFib.
If patient’s CHA2DS2VASC score is at least 2, he should be anticoagulated to reduce long term risk of systemic embolization
As far as choice of anticoagulation, ASA or ASA plus clopidogrel is significantly less effective than warfarin or target-specific oral anticoagulants like apixaban, dabigatran, rivaroxaban
Reflex syncope
AKA situational syncope. Neurally mediated syncope associated with specific triggers like micturition, defecation, cough. The triggers cause an alteration in the autonomic response and can precipitate a predominant cardioinhibitory, vasodepressor or mixed response.
Increased parasympathetic stimulation (cardioinhibitory) can manifest as profound bradycardia, varying degrees of AV block or asystole
Decreased sympathetic output can lead to vasodilation, hypotension or syncope.
What kinds of murmurs should worry us?
Diastolic and continuous murmurs are usually due to underlying pathology. Their presence should prompt further evaluation with a transthoracic echo which can find valvular regurgitation and evaluate for any associated structural abnormalities or hemodynamic consequences.
Midsystolic murmurs in otherwise young, ASx adults are usually benign and do not require further evaluation
High pitched blowing murmur. Gradually decreasing diastolic murmur. (decrescendo). Best heard along LSB at 3rd and 4th IC spaces with patient sitting up and leaning forward while holding breath in full expiration.
Aortic Regurgitation
Paroxysmal SVT
The most common paroxysmal tachycardia in people without structural heart disease.
Attacks begin abruptly and are characterized by HRs between 160-220 bpm. Most common mechanism underlying PSVT is re-entry into the AV node.
Mechanical and medical therapies for PSVT decrease AV node conduction.
Vagal maneuvers like valsalva, carotid sinus massage and immersion in cold water increase vagal tone and decrease conduction through AV node. This slows HR and can often break the rhythm.
Adenosine is a very short acting AV nodal blocker that is often used as well.
Atrial premature beats
AKA premature atrial complexes. Occur when there is premature activation of the atria originating from a site other than the SA node.
ECG will show early P wave. PACs by themselves represent a benign arrhythmia that can occur in healthy individuals and in patients with a variety of cardiovascular and systemic diseases.
They may occur singly or in a pattern of bigeminy. PACs are usually ASx. Sometimes, they can cause symptoms of “skipped” beats or palpitations. Sometimes they can precede AFib.
Tx is required only when symptoms cause distress or when there is SVT. B blockers are often helpful. Even in ASx patients, precipitating factors like tobacco, alcohol, caffeine and stress should be avoided.
Amiodarone side effects (10)
It is a class 3 antiarrhythmic drug. Often used for management of ventricular arrhythmias in patients with CAD and ischemic cardiomyopathy. Long term monitoring of PFTs and TFTs is recommended for early detection and recognition of potential side effects.
Cardiac
1) Sinus brady, heart block
2) Risk of proarrhythmias - QT prolongation and torsades
Pulm
1) Chronic interstitial pneumonitis (cough, fever, dyspnea, pulmonary infiltrates) most common
Endo
1) Hypothyroid
2) Hyperthyroid
GI/Hep
1) Elevated transaminases, hepatitis
Ocular
1) Corneal microdeposits
2) Optic neuropathy
Derm
1) Blue-grey skin discoloration
Neuro
1) Peripheral neuropathy
Pulm toxicity of amiodarone
A serious adverse effect of long term use that usually presents with chronic insterstitial pneumonitis (most common) but can cause ARDS.
Pulm toxicity correlates with total cumulative dose and usually occurs months to several years after initiation of drug.
Baseline CXR and PFTs are usually obtained prior to starting therapy and long-term surveillance is guided by development of signs of symptoms (cough, fever, dyspnea) suggestive of pulmonary toxicity
Apixiban mechanism
Oral factor 10a inhibitor (Stuart-Prower Factor)
How does CHF lead to hyponatremia?
Low CO along with decreased perfusion pressure at the baroreceptors and renal afferent arterioles leads to neurohormonal activation with the release of renin, NE and secretion of ADH.
ADH binds to V2 receptors in renal collecting ducts and promotes water reabsorption, while renin (via ATII) and NE increase proximal Na and water reabsorption and limit water delivery to the distal tubules.
These actions promote free water retention and lead to dilutional hyponatremia. This also contributes to hyperK.
Tx involves fluid restriction, ACEIs and loop diuretics.
Avoid salt tabs in edematous patients due to volume overload. Salt tabs are only used for hypoNa due to SIADH.
Mechanism for nitrates relieving pain in angina
Nitrates exert their effect by direct vascular smooth muscle relaxation causing systemic venodilation and an increase in peripheral venous capacitance.
Their primary anti-ischemic effect is mediated by systemic vasodilation (!!!) and decrease in cardiac preload (!!!) resulting in decreased LV EDV and LV ESV.
This leads to reduction in LV wall stress (!!!) which reflects afterload and is proportional to (pressure x radius all divided by thickness). Also, this decreases myocardial O2 demand (!!!) resulting in relief of anginal symptoms.
Monomorphic VTach
QRS complexes are wide and all match each other
Fusion beats
Capture of electrical signal though both the atrium and ventricle briefly leading to a hybrid of a normal and wide QRS complex (P waves precede fusion complex)
These are basically diagnostic for sustained monomorphic VTach (SMVT)
Management of patients with SMVT
Depends on symptoms and hemodynamic stability.
Patients with SMVT who are clinically and hemo stable can be initially managed with antiarrhythmic drugs. IV amiodarone is usually preferred, and other agents (procainamide, sotalol. lidocaine) are reserved for patients who do not respond to amiodarone.
Antiarrhythmics can convert SMVT to sinus rhythm and avoid need for urgent electrical cardioversion.
Synchronized electrical cardioversion is indicated for patients with persistent tachyarrhythmia who are severely symptomatic (AMS, acute HF or pulm edema, ischemic chest pain) or hemodynamically unstable (hypotension, signs of shock)
Meds to withhold prior to cardiac stress testing
1) Hold for 48h - B blockers, CCBs, nitrates. Should be continued though in patients with known CAD undergoing stress test to assess efficacy of antiangianal therapy.
2) Hold for 48h prior to vasodilator stress test - Dipyridamole
3) Hold for 12h prior to vasodilator stress test - Caffeine containing foods or drinks
4) Continue - ACEIs, ARBs, Digoxin, Statins, Diuretics
Gold standard for diagnosis of CAD
Coronary angiography - BUT it is expensive and invasive so first line in someone with low to intermediate probability pretest of CAD is stress testing.
DDx and features of various types of chest pain
CAD
1) Substernal
2) Radiation to arm, shoulder or jaw
3) Precipitated by exertion*
4) Relieved by rest* or nitro*
Pulm/pleuritic (pleurisy, pneumonia, pericarditis, PE)
1) Sharp/stabbing pain
2) Worse with inspiration
3) Pericarditis - worse when lying flat
4) PE, pneumothorax - respiratory distress, hypoxia
Aortic (dissection, intramural hematoma)
1) Sudden, severe tearing pain
2) Radiates to back*
3) Elderly men
4) HTN and risk factors for atherosclerosis
GI/esophageal
1) Nonexertional, relieved by antacids
2) Upper abdominal and substernal
3) Associated with regurgitation, nausea, dysphagia
4) Nocturnal pain*
5) Prolonged CP lasting more than an hour***, postprandial symptoms, associated heartburn or dysphagia (all point to esophageal etiology)
Chest wall/MSK
1) Persistent and or prolonged pain
2) Worse with movement or change in position
3) Often follows repetitive activity
AAA
Usually ASx and discovered incidentally. Found as a pulsatile abdominal mass.
AAA rupture is life threatening. All incidentally discovered aneurysms require close f/u.
Imaging modality of choice is abdominal US. It is nearly 100% sensitive and specific, allows size measurement, and can show presence of any associated thrombus.
AAA rupture
Patient with pulsatile abdominal mass, hypotension and abdominal pain. Forego imaging and get to OR right away.
CYP450 inhibitors (8)
Increase Warfarin effect (increased bleeding risk)
1) Acetaminophen, NSAIDs
2) ABx/Antifungals (metronidazole)
3) Amiodarone
4) Cimetidine
5) Cranberry juice, Ginkgo biloba, Vitamin E
6) Omeprazole
7) Thyroid hormone
8) SSRIs (fluoxetine)
CYP450 Inducers (5)
Decrease warfarin effect (lower efficacy)
1) Carbamazepine, phenytoin
2) Ginseng, St Johns Wort
3) OCPs
4) Phenobarbital
5) Rifampin
Ventricular aneurysm
Post MI complication (5d to 3mo) consisting of thin and scarred or fibrotic myocardium in remodeled areas affected by an ST segment elevation or a transmural MI. Patient presents with progressive decompensated CHF.
Usually, ST segment elevations go away within a few weeks of an MI. VAs present with ECG findings of persistent ST elevation after recent MI and deep Q waves in the same leads.
Large VAs can lead to progressive LV enlargement, causing heart failure, refractory angina, ventricular arrhythmias, mural thrombus with systemic arterial embolization, or mitral annular dilation with MR.
Dx confirmed by echo (thinned, dyskinetic LV portion in the area of prior MI)
Dressler
Acute pericarditis can present in first several days after MI and can cause diffuse ST segment elevation.
Post-cardiac injury syndrome (Dressler) is an immune-mediated pericarditis that can occur weeks to months post MI.
What might raise suspicion for free wall rupture after MI?
Large pericardial effusion. Usually causes cardiac tamponade (dyspnea, hypotension, pulsus paradoxus, high jugular pressure) and can progress rapidly to pulseless electrical activity.
Papillary muscle rupture following MI
Mechanical complication typically occurring 2-7d post MI. Presents dramatically with acute severe MR (hypotension, pulm edema, cardiogenic shock) and does not cause persistent ST segment elevations
Lung fields in setting of RV infarct
Clear. They usually have elevated JVPs and hypotension.
