UWorld 1 Flashcards
What arrhythmia is most specific for digitalis toxicity?
Atrial tachycardia with AV Block
Digitalis can increase ectopy in the atria or ventricles, which can lead to atrial tachycardia. Atrial tachycardia is distinguished from atrial flutter by its somewhat slower atrial rate (150-250 as opposed to 250-350).
P waves are present, but may appear different from p waves normally seen when conduction originates in SA node. In atrial tachy, the closer the ectopic focus is to the SA node, the closer the resemblance of its p waves to normal p waves coming from the SA node.
In addition to causing ectopic rhythms, digitalis can also increase vagal tone and decrease conduction through the AV node, potentially causing AV block. Since it is so rare for atrial tachy and AV block to occur at the same time, seeing them together is pretty specific for digitalis toxicity
How does digitalis cause AFib?
It doesn’t. In fact, it increases vagal tone and can be used to sometimes treat AFib if B-blockers or CCBs have not been completely effective.
Multifocal atrial tachycardia is often associated with dysfunction in which organ system?
Pulmonary
RV MI
30-50% of patients with acute inferior wall MI due to occlusion of RCA proximal to the origin of the RV branches.
Chest pain, autonomic signs and ECG findings of ST elevation in inferior leads II, III, and aVF.
May also have JVD and Kussmaul’s sign (increase in JVD with inspiration) along with clear lung fields, which are suggestive of RV failure.
Transient bradycardia or AV block can also occur with acute inferior MI due to enhanced vagal tone.
Dx is confirmed with at least 1mm ST elevation in R sided precordial leads V4R-V6R. RV failure leads to decreased preload and resultant hypotension. Therefore, in addition to standard MI therapy, such patients (without pulm congestion) are typically treated with bolus of IVFs (isotonic saline) to improve RV preload and help LV filling
IV septum rupture
Can lead to L-R shunt, which increases strain on RV and can result in RV failure. These patients usually have a loud holosystolic murmur on exam.
Pulm embolism on ECG
Tachycardia, nonspecific ST segment or T wave changes, new onset RBBB or S1Q3T3 pattern.
What drugs should be avoided in RV MI?
These patients are preload dependent, so avoid diuretics and nitrates.
STEMI management
1) O2 for arterial saturation less than 90
2) Nitrates - caution with hypotension, RV infarct, or severe aortic stenosis
3) Antiplatelets - Aspirin plus P2Y12 receptor blocker
4) Anticoagulation - unfractionated heparin, low molecular weight heparin, or bivalirudin
5) B blockers - contraindicated in overt HF; high risk for cardiogenic shock; bradycardia
6) Prompt reperfusion with PCI - ideal first medical contact for PCI in less than 90 minutes
7) Statin therapy ASAP
Crescendo-decrescendo systolic murmur along with left sternal border without carotid radiation in a young patient
This is the murmur of HOCM (hypertrophic obstructive cardiomyopathy), which is IV septal hypertrophy.
Common symptoms include syncope, dyspnea, and CP.
Syncope in HOCM is multifactorial. In large part, it’s due to outflow obstruction from the hypertrophied myocardium. But, syncope can also be secondary to arrhythmia, ischemia, and a ventricular baroreceptor response that inappropriately causes vasodilation
History of recent URI followed by sudden onset of cardiac failure in an otherwise healthy patient
Suggests dilated cardiomyopathy, most likely secondary to acute viral myocarditis.
Dilated cardiomyopathy is the end result of myocardial damage produced by a variety of toxic, metabolic, or infectious agents. Viral or idiopathic myocarditis is most commonly seen after Coxsackie B infection and occurs in about 3.5-5% of infected patients.
Other viruses commonly implicated include ParvoB19, HHV6, adenovirus, and enterovirus.
Viral myocarditis can cause dilated cardiomyopathy via direct viral damage and as a result of humoral or cellular immune responses to persistent viral infections.
The dx of dilated cardiomyopathy is made by Echo. It shows dilated ventricles with diffuse hypokinesia resulting in a low EF (systolic dysfunction). Tx is largely supportive involving mainly the management of CHF symptoms
Always think dilated cardiomyopathy in the acute heart failure patient. The other types take time.
Use Dependence
Refers to enhanced pharm effects of a drug during faster HRs and is seen with class I (esp in class 1C - Flecainide and propafenone) and IV (CCBs).
Class 1 antiarrhythmics block sodium channels and inhibit depolarization phase (phase 0) of AP.
IC drugs are occasionally used in tx of AFib (for maintenance of sinus rhythm) in patients with structurally normal hearts. They have the slowest rate of drug binding and dissociation from the sodium channel receptor. Under normal circumstances, flecainide does not cause any QRS or QT prolongation
BUT
In patients with faster heart rates, the drug has less time to dissociate from the sodium channels, leading to higher number of blocked channels. This leads to progressive decrease in impulse conduction and widening of QRS complex. This phenomenon is what is called Use Dependence. Seen most in Class 1C (less with 1A and rarely with 1B) and is the mechanism behind their efficacy against supraventricular arrhythmias
Digoxin mechanism
Inhibits ATPase-dependent Na-K pump and increases intracellular Na. This reduces Na-Ca exchanger activity, resulting in an increase in intracellular Ca.
It also enhances vagal tone and slows conduction through the AV node. These effects can cause bradyarrhythmias (younger, healthier patients) or enhance automaticity and delayed after-depolarization leading to ventricular ectopy and tachyarrhythmias (more common in older patients with underlying cardiac diseases)
Combo of exertional dyspnea, dry cough, and holosystolic murmur are most suggestive of what?
Mitral regurgitation. Exertional dyspnea and fatigue are common symptoms which are secondary to combo of lower CO and increased LA pressure.
Dry cough may relate to pulmonary congestion and edema. Indicates more severe disease that has resulted in LV dysfunction
Other common features are AFib and signs of HF.
MR murmur is holosystolic heard best over apex with radiation to axilla.
MR can occur as result of primary mitral valve diseases (RHD, infective endocarditis, trauma) or may be associated with other cardiac conditions (ischemic heart disease or hypertrophic cardiomyopathy)
CHA2-DS2-VASc Score
1) CHF - 1
2) HTN - 1
3) Age 75 and up - 2
4) DM -1
5) Stroke/TIA/thromboembolism - 2
6) Vascular disease (prior MI, peripheral artery disease or aortic plaque) -1
7) Age 65-74 - 1
8) Sex category (female) -1
Max score is 9.
Score of 0 - low stroke risk. No antrithrombotic therapy needed.
Score 1 - intermediate. None or ASA or oral anticoagulants. Oral anticoagulants are preferred.
Score 2 and up - high. Oral anticoagulants.
Lone AF
Patients with paroxysmal, persistent, or permanent AF with no evidence of cardiopulmonary or structural heart disease. These patients are usually less than 60 years old. By definition, their CHA2DS2VASc score is 0. Anticoagulant therapy is not needed.
Note: this is for nonvalvular AFib (as is the CHA2DS2VASc)
Acute limb ischemia
6 P’s
1) Pain
2) Pallor
3) Poikilothermia (cool extremity)
4) Paresthesia
5) Pulselessness
6) Paralysis
Most likely due to thromboembolic occlusion from L atrial thrombus due to AFib in a patient with preexisting peripheral vascular disease (multiple risk factors, intermittent claudication, diminished pulses).
Patients with suspected acute arterial occlusion leadng to an immediately threatened limb (sensory loss, rest pain, muscle weakness) should be immediately started on anticoagulation while further diagnostic procedures are done. Heparin prevents further thrombus propagation and thrombosis in the distal arterial and venous circulation. Put them on the drug first THEN confirm with arterial doppler study or duplex US.
Clinical features of cocaine use
Clinical
1) Sympathetic hyperactivity - tachycardia, HTN, dilated pupils
2) CP due to coronary vasoconstriction
3) Psychomotor agitation, seizures
Complications
1) Acute MI
2) Aortic dissection
3) Intracranial hemorrhage
Management of chest pain
1) IV Benzos* for BP and anxiety
2) Aspirin
3) Nitroglycerin and CCBs for pain
4) B blockers are CONTRAINDICATED* (cause unopposed alpha blockade and worsen coronary vasoconstriction)
5) Fibrinolytics not preferred due to higher risk of ICH
6) Immediate cardiac cath with reperfusion when indicated
Cocaine mechanism
It potentiates sympathomimetic actions by causing inhibition of NE reuptake into the sympathetic neuron. This causes stimulation of alpha and beta adrenergic receptors and can result in coronary vasoconstriction and increase in HR, systemic BP, and myocardial O2 demand.
It also enhances thrombus formation by promoting platelet activation and aggregation
Thoracic aortic aneurysm presentation
Look at the CXR. Shows mediastinal widening, increased aortic knob, and tracheal deviation. However, CXR cannot always distinguish TAA from tortuous aorta so get CT with contrast to confirm dx.
TAA can be ASx or present with chest, back, flank or abdominal pain depending on location.
Ascending aortic aneurysm (60%) starts anywhere from aortic valve to the innominate artery. Often due to cystic medial necrosis (usually occurs with aging) or connective tissue disorders (Marfan, Ehler-Danlos)
Descending arise distal to L subclavian. Usually due to atherosclerosis**. Risk factors include HTN, hypercholesterolemia, and smoking.
Electrical alternans
Think pericardial effusion. Recent URI is a clue since pericardial effusions are often secondary to viral pericarditis. Accompanying pleural effusions may be found as well. Enlargement of cardiac silhouette can also be seen on CXR.
Electrical alternans describes QRS complexes whose amplitudes vary from beat to beat on EKG. It is thought to be from heart’s swinging back and forth in an increased quantity of pericardial fluid.
Look out! JVD, muffled heart sounds and borderline BP indicate developing tamponade.
Causes of HF with preserved LV function
Diastolic HF
1) HTN with LVH
2) Restrictive cardiomyopathy
3) Infiltrative cardiomyopathy (sarcoid)
4) Hypertrophic cardiomyopathy
5) Occult CAD
Valves
1) AS or AR
2) MS or MR
Pericardial disease
1) Constrictive pericarditis
2) Cardiac tamponade
Systemic disorders (high output cardiac conditions)
1) Thyrotoxicosis
2) Severe anemia
Exertional dyspnea, orthopnea (choking sensation/dyspnea when lying flat), bibasilar rales, lower extremity edema, and normal EF on Echo
HFpEF (diastolic dysfunction) - remember that LV can be normal or increased in size on echo here
Patients have typical signs of CHF (exertional dyspnea, orthopnea, lower extremity edema) but normal or near normal LV EF (over 50%) with objective evidence of diastolic dysfunction (abnormal LV filling pressures) by Echo
What causes diastolic dysfunction?
It is caused by impaired myocardial relaxation!!! Or by increased LV wall stiffness (lower compliance) leading to increased LV End-Diastolic Pressure.
The increase in LVEDP is transmitted to the LA and pulmonary veins and capillaries, causing pulm congestion, dyspnea, and exercise intolerance
This is made worse by the loss of the atrial kick and short diastolic filling times in patients who develop AFib (look for a patient with palpitations and irregularly irregular HR)
What does Cor Pulmonale refer to?
Impaired RV function due to pulm HTN that occurs as a result of underlying pulmonary disease (COPD, Pulm vasculature disease, OSA). RV dysfunction would be seen on echo and would not cause bibasilar crackles.
High output heart failure can occur in what conditions?
1) Severe anemia
2) Hyperthyroid
3) Beriberi (B1/Thiamine def)
4) Paget Disease
5) AV fistula
High output is defined as a high cardiac output. Look for a cardiac index beyond normal range of 2.5 to 4L.
What is a feared complication of acute aortic dissection?
Cardiac Tamponade.
Look for sudden onset of severe chest pain radiating to the back and widened mediastinum on CXR (aortic dissection)
Hypotension, JVD, and respiratory variation in systolic BP (pulsus paradoxus) - this suggests cardiac tamponade
CT is a complication with rupture of aorta and rapid accumulation of blood in pericardial space. Abrupt accumulation of even small amounts of blood can significantly raise the pressure inside the pericardial cavity. Increased pericardial pressure causes compression of cardiac chambers and limits diastolic filling of the right sided chambers. This causes lower preload and reduced CO, resulting in hypotension and syncope
