UWorld 2

Question 1

Various maneuvers and their effects on HCM

Answer 1

1) Valsalva (straining phase), Abrupt standing (from sitting or supine), Nitro administration - All Lower Preload. This Increases murmur intensity
2) Sustained hand grip - Increases afterload. Lowers murmur intensity
3) Squatting (from standing position) - Increases afterload and increases preload. Reduces murmur
4) Passive leg raise - Increases preload. Reduces murmur.

Question 2

Hypertrophic cardiomyopathy clinical signs and genetics

Answer 2

Many patients are ASx and are detected when abnormal murmur or ECG abnormalities (Tall R wave in aVL, Deep S wave in V3 - these together are cornell criteria; repolarization changes in lateral leads I,aVL, V4, V5, V6)

1) Exertional dyspnea, chest pain, fatigue, palpitations, presyncope, or syncope
2) Harsh crescendo-decrescendo systolic murmur best heard at apex and lower left sternal border, with characteristics changes in intensity during physiologic maneuvers.

It is autosomal dominant genetic condition caused by mutations in one of several sarcomere genes encoding myocardial contractile proteins. Two most common mutations (70% of identifiable mutations) occur in cardiac myosin binding protein C gene and the cardiac beta-myosin heavy chain gene. First degree relatives of an affected patient with a known disease-causing mutation can be offered genetic testing to ID risk for developing HCM.

Question 3

In patients with CHF, activation of RAAS and production of ATII causes what?

Answer 3

Preferential vasoconstriction of efferent renal arterioles, which increases intraglomerular pressure in order to maintain adequate GFR

Question 4

ATII effects

Answer 4

1) Vasoconstriction of both the afferent and efferent glomerular arterioles, leading to increase in renal vasular resistance and a net decrease in renal blood flow
2) Preferential vasoconstriction of efferent renal arterioles which increases intraglomerular pressure in an attempt to maintain GFR
3) Direct stimulation of sodium resorption in prox tubule and increased secretion of aldosterone from adrenal glands, which in turn promotes further sodium resorption in the cortical collecting tubule. These actions lead to decreased sodium delivery to the distal tubule and an increase in extracellular fluid volume.

Question 5

Reasons for increased incidence of orthostatic hypotension in the elderly

Answer 5

Progressively decreasing baroreceptor sensitivity and defects in the myocardial response to this reflex. Arterial stiffness, decreased NE content of sympathetic nerve endings.

Question 6

Definition of orthostatic hypotension

Answer 6

Defined as postural decrease in BP by 20 systolic or 10 diastolic (sometimes goes with increased HR) that occurs with standing.

In general, comes from insufficient constriction of resistance and capacitance blood vessels in lower extremities on standing which may be due to a defect in autonomic reflexes, decreased intravascular volume, or medications.

Question 7

Normal changes to the aging heart

Answer 7

1) Decreased resting and maximal CO
2) decreased maximum HR
3) increased contraction and relaxation time of heart muscle
4) Increased myocardial stiffness during diastole
5) Decreased myocyte number
6) Pigment accumulation in myocardial cells.

Question 8

What kinds of arrhythmias are common after an MI?

Answer 8

Ventricular ones (ventricular premature beats, nonsustained or sustained VTach, and VFib) are quite common in the immediate post-MI period. VFib is the most frequent underlying arrhythmia responsible for sudden cardiac arrest in setting of acute MI. More than half occur within first hour of symptom onset.

Reentry is main mechanism responsible for ventricular arrhythmias in immediate post-infarct period. Underlying mechanism varies according to the time elapsed since onset of MI. If it’s within 10 minutes of coronary occlusion it is “immediate” or phase 1a ventricular arrhythmia. Acute ischemia causes heterogeneity of conduction with areas of marked conduction slowing and delayed activation which in turn predisposes to reentrant arrhythmias

Delayed or phase 1B happen 10-60 minutes after acute infarct and are the result of abnormal automaticity.

Question 9

Aortic Regurgitation murmur

Answer 9

Varies with severity. Early diastolic murmur if mild but holodiastolic if severe.

Bounding pulses (water hammer pulse). Bc AR is associated with an increased stroke volume, which produces an abrupt rise in systolic BP and rapid distension of peripheral arteries. Then, during diastole, there is a regurgitation of blood back into the LV, resulting in a low diastolic pressure and collapse of peripheral arteries. This hyperdynamic pulse is also associated with several other exam findings

Question 10

Pulsus paradoxus

Answer 10

Refers to a fall in the systemic arterial pressure by more than 10 during inspiration. Associated with cardiac tamponade. Also seen in asthma and COPD (don’t forget these pulm reasons too)

Question 11

Pulses in AS

Answer 11

Pulsus parvus (decreased pulse amplitude) and pulsus tardus (delayed pulse upstroke)

Question 12

CHF with proteinuria and easy bruising

Answer 12

Amyloidosis - look for extracardiac manifestations in addition to CHF. Examples are waxy skin, macroglossia, hepatomegaly, peripheral (carpal tunnel) and/or autonomic neuropathy (ortho hypo).

Suspect cardiac amyloid in patients with unexplained CHF (usually diastolic), low voltage on ECG, and Echo showing increased ventricular wall thickness with normal LV cavity dimensions (esp in patients without HTN). Patients may get syncope or presyncope due to conduction abnormalities

Tissue biopsy (abdominal fat pad, bone marrow, rectum, kidney, endomyocardial) can confirm dx by showing amyloid deposits.

Question 13

Hypertrophic cardiomyopathy Echo and effect on valves.

Answer 13

Increased LV wall thickness, most commonly noted in the basal anterior septum (asymmetric septal hyeprtrophy)

Some patients have systolic anterior motion of the mitral valve, leading to anterior motion of mitral valve leaflets toward IV septum. Contact btw mitral valve and thickened septum during systole leads to LV outflow tract obstruction and is responsible for the harsh systolic murmur best heard at the apex and left lower sternal border. Abrupt standing from a sitting position decreases venous return and enhances LVOT, resulting in an increase in intensity of murmur.

Question 14

What drugs can increase digoxin levels in blood?

Answer 14

Amiodarone (or verapamil, quinidine, propafenone). Can lead to toxicity in patient who has previously been on a stable digoxin regimen.

It is recommended that digoxin dose be decreased by 25-50% when initiating amiodarone therapy, with close monitoring of digoxin levels once weekly for the next several weeks.

Note: Acute digoxin toxicity typically presents with GI symptoms. Chronic digoxin toxicity typically presents with less pronounced GI symptoms but more significant neuro and visual symptoms (changes in color vision, scotomas, blindness)

Question 15

Initial therapy for AFib due to hyperthyroidism

Answer 15

Beta blockers. Continue until patient becomes euthyroid with thionamides, radioiodine and/or surgery.

This helps bc most of the systemic and cardiac manifestations of hyperthyroidism are due to an increase in sympathetic activity

Question 16

Single Photon Emission CT as tool to evaluate for CAD

Answer 16

Tc-99m perfusion agents (sestamibi or tetrofosmin) have half life of 6 hours, passively diffuse into perfused myocardial cells, have minimal redistribution afterward, and can provide an assessment of both myocardial function and perfusion.

Tc-99m is injected at rest and images are obtained during the gated SPECT scan. The patient then undergoes stress testing (physiologic or pharmacologic) and has repeat gated SPECT images. Patients with normal tracer uptake at both rest and exercise have excellent prognosis with less than 1% annual risk of CAD

Decreased tracer both at rest AND with exercise (fixed deficit) indicates likely scar tissue with decreased perfusion and CAD. A decreased tracer uptake with stress but normal uptake at rest (reversible defect) indicates inducible ischemia and likely CAD.

Current guidelines recommend antiplatelet (ASA) for prevention of MI (this is the preferred treatment), B blockers and modification of risk factors (smoking cessation, lipids, diabetes)

Question 17

Acute treatment of AFib in patients with WPW

Answer 17

Hemo unstable patients require immediate electrical cardioversion

For stable patients, rhythm control with anti-arrhythmic drugs such as IV ibutilide or procainamide is preferred.

AV nodal blockers such as B blockers, CCBs (ESP verapimil), Digoxin, and adenosine should be avoided as they can cause increased conduction through the accessory pathway. This can lead to degeneration of AFib to VFib.

In WPW, an accessory path conducts depolarization directly from the atria to the ventricles without traversing the AV node. AFib occurs in 10-30% of individuals with WPW, and is a potentially life threatening emergency. AF in WPW can bypass the usual rate limiting function of the AV node leading to very rapid ventricular response rates. Persistent AF with RVR in patients with WPW can ultimately deteriorate into VFib

Question 18

What to do with patient initially diagnosed with HTN

Answer 18

Although most patients with HTN have essential HTN, initial evaluation should assess possible secondary causes.

Detailed H and P. Also, get the following basic tests:

1) UA (for occult hematuria and urine protein/Cr ratio)
2) Chem panel (risk stratify for CAD)
3) Lipid profile (risk stratify for CAD)
4) Baseline ECG (evaluate for CAD or LVH)

Question 19

Scleroderma renal crisis

Answer 19

Marked HTN and AKI in setting of systemic sclerosis (scleroderma) suggests SRC, which can occur in up to 20% of patients with diffuse cutaneous systemic sclerosis (SSc).

SRC usually occurs within the first 5 years of SSc diagnosis. The likely mechanism involves increased vascular permeability, activation of the coagulation cascade, and increased renin secretion.

Patients typically develop sudden onset of renal failure (without previous kidney disease), and malignant HTN (HA, blurry vision, nausea). UA can be normal or show mild proteinuria. Peripheral blood smear can show microangiopathic hemolytic anemia (similar to HUS/TTP) or DIC with fragmented RBCs (Schistocytes) and low platelets.

Question 20

Burr Cells

Answer 20

Echinocytes. Spiculated appearing RBCs with serrated edges that can be seen in liver disease and ESRD.

Question 21

Howell-Jolly Bodies

Answer 21

Basophilic remnants of the nucleus that appear as small, black pellets in RBCs. They are seen in patients with a history of splenectomy or functional asplenia. Not seen in healthy people as normal spleen efficiently removes them.

Question 22

Spur cells

Answer 22

Acanthocytes. RBCs with irregularly sized and spaces projections are most often seen in liver disease

Question 23

Target Cells

Answer 23

RBCs with central density surrounded by pallor. Usually seen in patients with hemoglobinopathies (thalassemia) or chronic liver disease (esp obstructive liver disease)

Question 24

ACLS algorithm for VF and pulseless VT

Answer 24

Defibrillate! Then epi should be given. Epi is repeated every 3 minutes as CPR is ongoing. After a repeated attempt at defibrillation, use of antiarrhythmics (amiodarone, lidocaine, magnesium) is warranted.

VF and sustained VT are feared complications of MI, occuring in 10% of cases. VF can also occur in setting of lyte imbalances, myocarditis, cardiomyopathy, and as a drug side effect.

VF is recognized on EKG by fibrillatory waves and absence of regular QRS complexes.

Energy requires in defib is 200-360 J. Greater the length of time that transpires between onset of VF and use of defib, the lower the chance of survival.

In the case of witnesses arrests of less than 5 minutes duration, defibrillation should be performed immediately.

In unwitnessed arrests or witnessed arrests occuring more than 5 minutes before arrival of the defibrillator, a cycle of CPR should precede defibrillator

Question 25

Clinical features of AS

Answer 25

1) Exertional symptoms - CP, dyspnea, dizziness and syncope
2) Delayed and diminished carotid pulse
3) Single and soft S2, audible S4
4) Harsh ejection (crescendo-decrescendo) systolic murmur in second right IC space with radiation to carotids

A transthoracic ECHO should be obtained in all patients with syncope due to suspected structural heart disease (AS, HCM, LV dysfunction, Cardiac tamponade) to confirm dx and plan management.

Neuro is only 1% of the causes of syncope

Question 26

Acute CHF in an otherwise healthy young patient

Answer 26

Consider myocarditis. Coxsackie B is most common cause. Patients often (not always) have preceding viral-type symptoms.

Question 27

8 common etiologies of syncope and their clinical clues

Answer 27

1) Vasovagal or neurally mediated syncope - Triggers (prolonged standing or emotional distress, painfull stimuli), Prodromal symptoms (nausea, warmth, diaphoresis)
2) Situational syncope - Triggers like cough, micturition, defecation
3) Orthostatic hypotension - Postural change in heart rate/BP after standing suddenly
4) Aortic stenosis, HCM, Anomalous coronary arteries - Syncope with exertion or during exercise
5) Ventricular arrhythmias - Prior history of CAD, MI, cardiomyopathy, or low EF
6) Sick Sinus Syndrome, bradyarrhythmias, AV block - Sinus pauses, increased PR or Increased QRS duration
7) Torsades (acquired long QT syndrome) - HypoK, HypoMg, meds causing increased QT interval
8) Congenital long QT syndrome - FHx of sudden death, long QT interval, syncope with triggers (exercise, startle, sleeping)

Question 28

Torsades

Answer 28

A form of polymorphic VTach with a cyclic or sinusoidal alteration of QRS axis and/or morphology. Occurs in the setting of congenital or acquired QT interval prolongation.

Arrhythmic episodes can present with palpitations, presyncope, or syncope and may resolve on their own or degenerate into VFib and result in sudden cardiac death.

Immediate defibrillation is indicated in hemodynamically unstable patients with torsades. IV Magnesium is first line in conscious and stable patients with episodes of torsades. This is followed by identification and removal/correction of offending causes. IV Mag is effective even in patients with normal blood Mag levels.

Question 29

Causes of acquired QT prolongation (4 large groups, 17 causes)

Answer 29

Meds

1) Diuretics (due to lyte imbalances)
2) Antiemetics (ondansetron)
3) Antipsychotics (haloperidol, quetiapine, risperidone)
4) TCAs
5) SSRIs
6) Antiarrhythmics (amiodarone, sotalal, flecainide)
7) Antianginal drugs (Ranolazine)
8) Anti-infective drugs (macrolides, fluoroquins, antifungals)

Metabolic

1) Lyte imbalances (low K, low Mg, low Ca)
2) Starvation
3) Hypothyroidism

Bradyarrhythmias

1) Sinus node dysfunction
2) AV block (2nd or 3rd degree)

Others

1) Hypothermia
2) Myocardial ischemia/infarction
3) Intracranial disease
4) HIV

Question 30

Latex allergy

Answer 30

Can cause anaphylactic shock. Widespread use of latex in medical products has made it a common allergy. Development of hives after sexual intercourse likely due to sensitization to latex condoms. Look out for latex glove surgical exposure.

Pre-existing atopic dermatitis increases the risk of latex allergy. So does being a healthcare worker. So does being a surgical patient, esp those undergoing abdominal or GU surgery.

Question 31

Common side effect of CCBs

Answer 31

Peripheral edema. Incidence about 25% after 6 months of therapy. Edema is related to preferential dilation of precapillary vessels (arteriolar dilation) which leads to increased capillary hydrostatic pressure and fluid extravasation into interstitium.

Dihydropyridine CCBs (amlodipine and nifedipine) are potent arteriolar dilators and cause more edema than non-DHPs (Dilt and verapamil). Other major side effects with DHP CCBs are HA, flushing, dizziness.

RAS antagonists (ACE and ARBs) cause post capillary venodilation and can normalize the increased capillary hydrostatic pressure. Combo of CCBs with ACEIs was associated with less risk of CCB-associated edema.

Question 32

Most common side effects of HCTZ

Answer 32

Electrolyte imbalances (HypoNa, HypoK), renal failure, hyperuricemia (may precipitate acute gout) and high glucose and cholesterol levels.

Question 33

SVT

Answer 33

Regular, narrow complex tachy (QRS less than 120) at a rate of approximately 160 bpm. Usually no regular P waves since theyre buried in QRS. Can get retrograde P waves which are seen in beginning or end of QRS (pseudo R if in beginning, pseudo S if at end). They look like tiny spikes.

SVT refers to any tachycardia originating above the His bundle and includes:

1) Sinus tachy
2) Multifocal atrial tachy
3) Atrial flutter
4) Atrial fib
5) AV nodal reentrant tachy (AVNRT)
6) AV reentrant tachy (AVRT)
7) Junctional tachy

Patients usually present with palpitations, although some may have dizziness, lightheadedness, SOB, diaphoresis, CP, presyncope, or syncope.

Paroxysmal SVTs are SVTs with abrupt onset and offset. They include AVNRT and AVRT, atrial tacycardia, and junctional tachycardia.

In patients who are hemodynamically stable, next step is eval to ID type of SVT with the use of vagal maneuvers (carotid sinus massage, valsalva, eyeball pressure) or IV adenosine. Adenosine or vagal maneuvers temporarily slow conduction via the AV node and can aid in diagnosis by unmasking “hidden” P waves in patients with atrial flutter or atrial tachycardia. They can also cause a transient AV block and terminate AV node-dependent arrhythmias, including AVNRT and orthodromic AVRT.

Question 34

IV adenosine

Answer 34

Useful in initial diagnosis and management of patients with narrow QRS tachycardia.

It slows sinus rate, increases AV nodal conduction delay or can cause a transient block in AV node conduction.

It can be useful in identifying P waves to clarify diagnosis of atrial flutter or atrial tachycardia. It can also terminate paroxysmal SVTs by interrupting the AV nodal reentry circuit.

Question 35

Aortic regurgitation

Answer 35

Common causes

1) Aortic root dilation (Marfan, syphilis)
2) Post-inflammatory (RHD, endocarditis)
3) Congenital bicuspid aortic valve

Pathophys

1) Backflow from aorta into LV leads to increased LVEDV. Compensatory myocardial hypertrophy and ventricular enlargement initially maintain stroke volume and cardiac output.
2) Excessive LV stretching later leads to reduced SV, reduced forward blood flow and systolic HF
3) Increased LVEDP leads to pulmonary congestion

Clinical

1) Diastolic decrescendo murmur
2) Widened pulse pressure (increased SBP, lower DBP)
3) Collapsing/water hammer pulse
4) HF signs/symptoms
5) Left lateral decubitus position brings enlarged LV closer to the chest wall and causes a pounding sensation and increased awareness of heartbeat

Question 36

Acute pericarditis following MI

Answer 36

Complication of MI that typically occurs within the first several days after the event. It is characterized by sharp, pleuritic pain that is worse in the supine position and improved by sitting up and leaning forward.

Pericardial friction rub may be heard on exam. Diffuse ST elevations, esp with PR depressions are typical ECG findings in acute pericarditis.

Question 37

Ventricular aneurysm

Answer 37

Complication of anterior wall MI that can occur days to months after the initial infarct.

Presents with akinesis of the involved portion of the LV wall, ventricular arrhythmias, and systemic embolization.

Question 38

How does ASA produce antiplatelet effects?

Answer 38

Inhibits thromboxane A2

Early antiplatelet therapy with ASA reduces rate of MI and overall mortality in patients with ACS

Question 39

ASCVD risk calculator

Answer 39

Takes into account gender, race, SBP, Diabetes status, Age, Total cholesterol, HDL, Treatment for HTN (yes or no) and smoking status.

AtheroSclerosisCardioVascularDisease. A 10 year risk assessment.

Question 40

High intensity statin

Answer 40

1) Atorvastatin 40-80mg

2) Rosuvastatin 20-40mg

Question 41

Mod intensity statin

Answer 41

1) Atorvastatin 10-20mg
2) Rosuvastatin 5-10mg
3) Simvastatin 20-40mg
4) Pravastatin 40-80mg

Question 42

Fish oil supplements

Answer 42

High in omega 3 polyunsaturated fatty acids. Can effectively reduce serum triglycerides.

Statin is first line though for patients with mild to moderate hypertriglycerides for whom the goal of therapy is cardiovascular risk reduction.

Fish oil has not been shown to significantly improve CV outcomes or mortality

Question 43

Alcoholic cardiomyopathy

Answer 43

Look for certain signs. Like patient with signs of decompensated CHF but no evidence of CAD on angio. Look for macrocytic anemia, thrombocytopenia, more than 2 to 1 ratio of AST to ALT.

Alcoholic cardiomyopathy is a diagnosis of exclusion in patients with dilated cardiomyopathy and history of alcohol abuse in whom no other potential causes of cardiomyopathy (CAD, valvular heart disease) are suspected or identified.

The degree of LV dysfunction in alcoholic cardiomyopathy is directly related to the daily amount and overall duration of alcohol intake. Primary therapy for such patients is complete abstinence from alcohol use. This intervention is associated with improvement or normalization of LV function over time.

Question 44

Relative frequency of selected presenting symptoms in ACS

Answer 44

1) CP 80-85
2) Dyspnea 70-75
3) Nausea 40-55
4) Vomiting 15-20
5) Epigastric pain 10-15

Question 45

Which patients are most likely to have atypical presentations of ACS?

Answer 45

Women, elderly, and patients with diabetes. Up to 20% of these patients do not report any chest pain. Dyspnea, epigastric pain and n/v are common atypical presentations.

Always get an ECG in these groups if they have risk factors for ACS. This should be the first diagnostic test.

Question 46

11 factors associated with poor outcome after witnessed out of hospital sudden cardiac arrest

Answer 46

1) Time elapsed prior to effective resuscitation (delayed bystander CPR, delayed defib)**
2) Initial rhythm of pulseless electrical activity or asystole
3) Prolonged CPR (more than 5 minutes)
4) Absence of vital signs
5) Advanced age
6) Prior history of cardiac disease
7) 2 or more chronic illnesses
8) Persistent coma after CPR
9) Need for intubation or pressors
10) Pneumonia or renal failure after CPR
11) Sepsis, cerebrovascular accident, or class 3 or 4 HF

Question 47

Sudden cardiac arrest

Answer 47

Most common cause of out of hospital SCA in adults is sustained ventricular tachycardia or fibrillation due to acute myocardial ischemia or infarction.

Resuscitation for out of hospital SCA is successful in only one third of patients, and only about 10% of all patients are eventually discharged from the hospital

Question 48

Most important predisposing risk factor associated with development of aortic dissection

Answer 48

Systemic HTN.

Marfan is responsible for half of aortic dissections seen in patients under 40, but it is an uncommon cause in patients over 60.

Question 49

Meds that have been shown to improve long term survival in patients with LV systolic dysfunction

Answer 49

1) ACEIs
2) ARBs
3) B blockers
4) Mineralocorticoid receptor antagonists (MRAs) like spironolactone and eplerenone
5) In black people, combo of hydralazine and nitrates

Question 50

Spironolactone and eplerenone

Answer 50

MRAs. They block the deleterious effects of aldosterone on the heart and have been shown to improve overall survival and hospitalization for heart failure in symptomatic patients with LV systolic dysfunction.

MRAs are indicated in certain patients who have persistent HF symptoms despite use of ACE inhibitors/ARBs and BBs (LV EF less than 40 with recent STEMI and symptomatic HF)

Question 51

Third heart sound

Answer 51

Features

1) Ventricular gallop sound (after S2)
2) Heard during rapid filling of ventricles in diastole
3) Turbulent blood flow to the ventricles due to increased volume

Normal

1) Children
2) Young adults
3) Pregnancy

Abnormal/associated conditions

1) Age over 40
2) HF
3) Restrictive cardiomyopathy
4) High output states

Question 52

Fourth heart sound

Answer 52

Features

1) Atrial gallop sound (before S1)
2) Heard immediately after atrial contraction phase as blood is forced into a stiff ventricle

Normal
1) Healthy older adults

Abnormal/associated conditions

1) Younger adults, children
2) Ventricular hypertrophy
3) Acute MI (due to ischemia induced myocardial dysfunction)
4) Decreased LV compliance
5) HCM
6) AS

Question 53

Variant angina

Answer 53

AKA Prinzmetal’s Angina. Causes CP by coronary vasospasm.

Typically occurs in young females and the greatest risk factor for variant angina is smoking. Aside from smoking, affected patients often lack cardiovascular risk factors.

The episodes characteristically occur at night (from midnight to 8am) and can be associated with transient ST elevations on ECG.

Tx of this condition involves elimination of risk factors like smoking, as well as pharm therapy with CCBs or nitrates. These meds work in variant angina by promoting vasodilation and preventing vasoconstriction

Statins usually not needed bc they often lack other risk factors besides smoking

Avoid nonselective B blockers and ASA bc they can promote vasoconstriction

Question 54

uses of digoxin

Answer 54

Typically used to increase contractility in patients with CHF or as a rate control agent in patients with AFib or flutter

Question 55

Serum BNP

Answer 55

Can help distinguish between CHF and other causes of dyspnea. A value greater than 100 diagnoses CHF with a sensitivity, specificity and predictive accuracy of 90, 76, and 83.

BNP is released from ventricles in response to volume overload.

It is tough to tell the cause of worsening dyspnea in elderly patients, esp if there is a history of CHF and COPD, so this is helpful.