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Internal medicine rotations > Cardiovascular > Flashcards

Cardiovascular Flashcards

1
Q

Isolated systolic hypertension is defined as a systolic blood pressure > 140 with a diastolic < 90. What is the pathophysiologic mechanism leading to isolated systolic hypertension

A

-increased stiffness or decreased elasticity of the aortic and arterial walls in elderly patients

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2
Q

Renovascular HTN should be suspected in all patients with resistant hypertension and what other findings?

A
  • diffuse atherosclerosis
  • asymmetric kidney size
  • Recurrent flash pulmonary edema
  • elevation in serum creatinine > 30% from baseline after starting an ACEI or ARB
  • The presents of a continuous abdominal bruit has a high specificity for the presence of renovascular HTN
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3
Q

Early diastolic murmur best heard along the LEFT sternal border (3rd and 4th ICS)?

A

Aortic regurg due to valvular disease

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4
Q

Early diastolic murmur best heard along RIGHT sternal bordner

A

Aortic regurg due to aortic root disease

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5
Q

The development of a new conduction abnormality in patients with infective endocarditis should raise suspicion for what?

A

perivalvular abscess extending into the adjacent cardiac conduction pathways

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6
Q

Acute pericarditis is characterized by what?

A
  • Chest pain (sharp and pleuritis, improves by sitting up and leaning forward)
  • Pericardial friction rub
  • diffuse concave upward ST-segment elevations across precordial and limb leads on ECG
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7
Q

Mitral valve perforation can occur as a complication of mitral valve endocarditis. IT generally presents as what?

A
  • Acute congestive heart failure

- systolic murmur of mitral regurg

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8
Q

The tricuspid valve is the most frequent site of endocarditis in IV drug users. This presents with what murmur?

A
  • SYSTOLIC murmur: holosystolic murmur of tricuspid regurg that becomes accentuated with inspiration
  • cardiac abnormalities are uncommon in patients with tricuspid valve endocarditis
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9
Q

All patients with new-onset Afib should be worked up for what endocrine underlying cause?

A

Hyperthyroidism

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10
Q

progressive prolonged PR interval leads to a nonconducted P wave (“group beating”)

A

Mobits type I second degree AV block (Wenckebach)

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11
Q

PR interval remains constant with intermittent nonconduction P waves

A

Mobitz type II second degree AV block

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12
Q

Level of block in Mobitz type I

A

Usually AV node

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13
Q

Level of block in Mobitz type II

A

Below the level of AV node (e.g. bundle of His)

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14
Q

What does exercise of atropine to to Mobitz type I?

A

Improves

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15
Q

What does exercise or atropine do to mobitz type II AV block?

A

Worsens

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16
Q

What do Vagal maneuvers (carotid sinus massage) do to mobitz type I AV blocks?

A

worsen

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17
Q

What do Vagal maneuvers (carotid sinus massage) do to mobitz type II AV blocks?

A

Paradoxically improves

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18
Q

Risk of complete heart block in Mobitz type I?

A

Low risk

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19
Q

Risk of complete heart block in Mobitz type II?

A

Higher risk, indication for pacemaker

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20
Q

What drugs can block AV node leading to Mobitz type I AV block

A
  • digoxin
  • Beta blockers
  • CCB
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21
Q

Contrast the width of the QRS complex in a mobitz type II compared to Mobitz type I

A

can be wider

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22
Q

What is the most common cause of sudden cardiac arrest in the immediate post-infarction period in patients with acute myocardial infarction?

A

Reentrant ventricular arrhythmias (e.g. vintricular fibrillation)

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23
Q

describe the rash in toxic shock syndrome

A

erythematous and desquamating

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24
Q

Describe the management of chest pain due to cocaine use?

A
  • Benzodiazepines for BP and anxiety
  • Aspirin
  • Nitroglycerin and CCB for pain
  • Beta blockers CONTRAINDICATED
  • Fibrinolytics NOT preferred due to increased risk of intracranial hemorrhage
  • Immediate cardiac cath with reperfusion when indicated
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25
Q

Clinical features of Aortic dissection

A
  • Severe, sharp, tearing chest or back pain

- > 20 mm Hg variation in systolic BP b/t arms

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26
Q

Current guidelines recommend the used of primary percutaneous intervention for any patient with acute STEMI within what time frame?

A
  • within 90 minutes of the first medical contact in a PCI-capable hospital OR
  • within 120 minutes for patients who require transport to a PCI-capable hospital from another hospital
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27
Q

This refers to a transient systolic dysfunction of apical and/or mid segments of the left ventricle with hyperkinesis of the basal segements, causing a “balloon-like” appearance of the left ventricle in systole. It is seen predominantly in older adults in response to intense physical or emotional stress or acute medical illness (eg, unexpected death of a relative, grave medical diagnosis, arguments, significant loss)

A

Stress induced (Takotsubo) cardiomyopathy (apical ballooning syndrome, “broken heart” syndrome)

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28
Q

This is the first-line therapy in conscious and stable patients with episodes of Torsades de pointes (TdP), which is a form of polymorphic ventricular tachycardia

A

IV magnesium

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29
Q

This is primarily used for the acute termination of paroxysmal supraventricular tachycardia

A

Adenosine

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30
Q

This is a class III antiarrhythmic, and is used both fro atrial and ventricular tachycardia. It is used occasionally in patients with polymorphic VT (and normal baseline QT interval) due to myocardial ischmeia or infarction

A

Amiodarone

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31
Q

This is used in the treatment of symptomatic sinus bradycardia or AV nodal block

A

Atropine

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32
Q

This is useful for patients with cardiotoxicity due to hyperkalemia. It is occasionally used in patients with beta-blocker and/or calcium channel blocker overdose

A

Calcium gluconate

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33
Q

Describe the different levels of hyperkalemia and what is seen on ECG

A
  • 6 to 7: Tall peaked T wave and prolonged PR
  • 7 to 8: Tall peaked T wave, ST elevation, Loss of P wave
  • > > 8: Widened QRR (sine wave pattern, AV node block, Fascicle and BB blocks
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34
Q

This is useful in the management of patients with torsades de points due to quinidine use. IT is also beneficial in patients with cardiac arrest due to metabolic acidosis, hyperkalemia, and TCA overdose

A

Sodium bicarbonate

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35
Q

This is a class III antiarrhythmic agent that causes QT prolongation and Torsades de points. Patients being initiated on this therapy for other indications should be admitted to the hospital for serial ECG and cardiac rhythm monitoring

A

Sotalol

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36
Q

IV drug used with cough, fever, and weakness and numerous round alveolar infiltrates on chest imaging.

A

Tricuspid valve endocarditis with septic emboli to the lungs

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37
Q

Augmentation of intensity with inspiration was shown to have 100% sensitivity and **% specificity in differentiating what about systolic murmurs

A

differentated RIGHT sided systolic murmurs from all others

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38
Q

A fourth heart sound (S4) can be heard over the cardiac apex in the left lateral decubitus position in patients with what?

A
  • reduced ventricular compliance (or increased stiffness)
  • It can be heard in many healthy older adults and in patients with hypertensive hearts disease, aortic stenosis, and hypertrophic cardiomyopathy
  • An audible S4 is an abnormal finding in children and young adults
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39
Q

Aortic regurgitation causes an early and decrescendo diastolic murmur that begins immediately after A2 (aortic component of second heart sound). The murmur is high pitched and has a blowing quality. It is best heard along the left sternal border at the 3rd and 4th ICS when the patient is what?

A

-sitting up and leaning forward while holding the breath in full expiration

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40
Q

Standing from a supine position decreases venous return to the heart and worsens the dynamic gradient in patients with what?

A
  • Hypertrophic cardiomyopathy

- This increases the intensity of ejection systolic murmur in these patients

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41
Q

Normal splitting of second heart sound (A2 and P2) is best appreciated during inspiration over the 2nd ICS. Paradoxical or “reversed” splitting occurs when A2 follows P2, with maximal splitting noted during expiration and being less pronounced during inspiration. This is seen in what patients?

A

-patients with fixed left ventricular outflow tract obstruction (eg, aortic valve or subaortic stenosis, LBBB, right ventricular paced rhythm)

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42
Q

Etiology of acute pericarditis

A
  • Viral or idiopathic
  • Autoimmune disease (eg, SLE)
  • Uremia (Acute or chronic renal failure)**
  • Post MI: Early: Peri-infarction pericarditis, Late: Dressler syndrome
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43
Q

Clinical features and diagnosis of Acute pericarditis

A
  • Pleuritic chest pain (decreases when sitting up) +/- fever
  • Pericardial friction rub (highly specific)
  • ECG: diffuse ST elevation and PR depression
  • Echo: pericardial effusion
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44
Q

in Uremic pericarditis, elevated levels of BUN above what level can lead to inflammation of the visceral and parietal layers of the pericardium

A

> 60

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45
Q

Describe the sound of the pericardial friction rub heard on cardiac ausculation in pericarditis

A
  • high frequency grating or squeaking sound best heard at the left sternal border with the patient leaning forward
  • may occur during systole, diastole, or both
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46
Q

Describe how Uremic pericarditis differs from other etiologies on ECG and why

A
  • Does NOT typically cause diffuse ST elevation (or PR depression)
  • The inflammation does not affect the myocardium
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47
Q

Viral pleurisy is an inflammation of the lung pleura that typically presents with fever and pleuritis chest pain. A pleural friction rub may be present and is differentiated from a pericardial friction rub by what?

A

disappearance during breath holding

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48
Q

Describe cardiac, GI, and neurologic symptoms of digoxin toxicity

A
  • Cardiac: Life-threatening arrhythmias
  • GI: anorexia, N/V, abdominal pain
  • Neurologic: Fatigue, confusion, weakness, color vision alterations
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49
Q

What medications increase the serum levels of digoxin and can lead to toxicity in a patient who has previously been on a stable digoxin regimen?
What is recommended when starting these drugs?

A
  • Amiodarone, verapamil, quinidine, propafenone
  • Digoxin dose should be decreased by 25-50% with close monitoring of digoxin levels once weakly for the next several weeks
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50
Q

USPSTF recommendation on AAA screening

A

male active or former smokers age 65-75 years with a one-time Abdominal U/S

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51
Q

What are the normal changes to the aging heart?

A
  • decreased resting and maximal cardiac output
  • decreased maximum heart rate
  • increased contraction and relaxation time of heart muscle
  • increased myocardial stiffness during diastole
  • decreased myocyte number
  • pigment accumulation in myocardial cells
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52
Q

What are the main reasons for the increased incidence or orthostatic hypotension in the elderly

A
  • progressively decreasing baroreceptor sensitivity

- defects in the myocardial response to this reflex

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53
Q

Etiology of syncope?
Triggers: prolonged standing or emotional distress, painful stimuli
Prodromal symtpoms: nausea, warmth, diaphoresis

A

Vasovagal or neurally mediated syncope

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54
Q

Etiology of syncope?

Triggers: cough, micturition, defecation

A

situational syncope

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55
Q

Etiology of syncope? syncope with exertion or during exercise

A
  • Aortic stenosis
  • HCM
  • anomalous coronary arteries
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56
Q

Etiology of syncope? Prior hx or CAD, MI, cardiomyopathy, or Low EF

A

Ventricular arrhythmias

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57
Q

Etiology of syncope? Sinus pauses, Increased PR or QRS duration

A
  • Sick Sinus syndrome
  • Bradyarrhythmias
  • AV block
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58
Q

Etiology of syncope? Hypokalemia, hypomagnesemia, medications causing increased QT interval

A

Torsades de pointes (acquired long QT syndrome)

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59
Q

Etiology of syncope? Family hx of sudden death, increased QT interval, syncope with triggers (eg, exercise, startle, sleeping)

A

Congenital long QT syndrome

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60
Q

Clinical presentation of transient loss of consciousness along with loss of postural or motor tone during urination is consistent with situational (postmicturation) syncope, a form of reflex (neurally mediated) syncope associated with specifiec triggers (eg, micturition, defecation, cough). Describe pathophysiology

A
  • The specific triggers for reflex syncope cause an alteration in the autonomic response and can lead to a CARDIOINHIBITORY VASODEPRESSOR, or mixed response
  • Increased parasympathetic stimulation can manifest as profound bradycardia, varying degrees of AV block, or asystole
  • Decreased sympatheti output can lead to vasodilation, hypotension, or syncope
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61
Q

TIAs are an infrequent cause of syncope, as the TIA must affect where to cause syncope

A

posterior circulation and brainstem

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62
Q
  • Acute dyspnea, orthopnea, paroxysmal nocturnal dyspnea
  • HTN common; hypotension suggests severe disease
  • Accessory muscle use, tachycardia, tachypnea
  • Diffuse crackles with possible wheezes (cardiac asthma)
  • Possible S3, JVD, peripheral edema
A

Acute decompensated heart failure

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63
Q

Describe the treatment of Acute decompensated heart failure if normal or elevated blood pressure with adequate end-organ perfusion

A
  • Supplemental oxygen
  • IV loop diuretic (eg, furosemide)
  • Consider IV vasodilator (eg, nitroglycerin)
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64
Q

Describe the treatment of Acute decompensated heart failure if hypotension or signs of shock?

A
  • Supplemental oxygen
  • IV loop diuretic (eg, furosemide) as appropriate
  • IV vasopressor (eg, norepinephrine)
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65
Q

This is a ventricular gallop sound (after S2). It is heard during rapid filling of ventricles in diastole. Turbulent blood flow to the ventricles due to increased volume

A

Third heart sound (S3)

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66
Q

When is third heart sound normal

A
  • Children
  • YOUNG adults
  • Pregnancy
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67
Q

Abnormal or conditions associated with third heart sound

A
  • Age > 40
  • Heart failure
  • Restrictive cardiomyopathy
  • High-output states
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68
Q

This is an atrial gallop sound (before S1). Heard immediately after atrial contraction phase as blood is forced into a stiff ventricle

A

4th heart sound (S4)

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69
Q

When is 4th heart sound normal

A

Healthy OLDER adults

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70
Q

When is 4th heart sound abnormal or conditions associated with it

A
  • Younger adults, children
  • Ventricular hypertrophy
  • Acute MI
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71
Q

An abnormal S4 (atrial gallop) can be heard in most patients during the acute phase of MI due to what?

A

ischemia induced myocardial dysfunction

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72
Q

Pulsus paradoxus refers to an exaggerated drop in systolic BP (> 10 mm Hg) during inspiration. It is most commonly seen in patients with what?

A

cardiac tamponade but can also occur in severe asthma and COPD, hypovolemic shock, and infrequently with constrictive pericarditis

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73
Q

What are the possible mechanical complications following an acute MI? give time frames?

A
  • Right ventricular failure - Acute
  • Papillary muscle rupture - acute or within 3-5 days
  • Interventricular septum rupture - acute or within 3-5 days
  • Free wall rupture - 5 days to 2 weeks
  • Left ventricular aneurysm - up to several months
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74
Q

Which possible mechanical complication following an acute MI occur with RCA coronary artery involvement?

A
  • Right ventricular failure
  • Papillary muscle rupture
  • Interventricular septum rupture (basal septal)
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75
Q

Which possible mechanical complication following an acute MI occur with LAD coronary artery involvement?

A
  • Interventricular septum rupture (Apical septal)
  • Free wall rupture
  • Left ventricular aneurysm
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76
Q

Which possible mechanical complication following an acute MI? Hypotension, Clear lungs, Kussmaul sign (rise of JVD on inspiration)

A

Right ventricular failure

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77
Q

Which possible mechanical complication following an acute MI? Severe pulmonary edema, New holosystolic murmur

A

Papillary muscle rupture

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78
Q

Which possible mechanical complication following an acute MI? Chest pain, New holosystolic murmur, biventricular failure, shock

A

Interventricular septum rupture

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79
Q

Which possible mechanical complication following an acute MI? Chest pain, shock, distant heart sounds

A

Free wall rupture

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80
Q

Which possible mechanical complication following an acute MI? Subacute heart failure, stable angina

A

left ventricular aneurysm

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81
Q

Which possible mechanical complication following an acute MI? Echo shows hypokinetic RV

A

Right ventricular failure

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82
Q

Which possible mechanical complication following an acute MI? Echo shows severe mitral regurg with flail leaflet

A

Papillary muscle rupture

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83
Q

Which possible mechanical complication following an acute MI? Echo show left to right ventricular shunt and increase O2 level from RA to RV

A

Interventricular septum rupture

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84
Q

Which possible mechanical complication following an acute MI? Echo shows pericardial effusion with tamponade

A

Free wall rupture

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85
Q

Which possible mechanical complication following an acute MI? Echo shows think and dyskinetic myocardial wall

A

Left ventricular aneurysm

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86
Q

compared to interventricular septum rupture, the systolic murmur of acute mitral regurg from papillary muscle rupture is different how?

A

-is soft and no palpable thrill present

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87
Q

The diagnosis of Right ventricular MI is confirmed with >1 mm ST-segment elevation in the right sided precordial leads V4R -V6R. Right ventricular failure leads to decreased preload and resultant hypotension. Therefore, in addition to standard MI therapy, such patients, (without pulmonary congestion) are typically treated with what?

A

Boluses of IV fluids (isotonic saline) to improve RV preload and facilitate left ventricular filling
-Preload reducing meds such as nitrates and diuretics should be avoided

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88
Q

Massive PE can often present similarly to RV infarction. What does ECG typically show in a PE?

A
  • tachycardia
  • nonspecific ST-segment or T-wave changes
  • New onset RBBB OR
  • S1Q3T3 pattern
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89
Q

What is this and what is pathogenesis?

  • Angina episodes
  • Young patients (age < 50)
  • Smoking (minimal other CAD risk factors)
  • Recurrent chest discomfort: occurs at rest or during sleep; spontaneous resolution in 15 or less minutes
A
  • Vasospastic angina (formerly known as variant or prinzmetal)
  • Hyperreactivity of coronary smooth muscle
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90
Q

Describe how to diagnose vasospastic angina

A
  • Ambulatory ECG: ST elevation

- Coronary angiography: no CAD

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91
Q

Treatment of vasospastic angina

A
  • smoking cessation
  • CCB (preventative): like Diltiazem to dilate coronary arteries; Amlodipine and felodipine also effective
  • Sublingual nitroglycerin (abortive)
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92
Q

Why should Aspirin be avoided in patients with vasospastic angina?

A

-it can inhibit prostacycline production and worsen coronary vasospasms

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93
Q

Cilostazol is a phophodiesterase III inhibitor that causes arterial vasodilation and inhibits platelet aggregation. It is often used in what?

A

lower extremity claudication

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94
Q

As adrenergic stimulation of beta-2 receptors dilates coronary arteries and alpha-1 stimulation constricts them, these can worsen coronary vasospasm and should be avoided in patients with vasospastic angina

A

Nonselective beta blockers (eg, propranolol)

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95
Q

This is an antianginal drug that decreases myocardial calcium level by inhibiting late-phase sodium influx into ischemic cardiomyocytes. It is effective in treating stable angina due to atherosclerotic CAD

A

Ranolazine

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96
Q

Describe initiation of Statin in diabetics

A
  • Diabetic patients age 40-75 should be treated with statin therapy in addition to lifestyle modification and glucose control
  • Those with a 10-year risk of atherosclerotic cardiovascular disease <7.5% should receive moderate-intensity statin therapy, and those with a risk > 7.5% should receive high intensity statin therapy
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97
Q

A patient with NSTEMI (chest pain, ST depression troponin elevation) undergoes revascularization of the culprit coronary artery with a drug-eluting stent. Long-term medical therapy in such patients is aimed at prevention of recurrent coronary events (secondary prevention) and reduction of overall cardiovascular events. Medial therapy shown to improve morbidity and mortality in patients with known coronary hearth disease includes what?

A
  • DUAL antiplatelet therapy with aspirin and P2y12 receptor blockers (eg, clopidogrel, prasugrel, ticagrelor)
  • Beta blockers
  • ACEIs or ARBs
  • HMG-CoA reductase inhibitors (statins)
  • Aldosterone antagonists (eg, spironolactone, eplerenone) in patients with left ventricular EF <40% who have heart failure symptoms or DM
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98
Q

This is an adrenergic agonist with predominant activity on beta-1 receptors and minimal activity on beta-2 and alpha-1 receptors. It is used for the management of severe heart failure associated with severe left ventricular systolic dysfunction and cardiogenic shock.
What drug and what mechanism of action

A
  • Dobutamine
  • increased cAMP in cardiac myocytes –> enhanced calcium mediated binding of the actin-myosin complex to troponin and increased myocardial contractility (positive inotropic effect)
  • Heart rate is also increased via calcium channel activation (positive chronotropic effect)
  • The increase in myocardial contractility allows for forward ejection of a higher volume of blood and restuls in a decrease in left ventricular end-systolic volume
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99
Q

The 2 major treatment issues that need to be addressed in all patients with new-onset Afib includes what?

A
  • The choice between rate or rhythm control strategy and

- risk stratification for prevention of systemic embolization

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100
Q

The CHA2DS2-VASc score can be utilized to identify which patients with Afib are at greatest risk for thromboembolic complications and would benefit from antithrombotic therapy. What is this?

A
  • C: congestive heart failure - 1 pt
  • H: HTN - 1 pt
  • A2: Age 75 or older - 2 pt
  • D: DM - 1 pt
  • S2: Stroke/TIA/thromboembolism 2 pt
  • V: Vascular disease (prior MI, PAD, or aortic plaque) - 1 pt
  • A: Age 65-74 - 1 pt
  • Sc: Sex Category (ie, female) - 1 pt
101
Q

Describe the scoring of CHA2DS2-VASc scoring in coorelation with antithrombotic therapy

A
  • 0: low stroke risk. no therapy
  • 1: intermediate risk. None or aspirin or oral anticoagulants
  • 2 or more: high risk, oral anticoagulants
102
Q

Patient with fatigue, exertional dyspnea, lower extremity swelling in the absence of pulmonary edema is consistent with Right-sided heart failure. The predominant manifestation of restrictive cardiomyopathy (evidenced by thickened ventricular walls and diastolic dysfunction on echo). Systemic infiltrative disease is a common cause of restrictive cardiomyopathy; concomitant easy bruising and large proteinuria suggest underlying what?

A

amyloidosis

103
Q

what are the CYP450 inhibitors that increase warfarins effect and increases bleeding risk?

A
  • Acetaminophen, NSAIDs
  • Antibiotics/antifungals (eg, metronidazole)
  • Amiodarone
  • Cimetidine
  • Cranberry juice, Ginkgo biloba, vitamin E
  • Omeprazole
  • Thyroid hormone
  • SSRIs (eg, fluoxetine)
104
Q

What are the CYP450 inducers that decrease warfarin’s effects and decrease efficacy?

A
  • Carbamazepine, phenytoin
  • Ginseng, St. John’s wort
  • Oral contraceptives
  • Phenobarbital
  • Rifampin
105
Q

Beta blockers are first line therapy for alleviating symptoms and improving exercise tolerance in patients with stable angina. By what mechanism do they help with angina?

A
  • decreasing exertional heart rate and myocardial contractility, leading to reduction in myocardial oxygen demand
  • NONdihydropyridine CCBs (verapamil, diltiazem) treat angina primarily through the same mechanism
106
Q

Describe the mechanism of Valsalva on its effects on heart murmurs?

A
  • Decreases venous return during strain

- Increases during relaxation

107
Q

Describe the mechanism of standing on its effects on heart murmurs?

A

Decreases venous return

108
Q

Describe the mechanism of squatting on its effects on heart murmurs?

A
  • increases venous return
  • Increases afterload
  • Increases regurgitant fraction
109
Q

Describe the mechanism of Handgrip on its effects on heart murmurs?

A
  • Increases afterload
  • Increases blood pressure
  • Increases regurgitant fraction
110
Q

A short systolic murmur at the cardiac apex that disappears with squatting is most consistent with what?

A

mitral valve prolapse

111
Q

Describe the difference in the effects that squatting has on a mitral regurg murmur compared to mitral prolapse

A
  • Mitral regurg murmurs typically increase in intensity with squatting
  • Mitral prolapse decrease in intensity with squatting
112
Q

Exam findings in cor pulmonale (impaired function of the right ventricle caused by pulmonary HTN)

A
  • peripheral edema
  • Increased JVD with prominent a wave
  • Loud S2
  • Right sided heave
  • Pulsatile liver from congestion
  • Tricuspid regurg murmur
113
Q

What is the gold standard for diagnosis of cor pulmonale

A

right heart cath showing right ventricular dysfunction, pulmonary HTN, and no left heart dz

114
Q

The diagnosis of cor pulmonale is based primarily on clinical features and echo findings (eg, right ventricular hypertrophy, tricuspid regurg with right atrial enlargement). If necssary, definitive diagnosis can be made using right heart cath showing elevated what?

A

elevated pulmonary artery systolic pressure (> 25 mm Hg)

115
Q

The pulmonary capillary wedge pressure is an estimation of left ventricular end-diastolic pressure, and is elevated in patients with what?

A

left ventricular systolic and/or diastolic dysfunction

-patients with elevated PCWP typically have signs of pulmonary edema on lung auscultation

116
Q
  • Widened pulse pressure
  • Strong peripheral arterial pulsation (eg, brisk carotid upstroke)
  • systolic flow murmur
  • tachycardia
  • usually flushed extremities
  • The left ventricle hypertrophies and the PMI is displaced to the left
A

Arteriovenous fistula leading to high-output heart failure

117
Q

in an arteriovous fistula, shunting of a large amount of blood through the fistula does what do hemodynamics

A
  • Decreases systemic vascular resistance
  • Increases cardiac preload
  • Increases cardiac output
118
Q

In patients with mild-moderate hypertriglyceridemia (150-500) who have known or are at high risk for coronary artery disease, what is management?

A
  • Initiation of a high-intensity statin (eg, rosuvastatin, atorvastatin) is recommended first line pharmacologic therapy
  • In addition, lifestyle modifications targeting secondary causes should be pursued
119
Q

Niacin is effective at reducing triglyceride levels. Describe its use in combo with statins

A

-its use in combo with statins is associated with an increase in adverse effects (eg, GI upset) without improving cardiovascular outcomes

120
Q

What is the most effective pharmocologic therapy available for lowering triglyceride levels and are recommended in patients with SEVERE hypertriglyceridemia (>1000)? Describe its used in mild to moderate hypertriglyceridemia?

A
  • Fibrate (eg, gemfibrozil, fenofibrate)
  • Because of superior evidence for overall cardiovascular benefits, statins are the recommended first line therapy for patients with CAD and mild-moderate hypertriglyceridemia.
  • Due to increased rates of adverse effects (eg, myopathy) and lack of proven cardiovascular benefit, the addition of a fibrate to a statin is rarely indicated
121
Q

CHF due to left ventricular systolic dysfunction is characterized by what levels of Cardiac output/index, systemic vascular resistance, and left ventricular end-diastolic volume?

A
  • Low CI
  • High SVR
  • High LVEDV
122
Q

What is the most frequent location of the ectopic foci that cause Afib?

A

Pulmonary veins

123
Q

Origination of Afib in the pulmonary veins is therapeuitcally useful in patients who cannot achieve rate and/or rhythm control with standard medical therapy. Explain this?

A

-The myocardial tissue surrounding the pulmonary veins can be disrupted by catheter-based radiofrequency ablation, thereby electrically disconnecting the pulmonary veins from the left atrium

124
Q

describe location of conduction dysfunction in Wolff-Parkinson-White pre-ecitation syndrome

A

Accessory atrioventricular bypass tract

125
Q

describe location of conduction dysfunction in paroxysmal SVT

A

Atrioventricular nodal reentry tachycardia

126
Q

describe location of conduction dysfunction in sinus tachycardia

A

sinoatrial node

127
Q

The most common cause of atrial flutter is a reentrant circuit around what?

A

the tricuspid annulus, with slowing of the impulse through a region known as the cavotricuspid isthmus

128
Q

Decreased cardiac output due to decompensated systolic heart failure leads to what renal hemodynamics due to activation of RAAS system

A
  • Vasoconstriction of both Afferent and Efferent glomerular arterioles, leading to an increase in renal vascular resistance and net Decrease in renal blood flow
  • Preferential vasocontriction of Efferent arterioles, which increases intraglomerular pressure to maintain GFR
  • Direct stimulation of sodium resorption in the proximal tubules and increased secretion of aldosterone promotes further sodium resorption in the cortical collecting tubule. leads to DECREASED sodium delivery to distal tubule and an increase in extracellular volume
129
Q

What is the most effective nonpharmacologic measure to decrease BP in overweight individuals?

A
  • Weight loss

- reduce BMI < 25

130
Q

Describe the management of patient with PAD and claudication symptoms

A
  • A supervised graded exercise program is the most useful intervention to improve functional capacity and reduce symptomatic claudication
  • Antiplatelet agents (eg, aspirin, clopidogrel) reduce overal cardiovascular mortality
  • Lipid-lowering therapy with statins should be given to all patients with clinically significant atherosclerotic cardiovascular disease
131
Q

When is surgical revascularization used in PAD

A

reserved for patients with limb-threatening complications (eg, nonhealing ulcers), significant limitation in activities of daily living, or failure to respond to exercise and medication

132
Q

In observational studies, the strongest predictors of abdominal aortic aneurysm expansion and rupture are what?

A
  • Large aneurysm diameter
  • Rapid rate of expansion
  • Current cigarette smoking
133
Q

What are the current indications for operative or endovascular repair of AAA?

A
  • aneurysm size > 5.5 cm
  • Rapid rate of expansion (> .5 cm in 6 months or >1 cm/year)
  • Presence of symptoms (abdominal pain, or flank pain; limb ischemia) regardless of size
134
Q

What arrhythmia is most specific for digitalis toxicity?

A

Atrial tachycardia with AV block

135
Q

What is the classic clinical presentation of acute arterial occlusion (acute limb ischemia) . . 6 P’s

A
  • Pain
  • Pallor
  • Poikilothermia (cool)
  • Paresthesia
  • Pulselessness
  • Paralysis
136
Q

Patients with suspected acute arterial occlusion leading to an immediately-threatened limb (sensory loss, rest pain, muscle weakness) should be immediately started on what?

A
  • Anticoagulation while further diagnostic procedures are performed
  • Heparin prevents further thrombus propagation and thrombosis in the distal arterial and venous circulation
137
Q

Although most patients with HTN have essential HTN, initial evaluation should assess possible secondary causes. This basic workup includes investigating the duration of HTN, presence of precipitating/aggravating factors, extent of target organ damage, and cardiovascular risk factors. Basic laboratory analysis should include what?

A
  • UA (for occult hematuria and protein/creatinine ratio)
  • Chemistry panel
  • Lipid profile (risk stratification for CAD)
  • And baseline ECG (evaluate for CAD or left ventricular hypertrophy)
138
Q

This is a complication of cardiac catheterization and other vascular procedures. It is characterized by cutaneous findings (eg, “blue toe syndrome”, livedo reticularis), cerebral or intestinal ischemia, Acute kidney injury, and Hollenhorst plaques (bright, yellow, refractile plaques in the retinal artery)

A

Atheroembolism (cholesterol embolism)

139
Q

ECG findings of left ventricular Hypertrophy

A
  • high-voltage QRS complexes
  • Lateral ST segment depression
  • Lateral T wave inversion
140
Q

Which type of shock is the only type to have elevated mixed venous oxygen saturation? And what does this mean?-

A
  • Septic shock
  • Due to hyperdynamic circulation (as cardiac output is increased in resonse to reduced SVR to maintain peripheral tissue perfusion) with an inability of tissues to adequately extract oxygen (may develop lactic acidosis from tissue hypoperfusion)
141
Q

Bradycardia, AV block, Hypotension, and diffuse wheezing is suggestive of what overdose? Can also see hypoglycemia, delirium, seizures, and cardiogenic shock.

A

beta blocker overdose
-Intoxication with CCB, digoxin, and cholinergic agents could also cause similar symptoms but WHEEZING is more specific for beta blocker toxicity

142
Q

The first steps in management of Beta blocker intoxication are to secure the airway and give isotonic fluid boluses and IV atropine for initial treatment of hypotension and bradycardia. In patients with refractory or profound hypotension, the next step is to administer what?

A

IV glucagon

  • This increases the intracellular levels of cAMP and has been effective in treating both beta blocker and calcium channel blocker toxicity
  • Other therapies that can be used simultaneously or in succession include IV calcium, vasopressors (epinephrine or norepinephrine), high dose insulin and glucose, and IV lipid emulsion therapy
143
Q

Single photon emission CT scan is a useful tool to evaluate for coronary artery disease and indicates inducible ischemia when a reversible defect is noted on stress and rest images. What is the preferred treatment to prevent coronary artery disease in these patients?

A

Antiplatelet therapy

144
Q

elevated plasma levels of this has a high sensitivity for diagnosing CHF

A

BNP
-In studies of patients presenting with acute dyspnea, most patients with dyspnea due to CHF had plasma BNP levels > 400 whereas levels < 100 had a high negative predictive value for CHF as a cause of dyspnea

145
Q

Cutaneous flushing and intensive generalized pruritius are well-known side effects of high-dose niacin therapy (high dosage is required to treat lipid abnormalities) These effects are explained by niacin induced peripheral vasodilation. What is the mechanism behind this reaction?

A

drug-induced release of histamine and prostaglandins, not a truce hypersensitivity reaction
-The role of prostaglandins is confirmed by the fact that low-dose aspirin can greatly reduce or prevent cutaneous flushing and pruritis if taken 30 minutes before niacin

146
Q

Mitral valve prolapse is the most common cause of mitral regurgitation in developed countries. It usually causes mild Mitral regurg with mid-systolic click and mid to late systolic murmur. Patients with severe leaflet dysfunction and prolapse can develop severe Mitral regurg and holosystolic murmur on PE. Mitral valve prolapse occurs due to what?

A

Myxomatous degeneration of the mitral valve leaflets and chrondae

147
Q

What is the strongest predictor of stent thrombosis after intracoronary stent implantation within the first 12 months ?

A
  • Premature discontinuation of antiplatelet therapy
  • Such patients should be aggressively screened for, and counseled regarding, medication compliance to reduce the risk of stent thrombosis
148
Q

Most first degree AV blocks with NORMAL QRS duration occur due to conduction delay in the AV node and require what management?

A

no further evaluation unless there are significant associated bradycardic symptoms (eg syncope)
-Although it is considered a benign finding, the presence of first-degree AV block has been associated with a higher risk of heart failure, afib, and overall mortality

149
Q

The presence of first-degree AV block with a WIDE QRS duration (> 120 msec) can be associated with conduction delay below the AV node, most often in the bundle branches. These patients can have an unpredictable progression to advanced second-degree or complete heart block and should have what management?

A

electrophysiological testing to determine the site of conduction delay

150
Q

Some patients with first-degree AV block and marked prolongation of the PR interval can get an uncomfortable sensation with the awareness of heartbeat due to atrial contraction against a closed mitral valve during ventricular systole. What is this called and what is potential management?

A
  • “pacemaker syndrome”

- Potential candidates for pacemaker explantation

151
Q

these maneuvers tend to slow conduction in the AV node and decrease the pulse rate in SVT. They are useful in determining the site of conduction abnormality in patients with 2:1 AV block but provide no useful information in patients with first degree AV block

A

Vagal maneuvers

152
Q

This occurs in patients with lung cancer, thrombi, or fibrosing mediastinitis and can cause upper extremity edema. Arterial flow is preserved and no ischemia occurs

A

Superior vena cava syndrome

153
Q

Loop diuretics cause what electrolyte abnormalities?

What are the consequences of this?

A
  • Hypokalemia and hypomagnesemia

- These can cause ventricular tachycardia and also potentiate the side effects of digoxin

154
Q

Acute mitral regurgitation can occur due to papillary muscle displacement in patients with acute MI. Describe what this does to the left atrium and ventricle and contrast these findings to what happens with CHRONIC mitral regurg

A
  • Acute mitral regurg leads to abrupt and excessive volume overload, causing elevated left atrial and ventricular filling pressures and acute pulmonary edema
  • Unlike, chronic mitral regurg, Acute mitral regurg does not cause any significant change in left atrial or ventricular size and/or compliance
155
Q

Cardiac amyloidosis is a form of restrictive cardiomyopathy . . CHF with preserved ejection fraction. What does echo show?
Contrast this to hypertrophic cardiomyopathy?
What other findings suggest amyloidosis?

A
  • Concentric left ventricular hypertrophy
  • Hypertrophic cardiomyopathy is characterized by ASYMMETRIC SEPTAL hypertrophy
  • Other clinical manifestations: asymptomatic proteinuria/nephrotic syndrome, waxy skin, anemia, easy bruising with ecchymosis, hepatomegaly, GI bleeding, early satiety, subcutaneous nodules, enlarged tongue, and peripheral or autonomic neuropathy
156
Q

Thiamine deficiency can lead to beriberi heart disease, a form of high-output heart failure that leads to the development of what type of cardiomyopathy?

A

dilated

157
Q

Describe the management of Acute Aortic Dissection

A
  • Pain control (eg, morphine)
  • IV beta blockers (eg, esmolol)
  • +/- sodium nitroprusside (if SBP > 120 mm Hg)
  • Urgent surgical repair for ascending dissection
158
Q

What are the GOALS of initial therapy of aortic dissection

A
  • Adequate pain control
  • Reduction of systolic blood pressure to a goal of 100-120
  • Decrease in Left ventricular contractility to reduce aortic wall stress
159
Q

What are the IV beta blocker options? (for use in Acute Aortic Dissection for example)

A
  • Labetalol
  • Propranolol
  • Esmolol
160
Q

Describe the use of Hydralazine and Nitroprusside in the management of a Hypertensive patient with an acute Aortic dissection?

A
  • These are vasodilators sometimes used in hypertensive emergencies
  • However, they can cause reflex sympathetic stimulation with consequent rises in HR, LV contractility, and aortic wall stress.
  • These changes increase the risk of propagation of an aortic dissection
  • In patients with aortic dissection, nitroprusside is used as a Second line agent only if SBP remains above goal (ie, > 120 mm Hg) despide adequate beta blockade
161
Q

What is the most important predisposing factor associated with the development of Aortic dissection

A

Systemic HTN

162
Q

Marfan syndrome is responsible for almost 50% of the aortic dissections seen in patients what age?

A
  • <40

- However it is an uncommon cause in patients age > 60

163
Q

Describe the ECG findings for Premature atrial contractions (PACs)

A
  • rate: 60-100
  • Rhythm: irregular
  • P wave of the PAC often has a different shape from the one originating in the SA node
  • QRS is normal
164
Q

Other ECG findings in Wolff-Parkinson-White syndrome other than the “slurred” upstroke of QRS complex (“delta wave”)

A
  • Short PR interval ( < .12 seconds)

- Widened QRS complex

165
Q

Cardiac side effects of amiodarone?

A
  • Sinus brady, heart block

- Risk of proarrhythmias - QT prolongation and risk of torsades de pointes

166
Q

Pulmonary side effects of amiodarone

A

-Chronic interstitial pneumonitis (cough, fever, dyspnea, pulmonary infiltrates) most common

167
Q

Endocrine side effects of amiodarone?

A

-Hypo/Hyperthyroidism

168
Q

GI/Hepatic side effects of amiodarone?

A
  • Elevated transaminases

- hepatitis

169
Q

Ocular side effects of amiodarone

A
  • Corneal microdeposits

- Optic neuropathy

170
Q

Dermatologic side effects of amiodarone

A

Blue-Gray skin discoloration

171
Q

Neurologic side effects of amiodarone?

A

peripheral neuropathy

172
Q

Side effects of hydralazine?

A
  • Salt and fluid retention
  • Peripheral edema
  • Palpitations
  • Orthostatic hypotension
  • Drug-induced lupus-like syndrome
173
Q

All patients with persistent tachyarrhthmia (narrow or wide complex) causing hemodynamic instability (eg, hypotension, signs of shock, ischemic chest discomfort, mental status changes, acute pulmonary edema) should be managed how?

A

-immediate SYNCHRONIZED direct current cardioversion due to the risk of rapid clinical deterioration

174
Q

This provides a high-energy shock at a random point in the cardiac cycle and is used during resuscitation efforts in patients with pulseless cardiac arrest who have a shockable rhythm.

A

UNsynchronized cardioversion (defibrillation)

175
Q

This delivers a low-energy electric shock synchronized to the QRS complex

A

Synchronized direct current cardioversion

176
Q

What are the shockable ryhythms in which you can use UNsynchronized cardioversion (defibrillation)

A
  • Ventricular fibrillation

- Pulseless ventricular tachycardia

177
Q

Administration of an UNsyndhronized shock in circumstances that aren’t a shockable rhythm can lead to induction of what rhythm?

A

V fib

178
Q

This is a common cause of dilated cardiomyopathy in relatively young adults. Patients typically present with signs and symptoms of decompensated heart failure (eg, dyspnea, orthopnea, peripheral edema) and echo showing 4 chamber dilation

A

Viral myocarditis

179
Q

This cardiac auscultation finding is commonly heard in patients with CHF due to left ventricular systolic dysfunction (up to 99% specificity), and it correlates with elevated left atrial and/or ventricular filling pressures and serum BNP levels

A
  • The third heart sound (S3) is a low-frequency diastolic sound produced by the passive ventricular filling during early diastole
  • IT is best heard over the cardiac apex in the left lateral decubitus position
  • An abnormal S3 (louder and higher pitch, S3 GALLOP) is commonly heard in patients with CHF due to left ventricular systolic dysfunction
180
Q

Besides a harsh systolic murmur at the right upper sternal border with radiation to the carotid arteries, what other cardiac auscultation finding can occur with Aortic stenosis and why?

A
  • S4 occurs as the result of left atrial kick against a stiff left ventricle
  • The high resistance generated by the stenosed oartic valve causes concentric hypertrophy and stiffening of LV
181
Q

What are the 3 most common causes of Aortic stenosis in the general population?

A
  • Senile calcific
  • Bicuspid aortic valve
  • Rheumatic heart disease
182
Q

What is the cause of aortic stenosis in the majority of patients under 70 years old

A

Bicuspid Aortic Valve

183
Q

The murmur of hypertrophic cardiomyopathy can be easily confused with that of aortic stenosis. Both entities can cause a systolic crescendo-decrescendo murmur and an S4. However, the murmur of hypertrophic cardiomyopathy is different how?

A

-usually best appreciated in the lower left sternal border and it does not typically radiate to the carotids

184
Q

In WPW, an accessory pathway 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; Afib in WPW can bypass the usual rate-limiting function of the AV node, leading to a very rapid ventricular response rates. Persistent Afib with rapid ventricular response in patients with WPW can ultimately deteriorate into Ventricular fibrillatio. Acute treatment in patients wit hWPW is aimed at prompt control of ventricular response and termination of Afib with what?

A
  • Hemodynamically unstabe patients require immediate electrical cardioversion
  • For STABLE patients, rhythm control with anti-arrhythmic drugs such as IV ibutilide or PROCAINAMIDE is preferred
185
Q

What are the AV nodal blocking agents that should NOT be used for Afib in patients with WPW?
Why shouldn’t they be used?

A
  • Adenosine
  • Beta blockers
  • CCBs (especially verapamil)
  • Digoxin
  • They may promote conduction across the accessory pathway and lead to degeneration of Afib into Vfib
186
Q

What type of arrhythmias is lidocain indicated for

A

Ventricular

187
Q

An ECG is the essential first step in a patient with history and risk factors for coronary artery disease who has symptoms consistent with Acute coronary syndrome. There are a number of well-known atypical presentation (no over chest pain, dyspnea, epigastric pain, N/V) of ACS that should prompt a cardiac evaluation. Unfortunately, patients with atypical symptoms are more likely to have a delay in diagnosis and under treatment, which contributes to worsened outcomes. What demographic of people are more likely to have atypical symtpoms

A
  • Women
  • Elderly
  • Patients with diabetes
  • up to 20% of these patients do not report chest pain at the time of presentation
188
Q

Describe what cardiac auscultation reveals in Pulmonary stenosis?

A
  • Pulmonic ejection click (best heard during expiration)
  • Followed by a harsh crescendo-decrescendo systolic murmur over the Left 2nd ICS
  • The murmur intensifies with inspiration
  • The stenosis also causes the pulmonic valve to close later than usually resulting in widened splitting of the aortic and pulmonic components of the S2
  • The splitting is further increased during inspiration
189
Q

Atrial septal defect is a common congenital defect that leads to increased blood flow in the right side of the heart. Describe possible auscultation findings?

A
  • Patients can have a mid-systolic ejection murmur due to increased flow across the pulmonic valve
  • The S2 is widely split WITHOUT variation during respiration (Wide and fixed splitting)
190
Q

This type of murmur can occur in patients with anemia ((eg, due to menorrhagia)

A

A functional (benign) flow murmur due to increased flow across the aortic and pulmonic valves

191
Q

Patients with tricuspid regurgitation have a holosystolic murmur over the left mid-sternal border that is intensified by what?

A
  • An increase in venous return:
  • Leg raising
  • Deep inspiration
  • Hepatic compression
192
Q

In a nonobese individual. What lifestyle modification has the biggest effect on lowering blood pressure

A

DASH diet

-this is a combination diet rich in fruits, vegetables, legumes, low-fat dairy, and low saturated and total fat

193
Q

Takayasu arteritis is a chronic vasculitis that affects the aorta and major arterial branches of the Aorta. The pathogenesis is related to what

A

cell-mediated inflammation

194
Q

Describe the pathophysiologic mechanism of Raynaud phenomenon

A

-Characterized by cold- or stress-induced hyperreactivity of the digital arterial smooth muscle, leading to episodic vasospasm in the fingers and toes (similar mechanism to Vasospastic angina, formerly known as variant or Prinzmetal)

195
Q

Long term surveilance of patients on amiodarone

A
  • baseline chest radiography and PFT

- long term monitoring of Thyroid and pulmonary function

196
Q

Early onset HTN and bilateral upper abdominal masses

A

Polycystic kidney disease

197
Q

What is the preferred medication for HTN associated with Autosomal dominant polycystic kidney disease

A

ACEI’s

198
Q

Afib is a supraventricular tachyarrhythmia with unorganized atrial activity. Afib with RVR can present with ventricular rates as high as 150/min, and the symptoms are usually due to the fast ventricular rate rather than the arrhythmia itself. Stable patients can receive what medical therapy to control the ventricular rate?

A
  • Beta blockers
  • Diltiazem
  • Digoxin
199
Q

Post-MI acute pericarditis typically occurs in the first several days after the infarction. Dressler’s syndrome is pericarditis that can occurs weeks after an MI. It is believed to be due to immunologic phenomena. Malaise and sometimes fever are also characteristic. The ESR is typically elevated. What is the mainstay of therapy in Dressler’s syndrome?

A
  • NSAIDs

- Corticosteroids can be used in refractory cases or when NSAIDs are contraindicated

200
Q

Anticoagulation in Dressler’s syndrome?

A

Anticoagulation should be avoided to prevent development of a hemorrhagic pericardial effusion

201
Q

Describe the mechanism of how Adenosine (and its synthetic analogs regadenoson, apadenoson) or dipyridamole work to show ischmia during myocardial perfusion imaging?

A
  • Stimulates adenosine A2A receptors on vascular smooth muscle cells, causing coronary vasodilation and increased myocardial blood flow
  • There is a several-fold augmentation of blood flow in nonobstructed coronary arteries.
  • Blood flow is increased in stenosed coronary arteries as well but to a much lesser extent
  • This relative blood flow difference is magnified from rest, causing a detectable reduction in radioactive isotope uptake by myocardial cells in areas supplied by a stenotic coronary artery (appears as an ischemic defect on myocardial perfusion imaging)
202
Q

Adenosine stress testing allows evaluation for CAD in what patients?

A

-Those who are unable to perform adequate exercise (eg, due to amputation or severe OA)

203
Q

What is the underlying physiologic basis for exercise stress testing and dobutamine stress testing?

A

An increase in heart rate and/or myocardial contractility leads to an increase in oxygen demand

204
Q

Dobutamine stress testing (beta-1 agonist) is typically used in what patients

A

Patients who cannot exercise but have contraindications to vasodilator stress testing (eg, hypotension, Obstructive lung disease)

205
Q

Initial management of Vfib

A

immediate defibrillation

206
Q

Amiodarone and lidocaine in Vfib?

A
  • Amiodarone is indicated in patients with cardiac arrest due to VF or pulseless VT, but not until severeal attempts at defibrillation have been made
  • Lidocaine can be used as an alternate agent if amiodarone is not immediately available
207
Q

Epinephrine and Vfib?

A

-Should be administered every 3-5 minutes in patients who have persistent VF or pulseless VT following initial defibrillation and CPR

208
Q

Patients with a persistent, narrow or wide QRS complex tachyarrhythmia causing hemodynamic instability should be managed with SYNCHRONIZED cardioversion. Which rhythms is this indicated for?

A
  • Afib
  • Atrial flutter
  • VT with a pulse (SVT)
209
Q

NONexertional (or classic) heat stroke can have similar clinical features and potential complications. It occurs in the absence of strenuous activity and typically affects elderly patients with significant underlying comorbidities that limit their ability to escape or cope with excessive heat. How is the management of this different that that of exertional heat stroke?

A

-Evaporative cooling (eg, spraying lukewarm water while fans blow air on the patient’s skin), rather than ice-water immersion, which is associated with increased mortality in nonexertional heat stroke

210
Q

Describe how vagal maneuvers (eg, carotid sinus massage, cold-water immersion or diving reflex, valsalva, eyeball pressure) terminate Atrioventricular nodal reentrant tachycardia (Paroxysmal SVT)

A

increase parasympathetic tone in the hearts and result in a temporary slowing of conduction in the AV node and an increase in the AV node refractory period

211
Q

Describe nitroprusside and Cyanide poisoning

A
  • Cyanide toxicity can occur in patients receiving prolonged infusions or higher doses of nitroprusside, and is most common in patients with renal insufficiency
  • It is characterized by AMS, lactic acidosis, seizures, and coma
212
Q

Describe an excessive hypotensive response when treating hypertensive emergency

A
  • Mean arterial pressure should be lowered by 10%-20% in the 1st hour and by another 5% - 15% over the next 23 hours
  • An excessive drop in BP can lead to cerebral ischemia, with AMS and/or generalized seizures
213
Q

Involved Myocardium and vessel blocked in Acute MI?

- Some or all of leads V1-V6

A
  • Anterior MI

- LAD

214
Q

Involved Myocardium and vessel blocked in Acute MI?

-ST elevations in leads II, III, aVF

A
  • Inferior MI

- RCA or LCX

215
Q

Involved Myocardium and vessel blocked in Acute MI?

  • ST depression in leads V1-V3
  • ST elevations in leads I and aVL (LCX)
  • ST depression in leads I and aVL (RCA)
A
  • Posterior MI

- LCX or RCA

216
Q

Involved Myocardium and vessel blocked in Acute MI?

  • ST elevations in leads I, aVL, V5 and V6
  • ST depressions in II, III, and aVF
A
  • Lateral MI
  • LCX
  • Diagonal
217
Q

Involved Myocardium and vessel blocked in Acute MI?

-ST elevations in leads V4-V6R

A
  • Right ventricle MI (occurs in half of inferior MI)

- RCA

218
Q

Describe the relationship between acute MI involving the RCA and presence of AV block on ECG

A

-The RCA supplies blood to the AV node through the AV nodal artery in 90% of patients and RCA occlusion can cause AV block

219
Q

Describe relationship between acute MI involving the RCA and bradycardia?

A

-Inferior MI is most commonly associated with sinus bradycardia due to increased vagal tone in the first 24 hours after infarction and decreased RCA blood supply to the SA node

220
Q

What does the LAD supply and if its blocked what is seen on ECG?

A
  • supplies the anterior walls of the left ventricle as well as the anterior 2/3rds of the septum
  • ST-segment elevation in all precordial leads but most commonly in V1-V4
  • Second degree AV block can be seen
221
Q

What does the LCX supply and if its blocked what is seen on ECG?

A
  • Supplies the posterolateral wall of the left ventricle

- ST-segment elevation in leads I, II, III, and aVL

222
Q

Describe the consequences and ECG finding of an acute MI occluding the left main coronary artery

A
  • Usually a catastrophic event
  • presents as sudden cardiac death in the majority of patients
  • Occlusion of both LCX and LAD causes ST-segment elevations in anterior and lateral leads (I, AVL, V1-V6)
223
Q

Describe relationship between acute MI involving the RCA and hypotension?

A
  • The RCA also supplies blood to the right ventricle through RV marginal branches
  • RCA occlusion can lead to RV infarction/dysfunction resulting in hypotension
224
Q

Patient with paroxysmal Afib that spontaneously converted to normal sinus rhythm and otherwise completely healthy. What is management?

A
  • no additional therapy

- CHA2DS-VASc score of 0

225
Q

A left ventricular aneurysm can occur from scar tissue deposition following transmural MI. It can present several months after with Heart failure and angina, ventricular arrhythmia (eg, Vtach), or systemic embolism (eg, stroke). What is seen on ECG and Echo?

A
  • ECG: Persistent ST elevation, deep Q waves

- Echo: Thin and dyskinetic myocardial wall

226
Q

Current guidelines recommend primary PCI for patients with acute STEMI as follows:

A
  • within 12 hours of symptom onset AND
  • within 90 minutes from first MEDICAL contact to device time at a PCI capable facility OR
  • with 120 minutes from first medial contact to device time at a non-PCI-capable facility
227
Q

Describe the management of carotid atherosclerosis and stenosis in regards to symptoms and degree of blockage

A
  • All pts with carotid artery stenosis should recieve intensive medical therapy including antiplatelet agent, a statin, and careful BP control
  • SYMPTOMATIC (TIA or stroke) within 6 months: carotid endarterectomy with high-grade carotid stenosis (generally 70-99%)
  • If asymptomatic and high grade (80-99%) then maybe carotid endarterectomy but asymptomatic patients with < 80% blockage should be managed medically
228
Q

Describe the management of Afib due to suspected Hyperthyroidism?

A
  • Beta blockers (eg, propranolol, atenolol) are recommended as initial therapy to control heart rate and hyperadrenergic symptoms
  • In addition, propranolol decreases conversion of T4 to T3 in peripheral tissues
  • The beta blocker should be initiated as soon as hyperthyroidism is diagnosed and should be continued until the hyperthyroidism is adequately treated with thionamides, radioiodine, and/or surgery
229
Q

Lower extremity claudication and cardiovascular risk?

A
  • Cardiovascular disease is a major cause of morbidity and mortality in patients with PAD
  • Patients with PAD and intermittent claudication have an estimated 20% 5-year risk of nonfatal MI and stroke and a 15%-30% risk of death due to cardiovascular causes
  • Only 1%-2% of patients with PAD progress to develop critical limb ischemia with risk of limb amputation
230
Q

Acute limb ischemia after MI suggests what?

What is management?

A
  • Possible arterial embolus from Left ventricular thrombus
  • Management include immediate anticoagulation, vascular surgery consultation, and transthoracic echocardiogram to screen for LV thrombus and evaluate LV function
231
Q

Cardiac cath in patietns with cardiac tamponade typically reveals elevated and equilibrated intracardiac diastolic pressures. What should be done urgently?

A

-Urgent echo should be performed for definitive diagnosis and management

232
Q

Pericarditis can be due to an upper respiratory infection. Pericardial inflammation causes extra fluid within the pericardial cavity and leads to pericardial effusion the increased pericardial fluid compresses cardiac chambers and limits diastolic filling of the right-sided chambers. This causes a decrease in preload and reduces cardiac output, resulting in hypotension and syncope (due to decreased cranial blood flow). Exam shows tachycardia (compensatory), distended neck veins, pulsus paradoxus, and muffled heart sounds. What is the pathognomonic ECG finding and explain the mechanism?

A
  • Electrical alternans (varying amplitude of the QRS complexes)
  • It is due to the swinging motion of the heart in the pericardial cavity that causes a beat-to-beat variation in QRS axis and amplitude
  • Large pericardial effusions can also cause low voltage of QRS complexes
233
Q

A temporary transvenous pacemaker is used to pace the heart before a permanent pacemaker can be placed. It is indicated in what patients?

A
  • Sick sinus syndrome

- Symptomatic second-degree or third degree heart block

234
Q

This should be suspected in patients with Pulseless electrical activity (PEA) after a recent first MI and no signs of heart failure

A

Left ventricle free wall rupture

235
Q

What are the lab findings in Cholesterol crystal embolism (atheroembolism)

A
  • Elevated serum creatinine
  • Eosinophilia
  • Hypocomplementemia
  • U/A: typically benign with few cells or casts, may have eosinophiluria
236
Q

What is shown on skin or renal biopsy in cholesterol crystal embolism (atheroembolism)?

A
  • Biconvex, needle-shaped clefts within occluded vessels

- Perivascular inflammation with eosinophils

237
Q

imaging shows what in constrictive pericarditis?

A
  • pericardial thickening

- Calcification

238
Q

This is characterized by progressive peripheral edema, ascites, elevated JVP, pericardial knock (middiastolic sound), and pericardial calcifications on chest radiograph

A

constrictive pericarditis

239
Q

Describe the pathophysiological mechanism of the murmur in hypertrophic cardiomyopathy

A
  • Some patients have systolic anterior motion of the mitral valve, leading to anterior motion of mitral valve leaflets toward the interventricular septum
  • Contact between the mitral valve and the thickened septum during systole leads to left ventricular outflow obstruction and is responsible for the harsh systolic murmur best heard at the apex and left lower sternal border
240
Q

initial management in hemodynamically stable patient with widened mediastinum on chest x ray suggesting Aortic dissection with NO evidence of renal dysfunction

A
  • CT angiography

- this can reveal and intimal flap separating the true and false lumens in the aorta

241
Q

What is the preferred diagnostic study in patient with aortic dissection and hemodynamic INstability or renal insufficiency?

A

TransESOPHAGEAL echo . . . not transthoracic

242
Q
  • Shortness of Breath
  • Tachypnea
  • hypoxemia
  • S3
  • diagnosis and short term treatment?
  • Long term treatment?
A
  • Left ventricular heart failure
  • IV diuretics
  • Beta blockers in long term
243
Q

What is normal JVP height and CVP?

A

-1-3 cm . . . . 6-8 cm H2O

244
Q

definition of malignant hypertension

A

-Severe HTN with retinal hemorrhages, exudates, or papilledema

245
Q

definition of hypertensive encephalopathy

A

severe HTN with cerebral edema and non-localizing neurologic symptoms and signs

246
Q

Treatment in Stable Vtach wide complex

A

IV amiodarone

247
Q

This is an ultra-short acting beta blocker used for rapid rate control in atrial flutter or fibrillation

A

esmolol

248
Q

Describe the mechanism by which nitrates give pain relief in angina

A
  • Their primary anti-ischemia effect is mediated by SYSTEMIC vasodilation and decrease in cardiac preload resulting in a decrease in left ventricular end-diastolic and end-systolic volume
  • This, in turn, leads to a reduction in left ventricular systolic wall stress, which reflects afterload and is proportional to, and a decrease in myoocardial oxygen demand resulting in relief of anginal symptoms
249
Q

Physical exam findings suggestive of severe Aortic Stenosis

A
  • Delayed (slow rising) and diminished (weak) carotid pulse (“pulsus parvus and tardus”)
  • Presence of single and soft second heart sound (S2)
  • Mid to late peaking systolic murmur with maximal intensity at the second right ICS radiating to carotids

Internal medicine rotations (12 decks)

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