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UWorld - Cardio > Cardio > Flashcards

Cardio Flashcards

1
Q

What are the effects of LV Hypertrophy on:

  1. LV compliance
  2. Kidney perfusion and AngIiotensin II
  3. Beta-Myosin Heavy chain Expression
A
  1. Decreased LV compliance

2.

Decreased renal perfusion (due to dec. CO)

Increased AgII

  1. increased Beta-myosin heavy chain (to upregulate contractile sarcomere proteins)
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2
Q

Hyperacute Transplant Rejection

  1. Time of onset
  2. Mediators/cells
A
  1. Within minutes
  2. Pre-existing recipient Antibodies activate complement
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3
Q

Acute Transplant Rejection

  1. Time of onset
  2. Mediators/cells
A
  1. 1-4 Weeks
  2. T-cells and B-cells

(cellular and humoral response)

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4
Q

Chronic Transplant Rejection

  1. Time of Onset
  2. Cells/Mediators
A
  1. Months to years
  2. T and B cell response

(cellular and humoral)

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5
Q

Familial Dilated Cardiomyopathy

  1. Caused by what gene mutation?
  2. What protein does the gene code for?
  3. What is that proteins function?
A
  1. Mutation in the TTN Gene
  2. That gene is needed to make Titin

(these patients cannot make titin)

  1. Titin is needed to hold the sarcomere together

(lack of it causes myocardial dysfunction)

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6
Q
  1. When is wide splitting seen?
  2. How is it affected by breathing?
A
  1. Conditions that delay RV (pulmonic valve) empting?
  • pulmonic stenosis
  • right bundle branch block
  1. Pulmonic sound further delayed by inspiration
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7
Q

Normal Splitting

  1. Is S1 or S2 split?
  2. What are the order of sounds?
  3. How is it effected by breathing?
A
  1. Split S2 (in Aortic2 and Pulmonary2)
  2. S1–>A2–>P2
  3. Inspiration delays P2
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8
Q

Fixed Splitting

  1. When is heard?
  2. How is it effected by breathing?
A
  1. Heard in Atrial-Septal Defects (ASD)
  2. Not affected by breathing

(regardless of breath P2 is greatly delayed)

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9
Q

Paradoxical Splitting

  1. When is it heard?
  2. What are the order of sounds?
  3. How is it effected by breathing?
A
  1. Heart in conditions that delay aortic valve closure
  • aortic stenosis
  • Left bundle branch block

2.

S1 –> P2 –> A2

  1. Heard best on Expiration

(inspiration pushes P2 closer to A2)

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10
Q

What bacteria can cause endocarditis in already damaged heart valves and how?

A

Strep. Viridans

  1. Enter blood through mouth (ex: during dental procedure)
  2. Bacteremia (by binding to fibrin and platelets in blood)
  3. Adhere to valves
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11
Q

Whats are the effects of aging on the heart? (4)

A
  1. decreased LV chamber size
  2. sigmoid-shaped ventricular septum
  3. increased collagen content
  4. lipofuscin pigment within cardiomyocytes
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12
Q

What are the effects of LV hypertrophy on contractility?

A

Reduced contractility

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13
Q

Myxoma

  1. What is it?
  2. Where/how does it present?
  3. Histology
A
  1. Benign cardiac tumor
  2. Left Atrium, obstructs mitral valve
  3. Scattered cells with a mucopolysaccharide stroma
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14
Q

What heart pathology presents with:

  • Head bobbing
  • Bounding femoral and carotid pulses
A

Aortic Regurgitaion

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15
Q

What murmur is heard with aortic stenosis?

A

Crescendo-Decrescendo systolic ejection murmur

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16
Q

What murmur is heard with tricuspid/mitral regurgitation?

A

Holosystolic, high pitched “blowing murmur”

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17
Q

What murmur is heard with mitral valve prolapse?

A

Late systolic crescendo murmur with midsystolic click

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18
Q

What murmur is heard with a ventricular-septal defect?

A

Holosystolic, harsh sounding murmur

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19
Q

What murmur is heard with aortic regurgitation?

A

Early diastolic, blowing decrescendo murmur

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20
Q

What murmur is heard with a PDA?

A

Continuous machine-like murmur

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21
Q
  1. When is S3 heard?
  2. In what population is it normal?
A

1. Early diastole

  1. Normal in:
  • children
  • young adults
  • pregnant women
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22
Q

In what conditions (abnormal) do we hear an S3?

A
  1. Mitral Regurgitation
  2. Heart Failure
  3. Dilated Cardiomyopathy

​(Associated with increased filling pressures)

VOLUME OVERLOAD

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23
Q
  1. When is S4 heard?
  2. What is it associated with?
  3. In what population is it normal?
A
  1. Late diastole
  2. Ventricular Noncompliance
    (ex: hypertrophy/cardiomyopathy)
  3. Healthy older adults
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24
Q

Plaque Rupture

  1. What is the likelihood of plaque rupture dependant on?
  2. How can cells affect plaque rupture?
A

1. Plaque stability

(not size)

  1. Inflammatory Macrophages can secrete metalloproteinases destabilizing plaque and causing rupture
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25
Q

What is the relationship between blood flow (J) and vessel radius (r) ?

A

Flow (J) is proportional to the vessel radius raised to the 4th power

FLOW = r4

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26
Q

Cardiac Tissue Conduction Velocity

Place from fastest so slowest

  • Atrial Muscle
  • AV node
  • Ventricular muscle
  • Purkinje system
A
  1. Purkinje System
  2. Atrial Muscle
  3. Ventricular muscle
  4. AV node

Mnemonic: “Park At Venture AVenue”

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27
Q

What effect does squatting have on the on vasuclar resistance?

A

Squatting increases systemic vascular resistance

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28
Q

Why can squatting improve symptoms in a patient with a Tetralogy of Fallot?

A

Squatting increases the systemic vascular resistance which reduces right-to-left shunting which will allow more blood to enter the pulmonary circuit

(it will harder for unoxygenated blood to exit via the aorta so LV pressure will increase which will slow down shunt)

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29
Q
  1. What it pulsus paradoxus?
  2. How is it usually detected?
A
  1. A >10mm Hg drop in systolic BP during inspiration
  2. It is often detected when taking/measuring BP with a cuff

NOTE:

At high pressures we will only hear korotkoff sounds during expiration. At lower pressures we will hear korotkoff sounds during both expiration and inspiration

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30
Q

What can cause pulsus paradoxus? (4)

A
  1. Cardiac Tomponade (most common)

2. Pericardial Disease

  1. Severe Asthma
  2. COPD
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31
Q

How can blood flow from ischemic areas be shifted to non ischemic areas?

A

Via the use of Pharmacologic Vasodilators

  • adenosine
  • dipyridamole

(they mimic the vasodilation that occurs with exercise, shifting blood to areas of greater demand)

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32
Q

When cells within the heart, brain or skeletal muscle are injured, what enzyme leaks into circulation?

A

Creatine kinase

(due to cell membrane damage, the hallmark of irreversible damage)

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33
Q

Jugular Venous Pulse (JVP)

What does the a wave represent?

A

Right Atrial Contraction

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34
Q

Jugular Venous Pulse (JVP)

What does the c wave represent?

A

RV Contraction

(due to Bulging of Tricuspid Valve in to RA due to RV contraction)

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35
Q

Jugular Venous Pulse (JVP)

What does the x descent represent?

A

Right Atrial Relaxation

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36
Q

Jugular Venous Pulse (JVP)

What does the v wave represent?

A

Filling “villing” of right atrium

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37
Q

Jugular Venous Pulse (JVP)

What does the y descent represent?

A

passive empying of RA in RV once tricuspid opens

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38
Q

Marfan Syndrome

  1. How does it present?
  2. Major Complications
A
  1. Clinically presents as
  • Tall/thin build with long extremities
  • scoliosis
  • pectus excavatum (caved in chest)
  • Vision problems
  1. Major complications is heart problems
  • aortic dissection (most common cause of death)
  • mitral valve prolapse
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39
Q

What type of collagen is seen in scars?

(Any type of scar)

A

Type I collagen

(most common type in body)

NOTE: also seen in tendons, ligaments, bone, skin, blood vessels, etc.

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40
Q

What are the effects of Prostacyclin?

A

1. Inhibits platelet aggregation

2. Causes Vasodilation

(it opposes the effects of Thromboxane A2)

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41
Q

Cardiac Tamponade

  1. How does it clinically present? (3)
  2. What is it highly associated with?
A
  1. Presents as:
  • hypotension
  • elevated JVP
  • muffled heart sounds
  1. Pulsus Paradoxus
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42
Q

Why do we see a greater amount of Angiotensin II than Angiotensin I in the pulmonary vein compared to the pulmonary artery?

A

Since Angiotensin I gets converted into Angiotensin II when it enters the small pulmonary vessels in the lungs by ACE.

NOTE: RV–> pulmonary a. –> lungs –> pulmonary vein–>LA

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43
Q

Atrial Fibrillation

  1. How does it clinically present?
  2. How does it present on ECG
A
  1. Presents as:
  • Palpitations
  • Tachycardia
  • irregularly iregular heart rhythm
  1. varying R-R intervals with an abscense of p-waves
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44
Q

Acute Pericarditis

  1. How does it present?
  2. What is the most common cause?
A
  1. Presents as:
  • chest pain
  • friction rub on auscultation
  • ST elevation on ECG
  • pericardial effusion on echocardiogram

2. Viral infection

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45
Q

Hypertrophic Cardiomypathy

  1. Which part of heart is enlarged?
  2. When inherited, what genes/proteins are involved?
A
  1. Left Ventricle
  2. Sarcomere genes are affected
  • beta-myosin heavy chain proteins
  • myosin-binding protein C
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46
Q

What is strep. gallolyticus (formerly bovis) endocarditis associated with?

A

Colon Cancer

NOTE: Whenever S. gallolyticus is cultured in the blood, a colonoscopy must be done to check for colon cancer

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47
Q

What are the cardiovascular manifestations of SLE (lupus)?

A
  1. Atherosclerosis

2. Libman-Sacks Endocarditis

  • sterile vegetations that arise on BOTH surfaces of the mitral valve
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48
Q

Renal Artery Stenosis

  1. What usually causes it?
  2. How does it present?
  3. What can occur to kidneys over time and why?
A
  1. Atherosclerosis

2. Refractory/Resistant Hypertension

(hypertension that does not respond to drugs or normal treatment)

  1. Atrophy of kidneys due to chronic O2 and nutrient deprivation
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49
Q

Lipofuscin

  1. What is it a sign of?
  2. How does it occur?
  3. What does it look like?
  4. In who and where is it commonly seen?
A
  1. Aging and Wear+Tear
  2. Via lipid peroxidation or free-radical injury
  3. Yellow-brown intracytoplasmic granules
  4. In the heart and liver of aging, cachectic(wasting) or malnourished individuals
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50
Q

What is the most likely complication of having a bicuspid aortic valve?

A

They are much more likely to develop aortic stenosis in their 50s (10 years ealier than the aortic stenonis caused by calcification of the aortic valve)

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51
Q

What parameter must be the same in both the systemic circulation and the pulmonary circulation?

A

Flow must be the same

(the volume output of the RV must match the LV)

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52
Q

What does Adenosine do and how?

A

It decreases HR

(via decreasing the rate of spontaneous depolarization in cardiac pacemaker cells - phase 4)

It increases potassium condunctance and inhibts Ca2+

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53
Q

Stanford Type B Aortic Dissection

  1. In what part of aorta does it occur?
  2. From where does it originate?
A
  1. The Descending Aorta
  2. The Left Subclavian Artery
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54
Q

Stanford Type A Aortic Dissection

  1. In what part of aorta does it occur?
  2. From where does it originate?
A
  1. The Ascending Aorta
  2. The Sinotubular Junction
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55
Q
  1. Which Renal Vein can get compressed by the Aorta and SMA? (L or R)
  2. What can this result in?
A

The Left Renal Vein

Can cause retrograde blood flow to testes that can result in a Varicocele (dilation of pampiniform plexus)

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56
Q

Subclavian Steal Syndrome

  1. What causes it?
  2. What does it result in?
A
  1. stenosis of the subclavian artery
  2. It results in reversal in blood flow from the controlateral verterbreal artery to the affected vertebral artery
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57
Q

What affects does a Carotid Sinus Massage have on:

  1. Parasympathetic Tone
  2. SA node conduction
  3. AV node conduction
  4. AV node refractory period
A
  1. increased parasympathetic tone
  2. decreased SA Node conduction
  3. decreased AV Node conduction
  4. increased AV Node refractory period
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58
Q

Atrial Flutter

  1. How does it appear on ECG?
  2. What causes it?
  3. Where does it occur?
A
  1. Sawtooth pattern
  2. A large re-entrant circuit
  3. Between the Tricuspid Valve and IVC in the right atrium

(cavotricuspid isthmus)

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59
Q

Where is the AV node located?

Which artery supplies it?

A

in the Right Atrium, near the opening of the coronary sinus

Supplied by the PDA

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60
Q

What are the contents of the femoral triangle?

(from lateral to medial)

A
  1. Femoral Nerve
  2. Femoral Artery
  3. Femoral Vein

“NAV”

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61
Q

What can the pulmonary artery occlusion pressure be indicative of?

A

Left Atrial Pressure

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62
Q

Traumatic Aortic Rupture

  1. Where does it most commonly occur in the aorta?
  2. What normally holds that part in place?
A
  1. At the Isthmus of the aorta
  2. It is normally tethered to the ligamentum arteriosum
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63
Q

Atrial Fibrillation

  1. How does it present on ECG?
  2. What determines the ventricular contraction rate in a patient with AF?
A

1.

  • absent p-waves
  • irregularly irregular R-R intervals
  • narrow QRS complexes
  1. The AV node refractory period will determine the number of atrial impulses that reach the ventricles for contraction
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64
Q

What would an elevated PCWP be indicative of?

A

Increased Left Atrium Pressure

(most likely due to mitral stenosis)

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65
Q

What artery supplies the inferior surface of the heart?

A

PDA

(Inferior surface of heart = diaphragmatic surface of LV)

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66
Q

When the LAD is occluded, what vessel do we use as a graft?

A

The left internal mammary/throracic artery

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67
Q

Sodium Nitroprusside

  1. What does it do?
  2. How does it effect SV, CO and BP?
  3. Major Adverse effect?
A
  1. Balanced vasodilarion of veins + arteries
  2. Co: Same

SV: Same

BP: decreased

  1. Can cause cyanide poisoning
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68
Q

When coronary arteries (other than the LAD) are occulded, what vein do we use as a graft?

From where is it accessed?

A

The Great Saphenous Vein

Accessed inferolaterally to the pubic tubercle

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69
Q

When does the majority of blood flow to the following occur:

1. Left Ventricular Myocardium

2. Right Ventricular Myocardium

A
  1. Diastole

(due to LV coronary vessels being compressed during systole)

  1. It is constant

(RV contraction does not result in compression of its vessels)

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70
Q

What structure is dervived from the embryonic cardinal veins?

A

SVC

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71
Q

How and when can the LV Gallops (S3 & S4) best be heard?

A

They are best heard with the bell of the stethoscope with the patient in the lateral decubitus position at end expiration

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72
Q

Hand Grip Maneuver

  1. What effect does it have on heart pressures?
  2. How would it effect an Aortic Stenosis Murmur?
  3. How would it effect a VSD murmur?
A
  1. It would increase afterload (decrease SV)
  2. Decreased sounds
  3. Increased sounds
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73
Q

Neprilysin

  1. What does it do?
  2. Why is this significant?
A
  1. it inactivates ANP and BNP
  2. In HF with HTN, we give Neprilysin inhibitors (Sacubitril) and ARB’s which results in vasodilation and diuresis
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74
Q

What is typically seen in the lungs during heart failure?

A

Alveolar Hemosiderin-laden Macrophages

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75
Q

What are the 3 specific features that distinguish cardiac circulation form skeletal/visceral circulation?

A

1. The Left Ventricle is only perfused during diastole

2. Myocardial Oxygen extraction is very high

(takes 70% of O2 from blood)

  1. Myocardial Oxygen demand and coronary blood flow are tight coulples

(since the heart extracts so much O2, when it increases its O2 demands simply extracting more O2 isnt enough so flow must be increased)

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76
Q

What is the most deoxygenated blood in the body?

A

Cardiac venous blood

(since myocardium is best at extracting O2)

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77
Q

Where is the SA Node located?

A

At the junction of the SVC and Right Atirum

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78
Q

Atrial Natriuretic Peptide (ANP)

  1. From where is it secreted?
  2. What stimulates its secretion?
  3. What are its effects?
  4. What is it inhibited by?
A

1. Atrial Cardiomyocytes

  1. Stretching of atrium due to hypertension or hypervolemia
  2. peripheral vasodilation and increased urinary excretion of sodium and water

4. Sacubitril (a neprilysin inhibitor)

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79
Q

What it is the limiting factor for LV Myocardial blood supply?

A

Duration of Diastole

(since LV myocardium cannot be perfused during systole)

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80
Q

What is the normal pressure in the Left Ventricle?

What is the normal pressure in the Aorta?

81
Q

How does aortic regurgitation classically present?

A

- hyperdynamic pulse

- head bobbing

- wide pulse pressure

82
Q

What are the effects of aortic regurgitation on the following pressures:

  1. LV systolic pressure
  2. LV diastolic pressure
  3. Aortic systolic pressure
  4. Aortic diastolic pressure
A
  1. increased (>120)
  2. increased (>10)
  3. increased (>120)
  4. decreased (<80)

Aortic Regurgiation: LV(160/30) & Aorta(160/60)

83
Q

Why is the SA Node the de-facto pacemaker of the heart?

A

Because it stifles impulses generated by other cells in the conduction system since it fires more rapidly

84
Q

How does a First-degree AV block appear on ECG?

A

PR interval is prolonged (>200msec) but they are all equal

(usually asymptomatic)

85
Q

How does a Second-degree Mobitz Type 1 AV block appear on ECG?

A

Progressive lengthening of PR interval until a beat is dropped

(usually asymptomatic)

86
Q

How does a Second-degree Mobitz Type 2 AV block appear on ECG?

How is it treated?

Complications?

A

Dropped Beat without changes in PR interval

Treated with a pacemaker

May progress to a Third-degree block

87
Q

How does a Third-degree (complete) AV block appear on ECG?

How is it treated?

What is it associated with?

A

The atria and ventricles beat independently

(P waves and QRS complexes are not related)

Treated with a pacemaker

Associated with Lyme Disease

88
Q

What embryologic malfunction results in the Tetrology of Fallot?

A

Deviation of the infundibular septum

89
Q

What embryologic malfunction results in Transposition of the Great Vessels?

A

Failure of the aorticopulmonary septum to rotate

(remains linear instead of spiral)

90
Q

Why does Verapamil decrease cardiac myocytes contraction but not skeletal muscle?

A

Since Verapamil blocks L-type Calcium channels which are needed to provide the intial extracellular calcium influx into cardiomyocytes (Ca induced Ca release)

Skeletal muscle does not depend on extracellular calcium influx via L-type calcium channels for calcium release

91
Q

Isolated Systolic Hypertension

  1. What is it?
  2. In what population is it usually seen?
  3. Why does it occur?
A
  1. elevated systolic with normal diastolic BP
  2. Elderly (>60)
  3. Due to age-related stiffening and decreased compliance of the aorta and other major peripheral arteries
92
Q

What relieves symptoms in patients with a hypertrophic cardiomyopathy?

What pharmacology can be used to achieve this?

A

Increased LV Volume

Beta blockers (decrease HR giving more time for filling)

93
Q

What maneuvers decrease preload/volume in the heart?

What effect would these maneuvers have on a hypertrophic cardiomyopathy murmur?

A

Valsalva Maneuver & Standing up

Increase mumur intensity

(hypertrophic cardiomyopathy symptoms get relieved with increased blood in the left ventricle)

94
Q

What is the difference between a hypertensive urgency and emergency?

A

Hypertensive Urgency: severe HTN with no end-organ damage

Hypertensive Emergency: severe HTN with end-organ damage

(Note: severe hypertension is >180/120)

95
Q

What drugs are given in for a hypertensive emergency?

A
  • Clevidipine (Ca channel blocker)
  • Fenoldopam (Dopamine D1 agonist)
  • Labetalol (B-blocker)
  • Nicardipine (Ca channel blocker)
  • Nitroprusside (causes release of NO)
96
Q

Hypertrophic cardiomyopathy

  1. What makes it worse?
  2. Which medications should be avoided in these patients?
A
  1. Decreased LV Volume

2.

  • Vasodilators (dihydropyridine Ca blockers, Nitrates, ACEI)
  • Diuretics
97
Q
  1. What are the 3 Nitrate drugs?
  2. What do they do?
  3. How do they do it?
A

1.

  • Nitroglycerin
  • Isosorbide Dinitrate
  • Isosorbide Mononitrate
  1. Vasodilation (Veins>arterioles)
  2. Increase cGMP
98
Q

Hydralazine

  1. What does it do?
  2. How does it do it?
A

1. Vasodilation (arterioles>veins)

2. increase cGMP

99
Q

How do ANP and BNP work?

How is this related to erectile dysfunction?

A
  1. ANP and BNP increase cGMP which causes vasodilation
  2. ED can be treated with Sildenafil which inhibits PDE5 which decreases degradation of cGMP
100
Q

What are absolute contraindications to the use of Oral Contraceptives (OCP)? (6)

A
  1. Women older than 35 that smokes
  2. Hypertriglyceridemia
  3. Liver disease
  4. History of thrombolic event or stroke
  5. History of an estrogen-dependent tumor
  6. Pregnant
101
Q

Niacin

  1. What is its main use?
  2. What are its major side-effects and what mediates them?
  3. How can these side-effects be reduced?
A
  1. Raise HDL levels
  2. Skin flushing and warmth via prostaglandins
  3. Aspirin (inhibits prostaglandin production)
102
Q

Which type of Beta-blocker is best to use post-MI? Why?

A

B1-selective antagonists (names A–>M)

  • acebutolol
  • atenolol
  • betaxolol
  • bisoprolol
  • esmolol
  • metoprolol
103
Q

Digoxin

  1. What/When can it be used
  2. What is its mechanism?
A

1.

HF: can increase contractility

AFib: inc. parasympathetic tone via stimulation of vagus n.

2.

  • Inhibition of Na/K ATPase–>inhibition of Na/Ca exchanger
  • direct stimulation of vagus nerve
104
Q

Doxorubicin/Daunorubicin Chemotherapy

  1. What can it cause?
  2. How can this be prevented?
A

1. Dilated Cardiomyopathy

  1. Dexrazoxane (iron-chelating agent)
105
Q

How do nitrates cause vasodilation?

A
  1. Nitrate broken down into NO + S-Nitrosothiols
  2. They activate cGMP
  3. Dephosphorylation of light chain myosin
  4. Vascular smooth muscle relaxation

(large veins>small veins>arterioles)

106
Q

What type of drug would you give if you wanted to increase contractility and decrease vascular resistance?

A

A Nonselective Beta adrenergic agonist

(Isoproterenol –> B1=B2)

Trick: iso = equal

B1 stimulation: increase HR + contractility

B2 stimulation: vasodilation

107
Q

What major change is seen on ECG after administration of a Beta-Blocker?

A

Prolonged PR Interval

(due to decreased AV Node Conduction)

108
Q

Which anti-arrhythmic is best at treating ischemia-induced ventricular arrythmias?

A

Class IB Antiarrhythmics

(Lidocaine, Mexiletine, Phenytoin)

109
Q

Which drugs are best for treating the urinary symptoms of Benign Prostatic Hyperplasia (BPH)?

What else can they treat?

A

alpha-1 blockers

(Prazosin, Terazosin, Doxazosin)

They can also be used to treat hypertension

(alpha-1 stimulation causes increased SM contraction)

110
Q

Which medications reduce mortality in Heart Failure?

A
  1. ACE Inhibitors (“prils”)
  2. ARBs (“sartans”)
  3. B-Blockers (“ol”)
  4. Spironolactone

“Building AABS reduced mortality in HF”

111
Q

Cilostazol

What are its 2 major functions?

A
  1. inhibits platelet aggregation
  2. arterial vasodilator
112
Q

What is the major determinant of symptom severity in a patient with Tetralogy of Fallot?

A

The severity of the RV Outlow Tract Obstruction

113
Q

In an RCA Occlusion, what leads would be elevated?

A

Leads II, III, aVF

(inferior heart leads)

114
Q

In an LAD Occlusion, what leads would be elevated?

A

Leads V1, V2, V3, V4

(Anterior and Septal heart leads)

115
Q

In an LCX Occlusion, what leads would be elevated?

A

Leads I, aVL, V5, V6

(Lateral heart leads)

116
Q

At what point would a Mitral Stenosis Murmur be heard?

A

Point C

Mitral Stenosis results in a diastolic mumur

(opening snap followed by a mid diastolic murmur)

117
Q

The image below shows the % of O2 saturation is differing parts of the heart. What abnormality is likely seen in this patient?

(NOTE: abnormality not shown in picture)

A

Ventricular Septal Defect

(there is an increase in %O2 from the RA to RV)

118
Q

Before starting Statin Therapy, what test must be done?

A

Liver Transaminase levels should be measured before starting statin therapy

(Statins can cause hepatotoxicity and myalgias)

119
Q

Which cardiovascular abnormality/pathology is associated with ruptured cerebral aneurysms?

A

Coarction of the Aorta

(it is associated with increased berry aneurysms)

120
Q

Digoxin Toxicity

  1. What is its most lethal complication?
  2. How can it be treated?
A

1. Ventricular Arrythmias

  1. Class IB Antiarrythmics (Lidocaine, Mexiletine, Phenytoin)
121
Q

What are the symptoms of Digoxin Toxicity?

A

GI: anorexia, nausea, vomitting, abdominal pain

Neurologic: fatigue, confusion, color/vision disturbances

Cardiac: ventricular arrythmias

122
Q

What can be done to increase forward flow in mitral regurgitation?

What type of drug can be used to achieve this?

A

Decrease systemic vascular resistance

Vasodilators

123
Q

Milirinone

  1. What are its effects?
  2. How are they mediated?
A

1.

Cardiomyocytes: increase contractility

Vascular Smooth Muscle: vasolidation

  1. inhibits PDE-3 which reduces cAMP degredation

(increases cAMP)

124
Q

Coronary Sinus

  1. What does it do?
  2. To where does it deliver its blood?
A
  1. It collects blood from the myocardial veins
  2. It delivers the unoxygenated blood to the Right Atrium
125
Q

Enlarged Coronary Sinus

  1. What does it indicate?
  2. How is it most commonly caused?
A

1. Increased RA Pressure

2. Pulmonary Hypertension

126
Q
  1. What can be given to close a PDA?
  2. What can be given to keep open a PDA?
A
  1. Indomethacin

“Endomethacin Ends a PDA”

  1. Prostaglandins

“PGE keeps a PDA Going”

127
Q
  1. What are the cardiac manisfestations of Carcinoid Syndrome?
  2. What is measured to confirm carcinoid syndrome?
A

1. Right Heart Valvular Fibrous Plaques

(does not usually effect Left Heart)

  1. Urinary 5-HIAA

(5-hydroxyindoleacetic acid)

128
Q

How does a Restrictive Cardiomyopathy present?

A

Same as a Hypertrophic Cardiomyopathy

(both result in diastolic dysfunction)

-LA enlargement

-LV hypertrophy

-Normarl ejection fraction

129
Q

Alteplase Fibrinolytic Therapy

  1. How does Alteplase work?
  2. What is the most common adverse effect?
A

1.

Alteplase binds fibrin in the thrombus

It then activates plasmin which lyses the clot

  1. Hemorrhage (Intracerebral or GI)
130
Q

At the level of the mid-esophagus, what is:

a. Anterior to the esophagus
b. Posterior to the esophagus

A

a. Left Atrium

b. Descending Aorta

131
Q

What classically presents as:

-Tearing chest pain

-Unequal BP in arms

A

Aortic Dissection

(intimal tear of aorta)

132
Q

Blockade of which recepter can cause orthostatic hypertension?

A

alpha-1 adrenergic receptors

(terasozin, doxasozin)

133
Q

How does exercise affect the following?

  1. CO
  2. Arterial blood gas (O2/CO2)
  3. Venous blood gas (O2/CO2)
A
  1. increased CO
  2. Arterial blood gas remains the same

3. Venous O2 is decreased and CO2 is increases

134
Q

Septic Shock

  1. Hyperthermia or hypothermia
  2. Inc or Dec SVR
  3. Inc or Dec CO
A
  1. Either
  2. Decreased SVR
  3. Increased CO
135
Q

How would an occulusion of the Right Coronary Artery affect the following?

  1. CO
  2. PCWP
  3. CVP
A

1. Decreased CO

(since there is less blood in the left heart so SV will be down)

2. Decreased PCWP

(Since the RV cant pump as well so less blood in the LA)

3. Increased CVP

(due to impaired forward flow so blood is backed up)

136
Q

What are the 4 most common clinical findings in a Cardiac Tamponade?

A
  1. Hypotension
  2. Elevated JVP
  3. Muflled heart sounds
  4. Pulsus Paradoxus
137
Q

How come pregnant women can become hypotensive when lying in the supine position?

A

Compression of the IVC –>

Reduced venous return –>

Decreased CO –>

Hypotension

138
Q
  1. What is a Permissive Effect?
  2. What is a Additive Effect?
  3. What is a Synergistic Effect?
A
  1. When one hormone allows the other to exert its maximal effect
  2. When the combined effect is equal to the sum of the 2 individual effects
  3. When the combined effect is greater than the sum of the 2 individual effects
139
Q

How do Nitrates effect the following:

  1. LV End-diastolic pressure
  2. Systemic Vascular Resistance
  3. Peripheral Venous Capacitance
A

1. Decrease

(since they decrease cardiac preload - more blood in veins)

2. Decrease

(since they can modestly dilate arterioles)

  1. Increase
140
Q

Which drug class would this ‘new drug’ most ressemble?

A

Class IB Antiarrythmics

(Lidocaine, Mexiletine, Phenytoin)

NOTE: order from strongest to weakest: C A B

141
Q

In which cardiomyopathy do patients most likely develop a mural thrombus?

A

Dilated Cardiomyopathy

142
Q

What is the most frequent cause of death 2 hours post-MI?

A

Ventricular Arrythmias

143
Q

In the CT scan, what is:

B = ???

C = ???

A

B = IVC

C = Abdominal Aorta

144
Q

Patent Foramen Ovale

  1. How does it result?
  2. What can become a major complication of it?
A
  1. Failure of septum primum and septum secundum to fuse after birth
  2. If RA pressure increases above LA, it can cause a right to left shunt which can in turn result in a paradoxical emboli in the systemic circulation
145
Q

What statitistical method is best for comparing the means of 2 groups?

A

Two-sample T test

146
Q

An infant born with a flat facial profile, protruding tongue, small ears, upslanting palpebral defects and cardiac defects is most indicative of a child with what?

A

Down Syndrome

147
Q

How does down syndrome occur?

A

maternal meiotic nondisjunction

(fetus recieves 3 copies of chromosome 21)

148
Q

Would this holosystolic murmur be more indicative of mitral or tricuspid regurgitation?

A

Tricuspid Regurgitation

(the intensity increases with inspiration and inspiration increases the intensity of right heart sounds)

149
Q

A patient presenting with bacterial endocarditis following a cytoscopy (urinary procedure) is most likely infected with which bacteria?

A

Enterococcus

150
Q

What murmur is this?

Where would it be the loudest?

A

Aortic Regurgitation

  • loss of aortic dicrotic notch
  • steep diastolic decline of aortic pressure
  • High peaking LV and aortic systolic pressures

Point C

(just after closer of aortic valve)

151
Q

What is the pathway for which an embolus would be able to enter the retinal artery and cause vision impairment?

A

1. Internal Carotid –>

2. Opthalmic Artery –>

3. Retinal Artery

152
Q

How would atenolol affect the following:

  1. Cardiomyocite cAMP
  2. Juxtaglomerular cAMP
  3. Vasuclar smooth muscle cAMP
A

Atenolol is a beta-1 selective antagonist

  1. Decreased

(b1 found in cardiomyocytes –> dec. HR and contractility)

  1. Decreased

(b1 found in juxtaglmerular cells –> decreases Renin)

  1. No change

(b2 found in vascular smooth muscle)

153
Q

What are the effects of an AV shunt on the following:

  1. Preload
  2. EDV
  3. TPR
  4. Afterload
A

1. increased Preload

(increased venous return to heart)

2. Increased EDV

3. Decreased TPR

(less resistance since blood bypases arterioles)

4. Increased Afterload

154
Q

Which 2 endogenous factors are most responsible for controlling coronary blood flow?

A
  1. Nitric Oxide (NO) –> large coronary arteries, prearteriolar vessels
  2. Adenosine –> small coronary arteries
155
Q

What cardiovascular defect is ?? associated with:

1. Down Syndrome

2. Digeorge Syndrome

3. Friedreich Ataxia

A

1. ASD (ostium primum)

2. Tetralogy of Fallot

3. Hypertrophic Cardiomyopathy

156
Q

What cardiovascular defect is ?? associated with:

1. Kartagener Syndrome

2. Tuberous Sclerosis

A

1. Situs Inversus

2. Rhabdomyomas

157
Q

What cardiovascular defects are Turner Syndrome associated with?

A

Coarction of the Aorta

Bicuspid Aortic Valve

158
Q

What cardiovascular defects are Marfan Syndrome associated with?

A

Aortic Dissection

Aortic Aneurysm

Mitral Valve Prolapse

159
Q

What are the 2 ways/formulas to calculate Cardiac Output?

A

1.

CO = SV X HR

2.

CO = rate of O2 consumption / (Arterial O2 - Venous O2)

160
Q

Angioedema

  1. What is it?
  2. How is it usually caused?
A
  1. Swelling of the skin, most commonly of the tongue, lips and eyelids. Can also affect larynx (causing stridor)
  2. Side-effect of ACE inhibitors due to Bradykinin accumulation

(increases vascular permeability)

161
Q

If a patient with a heart transplant begins to reject the transplant 2 weeks after it was planted, what are the main features we would see in this type of rejection?

A

ACUTE REJECTION (1-4 weeks)

Vasculitis of graft vessels with a dense lymphocytic infiltrate (mainly T-cells)

162
Q

In a patient who has a holosystolic murmur that is best heard at the apex of the heart that radiates to the axilla, would he be more likely to develop an S3, S4, mid-systolic click or opening snap?

A

This patient has Mitral Regurgitation

(best heard at apex = mitral valve)

(radiates to axilla = blood is flowing back)

Mitral regurgitation is likely to result in an S3

(due to volume overload = S3)

163
Q

From hours 0-4 following a myocardial infarction what light microscopic changes would we most likely see?

A

None

(first changes begin after 4 hours)

164
Q

What does this patient have?

At which point would intensity of this murmur be loudest?

A

Aortic Stenosis

(LV pressure > aorta pressure, they should normally be equal)

Point B

(murmur will be loudest where we have the greatest pressure difference between the LV and aorta)

165
Q

What syndrome does this patient most likely have?

What causes it?

A

Wolf-Parkinson White Syndrome

(note the Delta Wave)

Caused by an accessory pathway (bundle of Kent) that bypasses the AV node

166
Q

Before intiating amiodarone therapy what must we first test?

A

Serum TSH levels

167
Q

A person wearing a tight short collar develops hypotension.

What nerve mediates the Afferent and Efferent Limb of this reflex?

A

Carotid Sinus Reflex

Afferent limb: Glossopharyngeal n.

(carotid sinus–>medulla)

Efferent Limb: Vagus n.

(medulla –> heart, parasympathetic stimulation)

168
Q

An arterial puncture above the inguinal ligament increases the risk of blood collection into where?

A

Retroperitoneal Space

169
Q

What medication improves survival in patients with HF?

A

ACE Inhibitors

ARBs

B-blockers

Spironolactone

170
Q

In what organ did this problem most likely originate? How?

A

The Heart

This is a splinter hemorrhage caused by endocartitis.

Caused by microemboli from the small valvular vegetations

171
Q

What should we inject into a patient who was recieving a venous drip of norepinephrine whose skin around the injection site has become cold hald and pale?

A

Phenotolamine (an alpha blocker)

The skin is sufferent from major alpha-1 mediated vasoconstriction due to norepinephrine

172
Q

In polyarteritis nodosa, the arteries of which organ are most commonly spared?

173
Q

In a patient with pulmonary hypertension, would we expect increased, normal or decreased values of the following:

  1. Thomboxane A2
  2. Nitric Oxide
  3. Prostacyclin
  4. Endothelin
A
  1. increased
  2. decreased
  3. decreased
  4. increased

pulmonary HTN occurs due to increased proliferative and vasoconstrictive mediators (endothelin, TXA2) and decreased antiproliferative and vasodilatory mediators (NO, Prostacyclin)

174
Q

A patient presents with pulsus paradoxus but has no pericardial disease, what is the next most likely cause?

A

Asthma or COPD

(obstructive lung disease results in hyperinflated lungs)

175
Q

A patient presents with a loud S2 and an accentuated palpable impulse at the left sternal border.

What is the most likely diagnosis?

A

Pulmonary Hypertension

Loud S2: forceful pulmonic valve closure

Palpable Impulse: RV hypertrophy due to increased pressure

(RV Heave)

176
Q

What is the most common trigger of atrial fibrilation?

A

Abberant electrical activity in the pulmonary veins

177
Q

Which part of the heart would most likely be affected in a patient who was stabbed in the left 4th intercostal space along the sternal border?

A

Right Ventricle

(makes up the majority of the anterior heart)

178
Q

What ions are represented in this photo

A

1 = Sodium

2 = Calcium

3 = Potassium

179
Q

What arteries are most suceptible to atherosclerosis?

A
  1. Abdominal aorta
  2. Coronary arteries
  3. Popliteal artery
  4. Carotid artery

“after an ABs workout, i grab a CORONa and POP my collar up to my CAROTID”

180
Q

What is mitochondrial vacuolization a sign of?

A

Irreversible cell injury

(it signifies that the mitochondria are permanently damaged and unable to make ATP)

181
Q

Whats the best way to assess the degree of mitral stenosis?

A

The A2-to-opening snap time interval

(the shorter the interval the more severe)

182
Q

A young woman presents with weak pulses, myalgias, arthralgias and fatigue.

What is the most likely diagnosis?

A

Takayasu Arteritis

(granulomatous thickening of large vessels)

183
Q

Which amino acid plays a role in vasodilation?

A

Arginine

(it is a precursor Nitric Oxide)

184
Q

A 4 yeard old asian child present with fever, bright red tongue, rash, and conjunctival injection.

What is the most likely diagnosis?

A

Kawasaki Disease

Conjunctival Injection

Rash

Adenopathy (cervical)

Strawberry Tongue

Hand and feet edema and rash

Fever (KAWASAKI motorcycles CRASH and Burn)

185
Q

What is the most significant complication that can lead to death in a patient with Kawasaki disease?

A

Coronary Artery aneurysms

186
Q

In a 14 year old girl whose 10th percentile for height and weight, has a short thick neck, broad chest and short 4th metacarpals, what cadiac defects is she most at risk for?

A

Turner Syndrome

- coarction of the aorta

-bicuspid aortic valve

187
Q

LV EDV = 125 ml

LV ESV = 75 ml

What is the Ejection Fraction?

A

EF = SV / EDV

= 50/125

= 40%

188
Q

What are the normal morphological changes in an aging heart?

A
  • decrease LV apex to base dimension
  • sigmoid shaped ventricular septum
  • increased collagen deposition
  • cytoplasmic lipofuscin (brown pigment) in cardiomyocytes
189
Q

A patient presents with neurological symptoms and signs heart failure, in what vitamin would he deficient?

A

Thiamine (Vit. B1)

Deficiency results in Beriberi

(peripheral neuropathy, heart failure)

190
Q

A genetic defect that prolongs the QT interval most likely effects which type of membrane channel?

A

Potassium Channels

191
Q

Pacemaker leads most commonly travel through what?

Where is this located?

A

Coronary Sinus

Atrioventricular groove

192
Q

What can cause a dilated cardiomyopathy?

A

Alcohol abuse

Beriberi

Chagas

Coxsackie virus

Cocaine use

Doxorubicin

“ABCCCDilated”

193
Q

Sick-sinus Syndrome

  1. what is it?
  2. how does it present?
  3. how it seen on ECG?
A
  1. age related degeneration of SA node

2.

bradycardia, reduced CO which can lead to syncope

3.

Delayed p-waves until a p-wave is dropped

194
Q

How is the chest pain seen in Costochondritis typically seen?

A

Chest pain that is reproducible with palpation and worsened with movement or changes in position

195
Q

Foam cells

  1. What do they lead to?
  2. What are they primarily composed of?
A

1.

Atherosclerotic plaque

2.

Macrophages

196
Q

Amyloid Cardiomyopathy

  1. What type of myopathy is it most likely to cause?
  2. How will the walls of the heart be effected?
  3. Systolic or diastolic dysfunction?
A
  1. Restrictive Cardiomyopathy

2.

Ventricular walls become thickened

Dilated left Atrium cavity size

Normal Left Ventricle cavity size

  1. Diastolic Dysfunction
197
Q

What will happen to this benign vascular tumor over time?

A

First in will increase in size

Then it will regress

198
Q

A patient presents with a loud S2 and a accentuated palpable impulse along the upper left sternal border.

What is the most likely diagnosis?

A

Pulmonary Hypertension

(RV Heave)

UWorld - Cardio (2 decks)

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