Final Review

Question 1

Myocardial oxygen supply and demand

Answer 1

Question 2

How do nitrates work as an anti-anginal therapy?

Answer 2

To reduce preload and thereby reduce myocardial wall stress.

They do also increase coronary dilation, however most patients with atherosclerotic disease have maximally dilated coronaries at baseline. For a patient with angina due to vasospasm, these effects are more significant.

Question 3

The ONLY two NDHP CCBs

Answer 3

verapamil and diltiazem

Act like beta blockers

Question 4

Evolution of STEMI and NSTEMI on ECG

Answer 4

Question 5

Anatomic localization of infarct by ECG

Answer 5

Question 6

58 year old man develops sharp left anterior pleuritic chest pain and has a cardiac rub on auscultation 1 week after MI.

What is the likely cause?

Answer 6

Pericarditis

Question 7

58 year old man develops sharp left anterior pleuritic chest pain and has a cardiac rub on auscultation 3 weeks after MI.

What is the likely cause?

Answer 7

Dressler syndrome (Type III Hypersensitivity)

Question 8

Aortic dissection may lead to ___

Answer 8

Aortic dissection may lead to aortic regurgitation

Question 9

Model for myelopoietic disorders

Answer 9

Question 10

In a patient with a healthy heart, if you push on the liver. . .

Answer 10

. . . the JVD won’t go up. Because, the right atrium and ventricle will just accept more blood.

It is really when the right heart is struggling against high pressure that this produces a hepatojugular reflux.

Question 11

Lovitch Leukocytosis Flowchart

Answer 11

Question 12

Lovitch Neutropenia Flowchart

Answer 12

Question 13

Lovitch Pancytopenia Flowchart

Answer 13

Question 14

General approach to leukopenia/leukocytosis

Answer 14

Question 15

Cardiogenic pulmonary edema

Answer 15

Question 16

Non-cardiogenic pulmonary edema

Answer 16

Question 17

NYHA Heart Failure grading

Answer 17

Question 18

Major factors that determine airway diameter (and therefore resistance)

Answer 18

• Long size (changes throughout respiratory cycle)
• Transmural pressure (Pin - Pout)

Question 19

Hemoglobin dissociation curve

Answer 19

Question 20

A patient with 60% oxygen saturation is put on oxygen and his oxygen improves, but his carbon dioxide increases substantially as well. What is the mechanism for his increased CO2?

Answer 20

Worsened V/Q mismatch

Question 21

Etiology of combined pre and post capillary pulmonary hypertension

Answer 21

Started with high wedge pressure due to poor left heart function, developed increased PVR over time, and eventually led to pre-capillary pulmonary hypertension

Question 22

Why is elevated pre- and post- capillary pulmonary hypertension so hard to treat?

Answer 22

When you give a pulmonary vasodilator, their pulmonary artery will relax and fill with fluid, but then the fluid will get stuck! It can’t make it through the high pressure barrier of the capillaries.

You will just precipitate pulmonary edema.

Note that these are the patients with chronic L heart diastolic dysfunction.

Question 23

Why is pulmonary infarction usually towards the periphery of the lung?

Answer 23

Because these areas benefit the least from the dual blood supply of the lung. They are the least perfused by the bronchial arteries, and rely heavily on the pulmonary arteries.

Question 24

____ is a major cause of dyspnea in patients who breathe at dynamic hyperinflation and is a way of measuring whether or not someone is breathing at an EELV above their FRC.

Answer 24

Constrained inspiratory capacity is a major cause of dyspnea in patients who breathe at dynamic hyperinflation and is a way of measuring whether or not someone is breathing at an EELV above their FRC.

Question 25

When it comes no nitrates. . .

Answer 25

**Low-dose nitrates** are selective venodilators **High-dose nitrates** are indescriminate vasodilators

Question 26

Full PAO₂ equation

Answer 26

PAO₂ = FiO₂ ( P_atm - 47 mmHg) - ( 1.25 \* PaCO₂ )

Question 27

The equation for estimated A-a gradient does not apply when. . .

Answer 27

. . . **the patient is on supplemental oxygen**

Question 28

Transfusion reaction summary

Answer 28

Question 29

Serologic types of autoimmune hemolytic anemia

Answer 29

Question 30

Model for drugging pulmonary hypertension

Answer 30

Question 31

Drug interactions for PAH

Answer 31

Question 32

What are some ways to differentiate TACO from TRALI?

Answer 32

Both produce an acute reaction involving severe dyspnea, tachycardia, and hypoxemia with new diffuse infiltrate on CXR. However, **TACO is not an inflammatory process**, and so **does not often cause hypotension or fever**. TACO is also more likely if transfused blood was from an **un-transfused male donor.** More often, **TACO causes hypertension**

Question 33

Approach to community acquired pneumonia

Answer 33

Question 34

Considerations for nosocomial pneumonia

Answer 34

* Patient gets pneumonia after ≥ 48 hours in the hospital * Identifying the pathogen is very important * CAP bugs + at risk for infection with a broader range of bacteria, including **gram negatives** (**Escherichia coli, Klebsiella pneumoniae, Pseudomonas**) and more resistant pathogens (**MRSA**) * Initial coverage often broad (ex. anti-pseudomonal cephalosporin + vancomycin) * Narrow regimen once pathogen identified

Question 35

Antibiotics that work against pseudomonas

Answer 35

Question 36

The HACEKs

Answer 36

A group of fastidious **Gram-negative bacilli** which normally live in the mouth, but which can also cause infective endocarditis.

Question 37

Treatment for HACEKs

Answer 37

Question 38

Treating outpatients for pneumonia

Answer 38

* **Treat empirically** (i.e., no sputum cx) * Regimen: * If **suspicion for possible S. pneumo** (lobar infiltrate, high fever, or sick appearing): Beta-lactam (ex. **amoxicillin**) * If **very low suspicion for S. pneumo**\* (interstitial infiltrate, not that sick): Tetracycline (ex. **doxycycline**) **OR** Macrolide (ex. **azithro**) * \*Rates of macrolide resistant S. pneumo high * If very elderly or with **substantial comorbidities,** treat more aggressively with **fluroquinolone** or **beta-lactam + macrolide**

Question 39

Treating inpatients for pneumonia

Answer 39

* Try to **obtain sputum cx** to guide treatment * **Empiric Regimen while awaiting** results: * **Fluoroquinolone** (ex. levofloxacin) OR **Beta-lactam + macrolide** \*\*\*These regimens cover atypicals (**beta-lactams don’t cover Legionella**, which is considered an “atypical organism” even though it generally causes a lobar infiltrate and makes people very sick) and provide extra coverage for macrolide-resistant S. pneumo

Question 40

Considerations for immunosuppressed states (impaired humoral, impaired cellular, AIDS, neutropemia, and asplenia)

Answer 40

* Impaired humoral immunity = bacteria * Impaired cellular immunity = bacteria, viruses, fungi, PJP, TB * AIDS = combo of the above * Neutropenia = bacteria, aspergillus * Asplenic = increased risk for infection with encapsulated organisms

Question 41

Symptoms of cardiac tamponade

Answer 41

* **Beck's triad**: Hypotension, JVD, distant heart sounds * Tachycardia (compensatory) * Elevated pulsus paradoxus * Forward failure (cold extremities, lightheadedness, somnolence)

Question 42

Treating cardiac tamponade

Answer 42

* Short term: * **Positive inotropes and IV fluids _if hypotensive_** * Allow tachycardia * **Don't do anything to decrease cardiac output** (no nitrates, no diuretics, no beta blockers, no CCBs) * **Pericardiocentesis** as soon as possible

Question 43

Constriction vs tamponade

Answer 43

Question 44

Kussmaul's Sign

Answer 44

A paradoxical rise in jugular venous pressure (JVP) on inspiration, or a failure in the appropriate fall of the JVP with inspiration. This is due to the constrianing effects of a diseased pericardium in constrictive pericarditis. It can also be due to R ventricular infarct, cor pulmonale, or other R heart diastolic failure. Present in 20-50% of patients with constrictive pericarditis

Question 45

Fick Equation

Answer 45

Question 46

Alveolar ventilation equation

Answer 46

Question 47

R and L axis deviation

Answer 47

Question 48

Why do patients with IPF have decreased oxygen saturation on exertion?

Answer 48

The primary mechanism for this is V/Q mismatch. Alveoli are partially destroyed due to fibrosis, and so the SA of any given alveolus is disrupted. Diffusion barrier is also a contributor, but is not as important as V/Q mismatch.

Question 49

A patient with chronic hypertension presents with this ECG. What is likely the cause of these anomalies?

Answer 49

Left ventricular hypertrophy Not necessarily ischemia

Question 50

Autoimmune hemolytic anemia table

Answer 50

Question 51

Endocarditis summary

Answer 51

Question 52

Modified Duke criteria

Answer 52

* Designed to provide a good guess of whether or not someone has IE * 2 major, 1 major + 3 minor, or 5 minor establish presumptive diagnosis if no other explanation is available * Major: 1) positive blood culture + confirmation, 2) evidence of endocardial involvement * Minor: 1) Predisposing heart condition *OR* IV drug use, 2) Fever, 3) Vascular phenomena (evidence of embolism), 4) Evidence of type III hypersensitivity, 5) Microbiologic evidence other than positive blood culture