Cardiology - important concepts - Sheet1

Question 1

How does a less negative membrane potential affect excitability? What are some situations in which you may have a less negative membrane potential?

Answer 1

As the resting membrane potential becomes less negative, less Na channel inactivation gates are open. There are now less Na channels available to be excitable. This reduces excitability and ultimately slows contractions. This situation can be seen in ischemia, situations with high extracellular K concentrations, and is mimicked when the drug TTX is given.

Question 2

Is degree of stenosis correlated with which lesions are most dangerous in unstable angina?

Answer 2

Nope. Not easy to tell which plaques are vulnerable, not related to degree of stenosis

Question 3

What is the role of anti-coagulants and anti-platelet agents in treatment of USA/NSTEMI?

Answer 3

Patients are treated based on risk stratification. Low-risk patients are managed medically and these anti-thrombotics prevent thrombosis after plaque rupture, reduce chances of occlusion.

Question 4

In what condition are intrramyocardial arterioreles hypertrophied?

Answer 4

Hypertrophic Cardiomyopathy

Question 5

Best drugs to increase SVR?

Answer 5

Norepinephrine, phenylephrine

Question 6

Best drugs to increase CO without increasing SVR?

Answer 6

Dobutamine and Isoproterenol (careful with iso because it can drop BP which is not good in CHF)

Question 7

What is the significance of lipophilicty vs. hydrophilicty in regards to autonomic antagonists?

Answer 7

Lipophilic = short half-life but greater risk of CNS toxicity due to greater ability to cross BBB, hydrophilic = longer half-life and usually renally excreted (careful with pts with renal failure!)

Question 8

Should you give beta-blockers to patients in cardiogenic shock? How about complete heart block?

Answer 8

Nope, beta-blockers are negative inotropes, so don’t give it to someone in HF until they are hemodynamically stable. They will slow conduction so don’t give it to someone in heart block until you have restored normal sinus rhythm.

Question 9

Holosystolic murmur?

Answer 9

Mitral regurgitation

Question 10

Crescendo/decrescendo systolic murmur?

Answer 10

Aortic Stenosis

Question 11

Decrescendo, high pitched diastolic murmur?

Answer 11

Aortic regurgitation

Question 12

Low pitched M shaped at axilla and apex?

Answer 12

Mitral stenosis

Question 13

How does extracellular potassium change in ischemia?

Answer 13

More extracellular potassium in inschemia, resting membrane potential is less negative

Question 14

Which layer of the heart is most susceptible to ischemic injury?

Answer 14

Subendocardium due to increased pressure during systole, decreased autoregulation and distance from arteries.

Question 15

What is the mutation in DiGeorge? What does it cause?

Answer 15

deletion of 22q11, results in neural crest migration defects. presents as thymus defects, parathyroid defects, CHD and defects in formation of aortic arch

Question 16

What causes the RVH in Tetralogy of Fallot?

Answer 16

The VSD (not the outflow tract narrowing!)

Question 17

What is the acute effect of diurectics? Long term action?

Answer 17

Natriuresis resulting in decreased blood volume. Compensatory mechanisms result in increased renin production, sodium retention and fluid restoration. Long term though, there is a decrease in ECF. Mechanism not known, could be due to long term decrease in pulmonary vascular resistance due to increased NO production

Question 18

What metric might tell you that there is a ventricular septal defect post MI?

Answer 18

Very high venous saturation as measured from PA (along with high pressures in RA/RV/PAWP)

Question 19

Are thin wavy myoctyes necessarly a sign of infarction?

Answer 19

Nope, can just be ischemic. Can’t know just by looking at them

Question 20

What channels are responsible for automaticity of the SA node? Purkinje fibers?

Answer 20

Sa node - delayed rectifier potassium channel and t-type calcium channel. purkinje - funny current

Question 21

What determines conduction velocity?

Answer 21

Magnitude of excitatory current, speed of excitatory current, resistance to flow (ex. in acute infarct, gap jxns are closed, increasing resistance to flow between myocytes)

Question 22

If there is low venous oxygen saturation, what assumption can we make about cardiac output?

Answer 22

Cardiac output is probably low as the tissues need to extract more oxygen from the blood due to decreased flow

Question 23

What is the equation for cardiac output as calculated by the fick principle?

Answer 23

Cardiac output = vo2 (o2 consumption)/avo2d (difference in o2 between arterial and venous measurements0

Question 24

What is the equation for systemic vascular resistance?

Answer 24

(SAP-RAP)/CO

Question 25

What is the equation for total pulmonary resistance?

Answer 25

PAP/CO

Question 26

What is the equation for pulmonary vascular resistance?

Answer 26

(PAP-LAP)/CO

Question 27

What must you check before starting a patient with CHF on a phoshodiesterase 3 inhibitor?

Answer 27

That they are volume overloaded, because PDEIs decrease preload and afterload, can result in hypotension.

Question 28

Why might you give someone with torsades des pointes isoproteronol?

Answer 28

It increases the HR which will shortern action potential duration and therefore the QT interval

Question 29

What conditions increase risk of using anti-arrhytmics?

Answer 29

1: Prolonged QT 2: slow sinus node 3: av block 4: systolic dysfxn (classes I, II, and IV are negative inotropes

Question 30

What is the hypothesized natriuretic hormone mechanism of HTN?

Answer 30

When intravsacular volume high, a hypothesized peptide blocks sodium/potassium pump resulting in increased sodium excretion in kidney but simulatneous increcased calcium concentration in vascular smooth muscle resulting in increased tone –> HTN

Question 31

What is the renal sympathetic mechanism of HTN?

Answer 31

Increased renal sympathetic activity in HTN results in decreased renal flood flow, sodium reabsorption and RAAS activation, renal denervation - possible treatment?

Question 32

What changes are seen in histology in benign HTN? Malignant HTN?>

Answer 32

Benign: hyaline arteriosclerosis, fibroblastic intimal hyperplasia, medial hypertrophy; Malignant: fibrinioid sclerosis, hyperplastic arteriolotiis “onion-skinning”, microangiopathic hemolytic anemia

Question 33

Other organ changes seen in benign HTN? Malignant HTN?

Answer 33

benign: LVH, nephrosclerosis, berry aneurysms, retinal microaneurysms; malignant: acute cortical necrosis, increased ICP, retinal flame shaped hemorrahges and papilledema,

Question 34

What are the criteria for metabolic syndrome?

Answer 34

3 of the following 5: increased abdominal adiposity, increased BP, increased fasting glucose, increased TG, decreased HDL

Question 35

In which cardiomyopathy would you see intramyocardial arteriolar hypertrophy?

Answer 35

HCM

Question 36

What is the hallmark of RCM as seen on a pressure wave form?

Answer 36

Rapid early diastolic filling with rapid decceleration slope