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Cardiovascular System - 3rd year > Clinical Medicine Review Q's (same Q's but via subject) > Flashcards

Clinical Medicine Review Q's (same Q's but via subject) Flashcards

Clinical aspects of hypertension (1-23) Cardiac arrhythmias (24-87) Heart failure (88-119) Acute coronary syndromes (120-148) Prevention of cardiovascular disease (149-163) Chronic ischemia (164-197) Valvular heart disease (198-247)

1
Q

A patient has a blood pressure of 169/90. Which hypertension grade is he in?

A

grade 2 (if one value crosses the threshold, thats enough to move into the stage)

grade 1 is 140/90 to 159/99

grade 2 is 160/100 to 179/109

grade 3 is 180/110 or higher

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2
Q

How much does the blood pressure have to increase to double the risk of CVD death? (2 fold risk increase)

A

systole increases by 20 and the diastole increases by 10mmHg

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3
Q

How does sleep apnea cause hypertension?

A

the body is afraid of hypoxia in sleep so it produces adrenaline, that leads to hypertension

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4
Q

A patient has a blood pressure of 159/90 and has two risk factors. What his risk of CVD death? How would you treat him?

A

moderate risk, treat with lifestyle changes for a few weeks then with drug if insufficient

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5
Q

A patient has a blood pressure of 159/90 and has more than 3 risk factors. What his risk of CVD death? How would you treat him?

A

high risk, start with drugs and lifestyle changes

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6
Q

What is a high normal BP?

A

130-139/85-89

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7
Q

Patient has BP of 150/111 what grade of hypertension is he in?

A

grade 3

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8
Q

At what age does most of the new onset of hypertension occur?

A

between the age of 30&40

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9
Q

T/F: blood pressure measurement are roughly equal no matter the location they are taken in

A

false; ambulatory/home measurements are less by 5mmHg. Some patients also have white coat hypertension, where their BP increases when encountering doctors.

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10
Q

A patient has a blood pressure of 181/90. What his risk of CVD death? How would you treat him?

A

high risk. immediately start with drugs and lifestyle changes.

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11
Q

What occurs if the BP cuff is slightly too tight for the patient? How will that affect the BP results?

A

if it was small it will give false high reading

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12
Q

What is “masked hypertension”?

A

a condition opposite of white coat, when BP is high at home but normal in the office

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13
Q

A patients father died at 60 due to CVD and his mother at the age of 70. Does this mean he has a family history of premature CVD?

A

no.

(tafree’3= if someone’s father got heart attack at the age of 50 he is considered to have family history of premature cvd. if someone’s father got heart attack at the age of 60 he is not considered to have premature cvd. if someone’s mother had heart attack at the age of 60 this is premature cvd for women because they usually get heart attacks 10 years after men.)

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14
Q

malignant hypertension vs accelerated hypertension

A

Accelerated hypertension is defined by retinal damage, including hemorrhages, exudates and arteriolar narrowing. A recent significant increase over baseline BP that is associated with target organ damage.

The additional presence of papilloedema constitutes malignant hypertension, which is usually associated with diastolic blood pressure greater than 180/120mmHg

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15
Q

When are ACE inhibitors contraindicated?

A
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16
Q

When are ARBs contraindicated?

A
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17
Q

When are beta blockers contraindicated?

A
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18
Q

When are diuretics contraindicated?

A
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19
Q

risks and benefits of:

Monotherapy vs combination therapy of hypertension

A

Monotherapy is using one drug, it was found that it doesn’t have a good control on BP and increases the side effects of that drug.

this is why we preferably start with a single-pill combination of 2 drugs. (use one pill because it increases compliance)

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20
Q

When do we use Monotherapy to treat hypertension?

A

when the patient has grade 1 hypertension, so we use
only ACEI or ARB alone

when patient is more than 80 yr old or fragile, so you don’t want to lower their BP significantly, so start with a single drug in a low dose

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21
Q

T/F: beta blockers are initiating drugs of hypertension treatment

A

False; beta blockers were used as initiating drugs, now we only use them in special circumstances

(ex/ angina and heart failure, and in heart failure we use a specific beta blocker)

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22
Q

Beta-blockers to give in heart failure patients are

A

carvedilol

metoprolol succinate

bisoprolol or nebivolol

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23
Q

When are calcium antagonists contraindicated?

dihydropyridines VS diltiazem VS verapamil

A
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24
Q

Which are objective?

a. palpitations
b. arrhythmias

A

b. arrhythmias

they’re measurable and not based on feelings. palpitations are subjective.

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25
Q

What’s the first organ to develop?

A

the heart

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26
Q

Which increases contractility?

a. Positive chronotropic effect
b. Positive inotropic effect

A

b. Positive inotropic effect

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27
Q

What maintains the polarity of myocardial cells?

A

voltage gated channels

(insures appropriate ion distribution)

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28
Q

What’s the AV guard?

A

the maximum amount ventricles can pump per minute

250bpm

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29
Q

What does mapping and tracing the R’s in an ECG do?

A

insures the R-R intervals are the same, if its a regular heart rate

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30
Q

What does it mean to be hemodynamically unstable?

A

insufficient oxygen to vital organs

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31
Q

T/F: we apply an electrical shock to hemodynamically unstable patients no matter what type of arrhythmias they have

A

true

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32
Q

How do you treat pathologically bradycardic patients?

A

pacemaker

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33
Q

How do you treat a hemodynamically stable patient with ventricular tachycardia?

A

shock them- because this condition has a tendency to destabilize quickly

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34
Q

How do you treat a hemodynamically stable patient with arrhythmia?

A

if hemodynamically stable, treat with pharmacotherapy!

(except if ventricular tachycardia, then shock them even if they’re stable- because they become unstable quick)

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35
Q

T/F: all class 1 antiarrhythmic drugs are used for septal defects of the heart

A

false, they’re only used in normally structured hearts

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36
Q

Which is given for a slow supraventricular pulse?

a. Amiodarone
b. Adenosine
c. Atropine
d. Sotalol

A

c. Atropine

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37
Q

appropriate vs inappropriate sinus tachycardia

A

appropriate = due to a secondary reason ex/ exercise

inappropriate = no cause

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38
Q

Whats the difference between Supraventricular Tachycardia (SVT) and Sinus Tachycardia?

A

Supraventricular Tachycardia (SVT) also known as paroxysmal supraventricular tachycardia (PSVT) occurs suddenly and stops suddenly. While Sinus Tachycardia occurs slowly and fades slowly.

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39
Q

AVRT versus AVNRT

AVRT = Atrioventricular reentrant tachycardia

AVNRT = AV-nodal reentrant tachycardia

A

AVRT→ anatomical reentry because of extra conducting tissue that ain’t the AV node (bundle of Kent is the conductor)

AVNRT→ functional reentry that occurs in the structurally normal AV node (the impulse is premature and it causes a circuit- activating the atria and ventricles at the same time + at a faster rate then SA)

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40
Q

paroxysmal supraventricular tachycardia (PSVT) occurs most commonly in…

A

young patients

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41
Q

Diagnose

A

Paroxysmal supraventricular tachycardia (PSVT)

no P waves, narrow QRS complex, ST depression, and regular but high heart rate

(AVNRT is the most common form of PSVT)

** technically you can only say its paroxysmal if you see it going from a normal rate to tachycardia… so this is SVT only

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43
Q

ST depressions are indicators of which pathology?

A

myocardial ischemia/ coronary artery disease

(but when its a young patient check PSVT because it also causes ST depression)

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44
Q

What’s the first line treatment of Paroxysmal supraventricular tachycardia (PSVT)?

A

carotid massage (because its a vegal maneuver that slows down the AV node)

+

adenosine (if no difference)

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45
Q

What’s the second line treatment of Paroxysmal supraventricular tachycardia (PSVT)?

A

IV Beta Blocker

IV Diltiazem (ca channel blocker)

IV Verapamil

(the goal is to interrupt the circuit at the AV node; Digoxin is also used because it has important parasympathetic effects, on the AV node)

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46
Q

What’s the definitive treatment of Paroxysmal supraventricular tachycardia (PSVT)/AVRT?

A

Radiofrequency​ Ablation therapy (aka rhizotomy) which is a type of minimally invasive procedure that uses heat to destroy abnormal tissue

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47
Q

What is the most common abnormal heart rhythm?

A

Atrial fibrillation

(more common as age increases)

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48
Q

What are some causes of atrial fibrillation (AF)?

(cardiac and noncardiac causes)

A

all cardiac diseases can lead to AF

non-cardiac reasons = drugs, alcohol, acute respiratory infections, hyperthyroidism, hormonal diseases

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49
Q

How many foci cause Atrial Fibrillation? Where are they located?

A

many supraventricular foci, especially at the junction of pulmonary veins

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50
Q

PSVT and Atrial fibrillation both don’t present P waves on ECG’s. Explain the mechanism of each.

A

PSVT doesn’t show the P waves because the QRS complex covers them due to the atrial and ventricles contracting simultaneously. (there technically IS a P wave)

Atrial fibrillation doesn’t have P waves because the atrial doesn’t contract (no atrial depolarization), it vibrates instead because of the many activations foci.

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51
Q

T/F: Atrial fibrillation (AF) is always paired up with tachycardia due to many impulses generated by the foci

A

False, the condition has varying heart rates. In AF young patients the AV node may conduct many impulses and cause tachycardia, but in AF older patients, the conductivity is reduced and the heart rate may be normal or reduced.

(so the only things that confirm AF is irregular R-R’s and no P waves, heart rate doesn’t play a factor)

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52
Q

What’s the major complication of Atrial Fibrillation?

A

blood clots forming in the atria (because they don’t contract) that can cause infractions or strokes

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53
Q

What is Valvular Atrial Fibrillation? How do you treat patients who have it?

A

Valvular Atrial Fibrillation is when a patient who has Atrial Fibrillation as well as Mitral valve stenosis. (both those conditions cause blood to stay in the atria- very high risk of stroke) Give anticoagulants

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54
Q

A patient has both atrial fibrillation and aortic stenosis, which does he classify into?

a. Valvular Atrial Fibrillation
b. Nonvalvular Atrial Fibrillation

A

b. Nonvalvular Atrial Fibrillation

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55
Q

In Which do you use the “CHA2DS2-VASc score” system to decide if he needs anticoagulants?

a. Valvular Atrial Fibrillation
b. Nonvalvular Atrial Fibrillation

A

b. Nonvalvular Atrial Fibrillation

(in Valvular you immediately give anticoagulants)

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56
Q

A male has a CHA2DS2-VASc score of 2, do you give anticoagulants?

A

yes, in males if above 1 then you give

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57
Q

reentry circuit of atrial flutter is 300 and it has a 3 to 1 AV block, what is the heart rate?

A

100bpm

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58
Q

What is a common atrial flutter rate?

A

150bpm (300 atrial circuit rate and 2:1 AV physiological block)

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59
Q

A female has a CHA2DS2-VASc score of 2, do you give anticoagulants?

A

no, for women it should be above 2 to administer anticoagulants

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60
Q

Diagnose. (What is that wave that’s different than the rest?)

A

Ventricular Tachycardia, with a capture beat (a normal looking SA beat). The ventricles are causing SA suppression, and the capture beat is evidence that the SA node is still functioning and can depolarize the heart.

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61
Q

T/F: Atrial flutter can be diagnosed due to its regularity

A

false, it is regular but the AV node may very in its conductivity. So it can conduct 2 to 1 then change to 4 to 1, which would make the rate appear irregular- that’s why we can’t use it.

(diagnose because of saw tooth appearance only, and it’s commonly 150bpm)

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63
Q

Diagnose. Explain the activity in the circle.

A

ventricular tachycardia, the circles indicate P waves when the SA node was able to depolarize the atria (but it wasn’t able to continue down the pathway to the AV node and bundle)

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64
Q

Which is more sensitive to shock?

a. atrial flutter
b. atrial fibrillation

A

a. atrial flutter

(that’s why they give 50J initially)

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65
Q

What are the three basic findings in an ECG that points to ventricular tachycardia?

A

wide QRS

no P waves

tachycardia

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66
Q

Diagnose. Is this monomorphic or polymorphic?

A

polymorphic ventricular tachycardia, also called torsades de pointes

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67
Q

diagnose

A

ventricular fibrillation

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69
Q

How many ventricular complexes must be present for the diagnosis of ventricular tachycardia?

A

3 or more

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70
Q

Mobitz I vs Mobitz II

A

both second degree heart blocks

Mobitz I= (PR interval prolonging + QRS missing)

Mobitz II= (PR interval constant + a QRS missing)

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73
Q

Who is most likely to have ventricular tachycardia?

A

people with structural heart disease (ex/ ischemic heart disease- most likely) and cardiomyopathy patients

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74
Q

Which of the following antiarrhythmic drugs only block Na in a depolarized state? What are two examples?

a. 1a
b. 1b
c. 1c

A

b. 1b

Lidocaine IV

Mexilitine

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75
Q

Which of the following antiarrhythmic drugs block N and K channels? What are two examples?

a. 1a
b. 1b
c. 1c

A

a. 1a

Procainamide IV

Quinidine

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76
Q

all class 1 antiarrythmatic drugs block which ion channel?

A

Na+

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77
Q

Diagnose

A

WPW syndrome/AVRT

When an accessory pathway is present, the sinus node action potential can pass through the bypass tract before the AV node, resulting in the ventricles becoming rapidly depolarized. This is termed “pre-excitation” and results in a shortened PR interval on the ECG.

The typical ECG finding of WPW is a short PR interval and a “delta wave.“ A delta wave is slurring of the upstroke of the QRS complex. This occurs because the action potential from the sinoatrial node is able to conduct to the ventricles very quickly through the accessory pathway, and thus the QRS occurs immediately after the P wave, making the delta wave.

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78
Q

What is a Delta wave? What does it look like? Why does it occur? When?

A

Delta wave is a slurred upstroke in the QRS complex often associated with a short PR interval. It is most commonly associated with (due to) pre-excitation syndrome such as Wolff-Parkinson-White syndrome.

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79
Q

Which of the following class 1 antiarrhythmic drugs are pure Na+ blockers? What are two examples of them?

a. 1a
b. 1b
c. 1c

A

c. 1c

Flecainide
Propafenone

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80
Q

Treatment of ventricular tachycardia

A
  1. shock ‘em with 100J
  2. pharmacological therapy (Procainamide, Sotalol, Lidocaine, Amiodarone)
  3. give magnesium sulfate if polymorphic VT
  4. correct contributing conditions
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81
Q

Patient comes in with supraventricular tachycardia. Which medications can be used to treat this condition?

A

Adenosine/Amiodarone

Beta Blockers

Calcium Blockers (Verapamil, Diltiazem)

Digoxin

(ABCD)

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82
Q

Patient comes in with ventricular tachycardia. Which medications can be used to treat this condition?

A

Beta Blockers

Amiodarone

Lidocaine

Sotalol

(BALS)

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83
Q

What is Wolff-Parkinson-White (WPW) Syndrome?

A

A condition in which there is an extra electrical pathway in the heart.The most common mechanism of tachycardia in patients with WPW is called atrioventricular reentrant tachycardia (AVRT)

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86
Q

How do you treat atrial fibrillation?

A

Control Rate with Beta Blockers, Calcium Channel Blockers, Digoxin

Control Rhythm (AF to Sinus rhythm) with either Electrical or Pharmacological methods.
pharma= Propafenone, Flecanide, Amiodarone

Or treat permanently with Ablation therapy

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87
Q

Sustained vs non-sustained ventricular tachycardia

A

sustained= 30 secs or more

non-sustained= less than 30 seconds

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88
Q

What is a pathognomonic symptom of heart failure?

A

Paroxysmal nocturnal dyspnea or paroxysmal nocturnal dyspnoea (PND) is an attack of severe shortness of breath and coughing that generally occur at night. It usually awakens the person from sleep, and may be quite frightening.

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89
Q

How do you treat patients that are cold and dry?

A

cold and dry means they have hypoperfusion but are not congested. Give them epinephrine to increase the cardiac output.

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90
Q

How do you treat patients that are warm and wet?

A

they’re congested. give diuretics.

(if cold and wet, give both diuretics and epinephrine)

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92
Q

Diagnose.

A

Pulmonary edema due to left ventricle systolic dysfunction

Kerley b lines are seen, indicates interstitial pulmonary edema.

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94
Q

a broadened/laterally displaced apical beat indicates…

A

a dilated heart

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96
Q

T/F: left ventricular systolic dysfunction is always present along with cardiomegaly

A

false, not always. If the systolic dysfunction is acute, the heart may not have has enough time to enlarge

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97
Q

What do high Natriuretic Peptides indicate? explain.

A

Natriuretic Peptides are high in heart failure. They’re released with the atrial pressure is high and its dilated, they act to reduce the BP. (by natriuresis- the excretion of sodium by the kidneys)

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98
Q

What conditions can increase the heart rate and mimic cardiac diseases?

A

anemia, high HR due to low RBC’s delivering oxygen

hyperthyroidism, can increase the metabolic rate so drastically that the body can’t keep up and thus increases HR

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99
Q

What test can prove and classify heart failure?

A

Echocardiography

classify it into heart failure with reduced ejection fraction OR with sustained ejection fraction

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100
Q

What is the normal left ventricular ejection fraction? How is it calculated?

A

50-75%

Ejection Fraction= SV/EDV

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101
Q

How do you treat patients with heart failure and sustained ejection fraction?

A

They have a filling issue and not a contraction error, so can minimally help them bu giving diuretics, controlling blood pressure, and heart rate.

102
Q

give an example of heart failure with reduced ejection fraction and with sustained ejection fraction.

A

reduced ejection fraction= dilated cardiomyopathy
sustained ejection fraction= Left ventricular hypertrophy

103
Q

How do neurohormones react to a decrease in CO?

A

SNS is activated and epinephrine is released to so it increases SV and HR via beta receptors. This aids the heart initially, but epinephrine is toxic to myocardial tissue

104
Q

How does the renin angiotensin aldosterone system react to low CO? How can this be bad?

A

due to the low CO and reduced renal perfusion, renin is released to increase the BP and volume. This acts to improve the CO initially, but then the volume increases the afterload, which decreases CO furthur.

105
Q

What are three ways to stop the actions of the renin angiotensin aldosterone system?

A

1- ACE inhibitor→ stop angII synthesis, increase bradykinin

2- angiotensin receptor blocker (ARB’s)→ stop the effects of angII by blocking its receptors (AT1)

3- Mineralocorticoid Receptor Antagonist (MRA)→ stop aldosterone from retaining Na and water

106
Q

T/F: digoxin and diuretics aid to improve survival in HF patients

A

false, they act to improve the symptoms (the neurohormonal antagonists are the ones improving survival)

107
Q

Which heart failure drug must you give the least effective dose?

A

drugs that only improve symptoms (digoxin and diuretics), you give as little as possible

108
Q

Which heart failure drugs must you give the highest tolerated dose?

A

Neurohormonal Antagonists

(they decrease death)

109
Q

hydralazine–isosorbide dinitrate (H-ISDN) is given to treat heart failure. What is the target population for the drug?

A

Black Americans (increases their survival rate more)

110
Q

When should you use ACE inhibitors and when should you use angiotensin receptor blockers (to treat HF)?

A

use angiotensin receptor blockers if ACE inhibitors are intolerated

111
Q

What does it mean when a heart failure patient is given optimal medical therapy (OMT)?

A

ACE inhibitors

beta-blockers

MRA (mineralocorticoid antagonists)

(the first 2 are given, then if symptoms persist, MRA’s also given)

112
Q

T/F: all beta blockers can be used in heart failure

A

false, there are four that can be used:

bisoprolol, carvedilol, nebivolol, metoprolol succinate XL

113
Q

Which of the following do Mineralocorticoid Receptor Antagonists (MRA) end with?

a. sartan
b. lol
c. one
d. pril

A

c. one

114
Q

Which of the following do Angiotension receptor blockers (ARB) end with?

a. sartan
b. lol
c. one
d. pril

A

a. sartan

115
Q

How do you treat a heart failure patient who’s still symptomatic after optimal medical therapy (OMT)?

A

give ARNI, a new class of drugs called angiotensin receptor neprilysin inhibitor

116
Q

What is angiotensin receptor neprilysin inhibitor (ARNI) made up of?

A

made up of Valsartan/Sacubitril

Valsartan= angiotensin receptor blocker

Sacubitril= neprilysin inhibitor

117
Q

Which of the following do beta blockers end with?

a. sartan
b. lol
c. one
d. pril

A

b. lol

118
Q

Which two systems does ARNI (Valsartan/Sacubitril) interfere with? How?

A

The natriuretic peptide system and RAAS system

Valsartan= angiotensin receptor blocker (↓vasoconstriction)

Sacubitril= neprilysin inhibitor

neprilysin is an enzyme that deactivates brain natriuretic peptide (BNP; which decreases BP). So if we stop the degradation of BNP we enhance its action.

119
Q

Which of the following do ACE inhibitors end with?

a. sartan
b. lol
c. one
d. pril

A

d. pril

120
Q

After a coronary occlusion, how long does it take for the myocardial tissue to start dying?

A

30 minutes

121
Q

What causes a STEMI?

A

ST segment elevation myocardial infarction most commonly occurs when thrombus formation results in complete occlusion of a major epicardial coronary vessel.

122
Q

What’s the cardinal symptom of acute coronary syndrome?

A

chest pain (severe pressure)

123
Q

What are some radiation sites of ischemic chest pain?

A

retrosternal

Ulnar aspect of left arm
Neck
Jaw
Epigastrium
Back (interscapular)

124
Q

T/F: radiation sites of ischemic chest pain can be the only/primary sight of pain

A

true (ex/ of someone who only has jaw pain)

125
Q

T/F: men and women have a likely chance of presenting with unusual ischemic pain

A

false, women have a higher chance of having unusual symptoms

126
Q

How do you differentiate between unstable angina pain and MI pain?

A

unstable angina= less than 30 minutes

MI= more than 30 min, severe, high troponin

127
Q

Women comes in due to chest pain that has been present for 5 months, but it has been getting worse recently that she has pain while resting. diagnose

A

unstable angina

(crescendo angina- escalating angina- and the fact that she has pain while resting indicates this)

128
Q

Patient comes in with chest pain. He points with one finger towards the left side of his chest to indicate the location of the pain. He says it hurts most when inhaling rapidly. Diagnose.

A

chest wall pain/ MSK pain/ costochondritis

129
Q

Patient comes on sudden chest pain. He described it as tearing pain that caused shortness of breath, faintness, and loss of vision. After checking his pulse, the right arm has a weaker pusle than the left. diagnose.

A

aortic dissection

130
Q

Whats the most common cause of chest pain?

A

chest wall pain

(MSK)

131
Q

Patient comes in with sharp pain on his sides that gets worse when he sneezes. He also has a fever and a productive cough. diagnose.

A

pneumonia

132
Q

Patient comes in with sharp chest pain that radiates to the shoulder (trapezius muscle). Pain improves when he leans forward.

A

acute pericarditis

133
Q

T/F: all unstable angina patients can be diagnosed with ECG

A

false, 1/3 have a normal ECG

(even MI patients may initially present with normal ECG- we treat them and keep checking ECG till we see abnormality)

134
Q

T/F: MI patient with ST deviation have a worse prognosis

A

true

135
Q

How long after MI does it take for troponin levels to elevate? How long will they stay high?

A

Modern assays can detect troponins as early as 3-4 hours after onset of myocardial damage. (the note says 4-6 hours)

stays elevated for 2 weeks

(this is why we use it to confirm the diagnosis)

136
Q

How do you diagnose MI?

A

elevated troponin levels + one of the following things

motion abnormality, myocardial viability, ischemia signs, ST-segment or Q wave abnormalities, thrombus

137
Q

What are some noncardiac reasons for increased troponin?

A

Renal failure, pulmonary causes, burns, severe illness, stroke, subarachnoid hemorrhage, sepsis

138
Q

You have a patient with a STEMI, whats the first thing you must do?

A

Dual Antiplatelet Therapy (Aspirin + P2Y12inhibitors Clopidogrel)

this is to prepare the artery for reperfusion

139
Q

Whats the best treatment for a STEMI?

A

Percutaneous coronary intervention (PCI or angioplasty with stent)

if that’s not possible then fibrinolysis therapy/ thrombolytic therapy

140
Q

Patient comes in with STEMI, you apply dual antiplatelet therapy and see that the closest hospital that has a facility for PCI is 150 minutes away. What’s the next course of action?

A

use the Fibrinolytic therapy (aka thrombolytic therapy)

Why? the PCI is the best treatment but it must be done within 2 hours- if thats not possible fibrinolytic therapy is the way to go.

141
Q

Patient comes in with a STEMI and hemophilia A. The closest PCI facility is five hours away. What is the next course of action?

A

travel the five hours for a PCI facility. fibrinolytic therapy is absolutely contraindicated.

142
Q

When is fibrinolytic therapy is absolutely contraindicated?

A

stroke or intracranial hemorrhage of unknown cause

ischemic stroke less than 6 months ago

recent head trauma (1 month)

recent GI bleeds

noncompressible punctures

aortic dissection

bleeding disorders

143
Q

How to treat an NSTEMI?

A

Dual Antiplatelet therapy + Parenteral anticoagulation

144
Q

When does fibrinolytic therapy stop being useful in treating a STEMI?

A

if the STEMI went on for 12 hours, the fibrinolytic therapy won’t do anything. PCI is the only option.

145
Q

After an MI the ejection fraction of the patient is below 40%. How do you treat this?

A

ACE inhibitor= to treat

aldosterone antagonist= secondary prevention drug

(if we keep the ejection fraction this low, remodeling will occur to compensate.)

146
Q

What is a Q wave MI?

A

myocardial infarctions that in a Q wave forming on the 12-lead ECG once the infarction is completed. Many Q-wave infarctions are often non-transmural, and conversely, transmurality may occur in the absence of Q-waves.

148
Q

A patient is suspected of having an MI. Lab tests also show elevated creatinine and glucose levels. What does this indicate?

A

elevated creatinine= renal impairment (maybe due to renal failure, which will increase the risk of MI)

elevated glucose= indicates necrosis (higher MI risk)

149
Q

Differentiate between primary and secondary risk prevention

A

primary risk prevention is preventing high risk patients from getting the first cardiovascular attack.

secondary risk prevention is for patients who already had a cardiovascular attack- we want to prevent further attacks from occurring

150
Q

What is considered a low 10 year ASCVD risk? What’s a high risk?

A

low risk =5% or less

high risk= 20% or more

151
Q

T/F: lifestyle modification of people with high MI risk includes banning salt completely from the diet

A

false, salt is still a necessary nutrient

152
Q

T/F: exercise reduces the risk of cardiovascular disease due to its effect on weight

A

false, exercise reduces the risk of cardiovascular disease independently on its affect on weight

153
Q

Drugs are mostly used in what type of prevention?

a. primary
b. secondary

A

b. secondary

154
Q

Which medications do you give all already established atherosclerotic cardiovascular disease patients?

A

aspirin

+

statin

155
Q

Patient has established CAD, an ejection fraction of 34%, and no signs of heart failure.

What should we give him?

A

beta blocker

ACEI

aldosterone antagonist

(Give these when CAD established + less that 40% EF)

156
Q

When should you give aspirin for primary prevention of CAD? How about statins?

A

aspirin can’t be used for primary prevention (due to bleeding risk)

statins are used when the patient has an intermediate or high risk (ex/ high LDL + diabetes)

157
Q

What are the qualifications needed for a patient to be given an implantable cardiovascular defibrillator (ICD) for primary prevention?

A

1- left ventricle ejection fraction 35% or less

2- is on optimal medical therapy (OMT) to increase the ejection fraction

3- NYHA Class II or III

4- nonischemic dilated cardiomyopathy

158
Q

A patient had an MI 20 days ago, his ejection fraction is 27%. You want to prevent further attacks by implanting an ICD (implantable cardiovascular defibrillator). Is this valid?

A

no, you have to wait for at least 40 days after the MI because the ejection fraction may improve with time. If you measure the ejection fraction again after 40 days and it’s still below 35%, an ICD is an appropriate secondary prevention.

159
Q

What is the prevention method for atrial fibrillation complications?

A

anticoagulant

(atria not contracting, so blood may pool and coagulate in them- then leaving the heart and embolizing in the body)

160
Q

Which is more dangerous, embolic stroke or ischemic stroke?

A

embolic stroke

161
Q

Which two kinds of patients should always be on anticoagulation?

A
  • patients who have artificial heart valves
  • patients who have Valvular Atrial Fibrillation (atrial fibrillation and mitral stenosis)
162
Q

What is Valvular Atrial Fibrillation?

A

Atrial Fibrillation with mitral stenosis

163
Q

What is the CHA2DS2-VASc Score used for?

A

the most commonly utilized method to predict thromboembolic risk in atrial fibrillation

(stroke risk)

164
Q

stable coronary artery disease vs. acute coronary syndrome

which one has a demand and supply mismatch?

A

both!

but in stable coronary artery disease, the mismatch occurs slowly while in ACS it happens suddenly

165
Q

How do each of these plaque features affect vulnerability?

thickness of fibrous cap

lipid pool size

amount of inflammatory cells

A

fibrous cap= thinner the cap, more vulnerable to rupture

lipid pool size= bigger pool size, more vulnerable to rupture

more inflammatory cells, the more vulnerable to rupture

166
Q

How does mitral regurgitation affect supply/demand of the heart?

A

mitral regurgitation→ increase contractility→ increases the hearts demand for blood

167
Q

How does hypertension affect supply/demand of the heart?

A

hypertension → increasing systolic wall tension→ increases demand

168
Q

Which of the following are more sensitive at detecting ischemia?

a. imaging techniques
b. ECG
c. symptoms (ex/angina)

A

a. imaging techniques

(imaging techniques based on perfusion, metabolism or wall motion are more sensitive)

170
Q

How long does the angina have to last for it to be labeled as chronic?

A

2 months

171
Q

What’s the best evaluation method of stable CAD?

A

history!

“It is possible to make a confident diagnosis on the basis of history alone”

172
Q

Typical duration fo ischemic chest pain

A

1-5 minutes

173
Q

patient comes in with substernal chest pain (quality= heavy, duration=1-5min) that is provoked by exertion but NOT relieved by rest. diagnose.

A

atypical angina (2/3 of the three characteristics)

174
Q

calssify the severity of the angina:

patient has marked limitation when climbing one flight of stairs

A

class III

175
Q

What are the three characteristics of typical angina?

(if patient meets all three then definite angina)

A
  1. substernal chest pain (quality= heavy, duration=1-5min)
  2. provoked by exertion
  3. relieved by rest or nitroglycerin
178
Q

What two cardiovascular conditions mimic angina? why?

A

Aortic Stenosis + Hypertrophic Cardiomyopathy
both cause obstruction of flow to outside of the ventricle, causing non CAD angina

179
Q

How do you diagnose patients with stable CAD? What are some obstacles?

A

patients with stable CAD often have normal physical exams and ECG’s

That’s why we do functional tests- to provoke cardiac ischemia by stressing the patient.

We also have anatomical tests (ex/angiography) so we can see the arteries

180
Q

What’s the strongest predictor of long-term survival?

A

LVEF is the strongest predictor of long-term survival as LVEF declines, mortality increases

(Patient with an LVEF <50% is already at high risk for CV death)

181
Q

What patients are recommended for ECG exercise testing?

A
  1. Patients with an intermediate pretest probability of IHD (not a high probability- if high then we don’t need the test)
  2. No major ECG changes or LBBB
  3. Are able to exercise
182
Q

blood pressure changes before and after exercise

in normal patients VS in patients with ischemic heart

A

in normal patients= after exercise BP increase

ischemic heart= BP decreases because heart doesn’t have strength to contract and raise BP

183
Q

You suspect patient of having stable CAD. When do you use…

Coronary computed tomography angiography

VS.

Catheterization & Coronary Angiography

A

CT angiography= its less invasive, so its done for patients with low/intermediate likelihood of CAD- when you’re not certain

Catheter coronary angiography= more invasive and involves catheterization, do it when patient has high CAD risk or taking optimal medical therapy (OMT) fails

184
Q

Risk stratification (of CAD) is done by evaluating 4 factors. What are they? how are they tested?

A

1-Risk stratification by clinical evaluation.

2-Risk stratification by ventricular function. (echocardiogram)

3-Risk stratification by response to stress testing.

4-Risk stratification by coronary anatomy. (angiography)

185
Q

Patient has ECG abnormalities, which is a preferred test?

stress imaging OR exercise ECG test

A

stress imaging

St ress Imaging has advantages over conventional Exercise ECG Test because it can be done even if there are resting ECG abnormalities

(exercise ECG test is done if ECG is normal****)

186
Q

Four ways stress imaging is better than exercise ECG

A
  1. can be done even with ECG abnormalities
  2. can be used if patient can’t exercise
  3. better sensitivity and specificity
  4. can quantify and localise ischemia areas
187
Q

Patient does a Stress Radionuclide Imaging and most of the anterior heart tissue appears red. What does this mean?

A

heart muscle tissue with a good blood flow will emit more gamma rays than areas with a poor blood flow or damaged tissue. So his heart has a good blood supply.

188
Q

Stress Radionuclide Image. diagnose.

A

with rest all areas get O2= complete horseshoe

with stress= the apex isn’t getting enough blood

189
Q

How does Stress Echocardiography work?

A

areas of the heart are given numbers (divided into segments), and when patient is exercising we see how each segment moves. (bad movement means ishemia)

hypokinetic means not moving well

akinetic means not moving at all

190
Q

Which of the following relief of anginal symptoms by increasing blood supply? How?
• Beta-blockers
• Calcium antagonists
• Nitrates

A

• Nitrates

by decreasing systemic will tension

191
Q

How does each of the following relief angina symptoms?
• Beta-blockers
• Calcium antagonists

A

they both decrease demand of blood by increasing heart rate and contractility

192
Q

first step to treating chronic angina? What happens if patient is resistant?

A

give OMT (optimal medical therapy)

if resistant, revascularize by PCI or CABG

193
Q

can revascularization therapy be used as first line treatment of CAD? if yes, when?

A

As first-line treatment in patients with :

Left main coronary artery disease (50% stenosis or more ).

Multivessel disease with severe or extensive ischemia.

Left ventricular dysfunction with EF of 35–50

194
Q

Coronary artery bypass surgery uses which two vessels to bypass the blockage?

A

internal mammary artery

saphenous vein

195
Q

Why do people suffer silent ischemia?

A

higher pain threshold

silent episodes reflect less severe ischmia

defect in pain preception

196
Q

How should silent ischemia be managed?

A

managed as angina

197
Q

T/F: Silent ischemia reflects less severe ischemia.

A

true

198
Q

T/F: pulmonary congestion starts as soon as the left atrium gets extra blood from the ventricle (due do regurgitation from mitral valve, causing increase in LA pressure)

A

false, LA adapts to the larger volume by dilating, which increases its compliance. This remodeling helps to limit the increases in LA pressure initially- but after a while it can’t keep up and pulmonary congestion occurs.

199
Q

How is the annulus affected by Chronic Renal Failure?

A

It undergos Calcification

200
Q

What 3 conditions cause Chordae Tendineae rupture?

A

Rheumatic Fever, Trauma, infective endocarditis

201
Q

Papillary muscle dysfunction is cause by (2)

A

Ischemia, LV dilatation

202
Q

How can mitral regurgitation lead to heart failure?

A

mitral regurgitation→blood leaks from LV to RV→RV has higher pressure→RV dilates to compensate→LV volume overload→ hyperdynamic LV→progressive LV dilation→ to heart failure

203
Q

Describe the left atrial pressure and ejection fraction during acute mitral regurgitation.

A

left atrial pressure= increases because the regurgitated blood causes an increase in volume; since its acute, the right atrium has no time to dilate (to compensate)

ejection fraction= it increases due to the increase in total stroke volume. The regurgitated blood causes an increase in preload, leading to a hyperdynamic state->SV increase

205
Q

Describe the left atrial pressure and ejection fraction during chronic compensated mitral regurgitation.

A

left atrial pressure= it’s slightly elevated. The left atria had time to dilate and accommodate the regurgitated blood, leading to a decrease in pressure (LAP is less than LAP in acute regurg.)

ejection fraction= high because the heart is pumping harder to provide adequate blood to body-> high total stroke volume -> high EF

206
Q

Describe the left atrial pressure and ejection fraction during chronic decompensated mitral regurgitation.

A

left atrial pressure= high because the atria dilated to it’s max

ejection fraction= low because the ventricle is dilated further due to the high pressure and now has a weak pump

207
Q

How can you determine the cause/severity of mitral regurgitation?

A

Echocardiogram

209
Q

Patient with mitral regurgitation has a severe infection and is symptomatic. What are the 2 surgical options? explain them.

A

Valve repair= artificial annulus (stop dilation) + stitch leaflets to repair them (this is the preferred surgery)

Valve replacement= remove old and put a new artificial valve

212
Q

Why is the blood velocity increased in mitral stenosis? What does it look like in echo?

A

due to stenosis, the blood gradient has to be high between atria and ventricle for the blood to pass through the stenotic valve. higher gradient means increased velocity, and that also means turbulent flow. this has a mosaic appearance in echo.

213
Q

When do you Surgically treat the heart valves?

A

when patient is Symptomatic and if the valve infection Severe

(2 conditions)

214
Q

describe ECG of mitral stenosis

A

The ECG in mitral stenosis is often normal early in disease. The most common finding is left atrial enlargement (p-mitrale)(however this finding disappears if the patient enters atrial fibrillation**) Right heart strain may produce findings of right axis deviation (and right ventricular hypertrophy)

**=valve stenosis is linked to a higher risk for atrial fibrillation

215
Q

Patient comes in with mitral regurgitation + symptoms. What is the pharmaceutical treatment?

A

Diuretics, ACE-I, warfarin (AF)

217
Q

Most mitral stenosis cases are due to

A

Rheumatic fever (99%)

218
Q

Normal mitral valve orfice area

A

5cm squared

(has to get to 2 to produce symptoms; if 1cm or smaller then its severe mitral stenosis)

220
Q

Mitral stenosis VS regurgitation

which heart chamber gets dilated in each?

A

Mitral stenosis= only L atria

Mitral regurgitation= both LV and LA

222
Q

Patient has AF as a complication of mitral stenosis. how do we treat?

A

warfarin, control heart rate

223
Q

Patient has pulmonary hypertension due to mitral stenosis. How so we treat?

A

by relieving the obstruction

via Trans-septal balloon valvotomy

OR

Mitral valve replacement

224
Q

How does aortic stenosis affect exercise?

A

The valve obstruction does not allow CO to increase during exercise

225
Q

Complications of aortic stenosis

A

stenosis causes left ventricular hypertophy→thick wall more susceptible to ischemia→ arrythmias→ heart failure

226
Q

Agre related calcific degeneration of aortic valve is more common in

A

developed countries

227
Q

Risk factors for the development of calcific Aortic stenosis

A

similar to those for vascular atherosclerosis:
elevated LDL cholesterol, diabetes , smoking, hypertension

228
Q

T/F: Calcific aortic stenosis increases risk of cardiovascular death only due to valve obstruction

A

False, Calcific aortic stenosis has a 50 % increased risk of
cardiovascular death and myocardial infarction even in the absence of valve obstruction

229
Q

T/F: Transcatheter Aortic-Valve Implantation (TAVI) is an invasive operation used to implant a new, synthetic aortic valve

A

false, it’s non-invasive (done by catheter)

230
Q

T/F: Bicuspid aortic valve disease is mostly discovered in childhood or adolescence

A

false, Usually functions normally in childhood. the abnormal structure causes stress which leads to calcifications later on (40’s+)

231
Q

T/F: Bicuspid aortic valve disease is more common in men

A

true 4:1 ratio

232
Q

Vascular complications of bicuspid aortic stenosis

A

Medial degeneration (damages connective tissue and results in the breakdown or destruction)

Aortic aneurysm

Aortic Dissection (rare)

233
Q

Patient has Aortic stenosis, aortic regurgitation, and mitral valve problems. What’s a likely diagnosis?

A

Rheumatic valve disease (can involve all left heart)

(If mitral stenosis alone—> mitral valve disease)

234
Q

What’s the best indicator of aortic stenosis prognosis?

A

the symptoms are the best indicator

no symptoms= good prognosis

symptoms=dismal prognosis

235
Q

symptoms of aortic stenosis. explain them

A
  1. chest pain
    • no blood in aorta, no blood in coronary arteries
  2. syncope
    • no blood reaching brain
  3. dyspnea
    • indicates heart failure= the worst symptom
236
Q

How can we determine the severity of the aortic stenosis?

A

mean pressure gradient

the higher it is, the more severe the stenosis

238
Q

pharma treatment of aortic regurgitation

A

Marfan syndrome: beta-blockers (may slow aortic root dilatation)

Hypertension, LV dysfunction when surgery is contraindicated or LV dysfunction persists: ACE, ARB

239
Q

medical treatment for severe symptomatic aortic stenosis

A

no medical treatment, just replace the valve via”

Transcatheter Aortic-Valve Implantation (TAVI)

240
Q

Management of severe asymptomatic aortic stenosis

A

adjust lifestyle (no vigorous physical activity)

observe clinically and by echo

prophylaxis for rheumatic fever (penicillin) and infective endocarditis (good hygine)

241
Q

What are factors that cause aortic regurgitation by affecting the wall of the aortic root?

A
  1. age-related (degenerative) aortic dilation
  2. cystic medial necrosis of the aorta (Marfan’s)***
  3. Syphilitic aortitis
  4. Ankylosing spondylitis

*** cystic medial necrosis= accumulation of basophilic ground substance in the media with cyst-like lesions

242
Q

What structural changes occur due to aortic regurgitation?

A

for Cardiac Output to be maintained, total volume pumped into aorta must increase, leading to LV dilatation

243
Q

aortic stenosis→ ? ventricular changes

aortic regurgitation→ ? ventricular changes

A

aortic stenosis→ hypertrophy

aortic regurgitation→ dilation

244
Q

When do the murmurs occur in each of the following condition?

Mitral regurgitation

Mitral stenosis

aortic regurgitation

aortic stenosis

A

Mitral regurgitation and aortic stenosis—> systolic murmurs

Mitral stenosis and aortic regurgitation—> diastolic murmurs

245
Q

carotid pulsations in

aortic regurgitation VS aortic stenosis

A

aortic regurgitation= prominent carotid pulsations

aortic stenosis= low/little carotid pulsations

246
Q

When do we surgically treat aortic regurgitation?

A

Symptomatic + severe —> surgery

Either repair or replacement but mostly replacement.

247
Q

What is a hibernating myocardium?

A

metabolically inactive myocardium (not dead, so if you improve the circulation to it, it gets activated)

248
Q

When is Implantable cardioverter-defibrillator (ICD) used?

A

used to prevent ventricular arrhythmia (the most common cause of sudden death). So we give them to patients with a reduced ejection fraction (below 35%) because we want to reduce the chance of sudden cardiac death.

(the device senses ventricular arrhythmia and sends a shock to the heart)

249
Q

When is cardiac resynchronization therapy (CRT) used?

A

For patient with electrical dissociation (ex/ right or left bundle branch block). So when the ventricles aren’t contracting at the same time, the CO and ejection fraction decreased.

This therapy makes the heart a new conduction system via wires. This is only used when conventional therapy fails and the ejection fraction is less than 25% or QRS complex is wide.

Cardiovascular System - 3rd year (23 decks)

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