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Cardiovascular > Cardio Flashcards 2 > Flashcards

Cardio Flashcards 2

1
Q

What is shock?

A

Clinical syndrome resulting from inadequate tissue perfusion and oxygen delivery to meet metabolic demands.

Results in global tissue hypoperfusion and metabolic acidosis

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2
Q

What occurs in cells in response to decreased systemic oxygen delivery?

A

Switch to anaerobic metabolism, causing systematic acidosis

ATP depletion causes ion pump dysfunction

Cellular edema and hydrolysis of cellular membranes occurs, resulting in cell death

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3
Q

What is the goal of the body in shock?

A

Maintain cerebral and cardiac perfusion

Vasoconstriction of splanchnic, musculoskeletal and renal blood flow

Can cause mulit-organ failure and death if the underlying abnormalities are not corrected

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4
Q

What is the ultimate outcome of shock, if underlying abnormalities are not corrected?

A

Multiorgan failure and death - caused by systemic metabolic lacti acidosis that overcomes the body’s compensatory mechanisms

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5
Q

What are useful hemodynamic parameters in shock?

A

Systemic vascular resistance

Cardiac output

Mixed venous oxygen saturation

Pulmonary capillary wedge pressure

central venous pressure

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6
Q

What is SVR?

A

Systemic vascular resistance

reflects degree of vasoconstriction/vasodilation in peripheral vasculature

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7
Q

What is CO?

A

Cardiac output

HR*Stroke volume

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8
Q

What is SvO2?

A

Mixed venous oxygen saturation

Saturation of systemic venous blood after delivering oxygen to peripheral tissues

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9
Q

What is PCWP?

A

Pulmonary capillary wedge pressure

surrogate for left arterial pressure

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10
Q

What is CVP?

A

Central venous pressure

surrogate for right atrial pressure

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11
Q

What hemodynamic measurement is a surrogate for left atrial pressure?

A

pulmonary capillary wedge pressure

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12
Q

Which hemodynamic measurement is a surrogate for right atrial pressure?

A

Central venous pressure

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13
Q

What is the normal value of right atrial pressure/central venous pressure?

A

0-6 mmHg

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14
Q

What is the normal value for systolic pulmonary artery pressure?

A

15-30 mmHg

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15
Q

What is the normal value for End-diastolic pulmonary artery pressure?

A

4-12 mmHg

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16
Q

What is the normal value for mean pulmonary artery pressure?

A

9-19 mmHg

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17
Q

What is the normal value for mean pulmonary capillary wedge pressure (PCWP)

A

i.e. left atrial pressure

4-12 mmHg

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18
Q

What is the normal value for cardiac output?

A

4-8 L/min

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19
Q

What is the normal value for mixed venous oxygen saturation (SvO2)?

A

>70%

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20
Q

What is the normal value for systemic vascular resistance?

A

800-1200 dynes*sec/cm^5

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21
Q

How is mean arterial pressure calculated?

A

MAP = CO x SVR

Recall, CO = HR * SV

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22
Q

What defines hypovolemic shock?

A

Heart pumps well, but not enough blood volume to pump

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23
Q

What causes hypovolemic shock?

A

decreased intravascular volume (preload) - causes decreased stroke volume

Hemorrhagic (trauma, GI bleed, AAA rupture)

Hypovolemic - burns, GI losses, dehydration, third spacing, diabetic ketoacidosis

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24
Q

What is another name for distributive shock?

A

Vasodilatory shock

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25
Q

What is distributive (or vasodilatory) shock?

A

Heart pumps well, but there is peripheral vasodilation due to loss of vessel tone

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26
Q

What caues distributive (vasodilatory) shock?

A

Loss of vessel tone

Can be caused by overwhelming inflammation (sepsis, toxic shock syndrome, anaphylaxis)

Can be caused by C-spine or thoracic cord injuries - decreased sympathetic tone

Toxins - cellular poisons (Carbon monoxide, methemoglobinema, cyanide)

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27
Q

What is cardiogenic shock?

A

Heart fails to pump blood out

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28
Q

What are causes of cardiogenic shock?

A

Decreased contractility (MI, myocarditis, cardiomyopathy)

Mechanical dysfunction (papillary muscle rupture post MI, severe aortic stenosis, rupture of ventricular aneurysms)

Arrhythmia (heart block, ventricular achycardia, supraventricular tachycardia, atrial fibrillation, etc.)

Caridotoxicity (β-blocker or CCB overdose)

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29
Q

Fill in the table:

A
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30
Q

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31
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32
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33
Q

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34
Q

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35
Q

Fill in the table:

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36
Q

What are the stages of shock?

A

Insult

Preshock

Shock

End organ dysfunction

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37
Q

What occurs during the insult stage of shock?

A

Splenic rupture, blood loss, MI, anaphylaxis, etc.

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38
Q

What occurs during the preshock stage of shock?

A

Hemostatic compensation to maintain MAP within normal ranges

(After insult)

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39
Q

What occurs during the shock stage of shock?

A

After preshock stage

Compensatory mechanisms fail and MAP declines

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40
Q

What occurs during the end-organ dysfunction stage of shock?

A

Occurs after shock stage

Cell death and organ failure

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41
Q

What is the definition of cardiogenic shock?

A

Systemic hypoperfusion secondary to severe depression of cardiac output and sustained systolic arterial hypotension despite elevating filling pressures

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42
Q

What are the three main keys to categorize someone as having cardiogenic shock?

A

Severe depression of cardiac output

Sustained arterial hypotension

Elevated filling pressures

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43
Q

How do patients with cardiogenic shock present?

A

Hypotension

Tachycardia/tachypnea

Elevated neck veins

Rales, gallop rhythm (S3)

New murmur

Cool extremities

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44
Q

Will patients in cardiogenic shock present with cool or warm extremities?

A

Cool extremities - physiological response to maintain perfusion to vital organs

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45
Q

What is the goal of medical treatment of shock?

A

Try to maintain mean arterial pressure

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46
Q

What agents are useful in the treatment of shock?

A

Dopamine - α1, β1, β2 and DA agonist

Dobutamine- α1, β1, β2 agonist

Norepinephrine - α1, β1, β2 agonist

Epinephrine - α1, β1, β2 agonist

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47
Q

How does dopamine help patients in shock?

A

Stimulates D1 receptors (coronary, renal, mesenteric and cerebral beds)

Promotes vasodilation and increased flow

Also direct precursor to norepinephrine

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48
Q

How does dobutamine help patients in shock?

A

Vascular smooth muscle binding results in β1 adrenergic agonism/antagonism and β2 stimulation with net vasodilation (low doses)

Tolerance can develop though

(not the best agent)

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49
Q

How does norepinephrine help patients in shock?

A

increases systolic, diastolic, and pulse pressure wtih minimal impact on cardiac output

Coronary flow is increased owing to elevated diastolic blood pressure and indirect stimulation of cardiomyocytes - release vasodilators

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50
Q

What are downfalls of adrenergic inotropes in shock patients?

A

Can further increase heart rate, afterload, and wall tension

Further exacerbating the problem

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51
Q

What non-pharmacologic treatmetns are available to treat shock?

A

Left ventricular assist devices (LVAD), which unload the heart, boost coronary and systemic flow, and promotes myocardial and end-organ recovery

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52
Q

What is an intra-aortic balloon pump (IABP)?

A

Inflates in diastole, deflates in systole

Displaces blood that is upstream towards the heart, increasing diastolic pressure

When deflated - draws blood volume downstream, reducing end-diastolic pressure and left ventricular afterload (creates suction)

Can also decrease LV volume, systolic work and myocardial oxygen consumption

Reduces end-diastolic and peak diastolic aortic pressure

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53
Q

What are the hemodynamic effects of IABP (intraaortic balloon pump)?

A

Reduce systolic pressure

Increase diastolic pressure

Reduces heart rate

Decreases pulmonary wedge pressure (LA pressure

Elevate cardiac output

Decrease LV wall stress

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54
Q

What is the most common cause of cardiogenic shock?

A

Acute MI

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55
Q

What two broad categories of pharmacologic treatment is available for the treatment of shock?

A

Vasopressors and inotropic agents

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56
Q

What are the two aortic valve diseases?

A

Stenois

Insufficiency

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57
Q

What is the normal aortic valve area?

A

3-4 cm^2

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58
Q

When do aortic valve stenosis symptoms start presenting?

A

Shen stenosis makes valve area 1/4 of normal area

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59
Q

What defines aortic stenosis and severe aortic stenosis?

A

When area becomes less than 2 cm^2 ( less than 1 cm^2 for severe)

Normal is 3-4 cm^2

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60
Q

What are three types of aortic stenosis?

A

Supravalvular - in ascending aorta

Subvalvular - from hypertrophic caridiomyopathy, for instance

Valvular

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61
Q

What are etiologies of aortic stenosis?

A

Congenital - leaflet cusps are deformed - can be unicuspid or bicuspid valve; or a fused tricuspid valve

Acquired - degenerative, rehumatic, or other

Congenital will present earlier than acquired or degenerative

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62
Q

What type of aortic stenosis do patients under 70 usually present with?

A

Congenital

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63
Q

What type of aortic stenosis do patients over 70 yo usually present with?

A

Acquired

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64
Q

What is the most common etiology of aortic stenosis that will be seen in the next 10-20 years?

A

Degenerative calcification - seen in patients in their 70s-80s, comorbid with risk factors for CAD

(because of aging population)

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65
Q

What is the effect of aortic stenosis on the left ventricle?

A

Imposes increased afterload

Causes concentric hypertrophy

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66
Q

What type of hypertrophy is seen in aortic stenosis?

A

Concentric left ventricular hypertrophy

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67
Q

What symptoms do you see in aortic stenosis?

A

Decreased outflow - dizziness, etc

Left heart failure symptoms - elevated left atrium pressures - backup to lungs - shortness of breath

Angina - increased work load of left ventricle

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68
Q

What type of murmur is heard in aortic stenosis?

A

Systolic crescendo/decrescendo - diamond shape

Ejection systolic murmur

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69
Q

What can happen to the second heart sound in aortic stenosis?

A

Can run into pulmonic valve sound - can even run past it and become paradoxical split

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70
Q

What occurs during paradoxical S2 splitting?

A

Occurs in Aortic Stenosis

Upon inspiration - split decreases. Upon exhalation, split increases

Normally - aortic first, pulmonary second; split on inspiration

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71
Q

What changes in the heart sounds do you see with aortic stenosis?

A

Systolic ejection murmur (crescendo decrescendo)

S2 sound changes - A2 delays - may even occur after P2 (reversal of splitting/timing)

More noticable upon expiration

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72
Q

What is the difference between the systolic murmur seen in aortic stenosis and in obstructive hypertrophic cardiomyopathy?

A

Aortic stenosis - there is a delay between S1 and murmur - also crescendo, decrescendo

HCM - starts at S1 and is relatively constant throughout

AS:

HCM:

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73
Q

How do you reduce the hypertrophic cardiomyopathy murmur sounds?

A

Squat

Opens up LV outflow

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74
Q

How do you increase the murmur from a hypertrophic cardiomyopathy?

A

Stand up from squating position

Valsalva maneuver to reduce size of LV

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75
Q

How do you exacerbate murmur seen in aortic stenosis?

A

Make patient run around and then you can hear it better - but does not help to differentiate from HCM

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76
Q

How do patients with aortic stenosis usually present?

A

Asymptomatic - onset of symptoms is a poor prognostic indicator

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77
Q

How good of a prognostic indicator is symptom onset in aortic stenosis?

A

Poor

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78
Q

What are the classical symptoms of severe aortic stenosis?

A

Dyspnea on exertion
Syncope - low forward cardiac output
Angina

Sudden death

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79
Q

What is DOE?

A

Dypsnea on exertion

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80
Q

What are physical findings of aortic stenosis?

A

Slow rising carotid pulse (pulsus tardus) and decreased pulse amplitude (pulsus parvus)

Soft and split second heart sound, S4 gallop

Systolic ejection murmur (crescendo-decrescendo

Other manifestations - bleeding, embolic events, CAD)

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81
Q

What are pulse findings in aortic stenosis?

A

Slow rising carotid pulse (pulsus tardus)

Decreased pulse amplitude (pulsus parvus)

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82
Q

What are heart sound findings in aortic stenosis?

A

Soft and split second heart sound and reverse split

S4 gallop due to left ventricular hypertrophy

Systolic ejection murmur - diamond shaped crescendo-decrescendo (peaks later as severity of stenosis increases)

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83
Q

What is pulsus tardus?

A

Slwo rising carotid pulse

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84
Q

What is pulsus parvus?

A

Decreased pulse amplitud

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85
Q

What is characteristic of the natural history of aortic stenosis after developing symptoms?

A

Sudden deaths soon after devleopment of symptoms if no valve replacement

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86
Q

What EKG findings do you see on AS?

A

Left axis deviation from hypertrophy

Conduction blocks from calcification

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87
Q

What can you see on chest x-ray in aortic stenosis?

A

Calcification

Other non-specific findings (hypertrophy)

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88
Q

What is the most specific diagnostic tool for diagnosing valvular heart disease?

A

Echocardiogram

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89
Q

Why must you perform cardiac catheterization on aortic stenosis patients?

A

Must ensure there is no coronary artery disease before undergoing surgery for valvular repair

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90
Q

What defines mild aortic stenosis?

A

Valve area > 1.5 cm^2

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91
Q

What defines moderate aortic stenosis?

A

Valve area 1-1.5 cm^2

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92
Q

What defines severe aortic stenosis?

A

Valve area < 1 cm^2

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93
Q

How do you manage patients with aortic stenosis?

A

Antibiotic prophylaxis in dental procedures or with prostetic valves or with patients with history of endocarditis

Few mediations - don’t want to give vasodilators because you’ll increase chances of syncope

Aortic valve replacement is definitive treatment

Aortic balloon valvotomy as a bridge to surgery

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94
Q

Why does aortic balloon valvotomy not work for aortic stenosis?

A

Too much calcium - can reclose or spread to brain

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95
Q

What are indications for surgery in aortic stenosis?

A

Any symptomatic patient with severe aortic stenosis

Any patient with decreasing ejection fraction

Any patient already undergoing CABG with moderate or severe stenosis

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96
Q

What is the only situation in which patients with moderate aortic stenosis are indicated for replacement surgery?

A

When they are already undergoing CABG

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97
Q

What is aortic regurgitation?

A

Leakage of blood back into the LV during diastole

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98
Q

What causes aortic regurgitation?

A

Ineffective coaptation of the aortic cusps

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99
Q

What is the pathophysiological result of aortic regurgitation?

A

Combined pressure and volume overload

Causes compensatory LV dilatation and hypertrophy

Progressive dilation leads to heart failure

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100
Q

What can cause acute aortic regurgitation?

A

Endocarditis - leaflet perforation or rupture from infection

Aortic dissection - can split aortic wall and continue through to the valve

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101
Q

What are avenues for treatment for patients with acute aortic regurgitation?

A

True surgical emergency

Medicines as a bridge to surgery:

Give positive ionotrope (dopamine, dobutamine)

Give vasodilators (nitroprusside)

Avoid beta blockers

NO balloon pumps

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102
Q

How do vasodilators help in the short-term treatment of aortic regurgitation?

A

Keeps blood in periphery and reduces amount of blood that flows back into heart

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103
Q

What are balloon pumps contraindicated in aortic regurgitation/aortic insufficiency?

A

Will only make it worse - make more blood flow backwards

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104
Q

What can cause chronic aortic regurgitation?

A

Bicuspid aortic valve (normally tricuspid)

Rheumatic

Infective endocarditis

Marfans

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105
Q

What type of murmur will you see in aortic regurgitation?

A

Early, low pitched diastolic murmur

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106
Q

What is the most common diastolic murmur?

A

Aortic regurgitation murmur

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107
Q

What changes in heart sounds will you see in aortic regurgitation?

A

Functional stenosis of aortic valve too - small crescendo-decrescendo systolic murmur

More importantly, low-pitched early diastolic murmur

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108
Q

What are differences in heart sounds between acute and chronic aortic regurgitation murmurs?

A

In acute - the diastolic murmur is very quick and faint - difficult to pick up

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109
Q

What are cliical features of aortic regurgitation?

A

Asymptomatic until 30s-40s

Progressive symptoms:

Dyspnea - exertional, orthopnea, PND

Angina

Palpitations - increased contractile force

No syncope

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110
Q

What clinical features of aortic stenosis are absent in aortic regurgitation?

A

Syncope - instead feel palpitations

Issue is increased volume!

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111
Q

What physical findings do oyu see in patients with aortic regurgitaiton?

A

Wide pulse pressure -very sensitive

Hyperdynamic and displaced apical impulse - can see chest wall excursion and feel it

Diastolic blowing murmur

Austin flint murmur - at apex - regurgitant jet impinges on anterior mitral valve leaflet causing vibration (resembles mitral valve murmur)

Systolic ejection murmur - increased flow across aortic valve

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112
Q

What is an Austin flint murmur?

A

Regurgitant jet impinges on anterior mitral valve leaflet causing vibration (resembles mitral valve murmur)

Heard best at apex

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113
Q

What pulse changes do you see in patients with aortic regurgitation?

A

Wide pulse pressure - very sensitive finding

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114
Q

When do you see Austin flint murmurs?

A

In aortic regurgitation

Regurgitant jet impinges on anterior mitral valve leaflet causing vibration (resembles mitral valve murmur)

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115
Q

What is Corrigan’s sign?

A

In aortic regurgitation - dancing carotids

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116
Q

What is Quincke’s pulse?

A

Exaggerated redennign and blanching of nail beds -pulsatile

seen in Aortic regurgitation

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117
Q

What is the main feature of aortic regurgitation that you can see signs of in almost all organs?

A

Hyperdynamism of the cardiac system - nail beds, chest excursion, etc

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118
Q

What do you see on chest x-ray in patients wtih aortic regurgitation?

A

Enlarged cardiac silhouette

Aortic root enlargement

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119
Q

What do you see on echocardiogram in patients with aortic regurgitation?

A

AV and aortic root measurements

LV dimensions and funciton

Can see flow-back via doppler

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120
Q

What do you do to manage aortic regurgitation in patients?

A

Prophylaxis for infectious endocarditis in dental procedures

Vasodilators (ACE inhibitors), Nifedipine improve stroke volume and reduce regurgitation (only if patient is symptomatic or hypertensive)

Surgical treatment is definitive

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121
Q

When do you perform surgery on patients with aortic regurgitation?

A

When there are any symptoms at rest or with exercise

Or in patients who are asymptomatic and whose ejection fraction drops below 50% or LV becomes dilated

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122
Q

What pharmacologic treatments are given to patients with aortic regurgitation?

A

Vasodilators (ACE inhbitors), Nifedipine to improve stroke volume

Only if patient is symptomatic or hypertensive

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123
Q

What is infectious endocarditis?

A

Infection of endocardial surface

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124
Q

What are the four classification groups of infective endocarditis?

A

Native valve endocarditis

Prosthetic valve endocarditis

IV druge abuse endocarditis

Nosocomial endocarditis

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125
Q

What are charactaristics of acute infectious endocarditis?

A

Fulminant - rapidly destructive

Affects normal heart valves

Metastatic foci

Commonly Staph

Usually fatal within 6 weeks if untreated

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126
Q

What are characteristics of subacute infectious endocarditis?

A

Often affects damaged heart valves

Indolent in nature - slower

Fatal if untreated, usually by one year

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127
Q

What is the common cause of acute infectious endocarditis?

A

Staph - staph aureus or coagulase negative

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128
Q

What type of endocarditis is caused by staphylococci?

A

Acute

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129
Q

What organisms are commonly implicated in subacute infectious endocarditis?

A

Streptococci species

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130
Q

What kind of endocarditis is seen with stretpococcal infections?

A

Subacute (viridans, enterococci, bovis, others)

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131
Q

What is IE?

A

Infectious endocarditis

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132
Q

What is the pathogenesis of IE?

A

Turbulent blood flow leads to the development of thrombus at site of injury

Bacteria that enters the circulation can adhere and colonize the injured surface

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133
Q

What is the most common non-bacterial thrombotic endocarditis seen?

A

In SLE - generalized state of inflammation

Libman-Sacks Endocarditis

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134
Q

What are cardiac lesions that predispose to endocarditis?

A

Rheumatic valvular disease

Acquired valvular lesions (left sided more common - higher shear stress)

Hypertrophic obstructive cardiomyopathy

Congenital heart disease

Surgically implantable intravascular hardware

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135
Q

Which side of the heart are lesions that predispose to endocarditis more commonly seen? Why? What is the exception?

A

On the left side - higher flow rates - more shear stress

On the right side in IV drug use

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136
Q

What are symptoms of acute IE?

A

High grade fever, chills

Shortness of breath

Arthralgias/myalgias

Abdominal pain (emboli)

Pleuritic chest pain (emboli)

Back pain (emboli)

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137
Q

What are symptoms of subacute IE?

A

Low-grade fever (indolent course)

Anorexia

Weight loss

Fatigue

Arthralgias/myalgias

Abdominal pain

N/V

(many non-specific symptoms)

Can be over days to weeks to months

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138
Q

What are signs of IE?

A

Fever

Clubbing - not specific

Splenomegaly

Neurological manifestations

Heart murmur - NEW

Peripheral manifestations - Osler’s nodes, Subungal hemorrhage, Janeway lesions, Roth Spots, petechiae

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139
Q

Why do you see splenomegaly in IE?

A

Attempting to clear the infection

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140
Q

What types of murmurs are seen in IE?

A

NEW murmurs

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141
Q

What are cardiac manifestations of IE?

A

New murmurs - regurgitations

CHF - valvular damage, myocarditis, intracardiac fistulas

Perivalvular abscesses

Fistula

Pericarditis

Heart block

essentially, all sorts of things

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142
Q

What are non-cardiac signs of IE?

A

Septic embolization - petechial hemorrhage, Janeway lesions, Oslers nodes

Infarcts in skin, spleen, kidney, meninges, skeletal system

Embolic strokes

Mycotic aneurysms - infetion of vasa vasorium of the blood vessel

Brain microabscesses

Glomerulonephritis

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143
Q

WHereaWhere can you see petechia from IE?

A

Skin, conjuntiva, palate

Mucous membranes and extremities

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144
Q

What are splinter hemorrhages?

A

Non-specific, nonblanching, linear reddish-brown lesions found under nail bed

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145
Q

What are Osler’s Nodes?

A

Extremely painful nodes in fingers

More specific for IE and more common in subacute

Erythematous

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146
Q

What are Janeway lesions?

A

Specific, erythematous, blanching macules that are not painful

On palms and soles

Seen in IE

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147
Q

What are Roth spots?

A

Seen on fundoscopic examination

Indicative of IE

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148
Q

What labs are helpful in identifying IE?

A

CBC showing anemia, leukocytosis

Blood cultures - from 3 different sites at least 1 hour apart

Evidence of brucella, bartonella, legionella, c. burnetti

Signs of inflammation:
Elevated ESR, CRP

Reduction of serum complement

Elevated Rheumatoid factor

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149
Q

What do you see in chest x-ray in IE?

A

Try to find clear lung fields to rule out pulmonary infections

May see multiple focal infiltrates and calcification

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150
Q

What can you see on EKG in IE?

A

May see ischemia or arrhythmias, or heart blocks

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151
Q

What can you see on echocardiography in IE?

A

Can see vegetations

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152
Q

What are major criteria for diagnosis of endocarditis?

A

Persistently positive blood culture for typical organisms

Vegetations, dehiscence, abscesses on echocardiogram

New valvular regurgitation murmur

Coxiella burnetii infection

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153
Q

What are indications of definite endocarditis?

A

2 major clinical criteria

1 major and any 3 minor

5 minor critera

Histology findings

+ Gram stain or cultures from surgery or autopsy

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154
Q

What are minor critera for the diagnosis of endocarditis?

A

Predisposing heart condition or IV drug use

Fever

Emboli to organs/brain, hemorrhages

Glomerulonephritis, Osler’s nodes, Roth spots, Rheumatoid factor

Positive blood cultures that don’t meet specific criteria

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155
Q

When do you treat a patient for infectious endocarditis?

A

Wait until blood samples come back from microbiology before treating with antibiotics - don’t want to conflate results

You can wait 24 hours

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156
Q

How do you treat IE?

A

4-6 weeks of IV parenteral antibiotics

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157
Q

When might surgery benefit a patient with IE?

A

If they are in congestive heart failure

If there is a prosthetic valve endocarditis

If it is caused by fungal or other highly-resistant organisms

If there are perivalvular infections with abscesses or fistula formations

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158
Q

When is prophylaxis indicated for IE?

A

Patients have:

Prosthetic heart valves

Prior history of IE

Unrepaired cyanotic congenital heart disease (shunts and gradients and non-laminar flow)

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159
Q

When do you give prophylaxis for IE?

A

To protect in the time frame during which bacteremia will happen - i.e. right before, through, and after a dental procedure

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160
Q

What procedures warrant prophylaxis for endocarditis?

A

Dental procedures

If there is evidence of infection during:

Upper respiratory tract procedures

GU or GI procedures

Procedures of skin, or MSK

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161
Q

If there is a gradient between the left atrium and left ventricle during diastole, which valve is affected?

A

Mitral

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162
Q

What type of murmur will be present in mitral valve issues?

A

Diastolic

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163
Q

What happens to S1 in mitral stenosis?

A

Fast mitral valve closure - S1 is loud

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164
Q

What happens to S2 in mitral stenosis?

A

Loud becuase of pulmonary hypertension

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165
Q

During which cardiac phase will you see a murmur in mitral regurgitation?

A

Systole - it is holosystolic (pansystolic)

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166
Q

What type of murmur do you see during mitral regurgitation?

A

Holosystolic (pansystolic)

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167
Q

Do you see a diastolic murmur in mitral regurgitation?

A

Yes - lots of blood that entered the atrium is trying to now enter the ventricle

Flow murmur (relative mitral stenosis, for the amount of blood that is flowing through)

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168
Q

Durign what stage of the cardiac cycle do we see murmurs during mitral valve prolapse?

A

Systole

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169
Q

What maneuvers can you perform to help diagnose mitral valve prolapse?

A

Delay the click - make the patient squat - this makes the venous return increase. SVR increases. LV dilates a bit and tightens. Valve has lesser tendency to prolapse and it takes longer in systole for it to prolapse

Accelerate the click - standing will bring it back

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170
Q

How do the murmurs of aortic stenosis and hypertrophic cardiomyopathy differ with valsalva/squatting?

A
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171
Q

Do dihydropyridines have more of a vasodilating or cardiac depressan effect?

A

Vasodilating

Decrease myocardial oxygen demand (venodilation and arterial dilation)

These are CCBs

172
Q

How do dihydropyridines work?

A

Vasodilate more than cardiac depressant

Decreased myocardial O2 demand by venodilating and dilating arteries

173
Q

how do nondihydropyridines work?

A

Cardiac depressants more than vasodilating

Reduce HR, contractility to lower O2 demand

Careful with β-blockers

174
Q

Do nondihydropyridines have more of a vasodilating or cardiac depressant effect?

A

Cardiac depressant

Reduce HR, contractility

(Calcium channel blocker)

175
Q

What is the effect of ranolazine on stable CAD?

A

Decreases anginal frequency

Improves exercise tolerane

Unclear how

176
Q

What drug can be given to CAD patients to decrease anginal frequency and improve exercise tolerance?

A

Ranolazine

177
Q

What is a benefit of a drug-eluting stent?

A

Reduces risk for restenosis and subsequent revascularization

May result in higher thrombotic risk

178
Q

What is a potential risk in drug-eluting stents?

A

Higher thrombotic risk

179
Q

What are indications for percutaneous coronary intervention?

A

Refractory symptoms despite optimizing medical therapy

Intolerance to medical hterapy

Always attempt medical therapy first!!

180
Q

What is a benefit from arterial vs venous grafts for coronary revascularization?

A

Higher patency at 10 years, but used for most critical epicardial stenoses

typically use saphenous veins from leg

181
Q

What is PCI?

A

Percutaneous coronary intervention (i.e. stent)

182
Q

What is CABG?

A

Coronary artery bypass graft

183
Q

What are advantages of PCI vs CABG?

A

Lower procedural risk

Minimal recuperation (more and more done on outpatient basis)

184
Q

What are advantages of CABG vs PCI?

A

Complete revascularization

No need for long term dual antiplatelet therapy (causing bleeding risk)

Has a proven mortality benefit

185
Q

What is antithrombin?

A

Plasma protein that inactivates thrombin (Factor IIa)

Heparan increases its efficacy 1000 fold

186
Q

What is the effect of heparan on antithrombin?

A

Increases efficacy 1000 fold

antithrombin inactivates thrombin (factor IIa)

187
Q

What is thrombomodulin/proteinC/protein S?

A

Trombin receptor present on endothelial cells

Bound thrombin is unable to convert fibrinogen to fibrin

The thrombin/thrombomodulin complex activates protein C which degrades Factors Va and VIIa

188
Q

What is tissue factor pathway inhibitor (TFPI?

A

Factor VIIa + TFPI initiate the extrinsic pathway of coagulation

This is inhibited by factor Xa (negative feedback)

189
Q

What is tissue plasminogen activator (TPA)?

A

Cleaves plasminogen to plasmin, which degrades fibrin clots

Is secreted by endothelial cells in response to clot formation

Important in clot lysis

190
Q

What are the components of a clot?

A

Platelets + fibrin

191
Q

What are clotting factors important in preventing thrombosis?

A

Antithrombin

Protein C/Protein S/Thrombomodulin

Tissue Factor Pathway Inhibitor (TFPI)

192
Q

What are endothelial anti-thrombotic mechanisms?

A

Platelet inhibition - prostacyclin and NO; ADP->adenosine conversion

Vasodilation

193
Q

What is the effect of prostacycin on thrombosis?

A

Prostacyclin released by endothelial cells inhibits platelet activation

Prostacyclin is also vasodilatory (minimizes contact between procoagulant factors (reducing propensity of thrombus formation)

194
Q

What is the effect of NO on thrombus formation?

A

NO inhibits platelet activation

NO is a vasodilator - minimizes contact between procoagulant factors, reducing propensity to form thrombus

195
Q

What is the major cause of coronary thrombosis?

A

Plaque rupture

196
Q

What can cause plaque rupture that leads to coronary thrombosis?

A

Chemical factors that destabilize fibrous cap (cytokines inhibit collagen synthesis, a key component; MMPs within plaques degrade matrix)

Physical stresses (shoulder region prone to rupture due to high stress; high BP; torsion from myocardial contraction)

Triggers (strenuous activity or emotional upset; early morning with high BP, viscosity, sympathetic tone)

197
Q

What are chemical factors that can estabilize a fibrous cap and cause plaque rupture?

A

T lymphocytes secrete cytokines that inhibit collagen synthesis

Enzymes in plaques degrade matrix - matrix metalloproteinases

198
Q

What are physical stresses that can cause plaque rupture and cause coronary thrombosis?

A

High stress on the shoulder region of the cap (most prone)

Intraluminal blood pressure

Torsion from myocardial contraction

199
Q

What are triggers of plaque rupture that can cause coronary thrombosis?

A

Strenuous physical activity or emotional upset

MIs usually occur in the early morning hours when physiologic stress is highest (BP, blood viscosity, sympathetic tone)

200
Q

What time of day is more likely for an MI to occur? Why?

A

Early mornin hours

Physiologic stress is highest - BP, blood viscosity, sympathetic tone

201
Q

What role does endothelium dysfunction play in the pathogenesis of coronary thrombosis?

A

Reduced secretion of NO and prostacyclin by endothelial cells results in a state where vasoconstriction is favored over vasodilation

Platelet products (thromboxane, 5-HT) and thrombin promote vasoconstriciton while ADP (vasodilatory) is attenuated in endothelial cell dysfunction

This increases hemodynamic stress on plaque and reduces coronary flow and normal clearance of procoagulant factors

202
Q

What are some triggers of acute plaque rupture?

A

Exertion
Sexual activity

Anger, mental stress

Cocaine use

Tobacco, marijuana use

Exposure to air pollution

Fever, specific infections (e.g. influenza)

203
Q

What are functional sequellae of MIs?

A

Impaired contractility (systolic dysfunction) - due to necrosis of functional myocytes (hypo-,a-, or dys-kinesis)

Impaired relaxation (diastolic dysfunction) - this is an energy-dependent process, thus impaired duringMI; Reduces compliance and increases filling pressures

Stunned myocardium - prolonged, but reversible period of contractile dysfunction; restored days-weeks later; adjacent to MI

Ischemic preconditioning - episodes of ischemia render tissue resistant to subsequent; seen in stable angina - increases ischemic threshold

204
Q

What is hypokinesis of the myocardium?

A

reduced contraction

205
Q

What is akinesis of the myocardium?

A

Loss of contraction

206
Q

What is dyskinesis of the myocardium?

A

Outward bulging during contraction

207
Q

Why is diastole dysfunctional after MI?

A

Diastole is energy dependent - thus MI causes problems (Oxygen, ATP, etc)

If compliance is reduced, filling pressures increase

208
Q

What is stunned myocardium?

A

Prolonged, but reversible period of contractile dysfunction seen after MI

Function is restored days to weeks after episode

Commonly seen in areas adjacent to region of MI

209
Q

What is ischemic preconditioning?

A

Episodes of ischemia render tissue resistant to subsequent episodes (sometimes)

Observed in the setting of stable angina, which causes an increase in the ischemic threshold with continued exercise

210
Q

What is ventricular remodeling?

A

Changes in cardiac size, shape, structure and physiology

May be physiological and adaptive during normal growth

Or pathological in the setting of MI, cardiomyopathy, HTN, or valvular heart disease

211
Q

What cardiac remodeling occurs initially, post-MI?

A

Fibrotic repair of necrotic area and scar formation and elongation

Thinning of the infarcted zone

LV volumes increase in the adaptive response - associated with increased stroke volume to maintain normal cardiac output

212
Q

What is the significance of infarct expansion in the context of MI?

A

Associated with higher mortality, incidence of non-fatal complications such as heart failure or ventricular aneurysm

Seen on echo

Can be severe and lead to systolic function deterioration, new/louder gallops, or new/worsening pulmonary congestion

213
Q

What remodeling occurs late, post-MI?

A

Hypertrophy

Myocytes hypertrophy due to neurohormonal activation, myocardial stretch, activation of local tissue RAS, an para-/autocrine factors

Ang II production locally, likely stimulates hypertrophy in non-infacted myocardium

214
Q

What is acute coronary syndrome?

A

Acute MI, unstable angina or sudden cardiac death

215
Q

What are non-atherosclerotic causes of acute coronary syndroem?

A

In young patients or in pts with no coronary risk factors:

  • Mechanical valves or infectious endocarditis (emboli resultin gin coronary occlusion)
  • Inflammatory disorders (vasculitis)
  • peripartum female (spontaneous coronary dissection)

Cocaine abuse - causes vasospasm (decreasing O2 supply), increases HR (increased O2 demand), and associated with increased atherosclerosis

216
Q

What is type 1 MI?

A

Classic case of plaque rupture with thrombus

217
Q

What is type 2 MI?

A

Supply/demand imbalance without a plaque rupture

218
Q

What is type 3 MI?

A

Sudden cardiac death - fixed atherosclerosis and supply/demand imbalance

219
Q

What is type 4/5 MI?

A

MI in the setting of revascularization procedures

220
Q

What is a transmural infarction?

A

(Q wave MI)

Necrosis spans the entire thickness of the myocardium

Caused by a total, prolonged occlusion of a coronary artery

221
Q

What is a subendocardial infarction?

A

(non-Q wave MI)

Subendocardium susceptible to ischemia, exposed to the highest pressures from the ventricles with few collaterals.

Vessels that supply O2 must pass through the contracting myocardium

222
Q

What is the most common cause of ACS (acute coronary syndrome)?

A

Rupture of an atherosclerotic plaque leading to superimposed thrombus

Plaque erosion may lead to thrombus

More common in younger women, smokers

223
Q

What demographics are more likely to have plaque erosion leading to thrombus as a cause of ACS?

A

Younger women

Smokers

224
Q

What is the result of a non-occlusive thrombus in the coronary vasculature?

A

Unstable angina

NSTEMI (non-ST-elevation MI)

Transient occlusion or distal imbolization may cause necrosis

225
Q

What is the result of an occlusive thrombus in the coronary vasculature?

A

ST-elevation MI (STEMI)

226
Q

What is the least severe on the spectrum of ACS?

A

unstable angina

227
Q

What is the most severe on the spectrum of ACS?

A

STEMI

228
Q

What is the spectrum of ACS?

A

Unstable angina -> NSTEMI -> STEMI

229
Q

What are the three classifications of unstable angina?

A

Rest angina - at rest and prolonged (>20 mins)

New-onset angina - <2 months

Increasing (crescendo) angina - previously diagnosed angina has become more frequent, longer, or worse in severity

230
Q

What is the effect of nitroglycerin on MI?

A

No improvement and minimal releif

231
Q

What are clinical symptoms in myocardial infarction?

A

More severe, longer, and more radiating chest pain, compared to stable angina

No improvement with rest and minimal releif with nitroglycerin

Sympathetic response (diaphoresis, nausea, tachycardia, cool skin)

25% may have no symptoms (diabetes)

Shortness of breath

232
Q

In what population of patients might you not see symptoms of MI?

A

Diabetics

233
Q

What are physical findings of MI?

A

S4 - atrial contraction into non-compliant LV (atrial kick)

S3 - volume overload (blood sloshing in)

Systolic murmur due to papillary muscle dysfunction causing MR or ventricular septal defect from rupture

Fever (low grade), as inflammatory response

234
Q

How is ACS (acute coronary syndrome) diagnosed?

A

Clinical symptoms, ECG findings, biomarkers of necrosis

Unstable angina/NSTEMI = T wave inversion; ST depression or normal :: elevated biomarkers in NSTEMI; normal in USA

STEMI = ST elevation, elevated biomarkers

235
Q

What ECG findings do you find in NSTEMI or unstable angina?

A

T wave inversion

ST depression or normal

236
Q

What ECG findings do you see in STEMI?

A

ST elevation

237
Q

What EKG findings do you find within minutes to hours after STEMI?

A

ST elevation and perhaps hyperacute T

238
Q

What EKG findings do you see hours-1 day after STEMI?

A

T wave inversion, elevated ST, depressed Q wave

239
Q

What EKG findings do you see ~1 week after STEMI?

A

Pronounced Q, ST elevation, T wave inversion

240
Q

What findings do you see months after STEMI?

A

Pronounced Q, ST elevation, marked T wave

241
Q

How is STEMI defined?

A

Angina unreleived by nitroglycerin with ST elevation on EKG and rise in biomarkers

242
Q

How is NSTEMi defined?

A

Angina at rest >20 minutes without ST elevation but with rise in cardiac biomarkers

243
Q

What is the pathophysiology of STEMI?

A

Total or near-total thrombotic occlusion of coronary artery

244
Q

What is the pathophysiology of NSTEMI?

A

Abrupt decrease in myocardial oxygen supply

Thrombus formation on an atherosclerotic plaque

245
Q

What are biomarkers of myocardial necrosis?

A

Troponin core complex (TnT, TnI, TnC)

Creatinine kinase myocardial band (CK-MB)

246
Q

What is the value of using troponin as a biomarker for MI?

A

They are generally not detected in blood of healthy individuals

Levels rise within 3-4 hours, peak between 18-36 hours and decline slowly (~2 weeks)

247
Q

What is the time course of troponin as a biomarker for MI?

A

Rises within 3-4 hours, peaks between 18-36, and declines slowly (up to 2 weeks)

248
Q

What is the value of creatinine kinase myocardial band (CK-MB) as a biomarker for MI?

A

Has sharper kinetics than troponin (peaks faster and returns to normal faster)

Good for identifying subsequent MIs after initial event

249
Q

What are the kinetics of CK-MB as a biomarker for MI?

A

Peak wtihin 24 hours and decline quickly (couple of days)

250
Q

What are the narrow complex tachycardias?

A

Sinus tachycardia

AVNRT/AVRT

Atrial fibrillation

Atrial flutter

Atrial tachycardia

Multi-focal atrial tachycardia

251
Q

How do you approach an EKG with narrow complex supraventricular tachycardia?

A

Regular or irregular R-R intervals?

P waves or no P waves

Long RP or Short RP? - transect R-R segment (P on left or right side?)

Response to adenosine -AV nodal blocker

252
Q

What is the classic irregular narrow complex tachycardia?

A

Atrial fibrillation

253
Q

What does an irregular narrow complex tachycardia tell you?

A

atrial fibrillation

254
Q

What does a regular narrow complex tachycardia tell you?

A

It’s NOT atrial fibrillation - check for long or short RP segments

255
Q

What does a short RP, regular narrow complex tachycardia tell oyu?

A

AVNRT/AVRT

256
Q

What does a long RP, regular, narrow complex tachycardia tell you?

A

Sinus tachycardia or atrial tachycardia - check nodal block effects

257
Q

What does a regular, narrow complex tachycardia with multiple p waves tell you?

A

atrial flutter

258
Q

What is AVNRT?

A

Narrow complex tachycardia seen in all ages

Manifests as palpitations “racing heart”

Re-entrant arrhythmia dependent on having dual AV nodal physiology

Psuedo R’ in V1

Pseudo S in II, III, aVF

no P wave (short RP) - P and QRS often on top of each other

259
Q

In AVNRT, the […] pathway has slower conduction and faster recovery

A

In AVNRT, the slow pathway has slower conduction and faster recovery

Fast pathway has faster conduction, slower recovery

If you walk a mile, you only need short rest

If you run a mile, you have to rest for a long time

260
Q

In AVNRT the […] pathway has faster conduction and slower recovery

A

In AVNRT the fast pathway has faster conduction and slower recovery

Slow pathway has slower conduction and faster recovery

If you walk a mile, you only need short rest

If you run a mile, you have to rest for a long time

261
Q

How do you treat AVNRT acutely?

A

Adenosine, Vagal maneuvers, AVN blocking agent

262
Q

How do you treat AVNRT chronically?

A

AVN blockers

Single dose during episodes, daily dosing

Class I and Class III anti-arrhythmics are effective

ABLATION of slow pathway is most efficacious (low risk)

263
Q

Which pathway (slow or fast) do you attempt to ablate to resolve an AVNRT?

A

slow!

264
Q

What is AVRT?

A

AV reciprocal tachycardia

Re-entrant arrhythmia

Dependent upon accessory pathway

Can be manifest on EKG = Wolff-parkinson-white (WPW)

Risk for sudden death

265
Q

What is WPW?

A

Wolff-Parkinson-White

Type of AVRT - re-entrant arrhythmia with accessory pathway

Characteristic Δ-wave on EKG and short PR interval

266
Q

What is atrial flutter?

A

Common arrhythmia in patients with heart disease

Can present with palpitations, dyspnea, heart failure, stroke

Re-entrant arrhythmia involving atria

Atria beating at 250-300 bpm, with ventricles at 2:1, or 3:1 or slower rate

Saw-tooth pattern P waves

267
Q

What is atrial fibrillation?

A

Highly prevalent arrhythmia

Risk factors are numerous (age, HTN, DM, etc)

Can be paroxysmal (in and out) or persistent

Variable symptomaticity

EKG is Irregularly irregular

Atria at >300bpm but uncoordinated

Originate from impulses from the pulmonary veins

Tx with AV nodal blockade, anti-arrhythmics, catheter ablation

268
Q

What are you thinking?

A

Atrial fibrillation

Irregularly irregular

Atria at >300 bpm

269
Q

What do you see here?

A

Atrial Flutter

Saw-tooth appearance

270
Q

What are clinical manifestations of lower extremity atherosclerosis?

A

Intermittent claudication

Critical limb ischemia

271
Q

What is intermittent claudication?

A

Pain, ache, or fatigue in the calf, thigh, hip, buttock, or low back that occurs on walking and is releived with rest

Location of symptoms correlates with level of obstruction

272
Q

What is critical limb ischemia?

A

Pain or paresthesia in the toes, foot, or leg at rest

Exacerbated by leg elevation or when supine

Releived with dependency

Persistent pain +/- ulceration with severe ischemia

273
Q

What is the Leriche triad?

A

Bilateral high claudication

Impotence

Global Atrophy

274
Q

What is aorto-iliac disease?

A

Peripheral artery disease characterized by the Leriche triad (bilateral high claudication, impotence, global atrophy)

Collaterals are typically well develope

There are multiple revascularization options with high patency

275
Q

What is Femoropopliteal disease?

A

Most frequent peripheral artery disease

Collaterals determine course of disease

Intermediate graft patency

276
Q

What is tibeal-peroneal disease?

A

Peripheral artery disease commonly seen in diabetes

Low graft patency without in-situ vein techniques

277
Q

What are trophic signs of acute limb ischemia on examination?

A

Ulceration

Petichae

Calf tenderness

Dependent edema

278
Q

What are trophic signs of chronic arterial obstructive disease?

A

Hair loss

Subcutaneous atrophy

Thickened nails

Dependent rubor

279
Q

How do you treat limb obstructive arterial disease pharmacologically?

A

Platelet inhibitors (aspirin, clopidogrel)

Lipid-lowering agents (statins)

ACE inhibitors

NO role for vasodilators

280
Q

What are etiologies of acute arterial occlusion?

A

In-situ thrombosis (ruptured atherosclerotic plaque)

Embolism from a proximal source

Arterial trauma

Vasculitis

Hypercoagulable state

Severe venous thrombosis

281
Q

What are sources of arterial emboli?

A

Atrial fibrillation

Valvular heart disease (rheumatic mitral stenosis, prosthetic valves, endocarditis)

Thrombus in cardiac chambers (left atrial appendage, LV mural thrombus)

Proximal arterial disease (AAA, atherosclerosis)

282
Q

What is a true aneurysm?

A

Intima, media and adventitia are in tact, but balloon out

283
Q

What is a false aneurysm?

A

Hole in intima and media that allows for hematoma to balloon the adventitia out and give the appearance of an aneurysm

284
Q

What are etiologies of aortic aneurysmal diseases?

A

Atherosclerosis

Cystic medial necrosis (primary, Marfan, Ehlers-Danlos)

Vasculitis

Dissection

Post-stenotic

Infections

Trauma

Congenital

285
Q

What are risk factors for abdominal aortic aneurysms?

A

Age

HTN

Tobacco smoking

Family history (males)

Hyperlipidemia

Atherosclerosis

286
Q

What is the natural history of an abdominal aortic aneurysm (AAA)?

A

Expand at 1-4 mm/ year

Predictors of expansion include initial size, active smoking, HTN)

287
Q

What are risk factors for aortic dissection?

A

HTN

Tobacco smoking

Cocaine use or stimulant use
Connective tissue disease (Marfans, Ehlers-Danlos)

Congenital structural abnormalities (bicuspid aortic valve, coarctation of aorta)

Inflammatory disease of aorta

Pregnancy

Weight lifting

Trauma

288
Q

What is Raynaud’s Phenomenon??

A

“asphyxiation of digits”

289
Q

What is primary raynaud’s disease?

A

most cutaneous vasospasm

Females more than males

15-40 year old onset

Symmetrical involvement of digits, earlobes, tip of nose, elbows, knees

Spontaneous improvement in 15%; progression in 30%

Ulceration is rare

290
Q

What is Buerger’s Disease??

A

Medium vessel vasculitis associated wtih tobacco smoking

Cessation of smoking is theapy

291
Q

What is Virchow’s Triad?

A

Stasis of blood flow

Endothelial injury

Hypercoagulable state

Describes factors that contribute to thrombosis

292
Q

Where are DVTs more common?

A

Calf > popliteal > femoral > iliac (more distal = more common)

293
Q

What sites of DVTs are more dangerous?

A

Proximal

Iliac > femoral > popliteal > calf

Deep > superficial veins

294
Q

What symptoms are seen in massive pulmonary embolism?

A

Syncope, profound dyspnea, cardiogenic shock, cardiac arrest

sub-massive = chest pain, dyspnea

295
Q

What symptoms are seen in sub-massive pulmonary embolism?

A

chest pain, dyspnea

massive = Syncope, profound dyspnea, cardiogenic shock, cardiac arrest

296
Q

What symptoms are seen in pulmonary infarction?

A

Hemoptysis (coughing blood), chest pain, dyspnea

297
Q

What are signs of chronic venous insufficiency?

A

Edema and induration

Hemosiderin pigmentation

Ulceration

298
Q

What are clinical syndromes associated with chronic venous insufficiency?

A

Superficial varicose veins

Deep venous incompetence

Postphlebitic syndrome

299
Q

What are symptoms of lymphedema?

A

limb swelling

heaviness

recurrent lymphanigitis or erysipelas

Skin changes

fungal infestation

300
Q

What are physical findings of lymphedema?

A

Non-pitting edema

Dorsal pedal hump

Elephantine distribution

Chronic induration without pigmentation

Lichenification

301
Q

What are causes of primary lymphedema?

A

Aplasia, hypoplasia or hyperplasia of lymphatic channels

Obstruction

Incompetence of lymphatic valves

302
Q

What can cause secondary lymphedema?

A

Malignancy

Radiation

Infection - pyogenic lymphangitis, filariasis

Surgery
trauma

303
Q

Where is the most common location for atherosclerotic aneurysms in the aorta?

A

Below renal arteries and above bifurcation of iliac artery

304
Q

How do β-blockers help in treating MIs?

A

Releive ischemic pain

Reduce infarct size and life-threatening arrhythmias

Presumed to decrease cardiac work and myocardial oxygen demand

305
Q

How do nitrates help treat MI?

A

They enhance coronary blood flow by coronary vasodilation

Decrease ventricular preload by increasing venous capacitance (reduce wall stress)

Contraindicated in pts with hypotension

306
Q

How do calcium channel blockers help MIs?

A

Symptom improvement

Nondihydropyridines reduce heart rate and contractility

Useful in pts with contraindications to β-blockers or ischemia refractory to β-blockade or nitrates

307
Q

What is the risk with antithrombotic therapies?

A

Can go too far, and thin blood, causing a bleeding risk

308
Q

What is the effect of Aspirin on MI?

A

Effective across all ACS categories

Give as soon as possible

Produces rapid antiplatelet effect

Reduces oronary occlusion and recurrent ischemic events after fibrinolytic therapy

309
Q

What is a drawback/issue with using clopidogrel?

A

There is substantial interindividual variability in the response

310
Q

How do glycoprotein IIb/IIIa receptor antagonists work/help in MIs?

A

Potent inhibitors of the final common pathway of platelet aggregation

Use has declined with advent of more potent antiplatelet drugs

Beneficial in highest risk patients undergoing PCI

311
Q

What is the goal of STEMI treatment?

A

To achieve reperfusion.

Restores flow in the infarct-related artery, limits infarct size and translates into early mortality benefit.

312
Q

What are treatment avenues for STEMI patients?

A

Fibrinolysis and invasive strategies are essentially equal in efficacy unless there are reasons not to do one (occupied cath lab, no access, delay to invasive, etc)

313
Q

What are complications of MIs?

A

Arrhythmias - signiicantly V. fib = sudden cardiac death;also supraventricular arrhythmias and conduction blocks

Pump failure

Free wall rupture/pseudoaneurysm

Papillary muscle rupture

Pericarditis

314
Q

What are left sided heart failure signs/symptoms?

A

Dyspnea, pulmonary rales, third heart sound

Diuretics can relieve volume overload

Standard heart failure meds indicated

315
Q

What are right sided heart failure signs/symptoms?

A

Elevations in JVD and hypotension (LV is underfilled)

Treat with volume expansion

Usually due to MI of RCA

316
Q

During what time scale does a free wall rupture typically occur after MI?

A

Within first 2 weeks

This is a surgical emergency, and usually fatal

317
Q

What is a psuedoaneurysm?

A

Caused by a contained myocardial rupture, still at risk for rupture

318
Q

What is a LV aneurysm?

A

Discrete dyskinetic area of LV wall with broad neck

Develops weeks to months after MI

No communication between LV cavity and pericardium

Complications include thrombus, arrhythmias, heart failure

Tissue bulges with cardiac contractions

LV aneurysm can be associated with ST elevation

319
Q

What are some issues with a papillary muscle rupture?

A

Complete rupture may result in severe mitral regurgitation -> heart failure or death

Partial rupture may cause moderate MR and symptoms of heart failure

320
Q

Which aspect of the papillary muscle is more susceptible to rupture?

A

Posteromedial papillary more susceptible than anterolateral

321
Q

What is acute pericarditis?

A

Inflammation that occurs early in the post-MI period taht extends from myocardium to pericardium

322
Q

What is Dressler syndrome?

A

Pericarditis that occurs several weeks after MI

autoimmune process may be contributory

323
Q

What is ischemic injury?

A

Injury resulting from reduced blood flow

324
Q

What are the effects of impaired blood inflow?

A

Inadequate oxygen supply

Insufficient availability of nutrients

325
Q

What are the effects of impaired blood outflow?

A

Insufficient removal of metabolites

326
Q

What is the etiology of most myocardial ischemia cases?

A

Obstructive coronary artery disease (CAD)

327
Q

What is myocardial infarction?

A

The irreversible myocardial muscle damage caused by prolonged ischemia resulting from a sustained imbalance of perfusion and demand

Discrete focus of ischemic muscle necrosis

328
Q

What cardiac areas does the right coronary arery supply?

A

Right atrium

Right ventricle

Bottom portion of left ventricle

Back of septum

329
Q

What cardiac areas does the left anterior descending artery supply?

A

Front and bottom of left ventricle

Front of the septum

330
Q

What cardiac areas does the circumflex artery supply?

A

Left atrium

Side and back of the left ventricle

331
Q

You find ischemia on the anterior wall of the LV and down to the apex of the heart. Where do you suspect a coronary artery occlusion?

A

Left anterior descending (LAD) branch of the left coronary artery

332
Q

You find necrosis on the posterior wall of the LV. Where do you suspect an occlusion of the coronary arteries?

A

Right coronary artery

333
Q

You find necrosis on the lateral wall of the left ventricle. Where do you suspect a coronary artery occlusion?

A

Circumflex artery - a branch of the left coronary artery

334
Q

Whhat is a transmural infarct?

A

ischemic necrosis that involves full or nearly full thickness of the ventricular wall in the distribution of a single coronary artery

335
Q

What is a subendocardial infarct?

A

Ischemic necrosis limited to inner 1/3 or 1/2 of the ventricular wall

Zone is least perfused and most vulnerable to any reduction in flow

Regional: transient obstructoin which is releived before necrosis extends across thickness

Circumferential: Prolonged, severe hypotension even without coronary stenosis

336
Q

What type of infarct can lead to pericarditis or ventricular rupture?

A

Transmural infarcts

Subendocardial infarts do not

337
Q

What do you see on pathology of an MI within 4 hours?

A

Nothing!

338
Q

What do you see on pathology of an MI after 1-3 days?

A

Mottling with yellow-tan infarct center

Seen maximally at 7-10 days

339
Q

When do you see yellow-tan areas in the myocardium following an MI?

A

After about 3-10 days

340
Q

What do you see on pathology of an MI after over 2 months?

A

Complete scarring

341
Q

How old is this MI?

A

~ 7 days

Note the yellow-tan zone of necrosis with the surrounding red granulation tissue.

342
Q

What are clinical findings in Giant Cell Arteritis?

A

Diminished temporal pulses/headache

Facial pain/jaw claudication

Impaired vision

Elevated inflammatory markers

Treat with high dose steroids before confirming diagnosis to save vision

343
Q

What is thrombangiitis obliterans?

A

Buerger disease

Smoking-related vasculitis that presents with triad of symptoms:

Distal arterial occlusion (corkscrew collaterals)

Raynaud’s phenomenon

Superficial vein thrombophlebitis

Smoking cessation is critical treatment

344
Q

You see corkscrew collaterals in a patient’s angiogram. What are you thinking?

A

Thrombangiitis obliterans (Buerger disease)

Stop smoking!

345
Q

What sex is affected more commonly by giant cell/Takayasu arteritis?

A

Females

Males are affected more by thrombangiitis obliterans (Buerger’s)

346
Q

What is the diagnosis?

A

A fibrillation

347
Q

What is the diagnosis?

A

Atrial flutter

348
Q

Which arrhythmia is dependent on having dual AV nodal physiology?

A

AVNRT

349
Q

What is the most likely diagnosis?

A

3rd degree heart block (complete heart block)

350
Q

What is the most likely diagnosis?

A

2nd Degree AVB - Mobitz I

351
Q

What do you see in this EKG?

A

Atrial fibrillation

Right Bundle Branch Block (RBBB)

3rd Degree AV Block (complete heart block) - no correlation b/w p waves and qrs complexes

352
Q

What are characteristics of WPW on EKG?

A

Short PR (less than 120ms)

Slurred QRS upstroke (delta wave)

Broad QRS

Secondary ST and T wave changes

353
Q

What is the diagnosis?

A

WPW

354
Q

What is an orthodromic AVRT?

A

Electrical activity occurs in a circle but proceeds down septum and around free walls and up to atria

355
Q

What is an antidromic AVRT?

A

Re-entrant arrhythmia where the electrical impulse passes from atria down free wall of ventricle and up through septum (backwards)

356
Q

What is the effect of hyperkalemia on the membrane resting potential of a myocyte?

A

Decreases it from -90 to -80 mV

357
Q

What changes are present on EKG in hyperkalemia?

A

Slowed conduction - fewer cells recruited

Everything delayed until it stops

358
Q

What is a clear EKG finding of hyperkalemia?

A

Pointy T waves

Prolonged QRS

Prolonged PR

359
Q

What is the diagnosis?

A

Hyperkalemia!

pointy T waves, prolonged QRS, PR

Give IV Ca

360
Q

What are the congenital long QT syndromes?

A

LQTS1 - Triggered by exercise, swimming

LQTS2 - triggered by auditory ques (doorbell)

LQTS3 - triggered by sleep

361
Q

What is the finding?

A

Long QT Syndrome

LQTS3 - found while sleeping

362
Q

What is this?

A

Torsades de Pointes

Causes sudden deaths in Long QT Syndromes when sustained

Can be OK if occurs briefly

363
Q

What is Brugada Syndrome?

A

Inherited syndrome that is most common cause of sudden death in southeast asian countries

EKG shows RBBB with downslowing ST segment elevation in the right precordial leads

Pts die from Torsades de Pointes

364
Q

What are you thinking?

A

Brugada Syndrome - downsloping ST segment elevation in right precordial leads

365
Q

What is the shared defining feature of all categories of vasculitis?

A

Inflammation of blood vessel walls at least at some time during the course of the disease

366
Q

What are the two broad etiologic categories of vasculitis?

A

Infectious (direct invasion and proliferation in vessel walls by pathogens)

Non-infectious (not known to be caused by pathogenic invasion)

367
Q

What are the vessels most frequently involved in polyarteritis nodosa (PAN)?

A

Renal vessels

Leads to arterial hypertension and ischemic nephropathy with renal failure

No glomerulonephritis

368
Q

What is Mucocutaneous Lymph Node Syndrome?

A

Sequellae associated with Kawasaki disease (medium vessel vasculitis)

Seen in infants and young children

369
Q

What is levocardia?

A

Heart to the left

370
Q

What is dextrocardia?

A

Heart to the right

371
Q

What is mesocardia?

A

Heart not left nor right

372
Q

What defines the right atrium?

A

The atrium with the broad triangular-shaped appendage (right atrium appendage)

Usually recieves connection from hepatic segment of IVC

Coronary sinus always opens into the morphologically right atrium

373
Q

What defines the left atrium?

A

The atrium that is not the right atrium

Flap valve of the foramen ovale is attached to its septal surface

Has a smaller finger-like appendage

374
Q

What defines the tricuspid valve?

A

Valve that serves the morphologically right ventricle, regardless of its leaflet morphology

Typically tri-leaflet valve with attachments of septal leaflet to septum via chordae

375
Q

What defines a mitral valve?

A

Defined as the valve that serves the morphologically left ventricle, regardless of its leaflet morphology (can be cleft and appear tricuspid)

Typically has two leaflets, connected by chordae to two free wall papillary muscle groups

376
Q

What defines a right ventricle?

A

Heavy trabeculations

Septal band

Prominent septal attachments of the tricuspid valve

Pyramidal shape

Moderator band

377
Q

What defines a left ventricle?

A

Fine trabeculation

Smooth septal surface

Absent septal connections to mitral valve (generally)

Prolate ellipsoidal shape

378
Q

What defines the pulmonary artery?

A

Great vessel that usually gives rise to branch pulmonary arteries (if present)

379
Q

What defines the aorta?

A

Great vessel which gives rise to at least one coronary artery and the aortic arch and its brachiocephalic vessels (though this may be interrupted)

380
Q

What is atrial situs solitus?

A

RA on the right and receives the hepatic IVC connection

LA on the left, as are attachments of septum primum - flap valve of foramen ovale

381
Q

What is atrial situs inversus?

A

RA on the left and receives the left-sided hepatic IVC connection

LA on the right, as well as attachments of septum primum

382
Q

What is atrial situs ambiguus?

A

Unclear - typically includes common atrium with multiple venous connection anomalies

383
Q

What is a d-looped ventricular loop?

A

Normal (Dextro-looping), but only for solitus atrial position in which the RV has developed to the right of the LV

384
Q

What is a L-looped ventricular loop?

A

Inverted ventricular loop, wherein the morphologically right ventrile is to the left of the morphologically left ventricle. Normal only for situs inversus of the atria

(left handed)

385
Q

What is x-looped ventricular looping?

A

For cases where there is a single ventricle, it is impossible to figure out the ventricular situs or loop (catch-all)

386
Q

What are the characteristics of normally related great arteries?

A

Aorta arises in fibrous continuity with the anterior mitral leaflet (no conus separating aortic valve from mitral)

Pulmonary valve is separated from tricuspid by subpulmonary muslce (conus)

LV with aorta; RV with pulmonic

Solitus: aortic valve to right and posterior of pulmonary valve

Inversus: aorta is leftward and posterior to pulmonary

387
Q

What does D mean with respect to the position of the great arteries?

A

Aortic valve is rightward of the pulmonary valve

388
Q

What does A mean with regards to the malpositions of the great arteries?

A

Aortic valve is anterior to the pulmonary valve

389
Q

What does L mean with regards to the malpositions of the great arteries?

A

Aortic valve is leftward and anterior to the pulmonary

390
Q

What does P mean with respect to the malpositions of the great arteries?

A

Aortic valve is posterior to the pulmonary valve, irrespective of right-left position

391
Q

What is AV discordance?

A

Morphologically right atrium connects abnormally with the morphologically left ventricle

Can be caused by solitus atria and L-looped ventricles or by inversus atria and d-looped ventricles

392
Q

What is V-A discordance?

A

When the morphologically left ventricle is aligned with the pulmonary valve

Refers to the great arterial malpositions (Transposition of great arteries, TGA; double outlet right ventricle, DORV; double outlet left ventricle, DOLV, anatomically corrected malposition of the great arteries, ACM, aortic atresia

393
Q

What does atresia mean?

A

“without an opening”

Refers to valves that do not form well - have no opening

394
Q

What is the conotruncus?

A

Segment which joins the ventricle to the great artery

395
Q

Why are ventral septal defects not diagnosed until a few days after birth?

A

Pulmonary resistance takes a while to decrease to “adult” levels. Once this happens, though, blood will flow to least resistance (pulmonary)

396
Q

What is the tetralogy of Fallot?

A

Pulmonary stenosis

Right Ventricular Hypertrophy

Overriding Aorta

Ventricular Septal Defect

PROVe

Cyanotic heart disease - Right to left shunting

397
Q

What is Rheumatic Fever?

A

Immunologic response to acute streptococcal pharyngitis (Group A strept)

Cross-reactivity b/w antigen and structural glycoprotein found in heart, joints, connective tissues)

Leads to chronic rheumatic valvular heart disease

398
Q

What are the Jones Critera useful for?

A

Diagnosis of Rheumatic Fever

2 major or 1 major and 2 minor; PLUS evidence of infection

399
Q

How do you treat Rheumatic Fever??

A

Penicillin

Anti-inflammatories (ASA, corticosteroids)

Treat complications

400
Q

What is Mitral Stenosis?

A

Obstruction of LV inflow that prevents proper filling during diastole

Normal MV area is 4-6 cm^2

Severe disease is <2cm^2

401
Q

What is the normal mitral valve area?

A

4-6 cm^2

402
Q

What is severe mitral stenosis valve area?

A

<2 cm^2

403
Q

What are etiologies of mitral stenosis?

A

Rheumatic heart disease - most common

Infective endocarditis

Mitral annular calcification

Congenital

404
Q

What would you hear on auscultation of mitral stenosis?

A

Loud S1

Opening snap after S2, with diastolic murmur with pre-systolic accentuation

405
Q

What are clinical manifestations of mitral stenosis?

A

Can be asymptomatic, but depends on degree of reduction of valve area

Dyspnea, reduced exercise tolerance, fatigue

Pulmonary congestion (orthopnea, paroxysmal nocturnal dyspnea)

RV failure

406
Q

What does a shorter S2 to opening snap time indicate about mitral stenosis?

A

More severe disease

Snap represents reachign maximally open aperture

407
Q

What are complications of mitral stenosis?

A

Pulmonary edema

Pulmonary HTN

Right heart failure

A fibrillation

Infective endocarditis

Systemic thromboembolism

408
Q

What can you see on EKG in a patient with mitral stenosis?

A

Maybe A. Fibrillation

Maybe LA enlargement and RV hypertrophy

409
Q

What do you see on chest x-ray in patients with mitral stenosis?

A

LA enlargement

Signs of pulmonary congestion

410
Q

What do you see on echo in a patient with mitral stenosis?

A

Can assess mitral valve mobility, and area

Can identify gradients and severity of disease

411
Q

How do you treat mitral stenosis?

A

Medicines do not prevent progression - useful for symptoms

β-blockers, CCBs, digoxin control HR and prolong diastole

Diuretics for fluid overload

Surgery is definitive treatment for patients with symptoms or pulmonary HTN

412
Q

What are causes of mitral regurgitation?

A

Abnormalities of valve leaflets (Rheumatic heart disease, infective endocarditis, myxomatous degeneration)

Abnormalities of mitral annulus (dilatation, calcification)

Abnormalities of chordae tendinae (congenital, infective, trauma)

Involvement of papillary muscles (CAD)

413
Q

What happens to LV/LA pressures in mitral regurgitation?

A
414
Q

How does the murmur in mitral regurgitation differ in acute vs chronic cases?

A

Acute - may not be holosystolic; is shorter and softer

Chronic - holosystolic

415
Q

What are differences between acute mitral regurgitation and chronic mitral regurgitation?

A

Acute - normal LA size and compliance, increased LA pressure causes backup into pulmonary system (edema)

Chronic - dilated LA, increased compliance; normal LA and pulmonary pressures with decreased CO

416
Q

What are symptoms of mitral regurgitation?

A

Can be asymptomatic

Palpitations

Fatigue

Dyspnea

Paroxysmal Nocturnal Dyspnea

Signs of RV failure

417
Q

What are clinical signs of mitral regurgitation?

A

Low, collapsing pulse

Heaving apex

Soft S1, loud P2 (pulmonary HTN)

S3 sound

Holosystolic murmur at apex that radiates to left axilla

Increased murmor on expiration, handgrip, squatting (increase resistance)

418
Q

How do you treat actue mitral regurgitatioN?

A

Diuretics, nitroprusside (reduce afterload to increase cardiac output that goes forward)

Balloon pump

Surgery (this is an emergency)

419
Q

How do you treat chronic mitral regurgitation?

A

Vasodilators for HTN, LV systolic dysfunction

MItral valve repair

420
Q

What can you see on EKG for a patient with mitral regurgitation?

A

LA enlargement, LV hypertrophy, A. Fib

421
Q

What can you see on chest x-ray of mitral regurgitation?

A

Chronic - cardiomegaly (LV, LA)

Acute - interstitial edema

422
Q

What can you see on echocardiogram for a patient with mitral regurgitation?

A

Estimate LA, LV size and function

Assess valve structure - Definitive for diagnosis

423
Q

What is mitral valve prolapse?

A

Autosomal dominant inherited disease that is associated with Marfan Syndrome, Ehler-Danlos syndrome

Pathophysiology includes enlarged valvular leaflets that prolapse into left atrium during systole

Can be asymptomatic, have chest pain or palpitations

Midsystolic click, late systolic murmur

Decreased murmur by squatting, increased by valsalva, standing, handgrip

424
Q

What are clinical signs of mitral valve prolapse?

A

Midsystolic click, late murmur

Heard best at apex

Decreased murmur with squatting.

Increased murmur with valsalva, standing, handgrip

425
Q

What can you see on echo for mitral valve prolapse?

A

Confirm the diagnosis

426
Q

How do you treat mitral valve prolapse?

A

Usually benign

Monitor to ensure no development of mitral regurgitation

427
Q

What are complications associated with mitral valve prolapse?

A

Rupture of choardae can cause mitral regurgitaiton, pulmonary edema

Infective endocarditis

Thromboembolism

Arrhythmias

Cardiovascular (2 decks)

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