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Cardiovascular > Cardio Flashcards 1 > Flashcards

Cardio Flashcards 1

1
Q

What are the cardinal symptoms of cardiac disease?

A

Chest pain - myocardium

Shortness of Breath - pulmonary artery HTN due to backup

Cough

Palpitation - awareness of heartbeat

Syncope - lost of posture/consciousness

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2
Q

What are non-specific symptoms of heart disease?

A

Abdominal pain/distention

Nasuea, vomiting

Polyuria, nocturia

Confusion, dizziness

Easy fatigability

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3
Q

What is systole?

A

Ventricular contration

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4
Q

What is diastole?

A

Atrial contraction, ventricular filling

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5
Q

What defines a pulse?

A

A wave along the arterial wall plus the reflected wave from the periphery, whose summation gives a waveform of the following form:

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6
Q

What defines tachycardia?

A

Resting HR greater than 100 bpm

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7
Q

What defines bradycardia?

A

Resting HR less than 60 bpm

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8
Q

What is pulsus alternans?

A

Seen in Left Ventricular systolic dysfunction

There is a change in strength of pulse from beat to beat

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9
Q

What is pulsus bigeminus?

A

Caused by regular bigemina dysrhythmias such as PVCs and PACs (premature ventricular/ premature atrial contractions)

normal + early beat due to premature contractions

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10
Q

What is pulsus bisferiens?

A

Seen in aortic regurgitation with or without stenosis, hypertrophic cardiomyopathy

Has multiple peaks at contraction - outflow obstruction with ejection occuring

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11
Q

What is pulsus paradoxus?

A

Seen in cardiac tamponade, constrictive pericarditis, obstructive lung disease

See changes in ventricular volume filling with breathing

Pericardial pressure exceeds chamber pressure of the sounds.

May hear heart sounds, but no pulse

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12
Q

What is a water-hammer pulse?

A

Seen in aortic regurgitation, fever, anemial, thyrotoxicosis, arteriovenous fistula, chronic alcoholism (all of these cause high volumes

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13
Q

What is jugular venous pressure and what is it useful for?

A

Internal jugular vein pressure - gives an assesment of Right Atrial pressure

Measured upright and at 30-45 degrees

Jugular Venous Distension (JVD) is an abnormal finding

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14
Q

What is the hepato-jugular reflex?

A

Assessment of RV function - press on abdomen, and you will normally see that the right heart accomodates for this within a heartbeat or two. Otherwise you may see prolonged JVD

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15
Q

Which segments of a jugular venous pressure waveform correspond to which aspects of a cardiac cycle?

A
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16
Q

What is S1 and where do you hear it best?

A

S1 is produced by the closing of the mitral and tricuspid valves

Best heard over the apex

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17
Q

Which heart sound is produced by the closing of the mitral and tricuspid valves?

A

S1

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18
Q

What conditions does an accentuated S1 heart sound indicate?

A

Shortened PR interval

Mid mitral stenosis

High cardiac output states

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19
Q

What conditions does a diminished S1 heart sound indicate?

A

Lengthened PR interval

Mitral regurgitation

Severe mitral stenosis

Stiff left ventricle (systemic HTN)

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20
Q

What is the S2 heart sound?

A

Produced by the closing of the pulmonary and aortic valve

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21
Q

What heart sound is produced by the pulmonary and aortic valve closure?

A

S2

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22
Q

What does a loud S2 indicate?

A

Aortic origin - systemic HTN, aortic aneurysm

Pulmonary origin - Pulmonary HTN, atrial septal defect

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23
Q

What does wide S2 splitting indicate?

A

Right bundle branch block or pulmonary stenosis

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24
Q

What does Fixed splitting of S2 indicate?

A

Atrial septal defect

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25
Q

What does paradoxical S2 splitting indicate?

A

Left bundle branch block or severe aortic stenosis

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26
Q

What is S3?

A

Dull, low pitched sound best heard with the bell of stethoscope that indicates volume overload or increased flow through mitral/tricuspid valve

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27
Q

What is S4?

A

Dull, low-pitched sound best heard with the bell of the stethoscope that indicates decrease in ventricular compliance resulting from ventricular hypertrophy

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28
Q

How do you describe a murmur?

A

Timing

Area of maximum intensity

Grading

Position best heard

Configuration (diamond shape, cresendo/decresendo….)

Respiratory variation

Conduction

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29
Q

What do the grades of systolic murmors correspond to?

A

Grade 1/6: barely audible (cardiologist)

Grade 2/6: faint but immediately audible (resident)

Grade 3/6: easily heard (med student)

Grade 4/6: with thrill (Four = four-nicate = its a thrill!)

Grade 5/6: very loud, heard with stethoscope lightly on chest

Grade 6/6: audible without the stethoscope on the chest

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30
Q

What are innocent murmurs?

A

Common in asymptomatic adults (common in pregnancy)

Heard on physical, but no other assoicated findings

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31
Q

What type of murmur is produced by aortic stenosis?

A

Systolic murmur

Has crescendo/decrescendo

Listen at right sternal edge, 2nd ICS w/ patient upright

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32
Q

What type of murmur is heard in mitral stenosis?

A

Diastolic murmur

Mid-diastolic murmur; augmented by rapid, deep inspirations or mild exercise

Listen to apex of heart w/ patient in left lateral position

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33
Q

What type of murmur is produced by mitral regurgitation?

A

Systolic murmur

Best heard at apex of heart with radiation to left sternal edge

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34
Q

What type of murmur is produced by aortic regurgitation?

A

Diastolic murmur

Best heard along lower left sternal border

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35
Q

What type of murmur is produced by a patent ductus arteriosus?

A

Continuous murmur

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36
Q

What information is given by a 12-lead EKG?

A

A recording of the electrical activity of the heart at a specific moment in time

Tells of depolarization and repolarization of the atria and ventricles

Can tell of heart geometry and metabolic state of the heart

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37
Q

What do you look for in an EKG reading?

A

Rate

Intervals (PR/QRS/QT)

Rhythm

Axis

Hypertrophy

Infarct/Ischemia

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38
Q

Which EKG leads are the precordial leads?

A

V1 to V6

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39
Q

Which EKG leads are the limb leads?

A

VI, VII, VIII, aVR, aVL, aVF

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40
Q

What is the placement of the six chest leads?

A
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41
Q

What is Einthoven’s triangle?

A

The comination of EKG leads VI, VII, and VIII

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42
Q

What is the directionality of VI?

A

Right arm to left arm:

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43
Q

What is the directionality of lead VII?

A

Right arm to left foot

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44
Q

What is the directionality of EKG lead VIII?

A

Left arm to left foot

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45
Q

What is the alignment of the limb leads on an EKG (i.e aVR, aVL, aVF, I, II, III)?

A
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46
Q

What is the p wave of an EKG?

A

Sequential depolarization of the right atria and left atria

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47
Q

What is the QRS complex of an EKG?

A

Right and left ventricular depolarization

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48
Q

What is the T wave of an EKG?

A

Ventricular repolarization

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49
Q

What is the PR interval?

A

Interval from onset of atrial depolarization to onset of ventricular muscle depolarization

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50
Q

What is the QRS interval?

A

Duration of ventricular depolarization

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51
Q

What is the QT interval?

A

Duration of ventricular depolarization

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52
Q

What is measured along x axis of EKG?

A

Time - usually 5mm = 0.2 seconds, 1mm = 0.04 seconds

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53
Q

What is measured along the y axis of the EKG?

A

Voltage

1mm = 0.1 mV

5mm = 0.5 mV

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54
Q

What is a normal PR interval?

A

120-200ms

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55
Q

What is a normal QRS interval?

A

<110ms

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56
Q

What is a normal QTc interval (QT interval)?

A

< 460ms

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57
Q

What is a good rule of thumb to calculate pulse rates on EKG?

A

Rate = 300 / # of boxes

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58
Q

What is a quick way to look at axis on EKG?

A

Lead I and Lead aVF (Is? Fine?)

Left hand first - thumbs up? (VI)

Right hand - thumbs up? (aVF)

Both good - normal

I good, aVF bad - left axis deviation

I bad, aVF good - right axis deviation

Both bad - extreme right axis deviation

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59
Q

How can you tell if there is left axis deviation on EKG?

A

Lead I is positive and aVF is negative

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60
Q

How can you tell if there is right axis deviation on EKG?

A

Lead I is negative and aVF is positive

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61
Q

How can you tell if there is extreme right axis deviation on EKG?

A

Both VI and aVF are negative

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62
Q

What causes right axis deviatioN?

A

Right Ventricular Hypertrophy (most common)

Chronic lung diseases, emboli, and others

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63
Q

What causes left axis deviation?

A

Left ventricular hypertrophy, left bundle branch block, and others

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64
Q

What assesments of cardiac function can you make from a chest x-ray?

A

Evaluate size of heart chambers and pulmonary consequences of heart disease

Dilations and gross anatomical deformations

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65
Q

What indicates enlarged heart on x-ray?

A

If the cardiac:thoracic ratio is over 0.5

Normal is 0.45

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66
Q

What is a normal cardiac:thoracic ratio?

A

0.45

Enlarged if greater than 0.5

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67
Q

What assesments of cardiac function can be made via an echocardiogram?

A

Anatomical relationships of movement

Valve and wall motion abnormalities

Doppler for blood flow direction, velocity, turbulence, and estimation of pressure gradients

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68
Q

What is special about trans-esophageal echocardiography?

A

Can get closer to the heart and use higher frequency in order to retrieve higher resolution images

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69
Q

What assesment of cardiac function can a CT scan perform?

A

Can look for calcium deposition in coronary arteries

Diseases of the pericardium

Aortic Dissection and aneurysm

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70
Q

What assessment of cardiac function does cardiac catheterization provide?

A

Measurement of the pressure in all of the chambers of the heart, the pulmonary artery, and the aorta

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71
Q

What are the normal pressures in the heart chambers and great vessels?

A

RA: 2-8

RV: 15-30/2-8

LA: 2-10

LV: 100-140/3-12

Aorta: 100-140/60-90

Pulm: 15-30/4-12

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72
Q

What is the normal pressure in the right atrium?

A

8-Feb

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73
Q

What is the normal pressure in the right ventricle?

A

15-30/2-8

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74
Q

What is the normal pressure in the pulmonary artery?

A

15-30/4-12

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75
Q

What is the normal pressure in the left atrium?

A

10-Feb

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76
Q

What is the normal pressure in the left ventricle?

A

100-140/3-12

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77
Q

What is the normal pressure in the aorta?

A

100-140/60-90

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78
Q

What assesment of cardiac function can contrast angiography provide?

A

Imaging of internal structures that are otherwise difficult to see on x-ray

Valvular insufficiency, intracardiac shunts, severity of coronary artery artherosclerosis

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79
Q

What is the definition of heart failure?

A

A structural or functional cardiac disorder that impairs the ability of the ventricles to eject blood (forward failure) or fill with blood (backward failure) or both

Not being able to move blood without higher filling pressure

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80
Q

What is forward failure?

A

An impairment in the ability of ventricles to eject blood

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81
Q

What is backward failure?

A

An impairment in the ability of ventricles to fill with blood

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82
Q

What are the mediators of cardiac output?

A

CO = HR x SV

SV = Stroke volume, comprised of Preload, Afterload, Contractility

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83
Q

Draw a normal Pressure-Volume Curve

A
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84
Q

What changes do you see in a pressure-volume loop with varying preload and constant pressure (afterload) and contractility?

A
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85
Q

What does this pressure-volume loop represent?

A

Varying preload with constant pressure (afterload) and contractility

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86
Q

What changes do you see in a pressure-volume loop with varying contractility and constant pressure (afterload) and preload?

A
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87
Q

What is the following pressure-volume loop indicative of:

A

Varying contractility with constant preload and pressure (afterload)

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88
Q

What do you see in a pressure-volume loop with varying pressure (afterload) and constant preload and contractility?

A
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89
Q

What is the following pressure-volume loop indicative of

A

Varying pressure (afterload) with constant preload and contractility

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90
Q

What type of heart failure do you see with decreased cardiac output, decreased left ventricular ejection fraction, or decreased contractility?

A

Systolic

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91
Q

What changes can you see in systolic heart failure?

A

Decreased cardiac output

Decreased LV ejection fraction

Dereased contractility

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92
Q

What is a normal ejection fraction?

A

Over 55%

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93
Q

What type of heart failure do you see elevated left, right end-diastolic pressures, with normal left ventricular ejection fractions?

A

Diastolic

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94
Q

What changes do you see in diastolic heart failure?

A

Elevated LV, RV end-diastolic pressures

Normal LV ejection fraction

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95
Q

How do you calculate/define ejection fraction?

A

EF = SV/EDV x 100

Stroke volume / End diastolic volume

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96
Q

What are potential etiologies of systolic heart failure?

A

Impaired contractility: CAD/MI, chronic volume overload(Mitral or Aortic Regurgitation), dilated cardiomyopathy

Increased afterload: Aortic stenosis, hypertension

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97
Q

What is the main difference between systolic and diastolic heart dysfunction?

A

Systolic dysfunction has reduced ejecton fraction (<50%)

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98
Q

What are potential etiologies of diastolic heart dysfunction?

A

Impaired diastolic filling: LV hypertrophy, restrictive cardiomyopathy, myocardial fibrosis, pericardial tamponade/constriction

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99
Q

What changes occur in the pressure-volume loops during systolic dysfunction?

A
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100
Q

What changes occur in the pressure-volume loops during diastolic dysfunction?

A
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101
Q

What are three compensatory mechanisms that can be activated during heart failure?

A

Frank-Starling Mechanism

Ventricular Hypertrophy

Neurohormonal Activation

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102
Q

What occurs during Frank-Starling compensation for heart failure?

A

Increase pressures to try to maintain cardiac output

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103
Q

During what type of heart failure do you see Frank-Starling compensation?

A

Systolic

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104
Q

How does hypertrophy help a failing ventricle?

A

Hypertrophy is a compensatory mechanism to reduce wall stress

Occurs more for diastolic heart failure

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105
Q

During which type of heart failure do you generally see hypertrophy as a compensatory mechanism?

A

Diastolic

Try to reduce wall stress by increasing thickness

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106
Q

What are two types of ventricular hypertrophy and when are they precipitated?

A

Eccentric - volume overload (chamber dilation): new sarcomeres are in series with old ones

Concentric - pressure overload: new sarcomeres in parallel with old ones

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107
Q

What is concentric hypertrophy?

A

Usually brought about due to pressure overload

Hypertrophy where new sarcomeres are in parallel with old

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108
Q

What is eccentric hypertrophy?

A

Ventricular hypertrophy brought about as a compensation for volume overload (chamber dilation)

New sarcomeres are in series with old

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109
Q

In what type of ventricular hypertrophy are new sarcomeres in parallel with old ones?

A

Concentric (pressure overload)

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110
Q

In what type of ventricular hypertrophy are new sarcomeres in series with old?

A

Eccentric (volume overload)

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111
Q

What type of ventricular hypertrophy does volume overload (chamber dilation) generally cause?

A

Eccentric

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112
Q

What type of ventricular hypertrophy does pressure overload generally cause?

A

Concentric

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113
Q

What are neurohormonal compensatory mechanisms in heart failure?

A

Adrenergic nervous system

Renin-angiotensin-aldosterone system (RAAS)

Antidiuretic hormone (ADH)

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114
Q

How does the adrenergic nervous system work to compensate for heart failure?

A

Systemic vascular resistance:

BP = CO + TPR

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115
Q

How does the Renin-Angiotensin-Aldosterone system work to compensate for heart failure?

A

NaCl and water retention increases circulating volume and therefore preload

Vasoconstriction maintains blood pressure but can add to afterload too

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116
Q

How does Antidiuretic Hormone act as a compensatory mechanism for heart failure?

A

NaCl and water retention whcih increases intravascular volume, increasing preload

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117
Q

What are some clinical manifestations (symptoms) of left sided heart failure?

A

Dyspnea (on exertion or at rest)

Orthopnea (needing to sleep erect)

Cough

Paroxysmal Nocturnal Dyspnea

Fatigue

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118
Q

What are some clinical manifestations (symptoms) of right sided heart failure?

A

Edema (peripheral, or ascites)

Right upper quadrant pain

Anorexia

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119
Q

Which side of the heart is likely to be failing when a patient presents with dyspnea, orthopnea, cough, paroxysmal nocturnal dyspnea, or fatigue?

A

Left sided heart failure

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120
Q

What side of the heart is likely to be failing if a patient presents with edema (peripheral or ascites), right upper quadrant pain, or anorexia?

A

Right sided heart failure

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121
Q

What are some signs on exam of left ventricular failure?

A

Tachycardia

Tachypnea

Rales

Pleural Effusion

Loud P2

S3 (systolic dysfunction)

S4 (diastolic dysfunction)

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122
Q

What are some signs on exam of right ventricular failure?

A

JVD

Hepatomegaly

Peripheral edema

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123
Q

If, upon exam, you find a patient has tachycardia, tachypnea, rales, pleural effusion, loud P2, S3 and/or S4, which ventricle do you suspect could be failing?

A

Left Ventricle

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124
Q

If, upon exam, you find a patient has JVD, hepatomegaly, and/or peripheral edema, which ventricle would you suspect to be failing?

A

Right ventricular failure

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125
Q

What are you likely to find upon chest x ray of a patient with heart failure?

A

Cardiomegaly

Vascular redistribution (interstitial edema)

Alveolar edema

Pleural effusion, bilaterally

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126
Q

What are goals of treatment for patients with heart failure with reduced ejection fraction?

A

Identify and correct underlying disease

Eliminate precipitating causes

Manage symptoms (decrease congestion, increase cardiac output)

Modulate neurohumoral response

Prolong long term survival

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127
Q

What are some therapies that can reduce mortality in heart failure?

A

ACE Inhibitors/Angiotensin Receptor Blockers

Beta blockers (acute - make it worse; chronic - may help)

Aldosterone antagonists

Hydralazine-Isosorbide dinitrate

ICD (implantable cardioverter defibrillator)

Cardiac resynchronisation + ICD

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128
Q

How/why are diuretics useful in treating heart failure?

A

Promote elimination of Na and water via the kidney

Reduce venous return to the heart, releive pulmonary congestion

There is no mortality benefit, only symptomatic releif

Overshooting it can lead to decreased CO

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129
Q

Do diuretics help reduce mortality in heart failure?

A

NO - only provide symptomatic releif

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130
Q

What is an example of a venous vasodilator?

A

Nitrates

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131
Q

What is an example of an arteriolar vasodilator?

A

Hydralazine

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132
Q

What is an examle of arteriolar and venous dilators?

A

ACE Inhibitors/Angiotensin Receptor Blockers (ARBs)

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133
Q

How do venous vasodilators work to treat heart failure?

A

Increase venous pooling, causing a decrease in the venous return to the heart

e.g. nitrates

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134
Q

How do arteriolar vasodilators work to treat heart failure?

A

Decreased systemic vascular resistance causes decreased LV afterload, increasing the stroke volume

e.g. Hydralazine

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135
Q

How do ACE inhibitors work?

A

Inhibit formation of Angiotensin II, decrease aldosterone

This increases the rate of Na+ elimination, decreasing the intravascular blood volume

As a result, this prevents the maladaptive ventricular remodeling of hypertrophy…

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136
Q

What are treatment options in the event that ACE inhibitors are not well tolerated?

A

ARBs

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137
Q

What are some beta blockers?

A

carvedilol, metroprolol, bisoprolol

improve overall and event free survival of all classifications of heart failure (NYHA classifications)

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138
Q

When are beta blockers contraindicated?

A

HR < 60 bpm

symptomatic bradycardia

Signs of peripheral hypoperfusion

COPD, Asthma

PR interval greater than 240 ms (2nd or 3rd AV block)

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139
Q

How does ionotropic therapy work?

A

Inhibits Na-K ATPase, causing an increase in intracellular Ca++, increasing contractility

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140
Q

When do you give ionotropic therapy?

A

In patients with heart failure in order to control symptoms

Significantly reduces hospitalization rates for heart failure, but does not provide benefit in terms of overall mortality

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141
Q

What is a phosphodiesterase inhibitor and when is it generally given?

A

Milrinone - only given in acute congestive heart failure

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142
Q

What is a beta agonist and when is it given?

A

Dopamine, dobutamine; only given in actue congestive heart failure

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143
Q

What are aldosterone antagonists and when are they given?

A

Spironolactone, eplerenone; act to increase diuresis and improves survival in congestive heart failure

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144
Q

What class of drug is spironolactone?

A

Aldosterone antagonist

Increases diuresis (improves survival in congestive heart failure)

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145
Q

What class of drug is eplerenone?

A

Aldosterone antagonist

Increases diuresis (improves survival in congestive heart failure)

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146
Q

What class of drug is dopamine?

A

Beta agonist - given in acute congestive heart failure

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147
Q

What class of drug is dobutamine?

A

beta agonist; given in acute congestive heart failure

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148
Q

What class of drug is milrinone?

A

Phosphodiesterase inhibitor; given in acute congestive heart failure

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149
Q

What class of drug is digitalis?

A

ionotropic

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150
Q

What class of drug is carvedilol?

A

Beta blocker - improves event-free survival of heart failure

contraindicated with heart rate <60bpm, symptomatic bradycardia, signs of peripheral hypoperfusion, asthma/COPD, PR interval greater than 240ms

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151
Q

What class of drug is metoprolol?

A

Beta blocker - improves event-free survival of heart failure

contraindicated with heart rate <60bpm, symptomatic bradycardia, signs of peripheral hypoperfusion, asthma/COPD, PR interval greater than 240ms

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152
Q

What class of drug is bisoprolol?

A

Beta blocker - improves event-free survival of heart failure

contraindicated with heart rate <60bpm, symptomatic bradycardia, signs of peripheral hypoperfusion, asthma/COPD, PR interval greater than 240ms

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153
Q

When are Implantable cardioverter-defibrillators (ICDs) used?

A

In patients with ischemic or non-ischemic cardiomyopathy and LVEF < 35%

provides significant survival benefit

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154
Q

What are the benefits of cardiac resynchronization?

A

Increased LV function

Increased Exercise capacity

Decreased heart failure exacerbation

Only indicated with patients with continued symptoms of heart failure while on maximum medical therapy, LVEF < 35%, prolonged QRS (>120 ms)

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155
Q

When are cardiac transplants indicated?

A

When all other medical treatments and managements have failed

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156
Q

How do you treat diastolic dysfunction?

A

Treat underlying condition - e.g. hypertension or pericardiectomy

Ionotropic agents are CONTRADICTED

Cautious use of diuretics for volume overload - stiff ventricles depend on high filling pressures to maintain cardiac output

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157
Q

What is the definition of a cardiomyopathy?

A

A structural or functional abnormality in the myocardium, independent of any other valvular, coronary, or myocardial involvement in systemic disease

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158
Q

What are the three main classifications of cardiomyopathies?

A

Dilated Cardiomyopathy (MC type): Features a reduced ejection fraction

Hypertrophic Cardiomyopathy: EF maintained, increased stiffness and diastolic dysfunction

Restrictive Cardiomyopathy: Infiltration by substances into myocardium marked by changes in compliance with preserved ejection fraction

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159
Q

What are the primary features of dilated cardiomyopathy (DCM)?

A

Cardiomegaly

Dilated ventricles

Impaired systolic function (decreased ejection fraction)

Increased myocardial mass

Increased predisposition to intra-cardiac thrombi

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160
Q

What is the etiology of dilated cardiomyopathy (DCM)?

A

Can basically be anything:

Idiopathic, familial, inflammatory (both infectious and non-infectious) toxic, metabolic, and neuromuscular

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161
Q

What is seen in the early stages of dilated cardiomyopathy (DCM)?

A

Tachycardia and inreased contractility to maintain cardiac output in light of a failure of the myocardium

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162
Q

What is seen in the later stages of dilated cardiomyopathy (DCM)?

A

Increased end-diastolic pressures along with decreased cardiac output.

This decreases renal perfusion which activates the R-A-A system to increase peripheral vascular resistance, further dilating all four chambers of the heart.

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163
Q

What are some symptoms of dilated cardiomyopathy (DCM)?

A

Dyspnea

Orthopnea

Paroxysmal Nocturnal Dyspnea

Weight gain

Edema

Decreased Exercise tolerance

Fatigue

Light-headedness

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164
Q

What are some physical findings (signs) of dilated cardiomyopathy (DCM)?

A

Cool extremities

Tachycardia

Displaced and diffuse apical impulse

Gallup rhythm

Rales

Signs of RV failure including JVD, hepatomegaly, edema, ascites

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165
Q

What do you see on chest x-ray in cases of dilated cardiomyopathy?

A

Cardiomegaly

Signs of heart failure including pulmonary vascular redistribution, interstitial and alveolar edema, pleural effusion

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166
Q

What do you see on EKG in cases of dilated cardiomyopathy?

A

Nothing specific, but may reveal a variety of abnormalities:

Chamber enlargement

Arrhythmias

Localized Q waves, dense fibrosis

Diffused ST, T wave abnormalities

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167
Q

What do you find on Echo in cases of dilated cardiomyopathies?

A

Chamber dilatation

Decreased ejection fraction (can be quantified here)

Presence or absence of intracardiac thrombus

Potentially concomitant valvular disease

Can be used to track pt progress

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168
Q

Why would you perform cardiac catheterization on a patient with dilated cardiomyopathy?

A

Useful to exclude coronary artery disease, valvular disease

Can perform a biopsy to confirm diagnosis of myocarditis

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169
Q

How do you treat dilated cardiomyoptahties (DCMs)?

A

Manage symptoms - medical treatment for systolic heart failure

Prevent complications such as arrhythmias or thromboembolic events

Prolong long term survival

Cardiac transplants

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170
Q

What is the prognosis for dilated cardiomyopathy patients?

A

1/3 will improve spontaneously

2/3 will have 5 year mortality of < 50% without cardiac transplant

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171
Q

What causes hypertrophic cardiomyopathy (HCM)?

A

Asymmetric hypertrophy of LV septum (not caused by chronic presure overload)

Inheritance is commonly autosomal dominant

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172
Q

What is seen on pathology of hypertrophic cardiomyopathy (HCM)?

A

Asymmetric LV septal hypertrophy

Disorganization of myocardial fibers in septum

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173
Q

What type of cardiomyopathy is suggested by asymmetric LV septal hypertrophy and findings of disorganized myocardial fibers in the septum?

A

Hypertrophic cardiomyopathy (HCM)

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174
Q

What are two different classes of hypertrophic cardiomyopathies?

A

HCMs with and wihtout outflow tract obstruction

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175
Q

What are some clinical symptoms of hypertrophic cardiomyopathy (HCM)?

A

Dyspnea

Angina

Syncope

Sudden cardiac death

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176
Q

What are some findings on exam (signs) of hypertrophic cardiomyopathy (HCM)?

A

Arterial pulse is abrupt and ill-sustained

S4 sounds

Double apical impuse

Signs of mitral regurgitation

Systolic murmor of HCM is distinct: crescendo and decrescendo at the lower left sternal border - increased with valsalva and standing, decreased with squatting

The obstruction is dynamic (increased afterload decreases obstuction; decreased afterload increases obstruction)

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177
Q

What do you find on chest x-ray in cases of hypertrophic cardiomyopathy (HCM)?

A

Nothing specific for HCM

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178
Q

What do you find on EKG in cases of hypertrophic cardiomyopathy (HCM)?

A

Left ventricular hypertrophy

LA enlargement

Q-wave and T-wave inversion

Arrhythmias

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179
Q

What do you find on echo on patients with hypertrophic cardiomyopathy?

A

Assymmetrical hypertrophy of the LV septum

Systolic anterior motion of the mitral valve

Intracavitary and subaortic pressure gradient

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180
Q

When do you perform cardiac catheteriation on patients suspicious for hypertrophic cardiomyopathy?

A

If the diagnosis is uncertain… This is usually not required

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181
Q

How do you treat hypertrophic cardiomyopathy (HCM)?

A

Beta blockers - negative inotropy (decrease oxygen demand, decrease LV outflow gradient during exercise, increase passive diastolic ventricular filling time, decrease frequency of ventricular ectopic beats)

Calcium channel blockers (instead of beta blockers)

Diuretics (in overt congestive heart failure)

Amiodarone (to treat arrhytmias)

ICD - family history of sudden cardiac death, ventricular wall greater than 30 mm, unexplained syncopal episodes, hx of tachyarrhytmia

Pacemakers

Surgical myomectomy

Percutaneous Septal Ablation

**** Avoid vasodilators, digitoxin****

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182
Q

How do beta blockers help in the treatment of hypertrophic cardiomyopathy (HCM)?

A

Decrease mocardial oxygen demand

Decrease LV outflow gradient during exercise

Increase passive diastolic ventricular filling time

Decrease frequency of ventricular ectopic beats

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183
Q

What is the natural history of hypertrophic cardiomyopathy?

A

Variable

Ranges from long life with few symptoms to rapid course with sudden death

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184
Q

When does sudden death occur in hypertrophic cardiomyopathy (HCM)?

A

When there are associated arrhythmias present

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185
Q

Which cardiomyopathy subtype is the least common?

A

Restrictive cardiomyopathy (dilated cardiomyopathy and hypertrophic cardiomopathy are more common)

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186
Q

What occurs in restrictive cardiomyopathy?

A

Diastolic dysfunction with preserved systolic function

Rigid myocardium - fibrotic or infiltrated

With end stage disease, the ventricular cavity may become obliterated

Cause of death at end stage is congestive heart failure

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187
Q

What is the etiology of restrictive cardiomyopathy (RCM)?

A
  • *Non-infiltrative** (idopathic, scleroderma)
  • *Infiltrative** (amyloid, sarcoid)

Storage diseases (Hemochromatosis, glycogen storage disease)

Endomyocardial diseases (endomyocardial fibrosis, hypereosinophilic syndrome)

Metastatic tumors

Radiation therapy

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188
Q

What is tropical endomyocardial firosis?

A

Unknown cause - seems to be related to troical environment

Disease in which firosis of ventricles occurs along with eosinophilia

Diastolic dysfunction and eventual obliteration of the left ventricle occur, and patients die by congestive heart failure

Treatments are often unsatisfactory, and surgeries (resections of oblierated tissue and valve repair) may only help in the short term

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189
Q

What is cardiac amyloidosis?

A

Primary: deposition of the Ig light chain (AL) fragments secreted by a plasma cell tumor (e.g. multiple myeloma)

Secondary: seen in variety of inflammatory conditions (Rheum. Arthr.)

Hereditary is autosomal dominant

Senile amyloidosis

In all: amyloid deposition is extracellular (between myocardial fibers, in the coronary arteries, veins and valves)

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190
Q

What are the different types of cardiac amyloidosis?

A

Primary: depositions of Ig light chain fragments secreted by plasma cell tumor

Secondary (to inflammatory condition, i.e. Rheumatoid Arthritis)

Hereditary (autosomal dominant)

Senile

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191
Q

What is the pathophysiology of restrictive cardiomyopathy (RCM)?

A

Rigid myocardium results in decreased ventricular filling (decerased cardiac output) and increased diastolic ventricular pressure (venous congestion)

As a result, you get symptoms of congestive heart failure (JVD< hepatomegaly, ascites, peripheral edema); and of decreased cardiac output (weakness, fatigue)

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192
Q

What are some clinical symptoms of restrictive cardiomyopathy (RCM)?

A

Dyspnea

Orthopnea

Paroxysmal Nocturnal Dyspnea

Weight gain

Decreased exercise tolerance

Edema

Fatigue

Light-headedness

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193
Q

What are some clinical exam findings (signs) of restrictive cardiomyopathy (RCM)?

A

Tachycardia

Rales

Kussmaul sign (Increased JVD with inspiration)

Other signs/symptoms of RV failure (JVD, hepatomegaly, edema, ascites)

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194
Q

What would a chest x-ray reveal for a patient with restrictive cardiomyopathy (RCM)?

A

Normal sized heart with signs of pulmonary congestion

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195
Q

What would an EKG reveal for a patient with restrictive cardiomyopathy (RCM)?

A

Non-specific ST-T changes, arrhytmias

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196
Q

What diagnostic test can you perform to differentiate a restrictive cardiomyopathy (RCM) from a constrictive pericarditis?

A

Cardiac CT or MRI

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197
Q

What is the treatment for restrictive cardiomyopathy?

A

There is a poor prognosis because treatment is mostly focused on treating the cause of the disease and symptoms; and often the causes are difficult to treat

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198
Q

Which cardiomyopathy is the most common?

A

Dilated cardiomyopathy (~90% of all cases)

199
Q

What is the most common age of onset for dilated cardiomyopathy?

A

In males between 20 and 50 years old

200
Q

What are findings on pathology of dilated cardiomyopathy?

A

Enlarged, flabby heart with dilatation of all chambers

Thin ventricles

Mural thrombi due to stasis

Absent valvular and vascular lesions that would cause secondary cardiac dilation

201
Q

What are histological findings of dilated cardiomyopathy?

A

Non-specific, including:

Hypertrophied myocytes with enlarged, boxcar nuclei

Irregular myocytes with varying degrees of interstitial and endocardial fibrosis

202
Q

What are common infectious causes of dilated cardiomyopathy?

A

Viral - Coxsackie, adenovirus, HIV, hep C, parvovirus

Parasitic - Trypanosoma cruzi (Chagas’ disease)

Bacteria - diptheria

Spirochete - Lyme disease (Boriella burgodrferi)

Rickettsial (Q fever)

Fungal (systemic)

203
Q

What can clue you in to a viral etiology of dilated cardiomyopathy?

A

Lymphocyte aggregates with myocyte necrosis

204
Q

What can clue you in to a fungal etiology of dilated cardiomyopathy?

A

Presence of hyphae on silver stain

205
Q

What are non-infectous causes of dilated cardiomyopathy?

A

Granulomatous inflammatory disease (giant cell myocarditis, sarcoidosis)

Hypersensitivity (to antibiotics, sulfonamides)

Collagen vascular disease (polymyositis, dermatomyositis)

206
Q

What histological features can identify giant cell myocarditis as the cause of dilated cardiomyopathy?

A

Multinucleated giant cells, interstitial infiltrate and myocyte necrosis

207
Q

What are some drugs/toxins that can cause dilated cardiomyopathy?

A

Alcohol

Cocaine, emetine, anabolic steroids

Chemotherapy agents (anthracyclines, trastuzumab, IFN)

Other (hydroxychloroquine, chloroquine)

Heavy metals (lead, mercury)

Occupational (hydrocarbons, arsenicals)

208
Q

What are the mechanisms of alcohol-related dilated cardiomyopathy?

A

Direct toxic effect of alcohol and its metabolites (acetaldehyde)

Secondary nutritional deficiency (thiamine)

Alcohol additives (cobalt)

209
Q

What are some metabolic causes of dilated cardiomyopathy?

A

Nutritinal deficiencies (thiamine, selenium, carnitine)

Electrolyte deficiencies (calcium, phosphate, magnesium)

Endocrinopathy (thyroid, diabetes, …)

Obesity

Hemochromatosis (iron storage disorder)

210
Q

What are some histological findings that can identify hemochromatosis as the cause of dilated cardiomyopathy?

A

Brown cytoplasmic iron pigments or a specific stain for iron

211
Q

What is the most important cause of suddenc ardiac death in the young and in atheletes?

A

Hypertrophic Cardiomyopathy (HCM)

212
Q

What are some causes of hypertrophic cardiomyopathy?

A

Genetic: genes encoding sarcomeric proteins (beta myosin heavy chain, for example)

213
Q

What is the inheritance pattern of genetic hypertrophic cardiomyopathy?

A

Autosomal dominant with nearly complete penetrance

214
Q

What are pathological features of the hypertrophy in hypertrophic cardiomyopathy?

A

Hypertrophy is asymmetric and confined to interventricular septum below the aortic valve in majority of patients

The interventricular septum is more hypertrophied than the free LV wall

215
Q

What is a difference on gross pathology between hypertrophic cardiomyopathy and hypertrophy from hypertension?

A

HCM causes a disproportionate hypertrophy of the interventricular septum as opposed to the free LV wall

216
Q

What are some microscopic/histologic freatures of hypertrophic cardiomyopathy?

A

Interstitial fibrosis and enlarged, box-car nuclei of the myocardial cells

217
Q

Which cardiomyopathy is the least common?

A

Restrictive Cardiomyopathy (RCM)

218
Q

What is the etiology of restrictive cardiomyopathy?

A

Primary: Tropical endomyocardial fibrosis - idiopathic

Secondary: infiltrative (amyloid, sarcoid, storage disorders), non-infiltrative (carcinoid, iatrogenic - i.e. due to radiation or chemo)

219
Q

What is the gross appearance of a heart in restrictive cardiomyopathy?

A

Ventricles are of approximately normal size or slightly enlarged

Myocardium is firm and of normal thickness

There is bilateral dilation due to poor ventricular filling and pressure overloads.

220
Q

What is Loeffler’s Endomyocarditis?

A

Restrictive cardiomyopathy that affects males in temperate climates

It results in death within months and can be identified on histology by an increased presence of eosinophils.

221
Q

How do you identify amyloid when you suspect it to be the cause of restrictive cardiomyopathy?

A

Polarized congo red stain - you can see apple green birefringence

222
Q

What is arrhythmogenic right ventricular cardiomyopathy (ARVC)?

A

A rare disease that is heritable and caused by mutations in desmosomal proteins (desmoplakin, plakophilin, desmoglein, desmocollin, plakoglobin)

Autosomal dominant, incomplete penetrance

Affects the right ventricle

Early phase is often clinically silent

Late phase predisposes to a disproportionate risk of arrhythmic events

223
Q

What mutations are seen in arrhythmogenic right ventricular cardiomyopathy (ARVC)?

A

Mutations in desmosomal proteins

224
Q

What is the inheritance pattern of arrythmogenic right ventricular cardiomyopathy?

A

Autosomal dominant

225
Q

What do you see pathologically in arrhythmogenic right ventricular cardiomyopathy (ARVC)?

A

fatty and fibrofatty replacement of heart muscle

226
Q

What is isolated left ventricular noncompaction (LVNC)?

A

Congenital myocardial disorder that is a common cause of cardiomyopathy in children

Presents with congestive heart failure, arrhythmia, or complications of thromboembolism

Persistence of the noncompacted endocardial layer is characteristic of the early fetal period before myocardial compaction is complete

Left ventricle is dilated or hypertrophied

227
Q

What do you find on pathology in cases of isolated left ventricular noncompaction (LVNC)?

A

Complex meshwork of trabeculations and recesses

Sponge-like appearance of the LV wall

Abnormal myocardial hypoperfusion

228
Q

What cells maintain the integrity and elasticity of arterial vasculature?

A

Endothelial cells and smooth muscle cells

229
Q

What are some key characteristics of endothelial cells?

A

Impermeable to large molecules (LDL-C)

Anti-inflammatory

Promote vasodilation

Resist thrombosis

230
Q

What are some important characteristics of smooth muscle cells?

A

Effect vasoconstriction/dilation in response to local or circulating molecules (provide tone)

Produce extracellular matrix that maintains vascular integrity (collagen provides strength; elastin provides flexibility)

They are contained within the arterial tunica media

231
Q

Where are smooth muscle cells of the vasculature located?

A

In the tunica media of arteries

232
Q

What is significant about a fatty streak?

A

It is a hallmark of early atherogenesis, and allows the entry of lipoprotein particles (LDL) into the sub-intimal space

This causes a recruitment of immunologic mediators (inflammation)

LDL is modified (oxidation or glycation)

mLDL is taken up by monocytes (foam cells), and these cells undergo necrosis

These lesions are apparent in healthy individuals by late teens

233
Q

What is a foam cell?

A

A monocyte that has taken up mLDL from an arterial subinimal space

This is generally unregulated

These cells gorge themselves on LDL and become the necrotic core of an atherosclerotic lesion

234
Q

What occurs during plaque progression of atherosclerosis?

A

Smooth muscle cells migrate to the sub-intimal space where they’re not supposed to be.

Smooth muscle cells proliferate and secrete extracellular matrix, producing the fibrous cap of the plaque.

This usually occurs outwardly and preserves the luminal diameter

Later on, this will occlude the vessel

235
Q

What distinguishes a vulnerable plaque from a stable plaque?

A
236
Q

What are characteristics of vulnerable atherosclerotic plaques?

A
237
Q

What are characteristics of stable atherosclerotic plaques?

A
238
Q

What occurs in atherosclerotic plaque disruption?

A

Fibrous cap ruptures as a consequence of hemodynamic stress and matrix degradation.

This is the most common mechanism for atherosclerotic-induced MI

This is a thrombogenic event, which causes a fibrin, red cell and platelet thrombus to form on top

Not all ruptures manifest clinically

239
Q

What are likely manifestations of atherosclerosis?

A

Ischemic stroke or transient ischemic attack

Myocardial infarction, angina, sudden death

Intermittent claudication, critical limb ischemia, gangrene, necrosis

Recall, atherosclerosis is a SYSTEMIC disease that manifests locally

240
Q

What are some risk factors for atherosclerosis?

A
  • *Traditional:**
  • Non-modifiable - *Age, Gender, Genetics;

*Modifiable - *Dyslipidemia, Smoking, Diabetes, Phisical Inactivity

Non-traditional:

Apolipoprotein (a)

C-reactive protein

Homocysteine

241
Q

What relationship does cardiovascular disease have with age and sex?

A

Increases linearly with age

Risk is higher among men than in women in youth, but reverses with age.

242
Q

What is the function of lipoprotein particles?

A

Transport cholesterol in serum

243
Q

What is HDL-C?

A

High Density Lipoprotein Cholesterol

This is “Good” cholesterol

Acts as a reverse cholesterol transporter (takes from periphery and brings it back to the liver)

244
Q

Why is HDL-C known as “good” cholesterol?

A

It participates in reverse cholesterol transport - takes cholesterol from the periphery to the liver

245
Q

What is LDL-C?

A

Low Density Lipoprotein Cholesterol

“Bad Cholesterol” that deposits in the arterial wall leading to atherosclerosis

It is the primary target of pharmacotherapy

246
Q

Why is LDL-C known as “bad” cholesterol?

A

It deposits in the arterial walls, leading to atherosclerosis

247
Q

How can one lower LDL-C levels?

A

Diet/Exercise (Therapeutic Lifestyle Changes)

Pharmacologic therapy: Niacin; bile acid sequestrans; fibric acid; statins (HMG-CoA Reductase Inhibitors)

248
Q

How do HMG-CoA Reductase Inhibitors (i.e. Statins) work?

A

Increase expression of LDL-C receptor in liver, thereby lowering serum levels of LDL-C

249
Q

What are some benefits of statins?

A

Benefit is proportional to the degree of lowering of LDL-C

Also, you can see a modest elevation of HDL-C (this is good)

Also, favorably modulates vascular tone, stabilizes plaques, and reduces inflammation

250
Q

What are some confounding factors that make it difficult to modulate LDL levels?

A

Cigarette smoking

Hypertension

Low HDL

Family history of coronary heart disease

Age

251
Q

What are the LDL targets for individuals with coronary heart disease, 2+ risk factors, or 0-1 risk factors?

A

CHD: <100

2+ : <130

0-1 : <160

252
Q

Is it a viable strategy to attempt to raise HDL-C levels?

A

Not really - many attempts have not been succesful or proven. Many have poor side effects

Best bet is to use non-pharmacologic methods (diet + exercise)

253
Q

What are some cardiovascular effects of diabetes mellitus?

A

Enhanced inflammation

Increased platelet reactivity, hypercoagulability

Endothelial dysfunction

Nonenzymatic glycation of lipoproteins

Vascular stiffness and arterial calcification

Sum total is ACCELERATED atherosclerosis in a genearlly PROthrombotic state

254
Q

What is meant by the statement that diabetes is a coronary heart disease “risk equivalent”?

A

It means that the risk for coronary heart disease among people with diabetes and no prior MI is equal to those who do not have diabetes but have had a prior MI

255
Q

What are good treatment strategies for the mitigation of the risk of cardiovascular disease in diabetic patients?

A

Glycemic control is key

But often times that is not enough - need to also aggressively control modifiable cardiac risk factors (hypertension, hyperlipidemia, obesity)

256
Q

What are some vascular effects of obesity/physical inactivity?

A

Inflammation - adipose tissue can secrete pro-inflammatory cytokines

Hypertension - increased cardiac output to meet increased metabolic demands of excess body weight + changes in vascular tone

Endothelial dysfunction

Insulin resistance - leading to diabetes

257
Q

How is BMI measured?

A

weight in kg/ (height in meters)^2

258
Q

What is the normal range of BMI?

A

18.5-24.9

259
Q

What defines obesity?

A

BMI over 30

260
Q

What is the relationship between BMI and mortality in US adults?

A

High mortality at both ends of BMI scale

Lower BMI mortality may be attributable to malnourishment, or frailty

261
Q

How is smoking a risk factor for coronary heart disease?

A

Smoking is associated with excess of fatty streaks and raised lesions in abdominal aorta

Causes endothelial damage

Exerts prothrombotic effects on platelet function

Causes coronary vasoconstriction

Produces oxidative modification of LDL-C

262
Q

What is homocysteine?

A

A biomarker of atherogenesis that may be linked to the pathophysiology of arteriosclerosis via oxidative stress, inflammation and platelet aggregation

Reduction of homocysteine does not correlate with reductions of cardiovascular risk

263
Q

What is lipoprotein (a)?

A

A variant of LDL that contains apolipoprotein apo(a)

May impair endogenous thrombolysis and promote inflammation

Higher Lp(a) levels correlate with higher risk for CV events, but therapeutic benefits are unclear

264
Q

What is C-Reactive Protein?

A

Acute phase reactant released by liver that is a good marker of inflammation

Has been associated with increased cardiac risk independent of cholesterol levels, but it is still unclear if CRP is a marker or mediator of atherosclerosis

265
Q

How do you diagnose hypertension?

A

Two independent readings with the patient not ingesting caffeine or smoking 30 minutes prior to measurements

Patient sitting for 5 minutes

266
Q

What are four determinants of blood pressure regulation?

A

Heart - provides cardiac output

Peripheral vasculature - vascular tone/resistance

Kidney - regulates intravascular volume, and is essential in the maintenence of chronic hypertensive states

Hormones/Reflexes - modulates all systems simultaneously

267
Q

What is an equation that represents blood pressure?

A

BP = Cardiac output * Total peripheral resistance

268
Q

What are the determinants of cardiac output?

A

Cardiac output = Heart rate * stroke volume

269
Q

What are two determinants of stroke volume?

A

contractility and venous return

270
Q

What are determinants of venous return?

A

blood volume and venous tone

271
Q

How do the kidneys regulate blood pressure?

A

Renin-Angiotensin-Aldosterone system

272
Q

What is pressure natriuresis?

A

Simple hemodynamics - more pressure = more in, increases GFR, increases Na and H20 excretion

Doesn’t involve sensors or circulating factors

In chronic hypertension, this is blunted… requires greater blood pressure to excrete a given salt load

273
Q

What role do baroreceptors play in blood pressure and its regulation?

A

Moment-to-moment regulation of BP

Found in aortic arch and carotid sinuses

Reflex response that works relatively instantaneously

274
Q

What is essential hypertension?

A

Elevation in BP without a readily identifiable cause

It is a syndrome rather than a disease with clear etiology

MOST COMMON form of HTN (~90%)

Diagnosis of exclusion - first need to rule out other potential causes that would secondarily produce hypertension

275
Q

What are some causes of essential hypertension?

A

Genetics - still unclear

Systemic abnormalities - vascular tone or sympathetic overactivity

Renal abnormalities - excess Na/H20 retention, or horomonal dysregulation (high baseline renin levels, for example)

276
Q

In younter patients, is essential hypertension usually systolic or diastolic?

A

Diastolic

277
Q

In older patients, is essential hypertension usually systolic or diastolic?

A

systolic

278
Q

What is secondary hypertension?

A

Hypertension in the setting of a clear structural/hormonal cause

Treatment may be curative

279
Q

What are clinical clues to a diagnosis of secondary hypertension?

A

Very young, or new hypertension after age 50

More severe with rapid onset

Physical signs/symptoms of renal disease, stenosis

280
Q

How can renal disease cause secondary hypertension?

A

Impaired ability of kidneys to excrete sodium/water causes a rise in intravascular volume which results in elevated cardiac output and blood pressure

281
Q

What are some laboratory findings that can identify renal causes of secondary hypertension?

A

Elevated serum creatinine, abnormal urinalysis

282
Q

What are renovascular causes of secondary hypertension?

A

Renal artery stenosis - atherosclerosis (in 2/3 of cases) or fibromuscular dysplasia (in 1/3 of cases, mostly in young women)

Stenosis causes reduced renal blood flow, which induces renin secretion and increased Angiotensin II (causing vasoconstriction) and increased aldosterone (causing sodium retention)

You can hear an abdominal bruit and you see an unexplained hypkalemia

283
Q

Why do you see hypokalemia in renovascular causes of secondary hypertension?

A

In these patients you have increased aldosterone which increases sodium retention (at the expense of potassium - Na/K pump)

284
Q

What are treatments for secondary hypertension due to renovascular causes?

A

Renal artery revascularization

ACE inhibitors

285
Q

How can aortic coarctation cause secondary hypertension?

A

Narrowing of aorta causes reduced blood flow to kidneys which stimulates RAAS and increases angiotensin II causing vasoconstriction

You can see BP discrepancy - arms vs legs and left vs right arm in some cases

286
Q

What are some endocrine causes of secondary hypertension?

A

Catecholamine-secreting tumors of neurendocrine cells in the adrenal medulla

Or excess mineralocorticoid secretion (aldosterone)

Or excess glucocorticoid secretion (cortisol)

287
Q

How do catecholamine-secreting tumors of neuroendocrine cells cause secondary hypertension?

A

Release epi/norepi - causes vasoconstriction/tachycardia that can come in waves

288
Q

How does excess mineralocorticoid secretion cause secondary hypertension?

A

Excess aldosterone - RAAS system activated

289
Q

What is Conn Syndrome?

A

Primary aldosteronism - causes secondary hypertension

290
Q

How does excess glucocorticoids cause secondary hypertension?

A

Cortisol - expands blood volume, stimulates RAAS

291
Q

What is Cushing Syndrome?

A

Excess cortisol - rounded facial appearance, central obesity, muscle weakness and hypertension

292
Q

How does hyperthyroidism cause hypertension?

A

Cardiac hyperactivity - increase in blood volume

293
Q

How does hypothyroidism cause hypertension?

A

Diastolic hypertensoin due to increase in peripheral vascular resistance

294
Q

What can be a cardiovascular side effect of oral contraceptives?

A

Hypertension - estrogen increases synthesis of angiotensinogen (RAAS)

295
Q

What are some drug-related causes of hypertension

A

Oral contraceptives

Glucocorticoids

Erythropoetin

Sympathomimetics (OTC cold remedies)

Alcohol

Cocaine

296
Q

What are some consequences of hypertension?

A

Physiologic/structural derangements that manifest chronically:

Increased workload of heart

Arterial damage (smooth muscle cell hypertrophy, endothelial dysfunction, loss of elasticity)

Organ damage (heart, cerebral vasculature, aorta, kidney, retina)

297
Q

What are cardiac effects of hypertension?

A

Ventricular hypertrophy - leads to ventricular stiffness and diastolic dysfunction

Systolic dysfunction (due to potential myocardial ischemia)

Coronary Artery Disease - HTN promotes development of atherosclerosis which decreases myocardial oxygen supply; alos, increased cardiac work due to elevated BP causes increased myocardial oxygen demand

298
Q

What are some cerebrovascular effects of hypertenison?

A

HTN is one of the strongest risk factors for stroke

Hemmorrhagic - rupture of microaneurysms

Ischemic - thrombosis due to atherosclerotic plaques and subsequent embolism

Treatment of BP reduces stroke-related deaths by 50%

299
Q

What are some aorta-related complications of hypertension?

A

Aneurysm - abdominal aorta below renal arteries

Dissection of ascending and descending, due to intimal tears - high mortality

300
Q

What is hypertensive crisis?

A

Urgency - BP > 180/110 with no end-organ damage; does not require hospitilization

Emergency - BP > 180/110 with signs of end-organ damage; Requires hospitalization

End organ damage can be hypertensive encephalopathy, dyspnea, eye damage

301
Q

What differentiates a hypertensive urgency from a hypertensive emergency?

A

In both cases, SBP > 180 or DBP > 110, but in emergency there is sign of end-organ damage whereas in urgency there is not

302
Q

What are components of a history/physical exam that can help identify hypertension?

A

Weight gain/loss, renal damage (history of UTIs)

Lifestyle behaviors such as alcohol or drugs

Medicaiton history of prescription and OTC

Murmurs, bruits, or BP discrepancies

303
Q

What are some laboratory findings that may be helpful in identifying hypertension?

A

Renal abnormalities (creatinine, urine analysis)

Serum potassium (hypokalemia may clue to increaed aldosterone)

Blood glucose

304
Q

What evidence of hypertension can be seen on electrocardiogram?

A

Evidence of LV hypertrophy

305
Q

What are some non-pharmacologic treatments of hypertension?

A

Weight reduction, exercise, diet modification, salt restriction, smoking/drinking cessasition

306
Q

What are some pharmacologic therapies for hypertension?

A

Diuretics (chepa, and ideal choice for management of uncomplicated hypertension)

Sympatholytic agents (Beta blockers) - reduce cardiac output and decrease renin secretion => Side effects include asthma, fatigue, and impotence

307
Q

Why do alpha-2 adrenergic agonists help in the treatment of hypertension?

A

Reduce sympathetic outlow

However, have a poor side effect profile and are rarely used

308
Q

Why are alpha-1 antagonists useful in treating hypertension?

A

Relax vascular smooth muscle and also have added benefit of reducing prostatic enlargement in older men

309
Q

What is the effect of calcium blockers in treating hypertension?

A

Reduce influx of calcium necessary for cardiac/vascular smooth muscle contraction - reduces contractility and resistance

(peripheral vasodilator)

310
Q

How do ACE inhibitors work in the treatment of hypertension?

A

Block conversion of angiotensin I to angiotensin II and block RAAS

Reduce mortality in high-risk cardiac patients

Side effects include dry cough and hyperkalemia

311
Q

What are some side effects of ACE inhibitors?

A

Dry cough, hyperkalemia

312
Q

What are ARBs?

A

Angiotensin-II receptor blockers

313
Q

What is the first line agent for uncomplicated hypertension?

A

Thiazide diuretics

Have proven benefits and low cost with an acceptable safety profile

314
Q

How do you choose a anti-hypertensive drug for a patient with complicated hypertension?

A

Consider co-morbidities and try to kill two birds with one stone:

E.g. avoid ACE inhibitors in women with child-bearing age (teratogenic)

Avoid diuretics in elderly - dehydration

315
Q

What effect does the rate of blood flow have on the development of thrombi?

A

In areas of high shear stress, endothelial cells generate an anti-thrombotic state

In slow-flow areas, the arterial walls are thickend and there is decreased luminal size

316
Q

What is the effect of endothelial derived relaxing factor (EDRF, a.k.a. NO) on the vasculature?

A

Inhibits smooth muscle contraction and proliferation

Inhibits platelet aggregation

Inhibits LDL oxidation

Decreases expression of adhesion molecules

Decreases endothelin production

317
Q

What is endothelin?

A

A factor produced by endothelial cells of the vasculature that promotes vasoconstriction and coagulation

318
Q

What is the role of endothelium in atherothrombosis?

A

Endothelium produces both pro- and anti- atherogenic substances:

Pro: vasoconstrictors, prothrombotics, pro-inflammatories, smooth muscle cell promoters

Anti: vasodilators, antithrombotics, anti-inflammatories, smooth muscle cell inhibitors

319
Q

What event causes platelet aggregation in the vasculature?

A

Release of NO (due to injury or other endothelial dysfunction)

This causes platelet adhesion and subsequent thrombus formation

320
Q

What is the difference between atherosclerosis and atherothrombosis?

A

People generally lives with atherosclerosis, but people die from atherothrombosis…

321
Q

What function does aspirin have on atherothrombotic disease?

A

Inhibits Arachidonic Acid pathway viea acetylation of Cyclogenase enzymes (COX1 and COX2)

Inhibits platelet aggregation and is an effective, safe, and inexpensive antithrombotic agent

322
Q

What is the efficacy of P2Y12 inhibitors vs aspirin?

A

More effective and efficacious in ASA-resistant patients

e.g. clopidogrel, prasugrel, ticagrelor

323
Q

What is clopidogrel?

A

ADP receptor inhibitor - blocks platelet activation

Used as antithrombotic therapy - in patients who are ASA intolerant

324
Q

What are diferent forms of pericardial disease?

A

Acute pericarditis

Pericardial effusion +/- cardiac tamponade

Constrictive pericarditis

325
Q

What are some causes of acute pericarditis?

A

Infectious: viral are most common (coxsackie and echovirus), but the least commonly identified; often labeled as idiopathic

Bacterial in the case of pneumonias

TB with immigrants

Non-infectious: Post MI, metabolic disorders, surgery, trauma, radiation, drugs, malignancies, collagen vascular disease

326
Q

What determines how much pericardial involvement there will be following an MI?

A

Infarct size

327
Q

What is the mechanism of pericarditis following an MI?

A

Early - inflammatory

Late stages - immune mediated (weeks to months later). This is autoimmune

Known as Post Cardiac Injury sydnrome or Dressler’s Syndrome

328
Q

What is Dressler’s Syndrome?

A

Post-MI autoimmune-mediated pericarditis

329
Q

What are some symptoms of acute pericarditis?

A

Chest pain (retrosternal, pleuritic - i.e. on breathing, positional - e.g. when leanign forward)

Dyspnea (because of pain on breathing)

Fever

330
Q

What are some signs of acute pericarditis?

A

Pericardial friction rub (ejection, early diastole, late diastole). This is best heard in expiration in a seated position

This is highly specific for pericarditis

331
Q

What tests would you order when suspecting pericarditis?

A

CBC

Bacterial culture if febrile

EKG - check for ST elevation or PR depression

CXR

Echo

332
Q

What findings do you find on EKG in acute pericarditis?

A

ST elevation in most leads (evidence of injury)

Depression of PR segment

Low voltage QRS

T wave inversion

333
Q

What is suggested by this EKG?

A

Acute pericarditis

334
Q

What is the treatment for acute pericarditis?

A

Bed rest

NSAIDs

Colchicine for the prevention of recurrent pericarditis (potent anti-inflammatory)

Steroids (only if recurring)

Treat for underlying etiology

335
Q

What are some complications of acute pericarditis?

A

Constriction - scarring and loss of elasticity of the pericardial sac

Tamponade - accumulation of pericardial fluid under pressure

Recurrent pericarditis (autoimmune role suspected)

336
Q

What can cause pericardial effusions?

A

Infections (viral, bacterial, TB)

Non-infectious - Malignancy, renal failure, hypothyroidism, radiation, trauma, aneurysim, AIDS

337
Q

What is a significant contraindiction in the treatment of pericardial effusions?

A

DO NOT DRAIN - take to the OR. Draining can cause patients to bleed out

338
Q

What are some symptoms of pericardial effusions?

A

Can be asymptomatic

Dyspnea

Cough

Dysphagia

Hiccup

Hoarseness

Abdominal fullness

339
Q

What are some signs of pericardial effusions?

A

Muffled heart sounds

Decreased intensity of heart sounds

340
Q

What is the appearance of pericardial effusion on x-ray?

A

Water-bottle heart

341
Q

What is this x-ray suggestive of?

A

Pericardial effusion

342
Q

What is cardiac tamponade?

A

A clinical syndrome of hypotension, tachycardia, and associated symptoms that occurs when intrapericardial pressure exceeds intracardiac pressure

343
Q

What is the difference between slowly and rapidly developing pericardial effusions with tamponade?

A

Slowly - pericardium can stretch and the tamponade occurs with a larger volume

Rapid - pericardium has no time to stretch and the tamponade occurs with a smaller volume

344
Q

How ist he pathophysiology of tamponade dependent on breathing?

A

Similar to constriciton

On inspiration, RV volume is greater than LV, on expiration, it is the opposite.

This is an exaggerated interventricular dependence

345
Q

What are some clinical symptoms of cardiac tamponade?

A

Dyspnea

Orthopnea

Fatigue

346
Q

What are some clinical signs of cardiac tamponade?

A

Tachycardia

Pulsus paradoxus

Increased JVP

Decreased Systolic BP with narrow pulse pressure

Muffled heart sounds

Dullness to percussion (Ewart’s Sign)

Kussmaul’s Sign (visible neck veins on inspiration)

Beck’s Triad - decreased arterial pressure, increased venous pressure, distant heart sounds

347
Q

What is Beck’s Triad?

A

Decreased arterial pressure

Increased venous pressure

Distant heart sounds

348
Q

What is Ewart’s Sign?

A

Dullness to percussion in left lung (collapse) in the context of cardiac tamponade

349
Q

What is Kussmaul’s Sign?

A

Visibility of neck veins on inspiration

350
Q

What are some characteristics of an EKG in the event of a cardiac tamponade?

A

Swigning heart - changes in electrical amplitude

351
Q

What is the treatment of cardiac tamponade?

A

Pericardiocentesis (drain it)

IV fluids and pressor agents

352
Q

What is constrictive pericarditis?

A

Pericarditis brought about by changes in the material properties of the pericardium

353
Q

What are some issues that arise with constrictive pericarditis?

A

Diastolic heart failure (ejection is maintained) due to non-elastic, thick pericardium. The myocardium is usually fine.

Symptoms include exertional dyspnea and the right side of teh heart is affected more than left - congestive heart failure

354
Q

What can cause constrictive pericarditis?

A

Heart surgery, radiation, idiopathic, connective tissue disease, infection, malignancy

355
Q

What are some clinical symptoms of constrictive pericarditis?

A

Dyspnea

Fatigue
Weight gain

Chronic edema

356
Q

What are some clinical signs of constrictive pericarditis?

A

Tachycardia

Hypotension

Elevated JVP

Kussmaul’s Sign

Pericardial Knock

Edema

Ascitis, hepatomegaly

Can look like jaundice

“sounds like a liver case, but looks like a heart case”

357
Q

What are some findings you might see on EKG in cases of constrictive pericarditis?

A

In chronic cases - atrial fibrillation

358
Q

What is somethign you might find on chest x-ray in a case of constrictive pericarditis?

A

Calcified pericardium

359
Q

What is suggested in this chest x-ray?

A

Calcified pericardium - constrictive pericarditis

360
Q

What is the most common source of prolonged A-V conduction?

A

Delays in the AV node

361
Q

When might you normally have prolonged AV conduction?

A

When you sleep - high vagal tone

362
Q

When might you normally have shorter AV conduction?

A

When you run - high sympathetic tone

363
Q

What can shorten AV conduction?

A

Sympathetic tone

364
Q

What is the effect of sympathetic tone on AV conduction?

A

Shortens

365
Q

What is the rule in classifying 1st, 2nd, and 3rd degree AV blocks?

A

1, 2, 3 correspond to all, some, or none with regards to QRSs conducted following P

e.g. some p result in QRS, but not all = 2nd degree AV block

366
Q

What is a 1st degree AV block?

A

prolonged, constant PR interval (longer than 200 ms) but every P has a QRS that follows

no real threat of sudden death

367
Q

What are some causes of first degree heart block?

A

High vagal tone (atheletes)

Medications (beta blockers, calcium channel blockers)

Aortic sclerosis

368
Q

What are some symptoms of first degree heart block?

A

Usually none, unless there is a severely prolonged PR interval

369
Q

What is the treatment for a first degree heart block?

A

usually none

370
Q

What are the three types of second degree heart block?

A

Mobitz 1 - progressive PR prolongation until dropped QRS

Mobitz 2 - sudden failure of conduction (and missed QRS)

2:1 conduction - something in between (every 2 P = 1 QRS)

371
Q

What characterizes a second degree heart block, Mobitz Type I?

A

Progressively longer PR intervals until you drop a beat

372
Q

What causes a Mobitz Type I second degree heart block?

A

High vagal tone (atheletes)

Medications (beta blockers, calcium channel blockers)

Aortic sclerosis/stenosis

373
Q

What are some symptoms of a second degree heart block, Mobitz type I?

A

Usually none, aside from a sensation of skipped beats

374
Q

What is the treatment for a second degree heart block, Mobitz type I?

A

Usually none

375
Q

Where is the level of block in a second degree block, Mobitz type I?

A

usually at AV node

There is no real threat of sudden death

376
Q

What is a second degree heart block, Mobitz Type II?

A

Sudden failure of conduction

377
Q

What are the causes of a second degree heart block, Mobitz Type II?

A

Medication toxicity (digitoxin)

Myocardial infarction

Lyme disease

Advanced conduction system disease

378
Q

What are some symptoms of a second degree heart block, Mobitz Type II?

A

Dizziness/syncope - but may be asymptomatic

predominantly asymptomatic

379
Q

What is the treatment for a second degree heart block, Mobitz Type II?

A

Pacemaker - this is a potentially life threatening condition and requires intervention

380
Q

Where in the conduction system is there a defect in a second degree heart block, Mobitz Type II?

A

Usually below the AV node, in the His-Purkinje system; Makes this a very dangerous condition with risk of sudden death

381
Q

What is a second degree heart block 2:1 AV conduction?

A

Condition where there is a 2:1 P:QRS ratio

Cannot be classified as either Mobitz 1 or Mobitz 2

382
Q

What is a third degree heart block?

A

A.k.a. complete heart block

P waves and QRS waves are dissociated

Atria and ventricles are not communicating and each are doing their own thing

383
Q

What type of heart block is seen in this EKG?

A

2nd Degree AVB - Mobitz II

no change in PR interval and some QRS are dropped

384
Q

What type of heart block is seen in this EKG?

A

2nd degree, Mobitz I

QRS are grouped together. PR progressively gets longer

385
Q

What type of heart block is seen in this EKG?

A

3rd degree - P and QRS are completely dissociated - no pattern

386
Q

Where does the right bundle course through?

A

The right side of the interventricular septum

387
Q

Describe the right bundle.

A

Long, thin, discrete structure that courses down the right side of the interventricular septum

388
Q

What is the result of a Right bundle branch block (RBBB)?

A

Delayed activation of the RV

This is common in the general population and usually has no prognostic significance

389
Q

What are diagnostic critera for a right bundle branch block?

A

QRS > 120

Broad, notched ‘secondary’ R waves in right precordial leads (Bunny ears)

Deep S waves in left precordial leads

390
Q

Where does the left branch course through?

A

The membranous portion of the interventricular septum near the aortic ring and then divides into three discrete branches: left anterior, left posterior, and left median fascicle

391
Q

What is significant about a left bundle branch block?

A

usually indicates underlying structural heart disease

Dramatically alters ventricular activation

Must work these patients up

392
Q

Describe the left branch.

A

More diffuse than the right branch. Courses through the membranous portion of the interventricular septum near the aortic ring and then divides into 3 discrete branches: left anterior, left posterior, and left median fascicles

393
Q

What are the diagnostic criteria for a left bundle branch block (LBBB)?

A

QRS > 120

Small or absent R waves in V1/V2 and deep S waves in V1/V2

Broad, notched monophasic R waves in V5/V6 and usually in leads I and aVL

394
Q

What is indicated by the following EKG?

A

LBBB

395
Q

What is indicated by the following EKG?

A

RBBB

396
Q

What does stable ischemic heart disease reflect in terms of the metabolic state of myocardial tissue?

A

An imbalance between the oxygen supply and demand

397
Q

What are the two components of myocardial oxygen supply?

A

Blood oxygen content (Hemoglobin level and oxygen saturation) - usually not the culprit

Coronary flow - more common culprit in coronary artery disease

398
Q

What are some determinants of coronary flow?

A

Q = P/R (directly proportional to perfusion pressure; inversely proportional to vascular resistance)

399
Q

What is the minimum diastolic pressure needed to ensure adequate flow to the coronary arteries?

A

60-65 mm Hg

400
Q

When during the cardiac cycle does coronary flow occur?

A

Diastole

401
Q

What are factors that affect coronary vascular resistance?

A

Vascular tone

Degree of coronary stenosis

402
Q

What are mediators of vascular tone?

A

Metabolic - adenosine, lactate, acetate, hydrogen ions, CO2

Neural Factors - Alpha (vasoconstriction) and Beta-2 (vasodilation) adrenergic receptors

Endothelial Factors - NO, prostacyclin, EDHF (vasodilators) ; endothelin-1 (vasoconstrictor)

403
Q

What is the most important metabolic mediator of vascular tone?

A

Adenosine

Produced during hypoxemia (during anaerobic work)

Binds to vascualr smooth muscle and causes vasodilation

404
Q

When is adenosine produced in the context of mediating vascular tone?

A

During hypoxemia

Causes vasscular smooth muscles to dilate, increasing vascular flow

405
Q

What is the effect of adenosine on vascular smooth muscle?

A

Vasodilation - causes increased coronary flow in coronary vessels

406
Q

What mechanisms of response to neural factors do coronary vessels contain?

A

Alpha (vasoconstriction) and Beta-2 (vasodilation) receptors

407
Q

Which neural factors cause vasoconstriction in the coronary arteries?

A

Alpha adrenergic receptors

408
Q

What neural factors cause vasodilation in the coronary vessels?

A

Beta-2 adrenergic receptors

409
Q

What are the endothelium-dependent vasodilators?

A

ACh, Serotonin, Shear stress

The endothelium produces NO, Prostacyclin, EDHF in response to these factors, and induces vascular smooth muscle relaxation

This results in vasodilation and increased blood flow

410
Q

What are the endothelium-dependent vasoconstrictors?

A

Thrombin, Angiotensin II, epinephrine

These cause the endothelium to produce endothelin 1 and causes vascular smooth muscle cell contraction

This results in reduced blood flow

411
Q

What does endothelium-dependence mean?

A

It means that a factor would not have the resulting effect if not for the presence of an in-tact endothelium

412
Q

What factors cause endothelial cells to produce NO, prostacyclin, and EDHF?

A

ACH, serotonin, shear stress

413
Q

In which direction (vasodilation/vasoconstriction) is the balance tilted towards in healthy states of coronary artery function?

A

Vasodilation

414
Q

In which direction (vasodilation/vasoconstriction) is the balance tilted towards in unhealthy states of coronary artery function (i.e. endothelial dysfunction)?

A

Vasoconstriction

415
Q

What is the effect of ACh on smooth muscle in the absence of normal endothelial function?

A

Vasoconstriction

416
Q

What is the effect of ACh in the presence of normal endothelial function?

A

Vasodilation

ACh alone causes vasoconstriction

However, the effect of ACh on the endothelial cells is to cause nitric oxide production (NO), which promotes vasodilation

The net effect is vasodilation

Abnormal response to ACh can suggest endothelial dysfunction

417
Q

What is suggested by a vasoconstriction response to ACh by vessel endothelium?

A

That there may be endothelial dysfunction

Normal function of ACh in the context of healthy endothelium is vasodilation

418
Q

What are determinants of myocardial oxygen demand?

A

Ventricular wall stress - wall stress promotes hypertrophy as a compensatory mechanism - more oxygen demand

Heart Rate - increased HR requires more oxygen demand

Contractility - stronger contractions requrie more energy/oxygen

419
Q

What is the relationship between heart rate and the oxygen demand of the myocardium?

A

Direct relationship - greater the heart rate, the more oxygen is required

420
Q

What is the relationship between the contractility of the myocardium and its oxygen demand?

A

Direct - more contractility (stronger/greater contractions) requires more oxygen

421
Q

What is the relationship between ventricular wall stress and the oxygen demand of the myocardium?

A

Pressure overload states increase wall stress

Volume overload states increase wall stress

Myocytes hypertrophy in response to increased wall stress; this requires more oxygen

422
Q

What are the determinants of ventricular wall stress?

A

P = pressure

r = radius

h = wall thickness

Hypertrophy (increase in h) is a response to increases in pressure/volume

423
Q

What is the effect of atherosclerotic plaques on the resistance to coronary blood flow?

A

Plaques increase resistance

The reduction in luminal diameter exerts a much greater effect on increasing resistance than does the length of the lesion:

where R = resistance

L = length

r = luminal radius

424
Q

What level of stenosis is requried to impair maximal blood flow under conditions of stress?

A

70% occlusion

425
Q

What level of stenosis is required to impair blood flow at rest?

A

up to 90%

426
Q

What characterizes endothelial cell dysfunction?

A

Release of endothelium-dependent vasodilators (prostacyclin/NO) may be impaired in response to normal stimuli (e.g. shear stress)

Vasodilatory effects of local metabolites (e.g adenosine) may be blunted

Vasoconstricting effects of catecholamines (e.g. ACh) predominates

Loss of antithrombotic effect of endothelial cells in response to stimuli (e.g. ADP, serotonin, thromboxane), resulting in a pro-thrombotic state in the setting of plaque rupture

427
Q

What are non-atherosclerotic causes of myocardial ischemia?

A

Reduced oxygen supply: aortic regurgitation (decrease in diastolic pressure reduces coronary artery perfusion), acute blood loss (GI bleeds)

Increased oxygen demand: tachyarrhythmias, acute rise in BP - increases stress and causes necrosis, severe aortic stenosis

428
Q

What are some medical issues that may cause reduced oxygen supply to the myocardium?

A

Atherosclerotic lesions of the coronary arteries

Aortic regurgitation - decreases diastolic pressure and reduces perfusing pressure of coronary arteries

Acute blood loss - for instance, due to a GI bleed

429
Q

What are some medical issues that may cause increased oxygen demand from the myocardium?

A

Tachyarrhythmias - like rapid atrial fibrillation

Acute rises in blood pressure - will cause increased wall stress and necrosis (hypertensive crisis)

Severe aortic stenosis

430
Q

What are potenial effects of ischemia on the myocardium?

A

Myocyte necrosis - irreversible cell death

Stunned myocardium - temporary dysfunction with function gradually restoring

Hibernating myocardium - chronic dysfunction that can have restored function with revascularization

431
Q

What is myocyte necrosis?

A

Sequella of ischemia that is marked by irreversible cell death in the context of a prolonged episode (infarct)

Can be detected by EKG (Q wave) and in cardiac imaging (akinetic, thinned wall on echo)

432
Q

What are signs of myocyte necrosis on EKG and Echo?

A

EKG - Q wave abnormalities

Echo - akinetic, thinned ventricular wall

433
Q

What is a stunned myocardium?

A

Temporary systolic dysfunction after an episode of transient ischemia - not necrosis

Magnitude depends on degree of insult

Function gradually recovers with therapy

434
Q

What is a hibernating myocardium?

A

Chronic ventricular dysfunction due to multivessel coronary artery disease in the setting of reduced blood supply (e.g. diabetes)

Revascularization restores ventricular function

435
Q

What defines a stable angina?

A

Retrosternal chest discomfort precipitated by exertion and relieved by rest

Usually occurs when stenosis is less than 70% of the lumenal size

Myocardial oxygen supply may be unable to meet the oxygen demands during exertion

This is reproducible

436
Q

What defines unstable angina?

A

New-onset SEVERE angina or increase in the severity and/or frequency of previously stable symptoms

Often caused by plaque rupture which leads to thrombosis, reducing myocardial oxygen supply

437
Q

What is variant angina?

A

Episodes of coronary spasm reduce oxygen supply

Occurs at rest while stable angina occurs with increased demand

May be caused by endothelial dysfunction or increased sympathetic activity

438
Q

What is Syndrome X?

A

Chest pain wtih positive stress test, and normal coronary arteries

Pain is significant

May be caused by microvascular dysfunction, spasm, or abnormal pain perception

439
Q

What is silent ischemia?

A

Ischemia without clinical symptoms

More common in Diabetes, women, and elderly

Do you treat? Trials ongoing to address this possibility

440
Q

What is most important in attempting to diagnose chronic stable angina?

A

History!

Quality, duration, location, associated sy mptoms, precipitants, and frequency

441
Q

How long does chronic stable angina usually last?

A

Usually a few minutes - pain lasting a few seconds is normally non-cardiac

442
Q

How is the pain in chronic stable angina localized?

A

Usually diffuse rather than focal sensation

Can radiate to left arm/neck

443
Q

What are symptoms associated with chronic stable angina?

A

Shortness of breath, fatigue, diaphoresis (sweating), nausea

444
Q

What are some precipitating factors that can be present in chronic stable angina?

A

Activities that increase myocardial oxygen demand - physical exertion, emotional stress

Usually relieved with several minutes of ceasing the activity

445
Q

What role does the physical exam play in diagnosing stable angina?

A

More of a screening for other non-coronary vascular diseases (peripheral vascular disease, aortic aneurysm, renovascular - i.e. bruits)

Has a limited role in diagnosis as symptoms occur with activity

446
Q

What diagnostic tests can help in diagnosing chronic stable angina?

A

EKG

Stress Test with Echo or Nuclear Perfusion

447
Q

What findings on EKG can help diagnose chronic stable angina?

A

ST segment depression and/or T wave inversions reflect myocardial ischemia

ST segment elevation reflects myocardial injury (infarction)

Can likely be completely normal (~50% of pts)

448
Q

What are two components of stress tests?

A

Stress - pharmacologic or exercise

Ischemic detection - via EKG, nuclear perfusion imaging, ultrasound

Exercise is always preferred as it allows for the assessment of functional capacity

449
Q

What is coronary angiography?

A

Invasive procedure requiring contrast media that allows for direct visualization of stenotic lesions

GOLD STANDARD in diagnosis of CAD

Drawback: can only visualize lesions that obstruct lumen; unable to asses atherosclerotic disease in vascular wall

450
Q

What is the gold standard in diagnosing coronary artery disease?

A

Coronary angiography

451
Q

What are the goals of treatment for patients with coronary artery disease?

A

Improve quality of life (reduce anginal symptoms)

Improve quantity of life (reduce risk of fatal events)

452
Q

How do you approach the treatment of stable coronary artery disease?

A

Drugs are the backbone and foundation of treatment in all patients

Revascularization in select patients - stents or bypass grafting

453
Q

How are nitrates effective in treating CAD?

A

Cause venodilation which reduces LV volume, wall stress, and myocardial oxygen demand

Causes maximal coronary vasodilation

Useful in patients with spasm

need to provide nitrate-free intervals since tolerance can develop

no long-term survival or reduction in MI risk; SYMPTOM RELEIF ONLY

454
Q

What is an important aspect of the dosing/prescribing of nitrates for chest pain?

A

To incorporate nitrate-free intervals since tolerance can develop

455
Q

How are beta blockers effective in treating CAD?

A

Reduce myocardial oxygen demand by slowing heart rate and decreasing force of contraction via beta 1

Increases duration of systole may also increase oxygen supply

Benefits symptomatic patients, those with prior MIs, and those with heart failure

456
Q

What are some side effects of beta blockers?

A

May provoke bronchospasm - use with caution in asthmatics

Heart block or significant bradycardia

Fatigue, sexual dysfunction

may mask reflexive tachycardia from hypoglycemia in insulin-treated diabetics

457
Q

How does the flow/resistance in the pulmonary circulation compare to that of the systemic circulation?

A

High flow, low resistance

Due to high capacitance that can acoomodate increases in cariac output

Pulmonary arterioles offer very little resistance (systemic arterioles offer 75% of total resistance)

458
Q

How does the pulmonary vascular resistance compare to systemic?

A

1/15th the resistance, due to the large cross sectional area.

(high flow)

459
Q

What are some causes of pulmonary hypertension?

A

Left heart disease

Chronic thrombotic and/or embolic diseases

Parenchymal lung disease and/or chronic hypoxemia

Otehrs

460
Q

What defines pulmonary hypertension?

A

Resting pulmonary artery pressures:

Systolic > 35

Diastolic > 15

Mean >25

And left atrial pressure < 15 mmHg (not transmitted from left heart back)

Pulmonary arteriolar resistance > 3 wood units

461
Q

What is the threshold of resting mean pulmonary arterial pressure for pulmonary hypertenison?

A

> 25 mmHg

Also must check that left atrial (LVEDP) pressure < 15 mmHg to ensure it is not being transmitted back

462
Q

What are three hallmark features of pulmonary arterial hypertension (PAH)?

A

Vasoconstriction

Smooth muscle and endothelial proliferation

Thrombosis (in situ)

463
Q

What changes happen to the pulmonary vasculature in the presence of pulmonary artery hypertensoin?

A

High flow, low resistance changes to low flow, high resistance

Due to proliferation of endothelial cells and vasoconstriction

464
Q

What are some mechanisms of PAH?

A

Homeostatic imbalance of vascular effectors (more vasoconstrictors, prothrombotics, and mitogenesis)

Environmental factors

Genetic factors

465
Q

What role does prostacyclin and thromboxane A2 play in PAH?

A

Prostacyclin is a vasodilator, inhibits platelet activation, antiproliferative

TXA2 is vasoconstrictor and platelet agonist

Levels of TXA2 >> Prostacyclin in PAH

466
Q

What is prostacyclin?

A

Vascular vasodilator, inhibitor of platelet activation, antiproliferative

Seen in low levels in PAH

467
Q

What role does serotonin play in PAH?

A

Vasoconstrictor - promotes smooth muscle cell hypertrophy

Seen in higher levels in PAH patients

Platelets have impaired 5HT reuptake in PAH patients

468
Q

What role does endothelin 1 play in PAH?

A

Endothelin 1 is a potent vasoconstrictor, stimulates smooth muscle cell proliferation

Plasma endothelin-1 levels are increased in PAH patients

Levels are inveresely proportional to magnitude of pulmonary blood flow

469
Q

What role does nitric oxide play in PAH?

A

Vasodilator, inhibitor of platelet activation adn smooth muscle cell proliferation

Endothelial isoform of NO synthase is decreased in patients with PAH

470
Q

What role does hypoxia play in the development of PAH?

A

Acutely - not so much

Systemically - induces vasodilation; Pulmonary bed - induces vasoconstriction

Chronically can lead to structural remodeling, smooth muscel cell proliferation, increased deposition of vascular matrix

471
Q

What are anorexigens?

A

Similar to methamphetamines

Found to be associated with higher risks for PAH

472
Q

What role do anorexigens play in PAH?

A

Found to be associated with higher risks of PAH

473
Q

What role do CNS stimulants play in PAH?

A

Cocaine, methamphetamines have been associated with medial hypertrophy of pulmonary arteries

474
Q

What role does the TGFβ receptor pathway play in PAH?

A

BMPR2 (bone morphogenic protein receptor type 2) modulates growth of vascular cells by suppressing it.

Mutations have been identified, but there is incomplete penetrance

475
Q

What role does the serotinergic pathway play in PAH?

A

Variant genes increase expression of 5HT receptor

Increases serotonin-dependent vascular remodeling

Higher prevalence of varinat genes among pts with PAH than controls

Still lots unknown

476
Q

What is the basic model of the development of PAH?

A

Risk factors + Genetic Predisposition leads to endothelial or smooth muscle cell dysfunction, leading to inflammation, thrombosis, remodeling and progression to disease

477
Q

Describe the hemodynamic progression seen in PAH.

A

\

CO - cardiac output

PAP - pulmonary arterial pressure

PVR - pulmonary vascular resistance

RAP - right atrial pressure

478
Q

What symptoms do we see in PAH patients?

A

Initially dyspnea, fatigue, maybe chest pain

Later - dyspnea, fatigue, chest pain, syncope, edema

479
Q

What symptom almost always predates a diagnosis of PAH?

A

Dyspnea

480
Q

What physical findings are present in PAH?

A

Elevated JVD

Tricuspid regurgitation

Pulmonary insufficiency (graham-steel murmur)

Accentuated S2

S3 gallup

Peripheral edema

Hepatomegaly, pulsatile liver, ascites

481
Q

What EKG findings can you see in PAH?

A

Only seen in fairly advanced cases

RV hypertrophy

Right axis deviation

Right atrial enlargement

482
Q

What evidence of PAH can you find on CXR?

A

Enlargement of central pulmonary arteries

Reduced caliber of peripheral vessels (pruning)

Cardiomegaly with RV enlargement

483
Q

What is the most effective diagnostic workup tool for PAH screening?

A

Echocardiogram

Can screen for elevation in pulmonary pressure and rule out left heart disease/congenital heart disease

Must confirm with catheterization

484
Q

What is the gold standard for diagnosing PAH?

A

Cardiac catheterization to measure pressures

485
Q

What general measures must you ensure patients with PAH are taking?

A

Maintain oxygen saturation (maybe give oxygen, minimize low oxygen environments)

Routine vaccination - flu, pneumovax

Avoid vasoconstrictors (nicotine, sympathomimietics)

Avoid deep valsalva maneuvers

Avoid pregnancy

486
Q

How can you treat PAH medically?

A

Diuretics to reduce volume overload

Digitalis may be useful in patients with LV dysfunction

Warfarin to mitigate prothrombotic state associated with PAH

Oxygen, when seen in chronic hypoxemia

487
Q

How do diuretics help PAH patients?

A

Treats symptoms of volume overload

488
Q

How does digitalis help PAH patients?

A

Unclear, but may be most useful with concomitant LV dysfunction

489
Q

How can warfarin help PAH patients?

A

Treat prothombotic state associated with PAH

490
Q

How can oxygen help PAH pateints?

A

Combats hypoxemic state that can worsen PAH

491
Q

How can calcium channel blockers help PAH patients?

A

Benefit is only seen in a minority of patients

Rationale is to vasodilate patients

492
Q

How do CCBs, endotheilal receptor antagonists, phosphodiesterase-5 inhibitors, and prostanoids help treat PAH?

A

Inhibit endothelin pathway, nitric oxide pathway, prostacyclin pathway that are all implicated in the development of PAH

493
Q

What are key pathologic features of PAH?

A

Vasoconstrition

Cellular proliferation

Thrombosis

494
Q

What are the targets of existing treatment approaches to PAH?

A

Reversing the underlying patholoic disturbances common in PAH

Cardiovascular (2 decks)

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