Clinical Cardio Exam Iv

Front 1

2 layers of pericardium

Back 1

Visceral - inner serosal layer, adheres to pericardium

Parietal - outer fibrous layer

Front 2

3 functions of pericardium

Back 2

- Fixes the heart within the mediastinum and limits its motion

- It prevents extreme dilatation of the heart during sudden rises of cardiac volume

- Barrier to spread of infection from adjacent structures ( lungs)

Front 3

Most common cause of acute pericarditis

Back 3

VIRAL

Front 4

3 types of infectious pericarditis

Back 4

- Viral or idiopathic

- Tuberculous

- Pyogenic bacteria

Front 5

Causes of non-infectious pericarditis

Back 5

- Post MI

- Uremia

- Neoplastic disease

- Radiation induced

-Connective tissue disease

- Drug induced

Front 6

2 types of post MI acute pericarditis

Back 6

Early- first few days after MI

Dresslers syndrome- weeks to months after MI

Front 7

Name drugs that cause acute pericarditis

Back 7

- Drugs associated with drug induced lupus syndrome

Procainamide
Methyldopa
Hydrolazine
Isoniazide
Phenytoin

Also minoxidil and anthracycline antineoplastic agents

Front 8

Name symptoms of acute pericarditis

Back 8

Chest discomfort - sharp, pleuritic, positional - better with sitting, worse with lying

Dyspnea

Fever

Front 9

-Auscultatory hallmark of acute pericarditis
-Sometimes heard in subacute or chronic pericarditis

Back 9

Frictional rub

Front 10

Describe pericardial friction rub

Back 10

Can have 3 components - systolic, mid diastolic or late diastolic, evanescent

Front 11

Where is pericardial friction rub should be heard, in which position?

Back 11

Left sternal border - ask patient to lean forward, take a deep breath, blow it all out and hold it out

Front 12

EKG findings of acute pericarditis

Back 12

-Diffuse, concave-upward ST segment elevation in many of the EKG leads
-PR segment depression in the same leads that have ST segment elevation*
-PR segment elevation and ST segment depression are often seen in lead aVR (& sometimes V1)*

Front 13

This EKG finding is very useful in differentiating ST segment elevation due to acute pericarditis from ST segment elevation due to other causes

Back 13

PR segment elevation and ST segment depression are often seen in lead aVR (& sometimes V1)

Front 14

Is chest x ray useful in diagnosis of acute pericarditis

Back 14

Usually normal (in idiopathic/ viral pericarditis)

Front 15

Is echo useful in diagnosis of acute pericarditis

Back 15

-Usually normal (in idiopathic/ viral pericarditis)
-Should be ordered to evaluate for possible coexisting large pericardial effusion

Front 16

CBC in patient with acute pericarditis will show _

Back 16

Mild leukocytosis, with mild lymphocytosis (if viral/ idiopathic)

Front 17

Is ESR level test useful in diagnosis of acute pericarditis

Back 17

-Modestly elevated in viral/ idiopathic pericarditis
-If markedly elevated, consider other causes

Front 18

If cardiac markers are elevated in patients with acute pericarditis what should you consider

Back 18

Concomitant myocarditis or MI

Front 19

Treatment for viral/idiopathic acute pericarditis

Back 19

NSAIDS

Oral corticosteroids

Oral colchicine

Rest

Analgesia

Front 20

What type of treatment should be avoided in patients with acute pericarditis due to MI

Back 20

NSAIDS and oral steroids- increase chance of free wall rupture

Front 21

These drugs are only used for pain refractory to NSAIDS and narcotic analgesia in patients with acute pericarditis (viral/idiopathic)

Back 21

Oral colchicine and oral corticosteroids

Front 22

Mainstay of therapy in treatment of acute viral pericarditis

Back 22

NSAIDS

Front 23

Treatment for tuberculous acute pericarditis

Back 23

Prolonged anti TB therapy

Front 24

Treatment for purulent acute pericarditis

Back 24

Catheter drainage + antibiotics

Front 25

Treatment for uremic acute pericarditis

Back 25

Dialysis

Front 26

3 complications for acute pericarditis

Back 26

Pericardial effusion

Pericardial tamponade

Constrictive pericarditis

Front 27

Accumulation of an abnormally large amount of fluid in the pericardial space

Back 27

Pericardial effusion

Front 28

Pericardial space normally contains _ of fluid

Back 28

15-50 cc of fluid

Front 29

Differential diagnosis for pericardial effusion

Back 29

Malignancy

Post cardiac surgery

Post PCI

Complication of pericarditis

Thoracic aortic dissection

Chest trauma

Front 30

Most useful test for pericardial effusion

Back 30

Echo

Front 31

3 determinants of symptom onset/ progression of pericardial effusion

Back 31

-Rate of accumulation of pericardial fluid
-Volume of pericardial fluid
-Compliance of the pericardium

Front 32

2 physical findings of large pericardial effusion

Back 32

Muffled heart sounds

Ewarts sign

Front 33

Ewarts sign (sign of pericardial effusion)

Back 33

Dullness to percussion over the angle of the left scapula due to compression of the left lung by the enlarged pericardial sac

Front 34

What do you see on EKG in large pericardial effusion

Back 34

Low voltage

Electrical alternance

Front 35

What do you see on x ray in moderate to large pericardial effusion

Back 35

Globular, symmetric enlargement of cardiac silhouette in moderate to large effusions
“Water bottle” heart

Front 36

Gold standard” test for detection, localization, and quantification of pericardial effusion

Back 36

Echo

Front 37

Treatment of pericardial effusion

Back 37

-Treat underlying cause (if known)
-Observation-If cause is known and patient is asymptomatic
-Pericardiocentesis-If cause is unknown (sample of fluid may be sent for analysis: “diagnostic pericardiocentesis”) or If patient is symptomatic or if there is evidence of pericardial tamponade (“therapeutic pericardiocentesis”)

Front 38

Cardiac chamber compression caused by pericardial effusion

Back 38

Pericardial tamponade

Front 39

Increase in RV volume during inspiration causes a slight shift of the interventricular septum _

Why does this occur?

Back 39

To the left

This leftward shift of the interventricular septum only occurs to a mild degree, as the compliant pericardium allows outward expansion of the right ventricle to accommodate most of the increased venous return during inspiration

Front 40

slight decrease in systolic pressure during inspiration which will increase during expiration

Back 40

Pulsus paradoxus

Front 41

Measuring pulsus paradoxus

Back 41

-Apply correct size BP cuff and quickly obtain baseline BP.
-Re-inflate BP cuff to about 20 mmHg above baseline systolic BP.
-Be sure that no sound is heard during expiration or inspiration.
-Slowly deflate the cuff until the first Korotkoff sound can be heard during expiration but not inspiration.
-Note this pressure.
-Slowly deflate the cuff until the sound can be heard during both expiration and inspiration.
-Note this pressure.
-The difference between these two pressures is the pulsus paradoxus

Front 42

Exaggerated pulsus paradoxus is a sign of _

Back 42

Pericardial tamponade

Front 43

Exaggeration (greater than 10 mm Hg during quiet breathing) of the normal decline in systolic arterial pressure during inspiration.

Back 43

Exaggerated pulsus paradoxus

Front 44

Is exaggerated pulsus paradoxus diagnostic of pericardial tamponade

Back 44

Although an exaggerated pulsus paradoxus is considered to be one of the classic physical signs of pericardial tamponade, it is not specific for pericardial tamponade.

Front 45

Potential causes of exaggerated pulsus paradoxus

Back 45

Pericardial tamponade Pulmonary embolism
Asthma
Emphysema
Constrictive pericarditis (about one-third of patients)
Hypovolemic shock
Other causes of acute hypotension
Pregnancy
Extreme obesity

Front 46

Most useful test for pericardial tamponade

Back 46

Echo

Front 47

Invasive measurement of intracardiac and intrapericardial pressures

Back 47

Cardiac catherization

Front 48

Patient presents with:

Exaggerated pulsus paradoxus
Hypotension*
Jugular venous distension*
Muffled heart sounds*
Tachycardia
Chest discomfort (sometimes)

Diagnosis?

Back 48

Pericardial tamponade

Front 49

Becks triad

Back 49

-Hypotension
-Jugular venous distension (or high central venous pressure)
-Muffled or distant heart sounds

Front 50

EKG changes of pericardial tamponade

Back 50

-Sinus tachycardia (unless pharmacologically suppressed)
-EKG signs of large pericardial effusion may or may not be present

Front 51

Cardiac cath of pericardial tamponade will show _

Back 51

-Invasive measurement of intracardiac and intrapericardial pressures
-Diastolic equalization of pressures
-All cardiac chambers will have equal diastolic pressures*
-Right atrial pressure tracing
BLUNTED Y DESCENT

Front 52

Definitive treatment of pericardial tamponade

Back 52

Pericardiocentesis

Front 53

Temporizing measure for pericardial tamponade

Back 53

IV fluids

Front 54

2nd line temporizing measure for pericardial tamponade

Back 54

IV inotropes

Front 55

Pericardial scarring leading to restricted diastolic filling of all four cardiac chambers

Back 55

Constrictive pericarditis

Front 56

Phases of impaired ventricular filling for pericardial tamponade

Back 56

Early, mid and late diastole

Front 57

Phases of impaired ventricular filling for constrictive pericarditis

Back 57

Mid and late diastole

Front 58

Used to be most common cause of constrictive pericarditis; rare cause in industrialized countries today

Back 58

TB

Front 59

Causes of constrictive pericarditis

Back 59

Idiopathic (presumed previous virus)
Post cardiac surgery
Post radiation
Tuberculosis

Front 60

Patient presents with

-Lower extremity edema
-Abdominal fullness/ discomfort
-Fatigue
-Dyspnea (later)

Back 60

Constrictive pericarditis

Front 61

Physical findings for constrictive pericarditis

Back 61

Hepatomegaly

Ascites

Peripheral edema

Pericardial knock

Jugular venous distention

Kussmauls sign

Front 62

Pericardial knock - early diastolic sound is caused by _

Back 62

Abrupt cessation of ventricular filling caused by rigid pericardium

Front 63

Pericardial knock is best heard at _

Back 63

Left sternal border or cardiac apex

Front 64

Kussmauls sign

Back 64

Jugular venous pressure increased during inspiration

Front 65

Kussmauls sign is the sign of _

Back 65

Constrictive pericarditis

Front 66

Increase in jugular venous pressure (distension) during inspiration (normally, JVP decreases during inspiration)

Back 66

Kussmauls sign - constrictive pericarditis

Front 67

Differential diagnosis for Kussmauls sign

Back 67

-Constrictive pericarditis*
-Restrictive cardiomyopathy
-Right ventricular infarction
-Right ventricular failure
-Acute pulmonary embolism
-Pericardial tamponade (occasionally)

Front 68

What do you see on chest x ray in patients with constrictive pericarditis

Back 68

-Normal or mildly enlarged cardiac silhouette
-Pericardial calcification seen in about 50 % of patients

Front 69

What do you see on cardiac cath in patients with constrictive pericarditis

Back 69

Invasive measurement of intracardiac pressures
Diastolic equalization of pressures
All cardiac chambers will have equal diastolic pressures*
Right atrial pressure tracing
PROMINENT RAPID Y DESCENT*

Front 70

Exaggerated y descent is a sign of _

Back 70

Constrictive pericarditis

Front 71

Cardiac cath

Right and left ventricular pressure tracings
“Dip and plateau” pattern in diastole*
A.K.A.: “square root sign”*


Diagnosis?

Back 71

Constrictive pericarditis

Front 72

Definitive treatment for constrictive pericarditis

Back 72

Pericardiectomy

Front 73

Symptomatic treatment for constrictive pericarditis ( should NOT delay surgery)

Back 73

Diuretics and salt restriction

Front 74

Rise in right atrial pressure due to right atrial contraction - wave?

Back 74

A wave

Front 75

Rise in right atrial pressure as the TR valve closes and bulges toward the right atrium - wave?

Back 75

C wave

Front 76

Rise in right atrial pressure during ventricular systole when the TR valve is (supposedly) closed- wave?

Back 76

V wave

Front 77

2 distinct components of S2 can be heard during inspiration but not expiration

Back 77

Physiological (normal) spliting of S2

Front 78

This heart sound is normal in children and young adults

Back 78

S3

Front 79

Causes for paradoxical splitting of S2

Back 79

LBBB

L ventricular obstruction of ventricular outflow - AS, HOCM

R ventricular pacemaker

R ventricular ectopic beat

Systemic HTN

Front 80

Auscultatory hallmark if ASD

Back 80

Fixed splitting of S2

Front 81

Cause of S3 in adults

Back 81

Sudden limitation of longitudinal ventricular expansion during early rapid ventricular filling

Front 82

Timing for S3

Back 82

Early to mid diastole

Front 83

Frequency of S3

Back 83

Low (dull thud)

Front 84

Location for listening to S3

Back 84

Apex (L), lower LSB/xiphoid (R)

Front 85

Cause for S4

Back 85

Late diastolic ventricular distention due to exaggerated active atrial contribution to ventricular filling resulting from reduced ventricular compliance

Front 86

Timing for S4

Back 86

Late diastole (presystolic)

Front 87

Frequency of S4

Back 87

Low

Front 88

Location for S4

Back 88

Apex (L), lower LSB/xiphoid (R)

Front 89

Altering hemodynamics by a variety of physiological and pharmacological maneuvers and observing their effects on auscultatory finding

Back 89

Dynamic auscultation

Front 90

_ increase in intensity (loudness) during inspiration except _

Back 90

All R sided pathological auscultatory findings

Pulmonic ejection sound (congenital pulmonary stenosis_

Front 91

What happens when you go from squatting to standing

Back 91

Decreased venous return

Decreased ventricular preload

Decreased systemic vascular resistance

Front 92

What happens when you go from standing to squatting

Back 92

Increased venous return

Increased ventricular preload

Increased systemic resistance

Front 93

Why do R sided problems increase in intensity on inspiration

Back 93

Inspiration increases venous return to R side of the heart increasing volume and flow in the right side of the heart

Front 94

What happens when you passively elevate legs while supine

Back 94

Increased venous return

Front 95

What happens in Valsalva maneuver

Back 95

Decreased venous return

Decreased ventricular preload

Front 96

What happens in Muller maneuver

Back 96

Increased venous return

Increased ventricular preload

Front 97

What happens in PVC in post ectopic beats

Back 97

Increase contractility (predominant effect)

Increase preload

Front 98

What happens in isometric exercise

Back 98

Increased:

- Systemic resistance
- Cardiac output
- Heart rate
- Arterial pressure
- L ventricular filling pressure
- L ventricular volume

Front 99

Potent vasodilator - used for dynamic auscultation - what happens?

Back 99

Amyl nitrate

1st 30 seconds- decreases systemic arterial pressure

After 30-60 seconds- Increased heart rate and increased cardiac output

Front 100

Cause hemodynamic effects opposite of amyl nitrite - should be avoided in CHF or systemic HTN

Back 100

Vasopressors - methoxamine and phenylephrine

Front 101

Murmurs result from _

Back 101

Turbulent flow

Front 102

What is grading system of murmurs based on?

Back 102

Loudness/intensity of murmur

Front 103

Grades _ murmurs have NO palpable thrill

Back 103

1-3

Front 104

Grades _ murmurs have palpable thrill

Back 104

4-6

Front 105

Very faint murmur, not usually heard during the first few seconds of listening - grade?

Back 105

1/6

Front 106

Faint murmur but heard immediately - grade?

Back 106

2/6

Front 107

Prominent but not loud murmur - grade?

Back 107

3/6

Front 108

Loud murmur usually associated with a palpable thrill - grade?

Back 108

4/6

Front 109

Very loud murmur, associated with palpable thrill audible with only one edge of stethoscope on the chest - grade?

Back 109

5/6

Front 110

Way loud murmur, associated with palpable thrill, audible with stethoscope removed slightly from contact with chest - grade?

Back 110

6/6

Front 111

What type of murmur begins with or after S1 and ends at or before S2

Back 111

Systolic

Front 112

What type of murmur begins with or after S2 and ends before the next S1

Back 112

Diastolic

Front 113

What type of murmur begins in systole and continues without interruption through the S2 into all or part of diastole

Back 113

Continuous

Front 114

What is more reliable in elucidating murmurs cause

Back 114

Timing, quality as well as associated findings ( NOT anatomical location)

Front 115

Which valves are open in diastole

Back 115

Mitral and Tricuspid

Front 116

Which valves are open in systole

Back 116

Aortic and Pulmonary

Front 117

Name systolic murmurs

Back 117

MR

TR

AS

PS

Front 118

Name diastolic murmurs

Back 118

AR

PR

MS

TS

Front 119

Name causes for systolic murmurs

Back 119

- Outflow obstruction from either ventricle - AS, PS, HOCM, any stenosis
- Insufficiency of either AV valve - MR, TR
- VSD
- Ventricular ejection in non compliant great vessel - aortic sclerosis
- Ventricular ejection in high flow states - innocent murmurs (child, young adult), pregnancy, anemia, hyperthyroidism

Front 120

2 types of systolic murmurs

Back 120

Systolic ejection murmurs - crescendo-decrescendo, midsystolic, AS, PS, HOCM, most innocent murmurs

Holosystolic murmurs - TR, MR, VSD

Front 121

Name holosystolic murmurs

Back 121

TR, MR, VSD

Front 122

Patient presents with classic holosystolic murmur - diagnosis

Back 122

Chronic mitral regurgitation

Front 123

Patient presents with early systolic crescendo-decrescendo murmur - diagnosis

Back 123

Acute mitral regurgitation

Front 124

Patient presents with midsystolic click, late systolic murmur - diagnosis

Back 124

Mitral valve prolapse

Front 125

- Holosystolic murmur
- DOES NOT get louder during inspiration
- Best heard at apex, sometimes radiating to L axilla
- Gets louder during isometric grip, sudden squatting or vasopressor administration

Back 125

Chronic mitral regurgitation

Front 126

Chronic mitral regurgitation murmur gets louder with _

Back 126

Isometric handgrip

Sudden squatting

Vasopressor administration

Front 127

Which murmur do you have with acute mitral regurgitation

Back 127

EARLY systolic CRESCENDO-DECRESCENDO murmur

Front 128

Which murmur do you have with MVP

Back 128

Midsystolic click, late systolic murmur

Front 129

Patient with MVP is standing, what happens to murmur

Back 129

Click occurs earlier - murmur is longer

Front 130

Patient with MVP is squatting - what happens to the murmur

Back 130

Click occurs later - murmur is shorter

Front 131

_ makes click later and murmur shorter (and louder) in MVP

Back 131

Squatting

Front 132

_ makes click earlier and murmur longer (and softer)

Back 132

Standing (or Valsalva)

Front 133

- Holosystolic murmur
- Gets LOUDER DURING INSPIRATION (Carvallos sign)

Back 133

Tricuspid regurgitation

Front 134

Classic triad of severe TR

Back 134

Carvallos sign

Pulsatile jugular venous distention (JVD)

Pulsatile liver

Front 135

Holosystolic murmur

Doesnt get louder with inspiration

Best heard at lower LSB

Often HARSH in quality

Back 135

VSD

Front 136

Auscultatory hallmark of bicuspid aortic valve

Back 136

Aortic ejection sound (click)

Front 137

Crescendo decrescendo murmur

Often heard best at 2nd RSB radiating to carotids

Pulsus parvus et tardus (diminished and delayed carotid upstroke)

Back 137

Aortic stenosis

Front 138

Paradoxical splittins of S2 + diminished or absent A2 (aortic component of 2nd heart sound)

Back 138

Aortic stenosis

Front 139

Crescendo decrescendo murmur that gets louder with Valsalva maneuver, standing (from squatting or lying) and amyl nitrite inhalation

Gets softer with isometric handgrip and squatting

Back 139

Hypertrophic cardiomyopathy

Front 140

Murmur of HOCM gets louder with _

Back 140

Valsalve maneuver

Standing (from squatting or supine)

Amyl nitrite

Front 141

Murmur of HOCM gets softer with _

Back 141

Isometric handgrip

Squatting

Front 142

Crescendo-decrescendo murmur which gets louder with squatting ( or lying, from standing) and amyl nitrite inhalation

Gets softer with standing, valsalva maneuver or isometric handgrip

Back 142

Aortic stenosis

Front 143

Crescendo decrescendo murmur

- Increases during inspiration
- often heard best at 2 LSB
- Doesnt radiate to carotids
- If ejection sound (click) is present (congenital PS), it gets softer during inspiration

Back 143

Pulmonic stenosis

Front 144

Which R sided problem gets softer during inspiration

Back 144

Congenital pulmonic stenosis (ejection sound - click)

Front 145

Causes of diastolic murmurs

Back 145

Insufficiency of either ventricular outflow - AR, PR

Stenosis of AV valves - MS, TS

Front 146

Early diastolic murmur, decrescendo, high pitched, " blowing" murmur, best heard with diaphragm of sthethoscope at 3 L or RSB with patient leaning forward, during held, deep end-exhalation

Back 146

Aortic insufficiency (regurgitation)

Front 147

Diastolic rumble, best heard with bell of stethoscope at apex - can be present in people with aortic insufficiency

Back 147

Austin Flint murmur

Front 148

Patients with aortic insufficiency in addition to primary murmur can have_

Back 148

Systolic ejection murmur - due to high flow states across aortic valve - from high stroke volume

Austin Flint murmur

Front 149

What is the cause of Austin Flint murmur

Back 149

Due to " functional" mitral stenosis resulting from aortic regurgitant jet forcing the anterior mitral leaflet into partially closed position ( also have been proposed that it results from fluttering of anterior mitral leaflet caused by aortic regurgitant jet)

Front 150

Duroziez sign

Back 150

Systolic murmur over femoral artery when stethoscope is compressed proximally and diastolic murmur over femoral artery when stethoscope is compressed distally

Front 151

Most predictive sign of severe aortic insufficiency

Back 151

Duroziez sign

Front 152

Signs associated with high stroke volume (aortic insufficiency)

Back 152

Wide pulse pressure

Quinckes pulse - phasic blanching of the nail bed

Hills sign - lower extremity SP exceeds upper extremity SP by > 20 mm Hg

Corrigan (water hammer) pulse - palpable abrupt upstroke and rapid fall of arterial pulsation

Traube sign - pistol shot sound over femoral artery

Mueller sign - pulsating uvula

Front 153

2 causes of pulmonic insufficiency (regurgitation)

Back 153

Pulmonary HTN - in absence of pulmonic valve deformity - GRAHAM STEEL MURMUR

- Deformity of pulmonic valve- congenital, acquired

Front 154

Early diastolic murmur
Begins with loud pulmonic component of S2
Decrescendo
High pitched
"blowing"
Gets louder during inspiration
Best heard at 2nd to 4th ICS, LSB

Back 154

Graham Steel Murmur - pulmonic insufficiency in absence of deformity of pulmonic valve

Front 155

Mid diastolic murmur
Begins AFTER pulmonic component of S2
Crescendo decrescendo
Low pitched
Gets louder during inspiration
Best heard at 3d-4th ICS, LSB

Back 155

Pulmonic insufficiency due to deformity of pulmonic valve

Front 156

Mitral stenosis is almost always a sequela of _

Back 156

Rheumatic fever

Front 157

Mid diastolic murmur (pre systolic accentuation if rhythm is sinus), holodiastolic if severe

LOW PITCHED

Best heard if patient is in left lateral position with the bell of stethoscope at apex

Back 157

Mitral stenosis

Front 158

This type of murmur has opening snap - high pitched sounds, occurs after S2 EARLY in diastole, as severity increases will move closer to S2

Back 158

Mitral stenosis

Front 159

Which R sided problem gets softer during inspiration

Back 159

Congenital pulmonic stenosis (ejection sound - click)

Front 160

Causes of diastolic murmurs

Back 160

Insufficiency of either ventricular outflow - AR, PR

Stenosis of AV valves - MS, TS

Front 161

Early diastolic murmur, decrescendo, high pitched, " blowing" murmur, best heard with diaphragm of sthethoscope at 3 L or RSB with patient leaning forward, during held, deep end-exhalation

Back 161

Aortic insufficiency (regurgitation)

Front 162

Diastolic rumble, best heard with bell of stethoscope at apex - can be present in people with aortic insufficiency

Back 162

Austin Flint murmur

Front 163

Patients with aortic insufficiency in addition to primary murmur can have_

Back 163

Systolic ejection murmur - due to high flow states across aortic valve - from high stroke volume

Austin Flint murmur

Front 164

What is the cause of Austin Flint murmur

Back 164

Due to " functional" mitral stenosis resulting from aortic regurgitant jet forcing the anterior mitral leaflet into partially closed position ( also have been proposed that it results from fluttering of anterior mitral leaflet caused by aortic regurgitant jet)

Front 165

Duroziez sign

Back 165

Systolic murmur over femoral artery when stethoscope is compressed proximally and diastolic murmur over femoral artery when stethoscope is compressed distally

Front 166

Most predictive sign of severe aortic insufficiency

Back 166

Duroziez sign

Front 167

Signs associated with high stroke volume (aortic insufficiency)

Back 167

Wide pulse pressure

Quinckes pulse - phasic blanching of the nail bed

Hills sign - lower extremity SP exceeds upper extremity SP by > 20 mm Hg

Corrigan (water hammer) pulse - palpable abrupt upstroke and rapid fall of arterial pulsation

Traube sign - pistol shot sound over femoral artery

Mueller sign - pulsating uvula

Front 168

2 causes of pulmonic insufficiency (regurgitation)

Back 168

Pulmonary HTN - in absence of pulmonic valve deformity - GRAHAM STEEL MURMUR

- Deformity of pulmonic valve- congenital, acquired

Front 169

Early diastolic murmur
Begins with loud pulmonic component of S2
Decrescendo
High pitched
"blowing"
Gets louder during inspiration
Best heard at 2nd to 4th ICS, LSB

Back 169

Graham Steel Murmur - pulmonic insufficiency in absence of deformity of pulmonic valve

Front 170

Mid diastolic murmur
Begins AFTER pulmonic component of S2
Crescendo decrescendo
Low pitched
Gets louder during inspiration
Best heard at 3d-4th ICS, LSB

Back 170

Pulmonic insufficiency due to deformity of pulmonic valve

Front 171

Mitral stenosis is almost always a sequela of _

Back 171

Rheumatic fever

Front 172

Mid diastolic murmur (pre systolic accentuation if rhythm is sinus), holodiastolic if severe

LOW PITCHED

Best heard if patient is in left lateral position with the bell of stethoscope at apex

Back 172

Mitral stenosis

Front 173

This type of murmur has opening snap - high pitched sounds, occurs after S2 EARLY in diastole, as severity increases will move closer to S2

Back 173

Mitral stenosis

Front 174

Opening snap of mitral stenosis softens or disappears with _

Back 174

Calcification (loss of mobility) of the body of mitral leaflets

Front 175

This type of murmur is associated with loud (accenuated) S1

Back 175

Mitral stenosis

Front 176

Name mitral stenosis - like murmurs

Back 176

Austin flint (AI)

Carey- Coombs murmur - active mitral valvulitis associated with acute rheumatic fever

Left atrial myxoma

Tricuspid stenosis

Front 177

This murmur sounds just like mitral stenosis except it gets louder during inspiration and best heard along lower LSB

Back 177

Tricuspid stenosis

Front 178

Most common cause of tricuspid stenosis

Back 178

Rheumatic heart disease

Front 179

Continuous murmurs causes

Back 179

PDA

Cervical venous hum

Mammary soufle

Hepatic venous hum

Arteriovenous connections

Ruptured aneurysm of sinus of Valsalva

Front 180

Congenital causes of aortic valve stenosis

Back 180

Unicuspid aortic valve

Bicuspid aortic valve

Tricuspid aortic valve

Front 181

Acquired causes of aortic valve

Back 181

Degenerative (senile) calcific

Rheumatic (post inflammatory)

Front 182

Causes severe obstruction to left ventricular outflow IN INFANCY, most common cause of fatal valvular aortic stenosis IN INFANCY

Back 182

Unicuspid aortic valve

Front 183

Most common congenital cardiac defect (1-2% of population), 4: 1 male to female, often not detected until adulthood

Back 183

Bicuspid aortic valve

Front 184

In people with bicuspid aortic valve obstruction develops after childhood due to _

Back 184

Turbulent flow (causes fibrosis and calcification of aortic cusps)

Front 185

If you have coarctation of aorta you have high chance of which congenital cardiac defect

Back 185

Bicuspid aortic valve

Front 186

Risk factors for degenerative (senile) calcific aortic stenosis

Back 186

- Hypercholesterolemia

- DM

- Pagets disease of bone

- End stage renal disease

Front 187

3 classic symptoms of aortic stenosis

Back 187

Angina

Syncope

CHF symptoms

Front 188

For aortic stenosis when will mortality increase dramatically

Back 188

With development of symptoms

Front 189

50% mortality for angina with aortic stenosis

Back 189

5 years

Front 190

50% mortality for syncope with aortic stenosis

Back 190

3 years

Front 191

50% mortality for CHF symptoms with aortic stenosis

Back 191

2 years

Front 192

Most common physical finding in acute stenosis

Back 192

Systolic ejection murmur that radiates to the neck

Front 193

Which heart sound would you hear in patient with aortic stenosis

Back 193

S4

Front 194

What would you see on EKG in patient with aortic stenosis

Back 194

LVH

Sinus rhythm

Front 195

If you see LVH in patient with atrial fibrillation - what should you consider

Back 195

Aortic stenosis with concomitant mitral disease

Front 196

What would you see on chest x ray in patient with aortic stenosis

Back 196

LV prominence

Dilation of ascending aorta

Calcification of aortic valve (lateral projection)

Front 197

This test allows localization of aortic stenosis, assessing LV size and function, coexisting mitral disease and assesment of severity - mean aortic valvular gradient and calculated aortic valve area

Back 197

Echocardiogram

Front 198

Coronary angiography should be performed in patients prior to aortic valve replacement EXCEPT

Back 198

Males < 40 years old without CAD risks

Females < 50 without CAD risk factors

Front 199

3 types of treatment of aortic stenosis

Back 199

Medical

Surgical

Percutaneous

Front 200

Is medical therapy a definitive treatment of AS

Back 200

NO

Front 201

Medical management of As

Back 201

SBE prophylaxis

Heart rate control - use negative chronotropes

Symptomatic treatment

Avoid physical exertion and extreme heat

Front 202

Which medications should be used with caution in patients with AS

Back 202

Nitrates

Diuretics

ACE inhibitors

ARB's

Hydralazine

Front 203

Only definitive treatment of aortic stenosis

Back 203

Aortic valve replacement

Front 204

Indications for aortic valve replacement

Back 204

Symptomatic severe AS

Severe AS with progressive LV dysfunction (regardless of symptoms)

Front 205

What should be performed in patients with significant mitral regurgitation before AVR

Back 205

Intraoperative TEE

Front 206

Indications for percutaneous (Balloon aortic valvuloplasty) intervention in patients with AS

Back 206

Bridge to AVR

Emergency non cardiac surgery

Palliation in non surgical candidate

Front 207

2 main causes of aortic insufficiency

Back 207

Valvular - structural valve problem

Aortic - dilated aorta

Front 208

2 causes of valvular aortic insufficiency

Back 208

Congenital - bicuspid aortic valve, VSD

Acquired - infective, rheumatic, degenerative

Front 209

2 causes of aortic AI

Back 209

Dissection - trauma, cystic medial necroiss

Dilation - systemic HTN, age, cystic medial necrosis

Front 210

Connective tissue diseases make you prone to which valvular problems

Back 210

Aortiic insufficiency

Front 211

Causes of acute AI

Back 211

Dissection

Infective endocarditis

Trauma

Front 212

Symtoms of acute AI

Back 212

Severe dyspnea

Weakness

Front 213

Physical findings of acute AI

Back 213

Hypotension

Tachycardia

Pulmonary edema

Front 214

Why dont you have classic findings of chronic AI in acue AI

Back 214

due to elevated LV end diastolic pressure

Front 215

Patient presents with severe dyspnea, weakness. Physical exam reveals hypotension, tachycardia and pulmonary edema - peripheral arterial signs are absent, pulse pressure is not widened and there is soft and short diastolic murmur

Back 215

Acute AI

Front 216

What would you see on EKG in patient with acute aortic insufficiency

Back 216

Sinus tachycardia

LVH may be absent

Front 217

What would you see on chest x ray in patient with acute aortic insufficiency

Back 217

Pulmonary edema (usually)

LV size is normal

Ascending aorta MAY be dilated (depending on the cause)

Front 218

Diagnostic test of choice in patient with acute aortic insufficiency

Back 218

Echo

Front 219

Patient presents with exertional dyspnea, reduced exercise tolerance, fatigue and uncomfortable"forceful" heartbeat

Back 219

Chronic AI

Front 220

Double systolic impulse in carotid or brachial artery

Back 220

Bisferiens pulse

Front 221

What would you see in patient with chronic AI on EKG

Back 221

LVH

Front 222

What would you see on chest x ray in patient with chronic AI

Back 222

LV enlargement

Ascending aorta MAY be dilated

Front 223

Excellent modality for long term follow up and timing of surgery in patient with chronic AI

Back 223

Echo

Front 224

Indicator of poor prognosis in patients with chronic AI

Back 224

- Presence of symptoms

- LVEF< 55%

- Significant LV dilation

LV end systolic dimension > 55

LV end diastolic dimension > 75

Front 225

Treatment for AI

Back 225

Prompt surgical intervention for hemodynamically unstable patients

Medical treatment while awaiting surgery

Front 226

Medical treatment while awaiting surgery for acute AI may include

Back 226

POSITIVE IV inotropic agents

IV vasodilators

Front 227

Which treatment is contraindicated in patients with acute AI

Back 227

Beta blockers

IABP

Front 228

Patient with acute AI secondary to active infective endocarditis is hemodynamically stable - treatment?

Back 228

Surgery deferred for 5-7 days of intensive antibiotic therapy

Front 229

Medical treatment of chronic AI

Back 229

- Antibiotic infective endocarditis prophylaxis
- Nifedipine - may delay the need for AVR surgery in asymptomatic patients with severe AI and normal LV systolic function

Front 230

Surgical indications for chronic AI

Back 230

- Decline in LV systolic function (rule of 55, LVEF< 55%)
- Increase in LV (end systolic>55, end diastolic > 75)

- Symptoms - significant fatigue, worsening exercise tolerance, CHF