Clinical Skills Exam--Cardiovascular System

Front 1

Patient with exertional chest pain with radiation to left side of neck and down left arm.

Back 1

angina pectoris

Front 2

Sharp pain radiating to back or neck

Back 2

aortic dissection

Front 3

Pt c/o transient skips and flipflops

Back 3

possible premature contractions

Front 4

Pt c/o regular beating of sudden onset and offset

Back 4

paroxysmal supraventricular tachycardia

Front 5

Regular rapid heart rate of less than 120 bpm (but more than 90)

Back 5

sinus tachycardia

Front 6

Orthopnea (dyspnea that occurs when the pt. is lying down)

Back 6

left ventricular heart failure or mitral stenosis (may accompany obstructive lung disease

Front 7

Paroxysmal noctournal dyspnea

Back 7

Left ventricular heart failure or mitral stenosis (mimicked by nocturnal asthma attacks)

Front 8

Accumulation of excessive fluid in interstitial tissue spaces especially the lowest parts of the body when sitting or the sacrum when lying down

Back 8

dependent edema (cardiac, nutritional, positional)

Front 9

enlarged waistline (swelling)

Back 9

ascites or liver failure (edema)

Front 10

Tight rings on fingers

Back 10

nephrotic syndrome (edema)

Front 11

Periorbital puffiness

Back 11

Edema

Front 12

Increased jugular venous pressure (JVP)

Back 12

Right sided heart failure (less commonly constrictive pericarditis, tricuspid stenosis, SVC obstruction)

Front 13

Unilateral distention of the external jugular vein

Back 13

Local kinking or obstruction

Front 14

a wave in JV pulse

Back 14

atrial contraction

Front 15

prominent a wave

Back 15

increased resistance to right atrial contraction (due to tricuspid stenosis, decreased compliance of a hypertrophied right ventricle)

Front 16

Absent a wave

Back 16

atrial fibrillation

Front 17

v wave of JV pulsation

Back 17

venous filling of JV

Front 18

Large v wave

Back 18

tricuspid regurgitation back into the JV

Front 19

Pressure volume curve manifestations of heart failure

Back 19

Reduced stroke volume-->less nutrition to the tissues of the body.
Ejection fraction decreases-->heart increases its filling pressures to increase preload (and thus to increase the force of contraction to increase EF)--> increases the water in the lungs.

Front 20

Four causes of dyspnea

Back 20

Heart disease, lung disease, anemia, insanity

Front 21

Dyspnea in heart failure. How ot define in pts?

Back 21

-Dsypnea relates to filling pressure: increased filling pressure-->pulm edema-->dyspnea.
-Ask: "How far can you walk/run?" (a question in terms of what they do daily)

Front 22

Orthopnea

Back 22

-Patient does not want to lie flat.
-If they lie flat, their dyspnea worsens.
-Lying flat puts more volume into central circulation
-This drives up the filling pressure
-This puts more water in the lungs

Front 23

Causes of orthopnea

Back 23

Heart or lung disease

Front 24

Paroxysmal noctournal dyspnea

Back 24

Pt went to sleep fine
At night woke up and had to sit upright and open a window.
Mechanism:
-Left heart failure increases central volume--> at night the mvmt of fluid back into the central circulation increases--> increases filling pressure on heart--> increases mvmt of fluid into alveolar spaces

Front 25

Causes of paroxysmal noctournal dyspnea

Back 25

-Heart failure
-Bronchospasm in asthma (but doesn't get better with sitting up)

Front 26

Causes of nocturia

Back 26

-Heart failure
-Enlarged prostate (goes to bed with lots of urine in bladder so wakes up having to pee)

Front 27

Mechanism of nocturia in heart failure

Back 27

-During day, person with heart failure is walking around, and the skeletal muscles consume most of the CO
-Deprives kidney of CO
-Lying down:
-increases central volume
-causes sk mm to go to sleep (don't need as much CO)

Front 28

Symptoms of left heart failure

Back 28

-Dyspnea
-Orthopnea
-Paroxysmal noctournal dyspnea
-Nocturia

Front 29

How does right heart failure arise from left heart failure?

Back 29

Increased filling pressures in the left heart indicate that something has to be working harder to get blood in there. The right ventricle is what has to work harder.

Front 30

Edema

Back 30

A symptom of right heart failure
Due to increased blood in the systemic circulation--> increased hydrostatic pressure in the periphery-->fluid leakage-->edema in legs and peritoneal cavity (ascites)

Front 31

INcrease in waistline/dress size in heart failure (right)

Back 31

ascites

Front 32

Does edema get better?

Back 32

Yes, when pt lies down

Front 33

Causes of edema

Back 33

-Liver diesease and nephrotic syndrome/kidney disease: oncotic pressure decreased due to loss of albumin
-Right heart failure

Front 34

How to tell edema is due to heart failure and not kidney or liver disease

Back 34

Evidence of right atrial hypertension (look at the JVP)

Front 35

Questions to ask to determine etiology of heart failure

Back 35

-Past MI
-Alcoholism
-HTN

Front 36

Where does angina occur

Back 36

"Between the bridge of the nose and the navel"
-Teeth
-Jaw
-Arm
-Left chest

Front 37

Angina

Back 37

-Occurs during EXERTION, goes away with REST!
-Squeezing
-Pressure
-Maybe pain

Front 38

Cause of angina

Back 38

Chronic stable plaque in coronary vessels builds up gradually and robs heart of blood during exertion

Front 39

Cause of heart attack

Back 39

-Plaque ruptures
-Crap in plaque gets squirted into artery
-Attracts and activates platelets
-Platelets form a clot
-Blood flow to heart is blocked

Front 40

Difference btwn pain of angina and pain of MI

Back 40

Angina pain goes away after about 10 minutes. MI pain does not go away b/c bld flow to heart is blocked.

Front 41

Symptoms of acute coronary syndrome (like an MI)

Back 41

1) Adrenergic NS revved up to maintain CO
-Pt may feel tremulous
-Feeling of impending doom
-Sweating
2)Parasymp NS activated (esp by inferior MI)
-Nausea
-Vomiting
-Acute dyspnea as heart failure increases filling pressures and decreases CO

Front 42

Low pulse pressure

Back 42

A clue that CO and SV are depressed
CHF

Front 43

Pulse of someone with heart failure

Back 43

around 100

Front 44

Thready weak carotid pulse

Back 44

suggests diminished stroke volume

Front 45

How to measure central venous pressure by distention of neck veins

Back 45

-First: it doesn't matter what angle you have the patient at. -You need to measure the height of the distention above parallel. Just tilt the patient up until you can see the neck vein distended.
-Manubrium is 5 cm above the right atrium
-You want to measure the height of the neck vein above the manubrium
-If the height of the neck vein is 2cm above the manubrium, then it is 2 + 5 = 7 cm above the right atrium.
-Thus central venous pressure = 7.

Front 46

When a vein in your hand gets above your left atrium, what happens?

Back 46

The vein collapses

Front 47

High central venous pressure

Back 47

Means that the right ventricle is working harder than it should against a higher than normal filling pressure (indicates right heart failure?)

Front 48

Causes of rales

Back 48

-Left sided heart failure--> increased filling pressure referred back to lungs--> alveoli fill with fluid--> rales/crackles on the left side (what about right side?)
-Lung diseases

Front 49

Where do you hear rales first?

Back 49

-In gravity dependent areas (base of the lungs)
-In severe pulmonary edema, they can be heard all the way to the apices

Front 50

Where do you hear the PMI?

Back 50

-Mid chest, 5th interspace
-Ask pt to breathe all the way out to get chest wall near the heart

Front 51

Enlarged heart: where is the PMI?

Back 51

Moves down and out toward the left 6th intercostal space

Front 52

S3

Back 52

-Large quantity of bld in left atrium is being forced down into the left ventricle at higher than normal filling pressure
-Means HEART FAILURE
-Lub da-dub (sloshing in)

Front 53

S4

Back 53

-Noise made when left atrium contracts to squeeze its bld into left ventricle (atrial kick)
-Da-lub dub
-A stiff heart
-Normal after age 50 (gradual onset of stiffer heart)

Front 54

Valvular heart disease

Back 54

-Hear murmurs (bld stream going through a smaller area)

Front 55

Edema + flat neck veins

Back 55

Something other than right heart failure is causing the edema

Front 56

Edema + elevated neck veins

Back 56

Right heart failure

Front 57

Normal distention of JVP

Back 57

less than 3-4 cm above the sternal angle

Front 58

How to diagnose pulmonary edema due to left heart failure

Back 58

Get a CXR

Front 59

Radiographic diagnosis of heart failure

Back 59

CXR shows pulmonary edema
EKG shows heart abnormalities
Echo shows problems in squeezing/flow/size of heart
Stress test for coronary disease

Front 60

Pt comes in complaining of dyspnea on exertion. He just had to start sleeping with an extra pillow because he has orthopnea. On PE, you find that he has flat veins, bibasilar rales, and an S3. Which chamber is involved? What causes of DOE can we now exclude? What's the first line of treatment? What do you give next?

Back 60

-The left chamber is involved, which is why the neck veins are not yet distended.
-We can exclude right heart failure (pulmonary hypertension) as cause of his dyspnea on exertion.
-First TX: diuretics to take the fluid out of the body (esp lungs)
-Next: ACE-inhibitors and beta blockers

Front 61

Murmurs you can hear with the diaphragm

Back 61

Aortic and mitral regurgitation

(also hear S2 and S2 because they are high-pitched)

Front 62

Murmurs you can hear with the bell

Back 62

Mitral stenosis

(also S3 and S4 because they are low-pitched)

Front 63

Cause of sustained amplitude of PMI

Back 63

left ventricular hypertrophy

Front 64

Cause of diffuse amplitude of PMI

Back 64

CHF

(or aortic or mitral regurgitation, according to book)

Front 65

Cause of increased diameter, amplitude, and duration of PMI

Back 65

CHF or ischemic cardiomyopathy

Front 66

PMI displacement to left

Back 66

pregnancy

Front 67

What murmur can you hear better if the patient is sitting, leaning forward, after full exhalation? Where do you listen?

Back 67

-Aortic insufficiency (soft decrescendo diastolic murmur)
-Listen along left sternal border and at apex

Front 68

What can you hear better in left lateral decubitus position?

Back 68

Low pitched sounds (listen with the BELL):
-Mitral stenosis (opening snap and diastolic rumble)
-S3
-Palpate PMI here if didn't feel it before

Front 69

Which murmur has an opening snap and diastolic rumble?

Back 69

Mitral stenosis

Front 70

Valvular problem that causes delayed upstroke of carotid pulse

Back 70

Aortic stenosis

Front 71

Valvular problem that causes bounding upstroke of carotid pulse

Back 71

Aortic insufficiency

Front 72

What does orthopnea suggest?

Back 72

-Left ventricular heart failure
-Mitral stenosis
-Obstructive lung disease

Front 73

What is a high risk group for CHD?

Back 73

Established CHD or CHD risk equivalent

Front 74

LDL goal for high risk group

Back 74

-<100 mg/dL (<70 optional)
-RX with drugs if LDL >= 100

Front 75

LDL goal for moderately high risk group

Back 75

-<130 mg/dL (<100 optional)
-RX with drugs if LDL >= 130
-These ppl have 2+ risk factors

Front 76

LDL goal for moderate risk group

Back 76

-<130 mg/dL
-RX with drugs if >= 160

Front 77

LDL goal for lower risk group

Back 77

-<160 mg/dL
-RX with drugs if >= 190
-These ppl have 0 or 1 risk factor

Front 78

Orthostatic hypotension

Back 78

With position change from supine to standing:
-Systolic BP decreases by >= 20 mmHg
-HR increases by >= 20 BPM

Front 79

When do you see absent a waves in jugular venous pulse (JVP)?

Back 79

atrial fibrillation

Front 80

When do you see prominent v waves in the JVP?

Back 80

tricuspid regurgitation

Front 81

Which murmurs cause palpable thrills in the left and right second interspaces close to the sternum?

Back 81

Aortic/pulmonic stenosis

Front 82

What can be palpaed in the left and right second interspaces close to the sternum?

Back 82

-pulsations of great vessels
-S2 accentuation
-thrills of aortic or pulmonic stenosis

Front 83

Alternating amplitude of pulse or sudden doubling of Korotkoff sounds

Back 83

Pulsus alternans
Indicates left ventricular heart failure

Front 84

Drop of greater than 10 mmHg during inspiration

Back 84

Paradoxical pulse
Consider obstructive lung disease, pericardial tamponade, constrictive pericarditis

Front 85

Valsalva maneuver

Back 85

Decreases ventricular filling

Front 86

What do you use Valsalva for?

Back 86

-Systolic click of MVP is earlier and the murmur lengthens
-Decreases murmur of aortic stenosis
-Increases murmur of hypertrophic cardiomyopathy

Front 87

Squatting

Back 87

increases ventricular filling

Front 88

What do you use squatting for?

Back 88

-Delays click and murmur of MVP
-Increases murmur of AS
-Decreases murmur of HC

Front 89

Loud S1

Back 89

Tachycardia
States of high CO
Mitral stenosis

Front 90

Soft S1

Back 90

First degree heart block
Reduced left ventricular contractility
Mitral regurgitation

Front 91

S1 and S2 at the base of the heart (right and left 2nd interspaces)

Back 91

S1 is softer than S2 at the base

Front 92

S1 and S2 at the apex of the heart

Back 92

S1 is louder than S2 at the apex

Front 93

Holosystolic murmur

Back 93

Mitral regurgitation

Front 94

Crescendo-decrescendo murmur in systole

Back 94

Aortic stenosis

Front 95

Diastolic rumble

Back 95

Aortic regurgitation

Front 96

Opening snap (opening of valve) in diastole with presystolic accentuation (due to atrial kick)

Back 96

Mitral stenosis

Front 97

Murmurs heard at base

Back 97

Aortic regurgitation and stenosis

Front 98

Murmurs heard at apex

Back 98

Mitral regurgitation and stenosis

Front 99

Systolic murmurs

Back 99

MR ASs
Mitral regurgitation
Aortic stenosis

Front 100

Diastolic murmurs

Back 100

MS AIds
Mitral stenosis
Aortic insufficiency

Front 101

How do pts with valve problems present

Back 101

Heart failure

Front 102

Regurgitation

Back 102

Always leads to volume overload--> eccentric LV hypertrophy

Front 103

Stenosis

Back 103

Always leads to pressure overload--> concentric LV hypertrophy

Front 104

Important complications of any valvular heart disease

Back 104

-Infective endocarditis (with dental surgery)
-Atrial fibrillation (dilated atria)--> embolism
-VT and SCD

Front 105

Type of aortic stenosis in ppl > 70 yoa vs in < 70 yoa

Back 105

- > 70 yoa: senile calcific ("degenerative")
- < 70 yoa: bicuspid aortic valve

Front 106

Aortic stenosis pathophysiology

Back 106

-Obstruction to LV outflow--> pressure gradient btwn LV and aorta
-LV pressure overload results in concentric LVH (ECG and echo)
-Acceleration of systolic flow--> systolic crescendo-decrescendo murmur at base radiating to neck

Front 107

Aortic stenosis: key physical exam findings

Back 107

Systolic murmur
Coarse
Crescendo-decrescendo
Left ICS 2-3
Radiates into neck
Slow carotid upstroke (bc ejection into carotid is hampered)
PMI forceful and sustained

Front 108

Classical clinical triad of aortic stenosis

Back 108

-Angina (LVH increases MVO2 thus outstripping O2 supply...ischemia and associated CAD reduces bld flow)
-Syncope/SCD (diseased myocardium prone to arrhythmias and heart block)
-Congestive heart failure (LV stiff; elevated LV diastolic and LA pressures cause pulmonary congestion...dyspnea

Front 109

Survival in AS

Back 109

Worst with heart failure
Better with syncope
Best with angina

Front 110

Acute and chronic aortic insufficiency

Back 110

Acute causes sudden diastolic retrograde flow into the LV resulting in heart failure (fulminant pulmonary edema). Chronic AI has a slowly-evolving leak allowing for compensation and a delay in the sx of heart failure.

Front 111

Why is S1 diminished in mitral regurgitation?

Back 111

S1 represents the closure of the mitral valve. If the mitral valve is regurgitant, the valve won't close as well as it should. A regurgitant mitral valve is immoble

Front 112

Why is S1 accentuated in mitral stenosis

Back 112

Mitral valve closes more loudly because it is stenotic

Front 113

Why is S2 accentuated in systemic hypertension or dilated aortic root

Back 113

S2 represents closure of the aortic valve, so if there is systemic HTN, the aortic valve will close harder because it is being pushed back harder.

Front 114

Why is S2 softer or absent in right 2nd ICS when someone has calcific aortic stenosis?

Back 114

The valve is immobile and thus it doesn't close as well, so S2 is softer/absent.

This is weird because when you have mitral stenosis, S1 is louder. Mitral valve stenosis is more like a heavy wooden door that slams harder the harder it is. Calcific aortic stenosis is more like a door with rusted hinges that won't close or open very well.

Mitral regurgitation is actually the valve that doesn't close well--> softer S1

Front 115

When is P2 softer or absent?

Back 115

Aging or pulmonic stenosis

Front 116

When is P2 louder?

Back 116

Pulmonary hypertension, dilated pulmonary artery, atrial septal defect

Front 117

What changes in blood pressure do you see with chronic aortic insufficiency?

Back 117

Wide pulse pressure (SBP-DBP rises)

Front 118

What change in PMI do you see in chronic aortic insufficiency

Back 118

Shifts left

Front 119

Most common c/o mitral stenosis

Back 119

Rheumatic heart disease

Front 120

Why is mitral stenosis a diastolic murmur?

Back 120

Turbulence occurs across the mitral valve as blood flows into the left ventricle during diastole

Front 121

Pathophysiology of mitral stenosis

Back 121

-Leaflets, chordae, papillary muscles scarred (due to rheumatic heart disease)
-LV preload reduced due to MV obstruction
-Elevated LA pressures cause pulmonary edema (dyspnea, orthopnea, and PND)
-Atrial fibrillation due to LA enlargement
-Diastolic "rumble" begins when mitral valve opens and coincides with flow thru stenotic MV

Front 122

Key clinical findings in mitral stenosis

Back 122

Dyspnea, fatigue, and sytemic embolism
Reduced S1
Loud P2 (due to pulmonary hypertension) followed by opening snap
Apical diastolic rumble after opening snap
Atrial fibrillation

Front 123

What does mitral insufficiency sound like?

Back 123

Monophasic systolic murmur

Front 124

Most common c/o mitral insufficiency

Back 124

Mitral valve prolapse

Front 125

Mitral valve prolapse

Back 125

Myxomatous degeneration (Barlow's syndrome) causes redundant leaflets that are posteriorly displaced during systole.
Mid-to-late systolic murmur

Front 126

Treatment of mitral insufficiency

Back 126

Drugs that relieve CHF symptoms and reduce afterload to encourage forward flow: ACEI, hydralazine, CCB

Front 127

Internal jugular pulsations

Back 127

-Rarely palpable
-Soft, rapid, undulating quality
-Two elevations and two troughs per heart beat
-Pulsations eliminated by light pressure on veins just above sternal end of clavicle
-Level of pulsations changes with position (drop as pt becomes more upright)
-Level of pulsations descends with inspiration

Front 128

Carotid pulsations

Back 128

-Palpable
-More vigorous thrust with single outward component
-Pulsations not eliminated by pressure
-Level of pulsations unchanged by position
-Level of pulsations not affected by inspiration

Front 129

Interesting fact that was on the test last time about JVP

Back 129

-Hypovolemic pt: may have to lie flat to see JV pulse
-Jugular venous pressure increased: may have to raise pt to 60 or 90 degrees to see the neck veins
-Sternal angle is always about 5 cm above the rt atrium

Front 130

Normal LV PMI

Back 130

-4th or 5th ICS
-7-10 cm lateral to midsternal line
-Discrete diameter, =< 2cm
-Brisk tapping amplitude
-Duration =< 2/3 systole

Front 131

Diffuse PMI

Back 131

volume overload, as in AR or MR

Front 132

More forceful RVI (right ventricular impulse)

Back 132

Pressure overload, as in pulmonic stenosis or pulmonary HTN
Hyperkinetic (anx, hyperthyroid, severe anemia)

Front 133

More forceful PMI

Back 133

Pressure overload: AS, HTN
Hyperkinetic: anxiety, hyperthyroidism, severe anemia

Front 134

Sustained PMI

Back 134

AS, HTN

Front 135

Sustained RVI

Back 135

Pulm stenosis, pulm HTN

Front 136

Short PMI

Back 136

hyperkinetic

Front 137

Normal RVI

Back 137

hyperkinetic

Front 138

RVI in left sternal border, extending toward left cardiac border; also subxiphoid

Back 138

volume overload due to ASD

Front 139

PMI displaced to left and possibly downward

Back 139

AR and MR

Front 140

Increased diameter of PMI

Back 140

AS, HTN
AR, MR

Front 141

Physiologic split of S2

Back 141

-Heard in 2nd or 3rd left ICS
-Aortic before pulmonic
-Accentuated by inspiration, disappears on expiration or when pt sits up

Front 142

Wide split of S2

Back 142

-Splitting during expiration
-Pulmonic stenosis (slows closure of pulmonic valve)
-RBBB (splits S2 into mitral and tricuspid components)
-Earlier-than-normal closure of aortic valve (mitral regurgitation)

Front 143

Fixed splitting of S2

Back 143

-Wide splitting that does not vary with respiration
-ASD
-RV failure

Front 144

Paradoxical/reversed splitting

Back 144

-Splitting appears on expiration and disappears on insiration
-Aortic valve closes after pulmonic in expiration
-Inspiration delays P2 so that split disappears
-LBBB!!!

Front 145

Mitral regurgitation

Back 145

-Located at apex of heart
-Radiates to left axilla
-Soft to loud, if loud feel an apical thrill
-Med-hi pitch
-Harsh, holosystolic quality
-DOES NOT BECOME LOUDER IN INSPIRATION
-S1 DECREASED
-Apical S3 due to volume overload in LV (hear at left lateral decubitus, remember)
-Apical impulse (PMI) diffuse, increased in amplitude and may be sustained

Front 146

Tricuspid regurgitation

Back 146

-Lower left sternal border
-Radiates to right of sternum, to xiphoid, midclavicular line
-Variable intensity
-Medium pitch
-Blowing, holosystolic quality
-Intensity may increase with inspiration
-Right ventricular impulse increased in amplitude and may be sustained
-S3 audible along lower left sternal border (due to incr vol?)
-JVP elevated with large v waves
-MC cause is RV failure and dilitation (pulm HTN or LV failure initiates)

Front 147

Ventricular septal defect

Back 147

-3rd, 4th, 5th left interspaces
-Wide radiation
-Very loud with a thrill (and thus must be 4-6 in intensity)
-High, holosystolic pitch
-Harsh quality
-A2 may be obscured by loud murmur

Front 148

Aortic stenosis

Back 148

-Rt 2nd interspace
-Radiates to carotids, down left sternal border, to apex
-Often loud with thrill
-Often harsh but more musical at apex
-Medium harsh midsystolic crescendo-decrescendo that may be higher at apex
-HEARD BEST WITH PT SITTING AND LEANING FORWARD
-A2 gets smaller and more delayed and may eventually lead to single S2 on expiration or a paradoxical S2 split
-S2 may be decreased
-Delayed carotid upstroke with small amplitude
-Hypertrophy of LV
-SUSTAINEDPMI, more foreceful, larger
-S4 from decreased compliance

Front 149

Hypertrophic cardiomyopathy

Back 149

-3rd and 4th left ICS
-Radiates down left sternal border to apex, base, NOT to neck
-Variable intensity
-Medium pitch
-Harsh quality
-Decreases with squatting or release of Valsalva (incr bld to heart decreases outflow obstruction)
-Increases with standing or straining with Valsalva (decreased bld to heart increases outflow obstruction)
-S3 may be present
-S4 at apex unlike in MR
-Sustained apicalimpulse with two palpable components
-Quick rise of carotid pulse unlike aortic stenosis
-May not even hear S2
-Associated with MR, outflow obstruction, unusually rapid ejection of bld from LV in systole

Front 150

Pulmonic stenosis

Back 150

-2nd and 3rd left ICS
-If loud radiates to left shoulder and neck
-Soft to loud intensity associated with thrill (like MR and VSD)
-Harsh quality
-Wide split of S2 in severe stenosis
-P2 diminished or inaudible
-Early pulmonic ejection sound common
-May hear right sided S4 (stiffness)
-RV impulse increased and SUSTAINED (due to vol overload in RV)
-High RV afterload
-ASD sounds like this sort of

Front 151

Aortic regurgitation

Back 151

-Diastolic decrescendo
-2nd to 4th left ICS
-If loud, radiates to apex and maybe rt sternal border
-Grade 1-3
-Blowing decrescendo may be mistaken for breath sounds
-High pitch-USE THE DIAPHRAGM
-Heard best with pt sitting, leaning forward, with breath held after exhalation (unlike aortic stenosis where don't have to hold breath)
-Ejection sound
-S3 or S4 if severe regurg
-increased amplitude, lateral and downward displacement, widened diameter, and increased duration of PMI
-Pulse pressure increases
-Arterial pulses often large and bounding
-Midsystolic Austin Flint murmur suggests large regurgitant flow

Front 152

Mitral stenosis

Back 152

-Usually apex
-no radiation
-Grade 1-4
-Dcrescendo low-pitched rumble (USE THE BELL)
-Place bell exactly on apical impuse. Turn pt into LEFT LATERAL DECUBITUS POSITION, exhalation, mild exercise--> make murmur more audible
-S1 accentuated; may be palpable at apex
-Opening snap follows S2 and initates murmur
-If pulm HTN develops, P2 accentuated and RVI palpable
-MR and aortic valve dz may be associated

Front 153

Atrial or nodal premature contractions (supraventricular)

Back 153

-Beat of atrail or nodal origin comes earlier than the next expected nodal beat. -Pause follows, and then rhythm resumes.
-S2 may differ in intensity from S1 of nl beats.
-S2 may be decreased.
-Both sounds otherwise normal
-Aberrant P wave, normal QRS and T

Front 154

Ventricular premature contractions

Back 154

-Beta of ventricular origin comes early than next expected normal beat
-Pause follows, then rhythm resumes
-S1 may differ in intensity from nl S1
-S2 may be decreased
-Both sounds likely to be split
-No p wave, aberrant QRS and T

Front 155

Sinus arrhythmia

Back 155

-Heart varies cyclicaly
-Ususally speeds up with inspiration and slows down with expiration
-The sound is normal but S1's sound may vary with the heart rate

Front 156

Atrial fibrillation and atrial flutter with varying AV block

Back 156

Ventricular rhythm is totally irrgular, but short runs of irrregular ventricular rhythm may seem regular.
-S1 varies in intensity