exam 4 new material (copy)

Mitral Stenosis

• Reduced E-F slope

• Early diastolic closing at a slower rate due to restriction of the LA emptying

Mitral Stenosis M-mode clues to look for when diagnosing:

1. Thickening of AML & PML

2. Anterior motion of posterior leaflet due to tethering (restriction)

3. Persistent high LA pressures

Most common cause of Mitral Stenosis

Rheumatic Fever

Complications of Mitral Stenosis

• MV Regurgitation

• Pulm hypertension (high BP)

• LA thrombus (7-15%) - most common in appendage

• A-Fib (bc LA can’t empty properly)

MV B-Bump

• Valve drifts shut with increasing LV end diastolic pressure (occurs during late diastole)

• Commonly seen with Dilated Cardiomyopathy

• Elevated LV end diastolic pressure is greater than 20mmHg

Systolic Anterior Motion

• Abnormal forward movement of AML toward the LVOT in systole

• Seen in hypertrophic cardiomyopathies such as:

  • ASH (asymmetrical septal hypertrophy)

  • IHSS (idiopathic hypertrophic subaortic stenosis)

  • HOCM (hypertrophic obstructive cardiomyopathy)

MV Prolapse

AKA Barlow’s syndrome

• Hammocking

• Posterior displacement of the MV leaflets beyond the MV annular plane during ventricular systole

• Paroxysmal Supraventricular tachycardia is a common arrhythmia that occurs in people with MVP

MV Flutter

• Caused by aortic regurgitation

• Diastolic flutter of AML with aortic regurgitation because aortic regurgitation jet slams into the AML

Premature closure of MV

• Closure on or before onset of QRS

• Associated with acute severe AOV regurgitation

Vegetation

• Infected mass

• Forms at sites where blood flow injury is most likely to occur

• Located on UPSTREAM side of infected valve

Aortic Stenosis etiology

• Acquired

  • Most common cause is Senile Calcification (8-9th decade of life)

  • Rheumatic AS is usually associated with MS - autoimmune & leads to chronic inflammation, commissural fusion, thickening & calcification of cardiac valves

• Congenital

  • Bicuspid - 1-2% of population

  • Unicuspid - very rare

Aortic Stenosis characteristics

• Reduced ACS

• Volume overload in LV & increased diastolic pressure - remodeling of LV

• LV’s response to pressure overload is a concentric hypertrophy

• EF<35% = increased risk of HF

Aortic Stenosis mimickers

Subvalvular stenosis (below/before)

• hypertrophic cardiomyopathy

• subvalvular membrane

Supravalvular stenosis (above/after)

• narrowing of ascending aorta

Bicuspid AOV

• Eccentric closure line (up or down from mid line)

• Valve thick

• RCC and LCC will be seen, no NCC

• Only diagnosed in systole

• In diastole, there may be raphe (seam or fibrous ridge of tissue between 2 cusps)

Premature closure of AOV

• Happens when there is a pressure change or drop from LV to Aorta

• Closing before onset of T-wave

• Associated with Idiopathic hypertrophic subaortic stenosis (IHSS)

• Thickened septum obstructs LVOT, which leads to pressure changes & premature closure

Dilated LA

Volume overload because of:

• MV regurgitation

• MV stenosis

• MV prolapse

• Significant LVEDP

• Chronic severe aortic insufficiency (aortic regurgitation)

LA Myxoma

• Benign tumor attached by stalk to IAS

• May completely or partially prolapse into LV during diastole, mimicking MV stenosis

• Larger myxoma = more it’ll encompass the window to EF slope

Dilated AOR

Etiology’s

• Marfan syndrome - proximal dilation of annulus, sinus of valsalva, & ascending aorta

• Hypertensive pt’s without proper meds

  • AOR and ascending aorta move into LA

  • Measurement should be taken from PSLA

LV hypertrophy

• Thickening of septal and/or posterior wall

• Symmetrical

  • Concentric hypertrophy

  • Concentric remodeling

  • Infiltrative disease

• Asymmetrical

  • Hypertrophic cardiomyopathy

    • Pressure overload

    • AOV stenosis

Paradoxical Motion

Movement away from opposite wall or stretching of wall during systole

• IVS away from free wall & posterior inferior away from pericardium

Due to:

• LBBB

• MV Prolpase

• RV hypertrophy & dilation

• Pressure gradient changes

• S/P (status post) cardiac surgery

Ischemia

• Abnormal septal motion

• Lack of blood to heart muscle

• Thin echogenic wall

• Reduced LVPW motion

Post Infarct

• Decreased wall motion

• Abnormal septal motion

• Thin echogenic wall

• No systolic thickening

Pericardial Effusion

Inflammatory

• Post MI

• Uremia

• Collagen Vascular Disease

• Post Cardiac Surgery

Infection

• Postviral pericarditis

• Bacterial

• Tuberculosis

Pleural Effusion

Below DA

• PE is ABOVE DA - peri effusion

• PL is BELOW DA - pleural effusion

Water pills to pee it out

RV gets crushed (with both)

Volume overload

• Chambers have large volume of close so can’t function properly

• LV overload leads to heart failure

• RV volume increases pressure and pushes on septum

• “D” shaped septum

Pulmonic valve - abnormalities

• Increased “a” wave = pulmonary stenosis

• Decreased “a” wave = pulmonary hypertension

• ***Pulmonary hypertension is known as “Flying W”