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www.cardionursing.com NTI 2009
CMC Review Course
NTI 2009
New Orleans
Cardiovascular
Pathophysiology
Cynthia Webner BSN, RN, CCRN-CMC
www.cardionursing.com
Valvular Heart Disease
Cynthia Webner BSN, RN, CCRN, CMC 1
www.cardionursing.com NTI 2009
Cardiovascular Pathology
Chronic Valve Disease
• Basic Tenants
– Early recognition is key to treatment
• Identified through routine cardiac auscultation
– Compensatory changes occur over years to
decades
– No treatment until symptoms or severe disease by
echocardiogram
– Treatment Options: Surgery
– Careful routine follow up
Aortic Stenosis:
Obstruction of flow at the level of the aortic valve
Classifications
Congenital Acquired
• Most common cause • Most common form of AS in those
>70
of AS in men under
• RHD
70 – Fibrosis of valve leaflets with
• More prevalent in commissure fusion
men – RHD impacts mitral valve as well
– Mitral valve affected
• Abnormal number of
• Senile Degenerative Calcification
valve cusps – Calcified nodules on valve leaflets
• Symptoms appear – Thickened leaflets
between ages of 40 - – Concomitant aortic regurgitation not
uncommon
60
Cynthia Webner BSN, RN, CCRN, CMC 2
www.cardionursing.com NTI 2009
Aortic Stenosis
Pathophysiology
Compensatory Mechanisms
Aortic Valve Orifice Narrows
____Afterload
____LV Workload
____LV Wall Mass
____LV Hypertrophy
___________ Dysfunction
Works well for years – even decades.
Compensatory system ultimately fails Symptoms
Cynthia Webner BSN, RN, CCRN, CMC 3
www.cardionursing.com NTI 2009
Aortic Stenosis
Symptoms
• Classic Triad
– Angina
• Left ventricular hypertrophy
• Imbalance in supply and demand
– Syncope: Hemodynamic response to exercise
• Arterial vasodilatation – decreased systemic vascular resistance
• Increased heart rate does not work to increase cardiac output ->
syncope
– Heart Failure
• Diastolic dysfunction
• Ultimately systolic dysfunction
Systolic Ejection Murmur
• May be present before any significant hemodynamic changes
occur
• More severe AS longer murmur
• Timing: Midsystolic
• Location: Best heard over aortic area (2nd ICS RSB)
• Radiation: Toward neck and shoulders
– May radiate to apex
• Configuration: Crescendo-decrescendo
• Pitch: Medium to high
• Quality: Harsh
Cynthia Webner BSN, RN, CCRN, CMC 4
www.cardionursing.com NTI 2009
Atrial Gallop - S4
• Occurs during late ventricular
diastole
• Caused by atrial contraction and
the propulsion of blood into a
noncompliant (stiff) ventricle.
• Associated with systemic
hypertension, restrictive
cardiomyopathy,ischemia, aortic
stenosis.
• Best heard with patient in left
lateral decubitus position.
• Location: Apex (5th ICS LMCL)
• Duration: Short
• Quality: Thud like
• Pitch: Low (Bell)
Diagnosis
• Echocardiogram
– Evaluate LV function and valve function
– Mean Pressure Gradient > 40 mmHg (Severe AS)
– Valve Area
• Severe AS Valve area <1.0 cm2
• Stress Test
– Assess for exercise capacity / induce symptoms
– Determine abnormal blood pressure response to exercise
– NOT INDICATED in symptomatic patients
– NOT INDICATED in severe disease by echo
• Cardiac Cath
– Verify absence/presence of CAD
– Evaluate pressure gradients
– Injection of dye arterial vasodilatation
Cynthia Webner BSN, RN, CCRN, CMC 5
www.cardionursing.com NTI 2009
Treatment
Medical Treatment Surgical Treatment
• Rarely needed • Mortality increase as LV dysfunction
decreases
• Treat diastolic dysfunction • AV Replacement with mechanical or
– Fluid balance bioprosthetic valve
• Assure oxygen delivery • Bileaflet valve most common
– Oxygen saturation / choice for mechanical valve in
Hemoglobin aortic position
• In severe or symptomatic • AV Replacement with an allograft
AS avoid (homograft) or heterograft valve
– ACE Inhibitors: Preload and – Stented heterograft most
afterload reduction common aortic valve prosthetic
– Beta Blockers: Decreases in US
sympathetic HR response – Homograft common with total
aortic root repair
• NTG with caution in severe • Aortic Valve Repair
of symptomatic AS
– Low dose: Impact on preload – Decalcification of valve
– Valvuloplasty
– High dose: Impact on
afterload
Endocarditis Prophylaxis
All Patients with Valve Disease
• Only for those with the highest risk for the
development of infective endocarditis.
• Population at the highest risk for the
development of infective endocarditis:
• 1. Prosthetic cardiac valve
• 2. Previous infective endocarditis
• 3. Congenital heart disease
• 4. Cardiac transplant recipients who
develop cardiac valvulopathy
Cynthia Webner BSN, RN, CCRN, CMC 6
www.cardionursing.com NTI 2009
Valve Replacement Options
All Valves Replacements
Mechanical Valves Tissue Valves
• More durable than tissue • Bioprosthetic
valves • Less durable than
• Require life-long mechanical valves
anticoagulation • Do not have risk of
• Post-op mortality related to mechanical failure
valve • No anticoagulation with
– Thromboembolism, warfarin required
hemorrhage, endocarditis,
periprosthetic leak • Homograft (Allograft)
• Ball and cage • Heterograft (Xenograft)
– Stented
• Single Leaflet Tilting Disc
– Stentless
• Bileaflet Valve
Percutaneous Balloon
Valvotomy
• Balloon placed across aortic valve
• Fractures calcium deposits in the leaflets
• Separate fused or calcified commissures
• Considered palliative in the aortic position
• May be used as a bridge to surgery
• All benefit gone in 6 months
• Development of or increased severity of
AR
• Not appropriate if AR > 2+ prior to procedure
Cynthia Webner BSN, RN, CCRN, CMC 7
www.cardionursing.com NTI 2009
Post Operative Considerations
• LV Hypertrophy regresses
• Diastolic dysfunction never returns to normal
• Patient experiences improvement immediately after
surgery
Endocarditis Prophylaxis
For All Valve Replacements
• Appropriate for all patients with prosthetic valves
• Procedures requiring prophylaxis
– Dental procedures involving manipulation of gingival tissue or periapical
region of teeth or perforation of oral mucosa
• Biopsies
• Suture removal
• Placement of orthodontic bands
– Respiratory procedures
• Involving incision or biopsy of respiratory mucosa
• No longer required
– GI or GU procedures
• Single dose 2 hours prior to procedure
• Amoxicillin or cephalexin (if penicillin or amoxicillin allergy)
• KEY TO PREVENTION
Cynthia Webner BSN, RN, CCRN, CMC 8
www.cardionursing.com NTI 2009
Endocarditis Prophylaxis
For All Valve Replacements
• Appropriate for all patients with prosthetic valves
• Procedures requiring prophylaxis
– Dental procedures involving manipulation of gingival tissue or periapical
region of teeth or perforation of oral mucosa
• Biopsies
• Sutures –placement or removal
• Placement of orthodontic bands
– Respiratory procedures
• Involving incision or biopsy of respiratory mucosa
• No longer required
– GI or GU procedures
• Single dose 2 hours prior to procedure
• Amoxicillin or cephalexin (if penicillin or amoxicillin allergy)
• KEY TO PREVENTION
Anticoagulation
For All Valve Replacements
• Mitral valve replacement highest risk for
embolization
• Mechanical Valve
– Warfarin for all patients
– Warfarin and ASA if high-risk for thromboembolism
– Consider warfarin and clopidogrel if allergy to ASA
• Tissue Valve
– Warfarin for 3 months post op in all patients
(especially MVR)
– ASA for all patients with no risk for
thromboembolism
Cynthia Webner BSN, RN, CCRN, CMC 9
www.cardionursing.com NTI 2009
Aortic Regurgitation (Insufficiency):
Valve cusps do not close completely
Blood travels retrograde through the valve during diastole
Classification
Chronic Acute
– RHD – Trauma
– Congenital – Acute infective
endocarditis
– Infective endocarditis
– Acute aortic dissection
– Marfan’s
– Inflammatory diseases
– Syphilis
– Severe systemic Hypertension
Aortic Regurgitation
Pathophysiology
Cynthia Webner BSN, RN, CCRN, CMC 10
www.cardionursing.com NTI 2009
Compensatory Mechanisms
In Aortic Regurgitation
During diastole there is backward filling of the LV from
the aorta and forward filling from the left atrium
___LV Volume
LV ___________ (size)
LV ____________ (muscle mass)
stroke volume __________
Works well for years – even decades.
Compensatory system ultimately fails
__________ Dysfunction Heart Failure
Chronic Aortic Regurgitation
Symptoms / Physical Exam
• Exertional dyspnea • Apical Impulse
• PND • Diastolic Murmur of
• Orthopnea AR
• Angina • Systolic Flow Murmur
• Aware of heart beat – • Austin Flint Murmur
especially when lying • Signs of
• Pulsatile sensation in Hyperdynamic
head Perfusion
Cynthia Webner BSN, RN, CCRN, CMC 11
www.cardionursing.com NTI 2009
Diastolic Murmur of AR
• Length of murmur correlates severity of AR
• Timing: Early diastole
• Location: left sternal boarder 3rd,4th ICS
• Radiation: Towards apex
• Configuration: Decrescendo
• Pitch: High
• Quality: Blowing
• Patient Position: sitting and learning forward at end
expiration
• Intensity: Increases with increased peripheral vascular
resistance
– Squatting, exercising, hand gripping
Systolic Flow Murmur
• Result of turbulent flow across valve during systolic
• Large volumes of blood from hyperdynamic perfusion
causes turbulence
• Timing: Mid systolic
• Location: Along left sternal boarder
• Configuration: Crescendo-decrescendo
• Pitch: Medium (best with diaphragm)
• Quality: Soft
• Intensity: May increase after coughing or when
elevating legs while in lying position
Cynthia Webner BSN, RN, CCRN, CMC 12
www.cardionursing.com NTI 2009
Austin Flint Murmur
• Very severe chronic AR or acute AR
• Diastolic murmur: functional mitral stenosis
• Severe AR
blood flow back through the aortic valve
regurgitant volume presses on open anterior leaflet of mitral
valve
moves the leaflet towards the closed position
functional MS
• Timing: Mid systolic
• Location: cardiac apex
• Configuration: Plateau
• Pitch: Low pitch
• Quality: Rumbling
• Intensity: Soft
Signs of Hyperdynamic Perfusion
• Warm, flushed, reddish mucous membranes
• Wide pulse pressure (>100mmHg)
• De-Musset Sign
– Head bobbing with each heart beat
• Water-Hammer pulse
– Rapid rise and collapse of the pulse upon palpitation
• Corrigan’s Pulse
– Large carotid pulsation in the neck
• Traube’s Sign
– Loud, sharp “pistol-shot-like” sound heard over the femoral
pulse
• Duroziez’s Sign
– Murmur heard over the femoral artery when compressed
• Quinke’s Sign
– Pulsitile blanching and reddening of the fingernails when
light pressure is applied
Cynthia Webner BSN, RN, CCRN, CMC 13
www.cardionursing.com NTI 2009
Acute Aortic Regurgitation
Pathophysiology
Sudden decrease in cardiac
output
Increased LV afterload
(increases regurgitation)
Increased LV preload
Pulmonary edema, cardiogenic
shock and acute decompensation
Diagnosis
• Cardiac Echocardiogram
– Grade of Severity (Severe 3-4+)
– Regurgitant Volume Evaluation of (amount
returned to LV each beat) (Severe 60-120ml)
– Evaluation of Left Ventricular Function
– Evaluation of Valve Leaflets
• Stress Testing
– Not needed to confirm diagnosis
– May test functional capacity, and response to
exercise
• Cardiac Cath
– Verify absence or presence of CAD
EF Evaluates what has been ejected and
does not consider volume that has been
displaced backwards!
Cynthia Webner BSN, RN, CCRN, CMC 14
www.cardionursing.com NTI 2009
Chronic Aortic Regurgitation
Treatment
Medical Treatment Surgical Treatment
• If normal LV function no – Replacement or
treatment repair as with
• Arterial Vasodilators aortic stenosis
– Decrease afterload
decrease regurgitation
– Not indicated in
asymptomatic patients
• Digoxin and diuretics
helpful with HF symptoms
• Avoid arterial
vasoconstrictors
Acute Aortic Regurgitation
Treatment
• Urgent Surgical Intervention
• STAT ECHO
• Reduce afterload
– Nitroprusside
• Reduce preload
– Help reduce fluid overload
• Beta blockers
– With caution
– Block sympathetic response of increased HR
• Inotropes
– Increase contractility for forward flow
Cynthia Webner BSN, RN, CCRN, CMC 15
www.cardionursing.com NTI 2009
Aortic Regurgitation
Outcomes
• LV function improves within first 10-14 days
• LV Function may improve for up to 2 years
• If LV function does not improve or only
minimally then symptomatic treatment will be
required.
Mitral Valve Disease
Normal Function of Mitral Valve
• Annulus
• Leaflets
• Chordae Tendineae
• Papillary Muscles
Cynthia Webner BSN, RN, CCRN, CMC 16
www.cardionursing.com NTI 2009
Normal Mitral Valve
Mitral Regurgitation (Insufficiency):
Valve cusps do not close completely
Blood travels retrograde through the valve during diastole
Classification
• Organic Processes • Functional
– Involve the structure of Abnormalities
the valve itself – Changes in other
– Mitral Valve Prolapse structures resulting in
– Rheumatic Heart Disease: changes in the valve
Fibrosis, leaflet shortening function
– Infective Endocarditis: – Left ventricular or atrial
Vegetation dilatation
– Collagen Vascular – Papillary muscle ischemia
Diseases or infective endocarditis
Cynthia Webner BSN, RN, CCRN, CMC 17
www.cardionursing.com NTI 2009
Mitral Regurgitation
Pathophysiology
Pathophysiology
During systole as the LV contracts blood is ejected from left
ventricle through the open aortic valve AND some is diverted
retrograde through dysfunctional mitral valve
______left atrial volume and pressure AND
left atrium responds by _________
atrium sends _________volume to ventricle
LV adjusts by ________________ AND
LV increases _____________to assure forward
flow
Works well for years – even decades.
Compensatory system ultimately fails __________ Dysfunction
Symptoms
Cynthia Webner BSN, RN, CCRN, CMC 18
www.cardionursing.com NTI 2009
Symptoms / Physical Exam
• Remain asymptomatic for • Decreased carotid pulse
years volume
• Most frequent • Apical impulse displaced
– Fatigue due to the dilation of the
– Dyspnea on exertion left ventricle
• Progress to include • Signs of heart failure
– Paroxysmal nocturnal • Signs of pulmonary
dyspnea hypertension – advanced
disease
– Orthopnea • Systolic Murmur of Mitral
– Palpitations from atrial Regurgitation
fibrillation • S3
• Initial diagnosis sometimes • Large V Waves on RA or
made with new onset AF PAWP trace
Systolic Murmur of MR
• Timing: Holosystolic
• Location: Mitral area
– May be louder in aortic
area depending on
leaflet involved
• Radiation: To the left
axilla or posteriorly
over lung bases
• Configuration: Plateau
• Pitch: High
• Quality: Blowing,
harsh or musical
Cynthia Webner BSN, RN, CCRN, CMC 19
www.cardionursing.com NTI 2009
Ventricular Gallop - S3
• Occurs during early
ventricular diastole
• Results from increased blood
volume or decreased
resistance.
• Most frequently associated
with systolic dysfunction
• Best heard with patient in left
lateral decubitus position.
• Location: Apex 5th ICS LMCL
• Duration: short.
• Quality: dull, thud like.
• Pitch: low (bell)
Large V Waves
PCWP Tracing with
Normal PCWP Tracing
Large V Waves
Cynthia Webner BSN, RN, CCRN, CMC 20
www.cardionursing.com NTI 2009
Acute Mitral Regurgitation
Papillary Muscle Rupture Endocarditis
Acute decrease in cardiac output
SVR
blood flow to area of least resistance (through non-
functional MV)
cardiac output (forward flow) and atrial volume
(fluid overload)
SVR and symptoms of volume overload
blood flow to area of least resistance
cardiac output (forward flow) and
atrial volume (fluid overload)
acute pulmonary edema & shock
Diagnosis
• Cardiac Echo
– Determine Grade of Severity (Severe 3-4+)
– Evaluation of Regurgitant Volume (60-120ml Severe)
– Evaluation of Left Atrium for left atrial dilation
• Stress Test
– Not helpful in diagnosis
• Cardiac Cath
– Assessment for CAD
– Right heart cath helpful in assessing pulmonary
hypertension
EF Evaluates what has been ejected and does not
consider volume that has been displaced backwards!
Cynthia Webner BSN, RN, CCRN, CMC 21
www.cardionursing.com NTI 2009
Treatment
Medical Treatment Surgical Treatment
• No treatment for • Mitral valve repair
asymptomatic patient • Mitral valve
with normal ventricular replacement with
function preservation of mitral
apparatus
• Rhythm Control
• Mitral valve
• Afterload reduction is replacement with
key to treatment. removal of mitral
• ACE Inhibitors apparatus
– Useful in non-surgical
candidates
– No benefit in
asymptomatic
patients
Treatment for Acute MR
• STAT Echo
• Surgery emergently
• IABP
• Afterload Reduction
– Nitroprusside
• Antibiotics
Cynthia Webner BSN, RN, CCRN, CMC 22
www.cardionursing.com NTI 2009
Outcomes
• Symptoms improve post operatively if no LV
dysfunction
• Those with MVP have best outcomes
• Endocarditis the same as with AS
• Anticoagulation the same as with AS
• Follow up the same as with AS
Mitral Stenosis:
Obstruction of flow at the level of the mitral valve
Classifications
• Rheumatic Heart Disease • Other causes
– Fibrosis and calcification of the – Rare
valve leaflets – Congenital mitral stenosis
– Valve commissures fuse – Atrial myxoma
together – Systemic lupus erythematosus
– Chordae tendineae thicken and – Bacterial endocarditis
shorten
– Combination of some or all of
these things results is a valve
orifice that is much smaller
than normal
– Normal mitral valve area is 4.0
to 5.0cm2
Cynthia Webner BSN, RN, CCRN, CMC 23
www.cardionursing.com NTI 2009
Mitral Regurgitation
Pathophysiology
Normal Compensatory
Mechanisms in Mitral Stenosis
Valve opening narrows
Passive filling from left atrium to left ventricle _______________
Left atrial pressure ________ in attempt to maintain normal flow
across the valve
_________ left atrial pressure transferred back to the
pulmonary vascular bed
Pulmonary pressures subsequently ___________
Left atrium ________ as forward flow _________
More difficult to empty atrium
Chronic ___________ in left atrial pressure
Pulmonary hypertension develops
Compensatory system ultimately fails Right ventricular
failure
Cynthia Webner BSN, RN, CCRN, CMC 24
www.cardionursing.com NTI 2009
Symptoms
• Symptoms at rest
– Valve area < 1.5cm2
• Dyspnea with exertion
• Pulmonary symptoms increase
• Development of orthopnea and
paroxysmal nocturnal dyspnea
• Develop cough and hemoptysis
• Ultimately RV Failure
Symptoms / Physical Exam
• Often discovered with • Signs of right ventricular
conditions that increase failure if disease process is
severe
heart rate
– Pregnancy
– Jugular venous distension
– New onset atrial fibrillation – Hepatomegaly
– Hyperthyroidism – Peripheral edema
– Fever – Ascites
• Stroke • Mitral Facies
– Enlarged atrium – Pinkish-purple discoloration of
– High risk for development of the cheeks
thrombi – Common with severe mitral
stenosis
• Atrial Fibrillation
– 50% of patients with MS
– Enlarged atrium
Cynthia Webner BSN, RN, CCRN, CMC 25
www.cardionursing.com NTI 2009
Physical Exam
• Opening Snap
– Not present if heavily calcified
– Location: Cardiac apex
– Timing: Just after S2
– Pitch: High
– Radiation: across precordium
– Often confused with S3
• S3 better heard with bell of stethoscope
• S3 louder during expiration than inspiration (OS does not
change)
• OS occurs closer to S2 than S3
• Diastolic murmur helps confirm OS
Diastolic Murmur
Mitral Stenosis
• Timing:
– Holodiastolic if severe MS
– Mid to Late diastole if moderate MS
• Location: Apex
• Configuration: Crescendo
• Pitch: Low
• Quality: Rumbling
• Best heard with patient in left lateral position
• Increases with isometric exercise, and expiration
Cynthia Webner BSN, RN, CCRN, CMC 26
www.cardionursing.com NTI 2009
Diagnosis
• Echocardiogram
– Evaluation of Pressure Gradient (Severe >10mmHg)
– Evaluation of Valve Area (Severe <1.0 cm2)
– Evaluation of Atrial Size
– Evaluation of Pulmonary Artery Pressures (Severe
>50mmHg)
– Evaluation of Valve Leaflets
• Cardiac Catheterization
– Assessment of need for coronary artery revascularization if valve
replacement is needed.
– Measure pulmonary pressures
– Measure left atrial pressure
Medical Treatment
• Limited treatment in asymptomatic patients in
NSR
• Atrial Fibrillation is poorly tolerated
• Heart Rate Control
– Heart rate should be maintained at less than
100 bpm
• Other Benefits of Beta-blockers and Calcium
Channel Blockers
– Decrease ventricular wall tension
– Improve filling from the atria
Key to Treatment: Passive ventricular filling is slowed therefore atrial
kick, long diastolic filling times and ventricular relaxation are essential.
Cynthia Webner BSN, RN, CCRN, CMC 27
www.cardionursing.com NTI 2009
Surgical Treatment
• Surgical Options
– Percutaneous mitral balloon valvotomy
– Closed surgical commissurotomy
– Open surgical commissurotomy
– Mitral valve replacement
Valvotomy
• Better long-term results for MV
than AV
• Inflated balloon causes fused
leaflets to split
• Best results in patient with no
valve calcification and strictly a
fusion of the commissures
• If LA is greatly dilated or the valve
is very calcified the results will be
suboptimal
• Should not be performed if also
have mitral regurgitation of 2+ or
more
Cynthia Webner BSN, RN, CCRN, CMC 28
www.cardionursing.com NTI 2009
Commissurotomy
• Commissures are cut apart
• Allows for increased movement of the leaflets
• Beneficial to patients with pliable leaflets and no calcification
• Closed repair or open repair
• Closed repair
– Cannot visualize the valve
– No cardiopulmonary bypass needed
– Valvotomy becoming more common
• Open repair is preferred method
– Can remove calcium deposits
and left atrial clots
– Amputation of left atrial appendage
– Open chest procedure
requiring the use of cardiac bypass
Outcomes
• Excellent outcomes with valvuloplasty and
commisurotomy
• Symptom improvement occurs as soon as
procedure is complete
Cynthia Webner BSN, RN, CCRN, CMC 29
www.cardionursing.com NTI 2009
Cardiomyopathy
Functional
AHA Definition 2006 Classification
• Heterogeneous group of • Pathological situation
diseases of the myocardium occurring regardless of
• Associated with mechanical cause
and /or electrical dysfunction • Provides a discussion based
• Usually (but not invariable) on patient presentation and
exhibit inappropriate related pathology
ventricular hypertrophy or • Cause often unknown
dilation • Describes the ventricular
• Due to a variety of causes changes that occur
• Classification – Restrictive Cardiomyopathy
– Primary (genetic) – Hypertrophic Cardiomyopathy
– Mixed (genetic and nongenetic) – Dilated Cardiomyopathy
– Acquired – Arrhythmogenic
– Secondary Cardiomyopathy
Restrictive Cardiomyopathy:
Rigidity of myocardial wall
Decreased ability of chamber walls to expand during diastole
Least common form of Cardiomyopathy
Causes
Primary Causes Secondary Causes
• Endomyocardial • Infiltrative disorders
Diseases – Amyloidosis
• 90% of RCM in North
– Eosinophilic America
Endomyocardial Fibrosis
– Sarcoidosis
– Endocardial Fibrosis – Radiation carditis
– Cardiac Transplant • Storage Diseases
– Anthracycline Toxicity – Hemochromatosis
• Idiopathic – Glycogen storage disease
• Loffler’s Endocarditis – Fabry’s Disease
Cynthia Webner BSN, RN, CCRN, CMC 30
www.cardionursing.com NTI 2009
Pathophysiology
• Ventricular chamber has limited ability to
expand during filling (diastolic dysfunction)
• Decreased volume available to eject
• Increased volume and pressure in atria
• Dilated atrium
• Increased volume and pressure in pulmonary
system
• Heart failure symptoms
Symptoms / Physical Exam
• Fatigue, weakness • S4
• Decrease in activity • Mitral insufficiency
intolerance – Dilation of atrium
• Hypotension – Papillary muscle
dysfunction
• Syncope – Fibrosis of leaflets
• Palpitations with – Murmur of mitral
arrhythmias regurgitation
– Atrial fibrillation
– Conduction disturbances
• Pale/ cool
• Peripheral pulses
decreased
Cynthia Webner BSN, RN, CCRN, CMC 31
www.cardionursing.com NTI 2009
Differentiation of RCM with
Constrictive Pericarditis
Clinical Features Constrictive Pericarditis Restrictive Cardiomyopathy
History Prior history of pericarditis or History of systemic disease (e.g..
condition that causes pericardial Amyloidosis, Hemochromatosis)
disease
Heart Sounds Pericardial knock, high Presence of loud diastolic filling sound S3,
frequency sound low frequency sound
Murmurs No murmurs Murmurs of mitral and tricuspid
insufficiency
Heart Pressures L (PCWP)& R (CVP) filling L sided filling pressures > R sided filling
pressures elevated and equal pressures
Chest X-ray Visualize pericardial calcification. Atrial dilation with normal ventricular size
Echocardiogram Normal ventricles and atria Atrial dilation with normal ventricular size
Pericardial thickening Amyloidosis: Speckled texture to
myocardium
Diagnosis
• ECHO • Cardiac Cath
– Chamber size – Full cath not necessary
– Wall thickness – Hemodynamic
– EF – Normal or high measurements valuable
– Valve functioning • Elevated LVEDP
• Elevated PAOP
– Speckled appearance on • Elevated RA Pressures
myocardium with • Elevated pulmonary
amyloidosis pressures
• Endomyocardial Biopsy
– Septal wall of RV
– Multiple sites
– Essential for diagnosis of
RCM
Cynthia Webner BSN, RN, CCRN, CMC 32
www.cardionursing.com NTI 2009
Treatment
• Reduce Diastolic Dysfunction • Treat Underlying Disease
– No direct medications Process
– Treat affect of restriction – No cure for Amyloidosis
• Steroids and chemo helpful in
• Careful control of volume slowing progression of disease
• Rate control process
• Rhythm control – Chelation for hemochromatosis
• Decrease afterload • Valve replacement
– Symptomatic relieve
• Conduction abnormalities – High mortality
• May require pacemaker • Cardiac Transplant
• Treat for Thromboembolic – Beneficial in idiopathic /
Complications familial
– Need heart and liver with
– Highest risk in endocardial fibrosis hemochromatosis
– High risk with enlarged atrium – Limited usefulness in
– High risk with AF infiltrative diseases: Disease
will affect new organs
– High risk with TR and MR
Outcomes
• Poorest mortality of all cardiomyopathies
• 90% mortality rate at 10 years (Kavinsky & Parrillo, 2000).
• Amyloid Heart
– 80% mortality at 2 years
Cynthia Webner BSN, RN, CCRN, CMC 33
www.cardionursing.com NTI 2009
Hypertrophic Cardiomyopathy
• 1 of every 500 (Maron et al, 2003)
• Effects men and women equally
• Hypertrophy of myocardial muscle mass
• Associated with decreased ventricular filling and
decreased cardiac output
• Most common cause of sudden death in young adults
• Cause unknown: 50% transmitted genetically
• Disarray of cardiac myofibrils with hypertrophy of
myocytes
• Cells take on a variety of shapes
• Myocardial scarring and fibrosis occurs
Hypertrophic
Cardiomyopathy
• Usually only effects LV
• Changes may be symmetrical
• Asymmetrical septal hypertrophy is
more common
• May involve entire septum or only a
portion of septum
Cynthia Webner BSN, RN, CCRN, CMC 34
www.cardionursing.com NTI 2009
Hypertrophic Cardiomyopathy
Pathophysiology
• Ventricular chamber size decreases as enlarging walls close in
on chamber
• Stiff walls resist filling (diastolic dysfunction)
• Passive filling is slowed
• Atrial kick more essential than normal
• Atrial dilatation due to increase in pressure and volume
• Transferred to pulmonary system
• Compensation for decreased filling -> hyperdynamic systolic
dysfunction: EF increases to 70-80%
• Mitral Regurgitation
– Hypertrophied papillary muscles
– Leaflets become calcified and thick
– Atrial dilatation enlarges mitral valve annulus
Hypertrophic Cardiomyopathy
OBSTRUCTIVE (HOCM)
• 30-50% of HCM patients
have obstruction
• Obstruction of outflow
tract
• Septal wall enlarges into
ventricular cavity
• Anterior leaflet of mitral
valve drawn towards the
septum during ejection
• Early closure of aortic
valve, decreased ejection
time, decreased cardiac
output
Cynthia Webner BSN, RN, CCRN, CMC 35
www.cardionursing.com NTI 2009
Symptoms / Physical Exam
Incidence of sudden death often • Bisferiens Carotid Pulse
first presentation
(HOCM)
• Identified during screening of
relative of patient with HCM – Brisk initial upstroke
• Symptoms related to severity of – Collapse of pulse then
diastolic dysfunction or mitral secondary rise
regurgitation – Must differentiate from AS –
• Dyspnea / activity intolerance delayed upstroke
• Palpitations • PMI forceful and brisk
• Chest pain • S4
• Syncope / Presyncope • MR murmur
• Systolic murmur with
obstructive disease process
Subvalvular Left Ventricular Outflow
Obstruction Systolic Murmur
• Timing: Mid systolic
• Location: best heard along left sternal boarder
• Radiation: usually does not radiate
• Configuration: crescendo-decrescendo
• Intensity: grade 3/6 to 4/6
• Pitch: medium
• Quality: harsh or rough
• Differentiating between HOCM and AS
– HOCM murmur increases with Valsalva maneuver
• Decreased preload results in decreased left ventricular
filling
• Decreased left ventricular filling results in increased
obstruction
– AS murmur decreases with Valsalva
Cynthia Webner BSN, RN, CCRN, CMC 36
www.cardionursing.com NTI 2009
Hypertrophic Cardiomyopathy
Diagnosis
• ECHO
– Wall thickness
– LV size
– Hyperdynamic LV function
– Atrial size
– MV leaflets
– LV outflow obstruction
• Cardiac Cath
– Not very helpful
– Do not usually find CAD with HCM
Treatment
Goals
Relief of symptoms
Preventing complications
Preventing or reducing risk of sudden death
No evidence supporting treatment of non-symptomatic patients
• Beta blockers
– 1st choice (with or without HOCM)
– Symptomatic benefit / improved exercise tolerance
– Changes in HR, contractility, and conduction
• Calcium Channel Blockers
– If BB not effective
– Verapamil (avoid in severe Pulmonary HPTN)
– Use with caution due to vasodilatation
Cynthia Webner BSN, RN, CCRN, CMC 37
www.cardionursing.com NTI 2009
Hypertrophic Cardiomyopathy
Treatment
• Antiarrhythmic Therapy
– AF
• Most common arrhythmia
• All efforts to convert to sinus
• Need atrial kick
– Norpace
• Negative inotrope and Class I antiarrhythmic
• Decreases SAM
• Decreases MR
• Use with BB to assist in HR control
• May cause ventricular arrhythmias – monitor QT
– Amiodarone
• Obstructive or non-obstructive OK
• Ventricular or atrial arrhythmias
– Anticoagulation
Hypertrophic Cardiomyopathy
Treatment
• Diuretics: With caution
• ACE Inhibitors and NTG
• Avoided in HOCM
• Decrease preload and afterload
• Increase in obstruction
• Positive Inotropes
• STRICTLY AVOID any medication that increases contractility in
OBSTRUCTVE disease
• Endocarditis Prophylaxis
– NO LONGER INDICATED (was previously indicated in obstructive disease
only)
• Pregnancy
– Not restricted
• Non-obstructive Disease Progression
– More difficult to treat
– Ultimately evolves into dilated cardiomyopathy
Cynthia Webner BSN, RN, CCRN, CMC 38
www.cardionursing.com NTI 2009
Surgical Treatment
Ventricular Septal Percutaneous Alcohol
Myectomy Septal Ablation
• Marked outflow obstruction • Symptomatic with full
• On maximum medical therapy
therapy • NYHA Class III or IV
• NYHA Class III or IV • Not appropriate if MVR
needed
• MV Replacement or repair at
same time (increases • Cath Lab Procedure
operative mortality) • Catheter in septal
perforator
• Improvement noted
immediately and last 20-30 • Ethyl alcohol injected
years • Myocardial infarction occurs
• Survival Rates 80% at 10 • Enlarged septum eventually
years shrinks
• May need pacer due to • Better for patients > 55
development of LBBB. • Often need pacemaker
Other Considerations
Risk for Sudden Death Family Evaluation
• One or more 1st degree • First degree relatives should
relative with an episode of be screened
SCD • Genetic testing best if
available
• Left ventricular wall
thickness greater than 35
• Screenings – annually from
age 12 -18 then every 5
mm years after that due to
• Prolonged or repetitive delayed adult onset
non-sustained ventricular – Not necessary in relatives
tachycardia on Holter < 12 unless a particularly
monitor high risk family profile or
• Hypotensive BP response a desire to play intense
competitive sports.
to exercise
• Screenings include:
• Syncope or near syncope – Physical exam
– 12 lead ECG
– ECHO
Cynthia Webner BSN, RN, CCRN, CMC 39
www.cardionursing.com NTI 2009
Other Considerations
Activity Outcomes
• No intense competitive • Normal life span
sports
• Once diagnosed –
• Most SCD occurs with
football or basketball
routine follow up
every 12 -18 months
• No “burst” exertion
• No restrictions in • SCD primary cause
patients with family of shortened life
history but no evidence span
of disease themselves – Prevention is key
• SCD may occur at rest
Dilated Cardiomyopathy
• Most common form of cardiomyopathy
• Causes
– Idiopathic
– Ischemic
– Genetic disorders
– Hypertension
– Viral / Bacterial Infection
– Hyperthyroidism
– Valvular Heart Disease
– Chemotherapy
– Peripartum Syndrome Related to Toxicity
– Cardiotoxic Effects of Drugs or alcohol
Cynthia Webner BSN, RN, CCRN, CMC 40
www.cardionursing.com NTI 2009
Physiologic Changes in Dilated Cardiomyopathy
Ventricular Dilatation
Decreased Ventricular Contractility
(Systolic Dysfunction)
Decreased Ejection of Ventricular Contents
↑ Ventricular Pressure
Dilated Mitral and Volume
Activation of
Valve Annulus
Neurohormonal Responses
↑ Atrial Pressure
and Volume
Mitral Regurgitation
Vasoconstriction
Atrial Dilatation
And Fluid Retention
Atrial Overload
↑ Pulmonary Pressures
and Volume
Dilated Cardiomyopathy
Presentation, Diagnosis, Treatment
Refer to Heart Failure Notes
Cynthia Webner BSN, RN, CCRN, CMC 41
www.cardionursing.com NTI 2009
Arrhythmogenic
Cardiomyopathy
• Inherited muscle disorder
• Manifest as an arrhythmia, heart failure, or
sudden death
• Genetic characteristics include autosomal
dominance inheritance with incomplete
penetration
• Most frequently affects the right ventricle
• Often referred to as arrhythmogenic right-
ventricular cardiomyopathy
• Some cases of arrhythmogenic left-ventricular
cardiomyopathy do exist
Pathophysiology
• Progressive loss of
cardiomyocyte
• Replaced with fibrofatty
tissue
• Same mechanism observed
in muscular dystrophies
• Arrhythmogenic
cardiomyopathy may be
associated with some forms
of muscular dystrophy
• Thinnest portions of the
right ventricle affected first
– Triangle of dysplasia: Inflow,
outflow, apical regions of RV
• If LV involvement
– Changes usually impact
thinner posterior lateral wall
– Septum usually not affected.
Cynthia Webner BSN, RN, CCRN, CMC 42
www.cardionursing.com NTI 2009
Contributing Factors
• Multiple bouts of myocarditis
• Altered mechanical coupling causing gap
junction remodeling
• Poor regeneration of myocytes
• Aneurysm formation
Arrhythmogenic
Cardiomyopathy
Cynthia Webner BSN, RN, CCRN, CMC 43
www.cardionursing.com NTI 2009
Arrhythmogenic
Cardiomyopathy Disease
Progression
• Four Phases
– Early / Concealed phase
• Subtle structural changes
• Often asymptomatic
– Overt Phase
• Noticeable structural and functional changes
• Palpitations, pre-syncope, syncope, arrhythmias
Arrhythmogenic
Cardiomyopathy Disease
Progression
• Four Phases
– Impaired contractility and right-sided failure
• Right ventricular dilation
• Decreased contractility
• Signs of fight sided heart failure
– Bi-ventricular failure
• Disease spreads to left ventricle
• Signs of biventricular failure
Cynthia Webner BSN, RN, CCRN, CMC 44
www.cardionursing.com NTI 2009
Diagnosis
• Difficult in concealed stage • ECG
• Differentiate between – Delayed depolarization
arrhythmogenic CM and – Epsilon waves
dilated CM – Inverted T Waves
• Common to find predominant • Echocardiogram
RV involvement – RV dilation
• Fibrofatty infiltrates – Wall motion
abnormalities
• Regional ventricular
– Systolic dysfunction
involvement and aneurysm
formation
• Sudden death frequently first
clinical presentation of
arrhythmogenic CM
• Evaluation of family
members
Right Ventricular Tachycardia
• Sustained Monomorphic VT
• Attributed to re-entrant circuits created by infiltrates
• Stimulus (myocarditis) triggers sudden death during
silent disease state
• Gap junction remodeling may cause RVT during
concealed state
Cynthia Webner BSN, RN, CCRN, CMC 45
www.cardionursing.com NTI 2009
Treatment
• Prevention of sudden cardiac death
• Implantable Cardiovertor Defibrillator
• Catheter ablation unsuccessful in treating
VT
Inflammatory Cardiovascular Disease
Pericarditis:
Inflammatory process involving the visceral or parietal
pericardium
Causes
• Rheumatoid arthritis
• Systemic lupus erythematosus (SLE)
• Myocardial Infarction
• Acute: Within 7 days of MI related to inflammation and healing
• Dressler’s Syndrome: 2 weeks or more after MI, thought to be autoimmune
• Uremia
• Radiation
• Infections (bacterial, fungal, TB)
• Cardiac OR
• Other Causes: Viruses
– Coxsackie A and B
– Mumps
– Influenza
– Epstein-Bar
– HIV
Cynthia Webner BSN, RN, CCRN, CMC 46
www.cardionursing.com NTI 2009
Signs and Symptoms
• Precordial or left pleuritic sharp/ stabbing CP
• Aggravated by inspiration, cough and supine
positionRelieved by sitting up and leaning
forward
• Dyspnea, cough, hemoptysis
• Tachypnea, tachycardia, low grade fever
• Pericardial Friction Rub
– Lower left sternal boarder
– Patient sitting and leaning forward
– High pitched
– Grating, scratchy, squeaking and leathery
– Louder during in inspiration
– Transient – only 50% of the time present
– Pericardial rub vs. pleural rub
ECG Signs of Pericarditis
• 4 Stages
– Only 50% experience all 4 stages
– Stage 1: ST-Elevation with concave upward ST
Segments
• Develops within hours of CP
• Usually noted in all leads except V1
– Stage 2: ST-segment returns to baseline with
flattening T-wave
– Stage 3: T-wave inversion without Q-wave
formation
– Stage 4: ECG normalization
Cynthia Webner BSN, RN, CCRN, CMC 47
www.cardionursing.com NTI 2009
Pericarditis
Signs and Symptoms
Diagnosis / Treatment
Diagnosis Treatment
• Labs • Non-steroidal anti-
– Elevated Sedimentation inflammatory
Rate • Indocin, ASA, Ibuprofen
(not after AMI)
– CK, Troponin may be
elevated • Upright position
– Elevated LDH, SGOT • Steroids if no response to
NSAIDs or if effusion
• Echocardiogram
– Modality of choice to
• Narcotics may be
R/O fluid accumulation necessary
– May appear normal • D/C anticoagulants (May
without fluid continue if AMI)
accumulation
Cynthia Webner BSN, RN, CCRN, CMC 48
www.cardionursing.com NTI 2009
Pericardial Effusion:
Abnormal amount and/or type of fluid in the pericardial
space
• Acute or chronic Causes
• Increase capillary • Idiopathic
permeability due to • Hydropericardium (HF, Valve
Disease)
inflammation may cause
fluid leak into pericardial • Neoplastic disorders
space • Infections
– >120cc can cause • Autoimmune or Connective
Tissue disorders (SLE,
tamponade if rapid Rheumatoid Arthritis)
– 2 Liters may not • Trauma
cause tamponade if • Uremia
slow
• Post op Open Heart Surgery
• Radiation
Symptoms / Physical Exam
• Chest Pain • Friction Rub
• Lightheadedness, • Tachycardia
syncope • Decreased breath sounds
– if subsequent pleural
• Palpitations effusions
• Cough, dyspnea, • Pulsus Alternans
hoarseness • ECG
• Hiccoughs – Diffuse low voltage, ST,
PR-segment depression
• Anxiety, confusion
Cynthia Webner BSN, RN, CCRN, CMC 49
www.cardionursing.com NTI 2009
Diagnosis
• Chest X-ray
– Enlarged cardiac silhouette
– Coexisting pleural effusions
• Echocardiogram
– Diagnostic test of choice
• CT Scan
– Determine composition of fluid
– Detects as little as 50 cc of fluid
– More reliable than echo – however patient’s condition
may not support transportation
• MRI
– Detects as little as 30 cc of fluid
– Difficult to do in an acute situation
Treatment
• Determine • Percardiocentesis
underlying – Diagnostic as well as
etiology treatment
– Corticosteroids / – Limited benefit
NSAIDs helpful in • 15-45% need further
autoimmune procedures
processes • 55% require reintervention
– Antineoplastic – Local anesthesia
therapy with – Complications
percardiocentesis • Pneumothorax
reduce recurrence of • Cardiac injury - perforation
malignant effusions • Recurrence of effusion
– NSAIDs – Instillation of sclerosing agent
– Indwelling catheter
– Balloon dilatation
Cynthia Webner BSN, RN, CCRN, CMC 50
www.cardionursing.com NTI 2009
Treatment
Subxiphoid Pericardiostomy Thoracoscopic Pericardiostomy
– Pericardial Window – Requires general anesthesia
– General anesthesia (may be – Useful if pleural effusions are
done under local) present
– Piece of pericardium removed – No outcome differences in two
procedures
– Pericardial drain may be placed
– Complications
• Bleeding Balloon Pericardiotomy
• Infection – Percutaneous procedure
• Incisional hernia – Balloon creates opening in
• Anesthesia complications pericardium
• Cardiac perforation – Fluid drains into pleural space
• Low mortality
Constrictive Pericarditis:
A thickened fibrotic pericardium, of whatever cause,
impedes normal diastolic filling
• Involves parietal pericardium Causes
• Can involve the visceral • Idiopathic
pericardium • Infections (TB)
• Acute and subacute forms
• May or may not be
• Radiation Therapy
symptomatic • Cardiac Surgery
• Usually begins with effusion • Neoplasms
that is reabsorbed
• Pericardium develops fibrotic • TB
scaring • MI
• Eventually calcifies
• Pericardial space adheres to
self
Cynthia Webner BSN, RN, CCRN, CMC 51
www.cardionursing.com NTI 2009
Diagnosis
• Chest x-ray
– Cardiac Calcification
• Echocardiogram
– Used to differentiate between constrictive pericarditis
(CP) and restrictive myopathy (RM)
– Provides information about ventricular filling
• CT Scan
– Can visualize pericardial thickness
– Normally 1-2 mm thick
– 3-4 mm thick considered abnormal
– Thickening of > 4mm supports CP over RM
• MRI
– Most sensitive for pericardial thickening
Symptoms / Physical Exam
• Dyspnea (most • JVD
common) • ST
• Fatigue • Apical impulse not
• Orthopnea palpable, distant or
• Chest Pain muffled
• Pericardial knock –
mistaken for S3
– Higher frequency
– Occurs earlier than S3
• Hepatomegaly
• Ascites
• Peripheral Edema
Cynthia Webner BSN, RN, CCRN, CMC 52
www.cardionursing.com NTI 2009
Treatment
– Steroids
– Avoid Beta-blocks
• Increased HR is a compensatory measure
– Diuretics – failure
• Watch cardiac output
– Treat cause
– Pericardectomy
• Avoid until absolutely necessary
• Complete resection of pericardium
– Mortality is 7-19%
• Bleeding
• Atrial and Ventricular arrhythmias
• Some diastolic filling problems may remain after OR
Myocarditis:
Inflammatory infiltrate of the myocardium with necrosis and /or
degeneration of adjacent myocytes
• Etiology: • Myocardial Damage in 2
– Viral infections Phases:
– Bacterial infections – Acute
– Parasitic infections • 1st 2 weeks
– Fungal infections • Direct myocyte destruction
– Radiation therapy to chest – Chronic
• Continued myocyte destruction
– Chronic Alcoholism
• Autoimmune
Cynthia Webner BSN, RN, CCRN, CMC 53
www.cardionursing.com NTI 2009
Signs and Symptoms Diagnosis
• Acute • Difficult to diagnose
– Look like acute • Rule out other causes
decompensated HF / • Careful history
cardiogenic shock • Elevated serum viral titers
• Sudden SOB, orthopnea, • Endomyopcardial biopsy
PND
• Chronic Treatment
– Non-specific symptoms • Withdrawal of offending
• Fatigue, dyspnea, chest pain agent
– Recent history of cold, – Decrease myocardial oxygen
fever, other flu-like consumption
symptoms – May need to treat for HF
– PND – Need to treat cause
– Orthopnea
Infective Endocarditis:
Infection of the endocardial surface of the heart
invading the endothelial lining
- Damage to endothelial surface from trauma or
hemodynamic abnormality that causes
turbulence in blood flow
- Endothelium no longer intact or turbulence
sets up environment for the collection of
platelet –fibrin thrombus -nonbacterial
thrombotic endocarditis lesions
- Lesions prone to adherence of bacteria
introduced by procedures
Cynthia Webner BSN, RN, CCRN, CMC 54
www.cardionursing.com NTI 2009
Classification
Native Valve Infective Prosthetic Valve Infective
Endocarditis Endocarditis
– Acute vs Subacute – More common than with native
– Abnormal native valve valve
• Mitral valve prolapse with – Most common with abnormal
regurge aortic valve
• Calcific aortic valve disease – Early: infection within 60 days of
• RHD of mitral valve implant
– Congenital heart disease – Late: >60 days
– HOCM – Pacemaker implant
– Marfan Syndrome with AI Nosocomial Infective
– IV drug abusers Endocarditis
• Normal valve – Secondary to invasive procedure
• Tricuspid most frequently • Pulmonary catheter placement
– Infection present 48 hours after
admission or within 4 weeks of
procedure
Cynthia Webner BSN, RN, CCRN, CMC 55
www.cardionursing.com NTI 2009
Classification
• Right Sided Infective Endocarditis
– Right side valves
– Embolization to the lungs
– More likely to have negative blood cultures
– Present differently due to hemodynamic
changes
• Left Sided Infective Endocarditis
– Left side valves
– Embolization to brain, spleen, kidneys\
– Greater hemodynamic compromise
Symptoms / Physical Exam
• Subacute • Murmurs
– Fever (low grade) – New murmur in presence of fever highly
suspect for IE
– Malaise • Peripheral signs of IE
– Fatigue – Petechiae
– Weight loss – Splinter hemorrhages
– Night sweats – Janeway lesions: Non-tender red-purple
– Back Pain macules on palms of hands and soles
offeet
– Flu-like symptoms
– Roth’s spot: Retinal hemorrhages
• Acute – Oslers Nodes: Small tender red-purple
– Sudden onset raised nodules on pads of fingers and
toes
– High grade fever
• Findings Associate with Embolic Events
– Signs of heart failure -
– Cerebral infarct
Right sided failure vs.
left sided failure – Splenic infarct
– Renal emboli
– Signs based on
embolization – Coronary infarct
– Pulmonary emboli
Cynthia Webner BSN, RN, CCRN, CMC 56
www.cardionursing.com NTI 2009
Diagnosis
• Blood Cultures
– 2 positive cultures over 12 hours apart
– 3 positive cultures
– A majority of 4 or more cultures greater
than one hour apart
– Negative cultures in 5%b of patients with IE
• Echocardiography
– Diagnostic method of choice
– TEE best for detection of vegetation and
emboli
Treatment
• Prevention • Surgery
• IE with heart failure that is not
• Goals: responsive to medical treatment
– Early recognition (NYHA Class III or IV)
– Eliminate cause • Recurrent or persistent infection
– Timely surgical • Large or hypermobile vegetation
interventions • Acute valvular dysfunction
• Antibiotics • A major embolic event
• New onset conduction abnormalities
– IV 4- 6 weeks
• Urgent surgery for severe heart
• Anticoagulation failure with significant aortic
– Not indicated regurgitation
• Any infected prosthetic valve should
be replaced.
• Fungal infection not responding to
medical therapy
Cynthia Webner BSN, RN, CCRN, CMC 57
www.cardionursing.com NTI 2009
Nursing Considerations Complications
– Monitor for signs of – Valve dysfunction
embolization. – Congestive heart failure
– Strict sterile technique – Myocardial (valvular) or
– Care of indwelling septal abscesses
catheters requires – Metestatic infection
meticulous attention. – Embolic events
– Assure good oral hygiene. – Organ dysfunction from
– Meticulous skin care embolic events
– Bed rest – metabolic – Pericarditis
demand – Myocarditis
– Monitoring temperature - – Glomerulonephritis and
recognize the response to acute renal failure
antibiotic therapy. – Mycotic aneurysm
– Monitor for heart failure
– IV drug abusers
– Emotional support
Follow Up Care Outcomes
• Repeat blood cultures • Fatal if untreated
• Education • Mortality rate significantly decreased
• Dependent on organism, valve & patient
– Reoccurrence • Improved outcomes
– Compliance with – Early diagnosis
antibiotics – Young age
• Antibiotic prophylaxis – Penicillin sensitive strep infections
– Young IV drug abusers
• Increased mortality with
– Acute cases
– Heart failure and renal failure
– Culture negative, gram-negative, fungal
– Multiple valve involvement
– Prosthetic valve involvement
– Left-sided involvement
– Aortic valve
– Systemic embolization
Cynthia Webner BSN, RN, CCRN, CMC 58
www.cardionursing.com NTI 2009
Final Thought:
Perfection may not be possible, but
in the pursuit of perfection
excellence may be found!
-Back of a Tee Shirt
Thank You!
www.cardionursing.com
Cynthia Webner BSN, RN, CCRN, CMC 59
