Cardiomyopathy

Cardiomyopathy: How Can One Name Mean So Many Things????
NTI 2010 Class Code 213
Cynthia Webner MSN, RN, CCNS, CCNS, CCRNCCRN-CMC

1
www.cardionursing.com
2010
NTI 2010 Class Code 213
Cynthia Webner MSN, RN, CCNS, CCRN-CMC 2010

Cardiovascular Nursing Education Associates www.cardionursing .com
No Disclosures
Mastery is not something that strikes in an instant, like a thunderbolt, but a gathering power that moves steadily through time, like weather.
- John Champlain Gardner Jr. (19331982)
4

Cardiomyopathy
Heterogeneous group of diseases of the myocardium Associated with mechanical and / or electrical dysfunction Usually (but not invariable) exhibit inappropriate ventricular hypertrophy or dilation Due to a variety of causes
Maron, B.J. et al Contemporary Definitions and Classification of the Cardiomyopathies: An American Heart Association Scientific Statement From the Council on Clinical Cardiology, Heart Failure and Transplantation Committee; Quality of Care and Outcomes Research and Functional Genomics and Translational Biology Interdisciplinary Working Groups; and Council on Epidemiology and Prevention Circulation, Apr 2006; 113: 1807 - 1816.
5 2009
AHA Classification of Cardiomyopathy

Primary (genetic) Mixed (genetic and nongenetic) Acquired Secondary
2009

Primary (Genetic) Cardiomyopathy

Previously idiopathic Processes confined to diseases of the heart muscle Hypertrophic cardiomyopathy Arrhythmogenic right ventricular cardiomyopathy / dysplasia Left ventricle noncompaction Conduction system disease Ion channelopathies
Long-QT syndrome Brugada syndrome Catecholaminergic polymorphic ventricular tachycardia Short-QT syndrome Idiopathic ventricular fibrillation
Mixed Cardiomyopathy
Genetic and non-genetic Dilated cardiomyopathy Primary restrictive non-hypertrophied cardiomyopathy

Acquired Cardiomyopathy
Myocarditis (inflammatory cardiomyopathy) Stress cardiomyopathy (Tako-Tsubo) Peripartum (postpartum) cardiomyopathy Alcoholic dilated cardiomyopathy
Secondary Cardiomyopathy
Infiltrative disorders Storage disease Toxicity Endomyocardial disorders Inflammatory disorders Neuromuscular/neurological disorders Nutritional deficiencies Autoimmune/collagen disorders Electrolyte imbalances Consequences of cancer therapy

Functional Classification of Cardiomyopathy

Pathological situation occurring regardless of cause Provides a discussion based on patient presentation and related pathology Cause often unknown Describes the ventricular changes that occur
Restrictive Cardiomyopathy Hypertrophic Cardiomyopathy Dilated Cardiomyopathy Arrhythmogenic Cardiomyopathy Stress Induced Cardiomyopathy (Tako-Tsabo)
Dilated Cardiomyopathy
12
2009

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
13 2009
Changes in Dilated Cardiomyopathy

Ventricular Dilatation Decreased Ventricular Contractility
Dilated Mitral Valve Annulus Mitral Regurgitation
Decreased Ejection of Ventricular Contents
Increased Ventricular Pressure / Volume
Activation of Neurohormonal Responses Vasoconstriction / Fluid Retention
Increased Atrial Pressure / Volume Atrial Dilatation Atrial Overload

Increased Pulmonary Pressure / Volume
Fluid Accumulates in Pulmonary Capillary Bed
Symptoms

Systolic vs Diastolic Dysfunction
15
Systolic Dysfunction
Impaired wall motion and ejection Dilated chamber 2/3 of HF Population Hallmark: Decreased LV Ejection Fraction< 40% Coronary artery disease is cause in 2/3 of patients Remainder other causes of LV dysfunction
16

Dilated Cardiomyopathy Presentation

Displace apical impulse S3 Murmur of Mitral regurgitation Crackles in lungs if fluid overloaded Diminished breath sounds with effusions JVD HJR Edema
Heart Failure
Heart Failure is a complex clinical syndrome resulting from any structural or functional cardiac disorder impairing the ability of the ventricle to either fill or eject
Cardiomyopathy not synonymous with HF
18

Clinical Syndrome Resulting in Clinical Manifestations

Dyspnea and fatigue
May limit exercise tolerance
Fluid Overload
May lead to pulmonary congestion and peripheral edema
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Impaired functional capacity and quality of life
2009
S3 Ventricular Gallop
Early diastolic filling sound Caused by increased pressure and resistance to filling. Most frequently associated with systolic dysfunction Associated with:
Fluid overload state Right or left ventricular failure Ischemia Aortic regurgitation Mitral regurgitation
20

Left or Right Sided S3

Patient position: left lateral decubitus position Location:
Left-sided S3 mitral area. Right-sided S3 tricuspid area.
Intensity
Left-sided heard best during expiration. Right-sided heard best during inspiration.
Duration: short. Quality: dull, thud like. Pitch: low. May be normal in children, young adults (up to 35-40) and in the 3rd trimester of pregnancy.
21
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

Dilated Cardiomyopathy Diagnosis

Echo Cath Chest X-Ray
Enlarged silhouette Congestion Pleural Effusion
ECG
Atrial Fibrillation Left Bundle Branch Block Large QRS Complexes Hypertrophy Abnormal P waves
Chamber size Not needed to diagnose DCM Wall thickness/shape Eccentric hypertrophy Usually thin Clot formation Ejection Fraction Normal 55-65% Mild Dysfunction 41-55% Moderate Dysfunction 26-40% Severe Dysfunction <26%
Stages of Heart Failure ACC / AHA

Stage A Stage B Stage C
Structural heart disease with prior or current symptoms of HF.
Stage D
Structural heart disease with prior or current symptoms of HF.
At high risk for HF Structural heart but without disease but structural heart without signs or disease or symptoms of symptoms of HF. Heart Failure HPTN CAD DM Obesity Metabolic syndrome Family HX CM Previous MI LV Remodeling including LVH and low EF A symptomatic valvular disease
Know structural disease and SOB, fatigue, reduced exercise tolerance.
Know structural disease and SOB, fatigue, reduced exercise tolerance.

Utilizing Stages as a Guide to Therapy

Stage A
Treat HTN Treat DM Smoking Cessation Treat Lipids Regular Exercise DC Alcohol / Drug Use ACE-I in select patients
Stage B
All measures as stage A
Stage C
All measures under stage A Dietary salt restriction Daily Weight Diuretics Digitalis Aldosterone Antagonists Cardiac Resynchronization Therapy -CRT
Stage D
All measures under stage A, B and C Mechanical assist Transplantation Palliative Care Hospice
ACE-I in select patients Beta Blockers in select patients Implantable defibrillators
Cardiac Resynchronization Therapy

Treatment modality for heart failure not just pacing Treatment modality in conjunction with drug therapy Goals:
Improve hemodynamics by restoring synchrony of ventricular contraction Improve quality of life Decrease mortality and morbidity
Significant reduction in all-cause mortality / hospitalization Survival benefits seen after 3 months Improved 6 minute walk tests Improvement by at least one NYHA class Clinical improvement in quality of life Improved ejection fraction Improved peak oxygen consumption 26

Indications for CRT

-
Stage C Heart Failure NYHA Class III EF< 35% QRS duration > 130 ms Optimal medical therapy ACE Inhibitor Beta Blocker Diuretic
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Normal Ventricular Depolarization
Ventricular Depolarization with LBBB
28

CRT Lead Placement
29
How do you know your patient is receiving resynchronization therapy by looking at the rhythm strip?
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32

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Implantable Cardiovertor Defibrillator Indications

Asymptomatic (NYHA Class I) LV dysfunction AND
EF < 30% and prior MI > 30 days or CABG > 3 months EF 31-35% and NSVT, CAD, prior MI, and inducible / sustained VT by EPS
NYHA II-III LV Dysfunction

EF < 35% Not recommended in Stage D Heart Failure
34

Acute Decompensated Heart Failure

Warm and Dry
Normal Perfusion No Congestion
Warm and Wet

Normal Perfusion Congestion
Cold and Dry

Low Perfusion No Congestion
Cold and Wet

Low Perfusion Congestion
35
Assessment of Skin and Lungs
Fluid Overload vs. Hypoperfusion

Fluid Overload
Weight gain Peripheral edema Jugular venous distention SOB Crackles in lungs
Hypoperfusion
Narrow pulse pressure Resting tachycardia Cool Skin Altered mentation Decreased urine output Increased BUN/Creatinine Cheyne Stokes Respirations
36

Treatment for Acute Decompensated Heart Failure

Congestion with adequate perfusion
Reduce Preload
Hypoperfusion with no congestion

Inotropic support
Assure adequate preload Assure decreased afterload Increase contractility
37
Cardiac Output
Heart Rate X Stroke Volume
Preload
Afterload
Contractility
38

Preload
End-diastolic stretch on myocardial muscles fibers
Determined by:
Volume of blood filling the ventricle at end of diastole Greater the volume the greater the stretch (muscle fiber length) Greater the stretch the greater the contraction Greater the contraction the greater cardiac output
39
TO A POINT
Afterload
Pressure ventricle needs to overcome to eject blood volume Blood pressure is major component of afterload but it does not equal afterload Other components
Valve compliance Viscosity of blood Arterial wall compliance
Aortic compliance
40

Contractility
Ability of myocardium to contract independent of preload or afterload
Velocity and extent of myocardial fiber shortening Inotropic state
Related to degree of myocardial fiber stretch (preload) and wall tension (afterload). Influences myocardial oxygen consumption contractility
myocardial workload myocardial oxygen consumption
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Dilated Cardiomyopathy Acute Treatment

Reduce Preload Diuretics Venous Vasodilators Low Dose NTG Neseritide Reduce Afterload Arterial Vasodilators High Dose NTG Neseritide Nitroprusside Intra Aortic Balloon Pump Increase Contractility Decrease afterload Positive Inotropes Dobutamine Milronone

Dilated Cardiomyopathy Outcomes

50% mortality 5 years after diagnosis
Progressive Heart Failure Sudden Death 40% Embolic Stroke
Restrictive Cardiomyopathy

Rigidity of myocardial wall Results in decreased ability of chamber walls to expand during ventricular diastole
Diastolic dysfunction
Least common form of Cardiomyopathy

5% of all primary heart muscle diseases
(Goswami & Reddy, 2003)
Diastolic Dysfunction
Filling impairment High pressure Normal chamber size 20 to 40% of patients with HF have preserved LV function Normal EF or elevated Caused by
Hypertension Restrictive myopathy Ischemic heart disease Ventricular hypertrophy Valve disease Idiopathic
Primarily disease of elderly women with HTN
46

Diastolic Dysfunction
Diagnosis is made when rate of ventricular filling is slow Elevated left ventricular filling pressures when volume and contractility are normal
In practice: the diagnosis is made when a patient has typical signs and symptoms of heart failure and has a normal or elevated ejection fraction with no valve disease.
47
Primary Causes
Endomyocardial Diseases
Eosinophilic Endomyocardial Fibrosis Endocardial Fibrosis Cardiac Transplant Anthracycline Toxicity
Secondary Causes
Infiltrative disorders
Amyloidosis
90% of RCM in North America
Idiopathic Lofflers Endocarditis
Sarcoidosis Radiation carditis
Storage Diseases
Hemochromatosis Glycogen storage disease Fabrys Disease

Physiologic Changes in Restrictive Cardiomyopathy

Ventricular chamber has limited ability to expand during filling
Decreased volume available for next ejection Decreased stroke volume and cardiac output Atrium dilates due to increased volume and pressure Increased volume and pressure in pulmonary symptoms Fluid Accumulates in Pulmonary Capillary Bed Symptoms of Heart Failure
Fatigue, weakness Decrease in activity intolerance Hypotension Syncope Palpitations with arrhythmias Pale/ cool Peripheral pulses decreased S4
Left Lateral Position Bell of Stethoscope
Murmur of Mitral Regurgitation

Systolic Murmur 5th ICS MCL
Mitral insufficiency
Dilation of atrium Papillary muscle dysfunction Fibrosis of leaflets

S4 Atrial Gallop
Late diastolic filling sound Caused by atrial contraction and the propulsion of blood into a noncompliant (stiff) ventricle. Most frequently associated with diastolic dysfunction Associated with:
Fluid overload state Systemic hypertension Restrictive cardiomyopathy Ischemia Aortic stenosis Hypertrophic cardiomyopathy
May be normal in athletes

51
Left or Right Sided S4

Patient position: left lateral decubitus position. Location
Left-sided S4 mitral area. Right-sided S4 tricuspid area.
Intensity
Left-sided louder on expiration. Right-sided louder on inspiration.
Duration: Short Quality: Thud like Pitch: Low

52

Diagnosing Restrictive Cardiomyopathy

Rule Out Other Causes of Diastolic Dysfunction
Aortic Stenosis Hypertrophic Cardiomyopathy Hypertensive Cardiovascular Disease
Differentiate from Constrictive Pericarditis
Differentiation of RCM from Constrictive Pericarditis

Clinical Features History Heart Sounds Murmurs Heart Pressures Constrictive Pericarditis
Prior history of pericarditis or condition that causes pericardial disease Pericardial knock, high frequency sound
History of systemic disease (e.g.. Amyloidosis, Hemochromatosis)
Presence of loud diastolic filling sound S4, low frequency sound
No murmurs
Murmurs of mitral and tricuspid insufficiency Arrhythmias L sided filling pressures > R sided filling pressures
L & R filling pressures up and equal (Elevated JVP)

Diagnosing Restrictive Cardiomyopathy

Echo
Chamber size Enlarged L Atrium Wall thickness Increased in infiltrative disorders Ejection Fraction Normal or high Valve functioning Speckled appearance on myocardium with amyloidosis
ECG
Chest X-Ray
Cardiac
Catheterization Low QRS voltage Dilated atrium No-specific ST-T wave Congestion if in HF Full cath not changes necessary Calcified P wave abnormalities pericardium can be Hemodynamic seen in constrictive measurements Arrhythmias pericarditis valuable Conduction Elevated LVEDP abnormalities Elevated PAOP Elevated RA Pressures Elevated pulmonary pressures
Restrictive Cardiomyopathy Diagnosis

Endomyocardial Biopsy
Septal wall of RV Multiple sites Essential for diagnosis of RCM

Restrictive Cardiomyopathy Treatment

Reduce Diastolic Dysfunction
No direct medications Treat affect of restriction Careful control of volume Diuretics - Fluid overload Decrease afterload -Arterial Vasodilators Careful with venous vasodilators
Treat Rhythm
AF Control Loss of atrial kick Decreased filling Digoxin cautiously in amyloidosis
Conduction Abnormalities
May require pacemaker
Ventricular Arrhythmias
Based on hemodynamic response
Restrictive Cardiomyopathy Treatment

Treat for Treat Underlying Thromboembolic Disease Process Complications No cure for
Highest risk in endocardial fibrosis High risk with enlarged atrium High risk with AF High risk with TR and MR Amyloidosis Steroids and chemo helpful in slowing progression of disease process Chelation for hemochromatosis
Valve Replacement
May provide symptomatic relieve High mortality
Cardiac Transplant
Beneficial in idiopathic / familial Need heart and liver with hemochromatosis Limited usefulness in infiltrative diseases Disease will affect new organs

Restrictive Cardiomyopathy Outcomes Poorest mortality of all cardiomyopathies 90% mortality rate at 10 years
Parrillo, 2000).
(Kavinsky &
Amyloid Heart
80% mortality at 2 years
Hypertrophic Cardiomyopathy

1 of every 500 (Maron et al, 2003) Primary genetic cardiomyopathy Effects men and women equally Hypertrophy of myocardial muscle mass in the absence of increased ventricular afterload Associated with decreased ventricular filling (diastolic dysfunction) 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

Usually only effects Left Ventricle Changes may be symmetrical Asymmetrical septal hypertrophy is more common
May involve entire septum or only a portion of septum

Physiologic Changes with Hypertrophic Cardiomyopathy

Ventricular chamber size decreases as enlarging walls close in on chamber
Stiff walls resist filling (diastolic dysfunction)

Compensation for decreased filling -> hyperdynamic systolic dysfunction
Passive filling from the atria is slowed Atrial kick more essential than normal Atrial dilatation due to increase in pressure and volume
EF increases to 70-80%
Mitral Regurgitation
Transferred to pulmonary system Symptoms of HF may develop
OBSTRUCTIVE Hypertrophic Cardiomyopathy

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

HOCM
Hypertrophic Cardiomyopathy Presentation

Many asymptomatic for years Incidence of sudden death often first presentation
Or identified during screening of relative of patient with HCM
Symptoms related to severity of diastolic dysfunction

Heart failure
Dyspnea #1 sign
Syncope / palpitations with activity Chest pain Supraventricular arrhythmias
Development of mitral regurgitation

Hypertrophic Cardiomyopathy Presentation Bisferiens Carotid Pulse (HOCM) Brisk initial upstroke Collapse of pulse then secondary rise Must differentiate from AS delayed upstroke PMI forceful and brisk S4 MR murmur Systolic murmur with obstructive disease process Differentiating between HOCM and Aortic Stenosis
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

Subvalvular Left Ventricular Outflow Obstruction Systolic Murmur

HOCM murmur louder during Valsalvas maneuver Valsava decreases venous return to the heart
Decreased preload left ventricular filling Decreased left ventricular filling obstruction
Any factor that decreases venous return to the heart increases the murmur in HOCM
Squatting increases venous return Standing decreases venous return
Aortic stenosis murmur becomes quieter during Valsalvas maneuver
Hypertrophic Cardiomyopathy Diagnosis

ECHO
Wall thickness LV size Hyperdynamic LV function Atrial size MV leaflets LV outflow obstruction
ECG
LV hypertrophy Deep symmetrical T wave inversions P wave abnormalities Arrhythmias
Cardiac Cath
Not very helpful Do not usually find CAD with HCM

Hypertrophic Cardiomyopathy Treatment Goals Relief of symptoms Preventing complications Preventing or reducing risk of sudden death No evidence to support treatment of non-symptomatic patients
Beta Blockers 1st choice (with or without HOCM) Symptomatic benefit / improved exercise tolerance Decreases HR Improves LV relaxation Helps control arrhythmias
Calcium Channel Blockers If Beta Blocker not effective Decrease LV wall tension Decreases HR Diltiazem or Verapamil (no nifedipine D/T vasodilatation)
Disopyramide
Negative inotrope Class I antiarrhythmic Use with BB to treat LV outflow track obstruction Assists in HR control May cause ventricular arrhythmias monitor QT
Anti arrhythmic Therapy

Atrial Fibrillation Most common arrhythmia Poorly tolerated Anticoagulation Amiodarone or sotolol Obstructive or non-obstructive OK Ventricular or atrial arrhythmias

Other Medications
Diuretics With caution ACE Inhibitors and NTG Avoided in HOCM Positive Inotropes Strictly avoid any medication that increases contractility in HOCM
Pregnancy
Not restricted in nonobstructive disease
Endocarditis Prophylaxis
NO LONGER INDICATED (was previously indicated in obstructive disease only)
Non-Obstructive Disease Treatment More difficult to treat if no symptoms Ultimately evolves into dilated cardiomyopathy
Surgical Myectomy
Marked outflow obstruction On maximum medical therapy NYHA Class III or IV MV Replacement or repair at same time (increases operative mortality) Improvement noted immediately and last 20-30 years Survival Rates 80% at 10 years May need pacemaker (2%)

Percutaneous Alcohol Septal Ablation

Symptomatic with full therapy NYHA Class III or IV Not appropriate if MVR needed Cath Lab Procedure Catheter in septal perforator Ethyl alcohol injected Myocardial infarction occurs Enlarged septum eventually shrinks May need pacemaker (20%)
Risk for Sudden Death

One or more 1st degree relative with an episode of SCD Left ventricular wall thickness greater than 35 mm Prolonged or repetitive non-sustained ventricular tachycardia on Holter monitor Hypotensive BP response to exercise Syncope or near syncope

Family Evaluation
Screen 1st degree relatives Genetic testing best if available Screenings Annually from age 12 -18 then every 5 years Not necessary in relatives < 12 unless a particularly high risk family profile or a desire to play intense competitive sports. Screenings include: Physical exam 12 lead ECG ECHO
Outcomes
Normal life span
Once diagnosed routine follow up every 12 -18 months
SCD primary cause of shortened life span

Arrhythmogenic Cardiomyopathy
Inherited muscle disorder Often referred to as Arrhythmogenic Right-Ventricular Dysplasia (ARVD) Manifest as an arrhythmia, heart failure, or sudden death Genetic characteristics include autosomal dominance inheritance (most common) Most frequently affects the right ventricle More often than thought also effects left ventricle More often males than females

Cardiomyocyte replaced with fibro fatty tissue Initially patchy infiltration Progressive loss of muscle leads to thinning of the ventricular wall, dilation and pump dysfunction Thinnest portions of the right ventricle affected first Triangle of dysplasia: Inflow, outflow, apical regions of RV
84

Disease Progression
Early / Concealed phase
Subtle structural changes Often asymptomatic
Overt Phase
Noticeable structural and functional changes Palpitations, pre-syncope, syncope, arrhythmias
Impaired contractility and rightsided failure

Right ventricular dilation Decreased contractility Signs of right sided heart failure
Bi-ventricular failure
Disease spreads to left ventricle Signs of biventricular failure
Arrhythmogenic Cardiomyopathy Presentation

Palpitations Presyncope Syncope Often episode of sudden cardiac death is first presentation Signs of heart failure are late sign

Diagnosis
ECG Echo
T Wave RV inversion in enlargement leads V1-V6 and dysfunction Epsilon wave VT with LBBB pattern Conduction delays through right bundle
Endomyocardial MRI / CT Biopsy Detect fatty infiltrate

Right Ventricular Tachycardia
90

Left Ventricular Ectopy Lead V1 Right Bundle Branch shaped

R wave with an early left peak (Rr) R wave with a single peak q wave followed by R wave
Clinical application: Amiodarone can affect morphology.

91
Right Ventricular Ectopy Lead V1

LBBB shaped
Primarily negative wide rS complex delay to the nadir
> 0.06 sec
r wave broader than 0.03 sec Slurring on the down stroke Note: LBBB shaped VT can come from RV or septum. VT from RV includes: Idiopathic VT, BB Reentrant VT,VT in inferior wall MIs Arrhythmogenic right ventricular dysplasia, VT from mechanical causes such as PA catheter
92

Right Ventricular Tachycardia
93
Left Ventricular Tachycardia
94

Arrhythmogenic Cardiomyopathy Treatment

No cure Goal: Manage arrhythmias Antiarrhythmics Implantable Cardiovertor Defibrillator Radiofrequency catheter ablation if unsuccessful in treating VT with antiarrhythmics Refrain from competitive / intense sports Screening of family members
1st and 2nd degree relatives
Outcomes
Progressive disease Long term prognosis continues to be evaluated

Tako-Tsubo Cardiomyopathy
Case Study Presentation

68 y/o female No previous cardiac history Smoker New onset chest pain Nausea and diaphoresis Husband recently placed in ECF after extended illness 6 daughters and 8 sisters
Appeared to be supportive family
98

ED ECG
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Hospital Course
Emergent cardiac catheterization
No obstructive coronary artery disease
Hemodynamic profile of cardiogenic shock

Intra aortic balloon pump Vasopressor support
100

ECG 36 Hours Later
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Echo Findings: 24 Hours After Admission

Moderate to severe systolic dysfunction of LV which is segmental
Only proximal segment of IV septum and anterolateral wall are contracting normally Ballooning of distal ventricle EF estimated at 20% Consistent finding of Takotsubo Syndrome
Moderate mitral regurgitation
102

Transient left ventricular apical ballooning Abrupt onset of ballooning or dilatation of left ventricle Post menopausal women Occurs after psychosocial or physical stressors Also referred to as Stress Cardiomyopathy Cause unknown
Related to excessive catecholamines
Chest Pain mimicking acute MI ST-segment changes similar to anterior MI Elevated cardiac biomarkers Dyspnea Hypotension Signs of left ventricular failure

Tako Tsubo Cardiomyopathy Diagnosis

ECG
ST elevation mimicking AMI Prolonged QT interval
Cardiac Biomarkers
Mildly elevated Do not follow same rise and fall as AMI
Cardiac Cath
No significant coronary artery disease Visualize ballooning of LV
Echocardiogram
LV Dysfunction with decreased ejection fraction Visualize ballooning of LV
106
2009

Treatment
Goals: Similar to patients with Acute MI Treat Left Ventricular Failure Cardiogenic Shock IABP Arrhythmias Hypotension Avoid inotropes Cardiac Rehabilitation Stress Reduction
Cardiomyopathy: Sorting Through the Differences

Heterogeneous group of diseases of the myocardium associated with mechanical and / or electrical dysfunction Usually (but not invariable) exhibit inappropriate ventricular hypertrophy or dilation
THINK FUNCTIONAL CARDIOMYOPATHY

Pathological situation occurring regardless of cause Provides a discussion based on patient presentation and related pathology Describes the ventricular changes that occur

A Final Thought:
We must not, in trying to think about how we can make a big difference, ignore the small daily differences we can make which, overtime, add up to big differences that we often cannot foresee. -Marian Wright Edelman
Thank You!
Handouts will be available on the internet at www.cardionursing.com on Monday.

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Cardiomyopathy: How Can One Name Mean So Many Things????

NTI 2010 Class Code 213

Cynthia Webner MSN, RN, CCNS, CCNS, CCRNCCRN-CMC

NTI 2010 Class Code 213

Cynthia Webner MSN, RN, CCNS, CCRN-CMC 2010

Cynthia Webner MSN, RN, CCNS, CCRN-CMC 2010

AHA Classification of Cardiomyopathy

Cynthia Webner MSN, RN, CCNS, CCRN-CMC 2010

Primary (Genetic) Cardiomyopathy

Cynthia Webner MSN, RN, CCNS, CCRN-CMC 2010

Cynthia Webner MSN, RN, CCNS, CCRN-CMC 2010

Functional Classification of Cardiomyopathy

Cynthia Webner MSN, RN, CCNS, CCRN-CMC 2010

Changes in Dilated Cardiomyopathy

Increased Ventricular Pressure / Volume

Activation of Neurohormonal Responses Vasoconstriction / Fluid Retention

Increased Atrial Pressure / Volume Atrial Dilatation Atrial Overload

Cynthia Webner MSN, RN, CCNS, CCRN-CMC 2010

Systolic vs Diastolic Dysfunction

Cynthia Webner MSN, RN, CCNS, CCRN-CMC 2010

Dilated Cardiomyopathy Presentation

Cardiomyopathy not synonymous with HF

Cynthia Webner MSN, RN, CCNS, CCRN-CMC 2010

Clinical Syndrome Resulting in Clinical Manifestations

Impaired functional capacity and quality of life

Cynthia Webner MSN, RN, CCNS, CCRN-CMC 2010

Left or Right Sided S3

Cynthia Webner MSN, RN, CCNS, CCRN-CMC 2010

Dilated Cardiomyopathy Diagnosis

Stages of Heart Failure ACC / AHA

Know structural disease and SOB, fatigue, reduced exercise tolerance.

Know structural disease and SOB, fatigue, reduced exercise tolerance.

Cynthia Webner MSN, RN, CCNS, CCRN-CMC 2010

Utilizing Stages as a Guide to Therapy

ACE-I in select patients Beta Blockers in select patients Implantable defibrillators

Cardiac Resynchronization Therapy

Cynthia Webner MSN, RN, CCNS, CCRN-CMC 2010

Indications for CRT

Normal Ventricular Depolarization

Ventricular Depolarization with LBBB

Cynthia Webner MSN, RN, CCNS, CCRN-CMC 2010

CRT Lead Placement

Cynthia Webner MSN, RN, CCNS, CCRN-CMC 2010

Cynthia Webner MSN, RN, CCNS, CCRN-CMC 2010

Implantable Cardiovertor Defibrillator Indications

NYHA II-III LV Dysfunction

Cynthia Webner MSN, RN, CCNS, CCRN-CMC 2010

Acute Decompensated Heart Failure

Warm and Wet

Cold and Dry

Cold and Wet

Assessment of Skin and Lungs

Fluid Overload vs. Hypoperfusion

Cynthia Webner MSN, RN, CCNS, CCRN-CMC 2010

Treatment for Acute Decompensated Heart Failure

Hypoperfusion with no congestion

Heart Rate X Stroke Volume

Cynthia Webner MSN, RN, CCNS, CCRN-CMC 2010

Cynthia Webner MSN, RN, CCNS, CCRN-CMC 2010

Dilated Cardiomyopathy Acute Treatment

Cynthia Webner MSN, RN, CCNS, CCRN-CMC 2010

Dilated Cardiomyopathy Outcomes

Cynthia Webner MSN, RN, CCNS, CCRN-CMC 2010