Transcript Introduction to Cardiology

Cardiology
Review
Craig Ernst MHS, PA-C
Lock Haven University
Heart Function
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Heart: A blood pump which sends oxygen
rich blood to every living cell in the body.
William Harvey (1578-1657) “On the Motion
of Heart and Blood” -First physician who
accurately described heart function, systemic,
and pulmonary circulation.
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"...I found the task so truly arduous... that I was almost tempted to
think... that the movement of the heart was only to be comprehended
by God. For I could neither rightly perceive at first when the systole
and when the diastole took place by reason of the rapidity of the
movement..."
The Burden of CV Disease
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1900: CV disease < 10 % all deaths worldwide
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rheumatic valvular & nutritional cardiomyopathies
infectious disease & malnutrition
2000: CV disease ~ 50% all deaths in developed
countries and 25 % in developing world
by 2020: CAD disease will surpass infectious
disease as world’s # 1 cause of death and disability
US Epidemiology of CV Disease
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#1 cause of death in the United States
10 % of acute complaints in medical clinic
8 % of ER visits
60 % of a provider’s time treating CV disease
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hypertension
heart failure
arrhythmias
coronary artery disease
valvular heart disease
Physician Assistant Certification
 Cardiology:
 up
to 30-40 % of your
certification exam!
Scope of this review
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Hypertension
Ischemic disease
MI
CHF
Cardiomyopathy
Hypertension
EPIDEMIOLOGY
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Hypertension affects ~50 million individuals in USA
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Affects ~1billion world wide.
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As the population ages, the prevalence of hypertension
is expected to increase.
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Most common reason for office visits and medications
in the USA.
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35 million office visits as primary diagnosis.
EPIDEMIOLOGY
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Both genetic predisposition and environmental
factors (increased salt intake, obesity, smoking,
ETOH)
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African Americans affected at higher rates.
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Lowest BP control rates are seen in Mexican
Americans and Native Americans.
Prevalence
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Variable by race and criteria
Framingham data in predominately white
population revealed incidence of 1:5
Higher prevalence in:
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Males
African Americans
Smokers
Sedentary lifestyle
Female prevalence closely related to age
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> 50 y.o. = increased incidence
Why Hypertension?
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Major contributing factor in:
 CAD
 CHF
 Renal failure
 Bigest risk factor for stroke
Only 50% of patients with hypertension are
treated
Only 30% treated achieve goals
Hypertension
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Essential or Primary Hypertension
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Hypertension without an identifiable cause
Secondary Hypertension
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Hypertension secondary to a known underlying
cause
Hypertension
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Hypertensive emergency
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Malignant Hypertension
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BP greater than 180/120 plus hypertensive
encephalopathy, nephropathy, intracranial
hemorrhage, aortic dissection, eclampsia, pulm
edema, UA, MI
Requires the presence of papilledema
Refractory Hypertension
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BP of greater than 140/90 despite maximal doses
of two or more medications
Primary HTN
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>90% of all hypertension is primary
Diagnosis made on basis of average blood
pressure determination on two or more properly
measured, seated BP readings on each of two or
more office visits.
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Unless end organ damage already exists
Standards for blood pressure follow-up set by
Joint National Commission Seventh Annual
Report
Taking a BP
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Patient seated for 5 min in a chair, arm
supported at heart level
Appropriate sized cuff for arm
Two meaurements
Provide readings verbally and in writing to the
patient
JNC 7 BP Classification
BP Classification
SBP (mmHg)
DBP (mmHg)
Normal
< 120
And
< 80
Prehypertension
120 – 139
Or
80 – 89
Stage 1 Hypertension
140 – 159
Or
90 – 99
Stage 2 Hypertension
≥ 160
Or
≥ 100
New classification of “prehypertension” recognizes risk of progressing to HTN
and signals a need for increased education of health care professionals and the
public to reduce BP levels and prevent the development of hypertension in
general populations.
JNC 7 Key Messages
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For persons over age 50, SBP >140 is a much more important
CVD risk factor than DBP.
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Starting at 115/75 mmHg, CVD risk doubles with each
increment of 20/10 mmHg throughout the BP range.
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Persons who are normotensive at age 55 have a 90% lifetime risk
for developing HTN.
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Those with SBP 120–139 mmHg or DBP 80–89 mmHg should
be considered prehypertensive and require health-promoting
lifestyle modifications to prevent CVD.
JNC 7 Key Messages
 Thiazide-type diuretics should be initial drug therapy for most
with uncomplicated HTN, either alone or combined with other
drug classes.
 Certain high-risk conditions are compelling indications for other
drug classes.
 Most patients will require two or more antihypertensive drugs to
achieve goal BP (<140/90 or <130/80 if DM or CKD).
 If BP is >20/10 mmHg above goal, initiate therapy with two
agents, one usually should be a thiazide-type diuretic.
JNC 7 Key Messages
 The most effective therapy prescribed by the careful clinician
will control HTN only if patients are motivated.
 Motivation improves when patients have positive experiences
with, and trust in, the clinician.
 Empathy builds trust and is a potent motivator.
 The responsible physician’s judgment remains paramount.
Secondary Causes
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Pheochromocytoma
Coartcation of the aorta
Renal disease
RAS
Hyperaldosteronism
Drugs/Medications
Thyroid disorder
Obstructive sleep apnea
Symptoms
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Typically asymptomatic
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“Silent killer”
Headache – (most common) behind the eyes,
particularly in the AM
Dizziness
Visual disturbances
N/V
Confusion
Fatigue
Dyspnea
Symptoms associated with secondary causes
Signs
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????
Studies
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Initial Workup
 ECG (LVH)
 Hematocrit
 BMP (glucose,
creatinine,
electrolytes)
 Lipids
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Secondary workup
 Thyroid studies
 Serum
Aldosterone /
plasma renin
 Echo
 Renal artery
doppler
Non-Pharm Management
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First line for prehypertension and adjunct for mod-severe
 Na restriction
 Weight reduction
 Moderation of ETOH consumption
 Smoking cessation
 Physical Activity/Aerobic exercise
 Dietary Approaches to Stop Hypertension (DASH)
 Rich in fruits, vegetables, lowfat dairy, with reduced sat.
and total fat
 Address all CVD risk factors
Pharm Management of HTN
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Diuretics
B-blockers
Ace Inhibitors
Calcium channel blockers
Alpha blockers
Angiotensin receptor blockers
Direct Aldosterone inhibitors
…More
Ischemic Heart Disease
Atherosclerosis
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Lipid deposition, fibrosis, plaque formation
within the intima of arteries
Associated with premature CAD, PVD
Men affected 4 x more than women but by
age 70 risk is equal.
Risks are:
Ischemic Heart Disease
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Insufficient oxygen supply to cardiac tissue
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Atherosclerotic narrowing of arteries
Risks: ??
Clinical features
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Angina pectoris
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Stable angina
Prinzmetal’s or Variant
Levine’s sign
Radiation
Ischemic Heart Disease
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Studies
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ECG findings
Stress ECG
Nuclear scan or Stress echocardiogram
MRI or 64 slice CT scan
Coronary angiography: GS
Ischemic Heart Disease: Treatment
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Preventive???
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Reversible Risks
Diet
Activity
Medical therapy
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Nitrates
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Adverse reaction?
Beta Blocker
Platelet inhibition
ACE Inhibitor
Statins
MI
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Result of prolonged myocardial ischemia
Generally a result of ruptured atherosclerotic
plaque and subsequent thrombus formation
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1/5th of all die before reaching a hospital
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Also a result of thromboemboli
Rhythm?
Up to 1/4th of pts have silent MIs
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Women and DM most likely to have atypical sx
Clinical Features
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Severe chest pain
Diaphoresis
N/V, weakness, syncope, dyspnea, restlessness
Dysrhythmias
Hypo or hypertensive
Lungs: clear to rales and wheezing
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Signs of HF?
JVD, S4
Pericardial friction rub after 24 hours
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Dressler’s syndrome (post MI)
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Pericarditis, fever, leukocytosis and either pericarial or pleural effusion
MI
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Labs/Tests
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ECG findings
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Location of MI
Cardiac enzymes
Echocardiogram
MI
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Treatment
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MONA
PTCA or PCI
Thrombolytic therapy
CABG
Studies
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EKG progression
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Early peaked T waves
ST elevation
T wave inversion
Q waves
Studies
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Cardiac Enzymes
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Total CK
CKMB
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Rapid fall to baseline
Troponin
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More specific for AMI
Cardiac Enzymes
Test
Onset
Peak
Duration
CK - Total &
MB
3-12 hours
18-24 hours
36-48 hours
Troponins
3-12 hours
18-24 hours
Up to 10
days
Myoglobin
1-4 hours
6-7 hours
24 hours
LDH
6-12 hours
24-48 hours
6 -8 days
EKG Localization of MI
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RV infarct: ST elevation in V1, V4R
I
Lateral
aVR
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V1 Septum
V4 Anterior
II Inferior
aVL Lateral
V2 Septum
V5 Lateral
III Inferior
aVF Inferior
V3 Anterior
V6 Lateral
??
??
Heart Failure
Heart Failure
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Inability of the heart to pump blood
adequately to meet the metabolic demands of
the body
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Abnormalities of filling
Abnormalities of pumping
Structural heart disease with abnormal blood /
oxygnation
Epidemiology
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Prevalence
 Symptomatic HF Affects 6 million Americans
currently, expected to double over the next 7
years
 Many millions more have asymptomatic LV
dysfunction or medical conditions predisposing
them to HF
Cost
 Annual direct cost is >10 billion dollars
Frequency
 It is the most common inpatient diagnosis in the
US for patients over 65 years of age
Heart Failure Types
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Low output
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Systolic (abnormal pump)
Diastolic (abnormal filling)
Right heart failure (cor pulmonale)
High output failure (normal heart)
Flavors of heart failure
NYHA Classification
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Class I - symptoms only at activity levels that
would limit normal individuals
Class II – only mild symptoms with daily
activities
Class III – marked symptoms with daily
activities
Class IV - symptoms at rest
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GOAL: treat to minimize sx
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Evaluation and Management
1.
2.
3.
4.
Determine the etiology of HF
Detailed history and physical
Identify current class
Determine therapeutic plan
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Diagnostics
Therapeutics
Prognostics
Symptoms
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Dyspnea
Orthopnea, PND, sleep disturbance
Abdominal discomfort, ascites
Nausea, early satiety, anorexia
Edema
Weight gain
Chest pain
Signs
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Volume and/or Pressure Overload
 JVD
 HJR
 Ascities
 S3
 Hepatomegaly
 Pleural effusion
 Edema
 Pulmonary rales
 Resting tachycardia
 Weight gain
Diagnostics
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CBC/diff
CMP
U/A
TSH
BNP
Iron studies (if suspect
hemochromatosis)
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CXR
EKG
ECHO
CATH
Therapeutics: GOALs
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Improve survival
Improve symptoms
Slow progression
Avoid adverse events
Decrease use of resources (hospitalization)
Therapeutics: non-pharm
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Salt restriction
Exercise
Smoking cessation
Weight loss
Treat OSA
Fluid restriction*
* In select pts
Therapeutics
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ACE
Beta-Blocker
Digoxin and diuretics
Coronary revascularization
Valvular repair
End of life/Hospice counseling
Cardiomyopathy
Cardiomyopathy
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General term indicating disease of cardiac
muscle resulting in abnormal function
Divided into three types:
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Dilated cardiomyopathy-ventricular dilation
Hypertrophic cardiomyopathy-myocardial
hypertrophy
Restrictive cardiomyopathy-impaired
ventricular filling
Can have characteristics of more than one
Incidence and Prevalence
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Incidence
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Dilated cardiomyopathy: 148/100,000/year
Prevalence
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Dilated cardiomyopathy: 920/100,000
Hypertrophic cardiomyopathy: 50-200/100,000
Restrictive cardiomyopathy is the most rarely
encountered form of heart muscle disease in the
western world
Dilated Cardiomyopathy (DCM)
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Characterized by dilation and impaired
systolic function of left &/or right ventricle
Most common DCM is ischemic
cardiomyopathy
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Idiopathic (ICM) next most common
Pattern of familial inheritance in 20% of
cases.
Role of coxsackie/adenovirus and immune
mediated etiology unknown.
DCM
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Common causes:
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Ischemic
Hypertensive
Idiopathic
Genetic
Alcoholism
Tachycardia-induced
Drug abuse (cocaine,
methamphetamine, and
heroin
Chemotherapeutic
agents
Pregnancy
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Hemochromatosis
HIV and antiretroviral
agents used to treat
Infectious disease
(coxsackievirus,
adenovirus,
cytomegalovirus, Rocky
Mountain spotted fever,
toxoplasmosis, trichinosis,
leptospirosis, Lyme, chagas
disease)
DCM- Rare Causes
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Exposure to toxins,
heavy metals
Nutritional deficiency
involving thiamine,
selenium, etc.
Endocrine disorders
like hypothyroidism,
hyperthyroidism,
adrenal insuff
Electrolyte abn
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Connective tissue
disease: SLE, RA,
scleroderma
Hematologic disordersSickle cell, thalassemia
Muscular dystrophies
Sarcoidosis
DCM
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Clinical features:
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R/L heart failure
Arrhythmia
Thrombus/Emboli
Cardiomegaly
Tachycardia
JVD
3rd heart sound
basiler crackles
displaced PMI
DCM
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Evaluation
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CXR: cardiomegaly
EKG: diffuse non specific ST-T wave changes,
LBBB common, tachycardia, conduction
abnormalities, arrhythmias
Echo: poor chamber contraction and dilated
chambers
If CAD suspected, cardiac catheterization
Endomyocardial biopsy for research only.
DCM
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Treatment
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Beta blcokers
Ace Inhibitors
Anticoagulation for A.fib/mural thrombus.
Diuretics
CRT-D (Bi-V AICD)
Transplant
Sudden death –
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Due to V. Tach. or V. Fib
Hypertrophic Cardiomyopathy (HCM)
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Unexplained myocardial hypertrophy
(disproportionate to hemodynamic load)
with disarray of muscle fibers
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Principal abnormality is impaired ventricular
compliance
Outflow tract obstruction present in only
25% of cases (HOCM, IHSS, ASH)
Inherited in 50-75% of cases
Most common cardiovascular cause of
death in athletes
Hypertrophic Cardiomyopathy
Diastolic dysfunction
 Outflow tract obstruction
 Myocardial ischemia
 Arrhythmia
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Symptoms:
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Asymptomatic
Dyspnea
Chest pain (angina)
Syncope/Pre-syncope (typically with
exertion)
Palpitations
Sudden Death (arrhythmia)
Left Ventricular Outflow Tract
Obstruction
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Subvalvular obstruction
Different from aortic stenosis (pressure
gradient across valve)
Exam to distinguish the systolic murmur of
AS from systolic murmur of HOCM
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Valsalva- Decreases preload and volume is no longer
holding back the septal wall, obstruction gets worse
resulting in a louder murmur (softer with AS)
Squat- increases preload and obstruction gets better
resulting in a softer murmur (louder with AS)
Murmur does not radiate to the neck
HCM
Evaluation
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EKG-LVH with ST-T wave changes
CXR-normal
ECHO is diagnostic
XST/Holter
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Screen first degree relatives (echo)
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Treatment
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B-Blockers
Dual chamber pacer
Myomectomy
Catheter directed ETOH ablation
AICD
Restrictive Cardiomyopathy (RCM)
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Restrictive ventricular filling and reduced
diastolic volume with normal or nearnormal wall thickness “stiff ventricle”
Uncommon in USA
Presents with diastolic dysfunction
Fewer than 10% of patients live more than
10 years after the initial diagnosis
A leading cause of transplant
Restrictive Cardiomyopathy
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Amyloidosis (most common in USA)
Sarcoidosis
Idiopathic
Radiation fibrosis
Hemochromoatosis
Drug inducing fibrosis
Endomyocardial fibrosis
Restrictive Cardiomyopathy
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Clinical Features
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Dyspnea
Fatigue
Elevated venous pressures
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JVD
Hepatomegaly
Edema
Ascites
Restrictive Cardiomyopathy
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EKG
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low voltage and ST-T wave abnormalities
atrial dilation
atrial fibrillation (clot formation common)
Echo
Endomyocardial biopsy may be useful.
Is it restrictive pericarditis?
Restrictive Cardiomyopathy
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Treatment
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Management of diastolic dysfunction
Treat underlying cause
Those with amyloidosis may recur after
transplant
Amyloidosis
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Abnormal proteins (amyloid) are produced
by plasma cells in the bone marrow
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Secondary to cancer (multiple myeloma),
systemic disease, or genetic disorders
Deposits in tissues and organs cause
structural and functional damage
Hypertrophy and restrictive cardiomyopathy
Characteristic low voltage on EKG despite
hypertrophy on echo
Hemochromatosis
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Inherited disorder of iron metabolism causing the body
to absorb/store excess iron resulting in “iron overload”
Accumulation in:
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Liver (cirrhosis and hepatocellular carcinoma)
 Pancreas (bronze diabetes)
 Heart (cardiomyopathy)
 Gonads (atrophy)
 Skin (bronze or silver-grey)
 Joints (arthritis)
Restrictive or dilated cardiomyopathy
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