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Clinical Medicine 3 > Lecture 4 (Cardiomyopathy)-Exam 1 > Flashcards

Lecture 4 (Cardiomyopathy)-Exam 1 Flashcards

1
Q

Cardiomyopathy
* What are they?
* In essence they are problems with what?
* When it occursbecause of what?

A
  • Cardiomyopathies are diseases of the heart muscle. (form of HF)
  • In essence they are problems with the myocardium or the surrounding layers that can make it harder for the heart to pump blood effectively.(Not Systemic Resistance)
  • When it occursbecause of hypertension or valvular diseases, then it is called secondarycardiomyopathy but when by itself, it is called primarycardiomyopathy.
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2
Q

What are the Types of Cardiomyopathy?

A
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3
Q

Dilated Cardiomyopathy:
* Dilated cardiomyopathy generally placed into category of what?
* Both ventricles are what?

A
  • Dilated cardiomyopathy generally placed into category of HF with reduced EF where the ejection fraction can fall below 20% but generally between 20-40%.
  • Both ventricles are dilated with left ventricular systolicfunction is impaired (reduced ejection fraction)
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4
Q

Dilated cardiomyopathy
* What are the different causes? (6)

A
  • Large proportion of dilated cardiomyopathy causes are idiopathic, likely genetic variants thatmay be responsible.
  • Alcohol has a strong link as alcohol and its metabolites have a direct effect on the myocardium.
  • Other causes include bacterial/viral infections.
  • Endocrine, inflammatory, and metabolic causes which includes obesity, diabetes as well as obstructive sleep apnea.
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5
Q

What is the trick to remember the causes for dilated cardiomyopathy?

A
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6
Q

Dilated Cardiomyopathy: pathophysiology
* Increased hemodynamic overload and ventricular remodeling causeswhat?
* What leads to to biventricular congestive heart failure?
* What happens to the valves?

A
  • Increased hemodynamic overload and ventricular remodeling causesall four chambers of the heart to dilate or get bigger. Sarcomeres are added in series which makes the walls thin in comparison to the chamber size, with less muscle to use for contraction.
  • Weak contractions and reduced stroke volume leads to biventricular congestive heart failure.
  • Valves are stretched apart also due to the increase in chamber sizes, and this leads to both mitral and tricuspid regurgitation.
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7
Q

Dilated Cardiomyopathy: pathophysiology
* Essentially poor contractions leads to what?

A
  • Essentially poor contractions leads to reduced stroke volume and ejection fraction - hemodynamic overload occurs - then ventricular remodeling as a response to maintain cardiac output through the Frank-Starling mechanism which produces the thin-walled dilated left ventricle appearance.
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8
Q

Dilated Cardiomyopathy: pathophysiology
* Increased ventricular preload augments what? What can temporarily increase CO?

A

Increased ventricular preload augments contractions, but excessive pressure and volume (over time) can lead to a reduction in myocardial contraction which leads to left ventricular remodeling.
* A fluid bolus is effective in using Frank-Starling mechanism to temporarily increase cardiac output.

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9
Q

Dilated Cardiomyopathy: pathophysiology
* If during the time of childbirth then what can happen?

A
  • If during the time of childbirth then dilated cardiomyopathy may occur towards the end of pregnancy or in the months after delivery, likely because of pregnancy induced hypertension.
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10
Q
A
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11
Q

What is this?

A
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12
Q

Dilated cardiomyopathy
* What are the sxs?

A
  • Symptoms of heart failure develop gradually.
  • Exertional intolerance.
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13
Q

Dilated cardiomyopathy: PE
* What happens with the lungs?
* Elevated what?
* What happens with the heart?
* What happens to the extremities?
* What happens in the abdomen?

A
  • Pulmonary rales
  • Elevated jugular venous pressure
  • S3 gallop rhythm (third heart sound, caused by blood rushing into the ventricles and slamming againstdilated ventricular walls during relaxation)
  • Murmurs of mitral or tricuspid regurgitation
  • Peripheral edema
  • Ascites
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14
Q

Dilated cardiomyopathy:
* What does the ECG and chest crx?

A
  • Sinus tachycardia is common – hearts response to try to improve blood flow to meet oxygen demands.
  • Left ventricular hypertrophy (rhythm, not the thickening) , other various types of rhythms which are caused by the irritation of the heart muscles as a result of the stretching due to the dilation.
  • Chest radiograph reveals cardiomegaly and pleural effusions.
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15
Q

What does this show?

A

Dilated cardiomyopathy
* Sinus tachycardia is common – hearts response to try to improve blood flow to meet oxygen demands.
* Left ventricular hypertrophy, other various types of rhythms which are caused by the irritation of the heart muscles as a result of the stretching due to the dilation.
* Chest radiograph reveals cardiomegaly and pleural effusions.

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16
Q

Diagnostics Studies of Dilated Cardiomyopathy
* Those with dyspnea should have what measured?
* What is used to see EF?

A
  • Those with dyspnea should have a BNP(used to rule in or out heart failure) measured to help establish prognosis and disease severity.
  • Echocardiogram – to confirm the presence of ventricular dilation as well as the ejection fraction.
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17
Q

Diagnostics Studies of Dilated Cardiomyopathy
* Cardiac MRI is helpful in what?
* Cardiac catheterization is what?
* Myocardial biopsy is what?

A
  • Cardiac MRI is helpful in inflammatory or infiltrative processes, such as sarcoidosis.
  • Cardiac catheterization is seldom of specific value unless myocardial ischemia is suspected.
  • Myocardial biopsy is rarely useful in establishing a diagnosis.
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18
Q

BNP measures what?

A

the levels of protein in the blood which the heart produces when it has to work harder and higher levels can be attributed to heart failure.

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19
Q

What is this?

A
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20
Q

Dilated Cardiomyopathy txt:
* Identify what?
* Treat as what?

A

Identify behaviors that might predispose patients to the disease such as alcohol abuse, early genetictesting.

Treat as heart failure
* ACE/ARB, beta blocker, loop diuretics, all which help to decrease the workload of the heart.

Standard therapy includes control of the blood pressure and of contributing factors such as obesity, smoking, diabetes, sodium restriction. Treating the underlying cause is the mainstay of therapy.

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21
Q

Dilated Cardiomyopathy txt:
* Standard therapy includes what? What is the mainstay therapy?

A

Standard therapy includes control of the blood pressure and of contributing factors such as obesity, smoking, diabetes, sodium restriction. Treating the underlying cause is the mainstay of therapy.

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22
Q

Dilated Cardiomyopathy txt:
* To prevent sudden cardiac death, what should be placed?
* Placement of what?
* Extreme measures would be what?

A
  • To prevent sudden cardiac death, an ICD is reasonable incardiomyopathy patients with an LVEF of less than 30%
  • Placement of a left ventricular assist device as well (LVAD)
  • Extreme measures would be a heart transplant.
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23
Q

What is this?

A
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24
Q

prognosis
* Prognosis of dilated cardiomyopathy without clinical heart failure is what?
* What is the Mortality rate?

A
  • Prognosis of dilated cardiomyopathy without clinical heart failure is variable, some remain stable, some deteriorating gradually, and others declining rapidly.
  • Mortality rate is around 11-13%
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25
Q

prognosis
* Patients with pregnancy induced what?
* In general, cardiomyopathy due to what?

A
  • Patients with pregnancy induced cardiomyopathy or stress-induced cardiomyopathy appear to have a better prognosis than those with other forms, resolves on its own.
  • In general, cardiomyopathy due to infiltrative myocardial diseases, have poor prognosis.
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26
Q

Hypertrophic Cardiomyopathy
* When does it occur?
* Growth is generally what?
* Walls become thicker which take up what?

A
  • Hypertrophic cardiomyopathy occurs when the wallsget thick and heavy and hypercontractile. Heart muscle gets thicker as the sarcomeresline up in parallel to each other, usually affects the left ventricle.
  • Growth isgenerally asymmetrical, with left vetricular hypertrophy observed.

THICK

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27
Q

Hypertrophic Cardiomyopathy
* Walls become thicker which take up what?

A
  • Walls become thicker which take up more room and become stifferleading to less ventricular filling, leads to reduced stroke volume and diastolic heart failure – the left ventricle loses its ability to relax normally and cannot fill with blood properly.
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28
Q

Diastolic heart failure is also described as what?

A

heart failure with preserved ejection fraction

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29
Q

Hypertrophic cardiomyopathy:
* Larger muscles gets in the way of what?
* Obstruction to the flow usually causes what?

A
  • Larger muscles gets in the way of the left ventricular outflow tract during contraction. The blood rushing through the outflow tract increases in velocity and pulls the mitral valve towards the septum – further obstructs the outflow tract.
  • Obstruction to the flow usually causes increases in pressure in the heart which is responsible for exercise limiting symptoms of exertional dyspnea.
30
Q

Hypertrophic cardiomyopathy:
* In non-obstructive hypertrophic cardiomyopathy, there is an absence of what?

A
  • In non-obstructive hypertrophic cardiomyopathy, there is an absence of an outflow gradient both at rest and with a variety of physical and nonphysical actions and drugs.
31
Q

Hypertrophic Cardiomyopathy
* Left ventricle outflow tract is usually narrowed during what?
* Worsened by factors that do what?

A
  • Left ventricle outflow tract is usually narrowed during contraction due to the hypertrophied septum – as blood passes through this short opening, it pulls themitral valve closer to the septum – Venturi Effect
  • Worsened by factors that increase contradiction or decrease left ventricle filling such as the Valsalva maneuver or peripheral vasodilators.
32
Q

What is this?

A
33
Q

Hypertrophic Cardiomyopathy
* What can be a cause?
* Patients usually present with sx when?

A
  • It is an inheritedautosomal-dominant trait that passes from one parent to their child – affects the gene responsible for sarcomere development.
  • Patients usually present early in adulthood – may be identified through sport related assessments, physical activity.
34
Q

Hypertrophic Cardiomyopathy
* Elite athletes may demonstrate what?

A
  • Elite athletes may demonstrate considerable hypertrophy that can be confused with hypertrophic cardiomyopathy but there is no diastolic dysfunction.
35
Q

Hypertrophic Cardiomyopathy: Symptoms and Signs
* Frequent symptoms are?
* What happens with respiratory?
* Syncopal episodes are also most common typically what?
* If they also present with what arrhythmia?
* Ventricular arrhythmias are also common – leading to what?

A
36
Q

Hypertrophic Cardiomyopathy
* The highest incidence of SCD in who?
* Triggers such as what?

A
  • The highest incidence of SCD in young athletes is among those participating in sports like basketball, football, track, and soccer.
  • Triggers such as extreme physical exertion coupled with underlying structural heart disease constitutes the pathologic basis of SCD in athletes.
37
Q

Hypertrophic Cardiomyopathy: Symptoms and Signs
* What type of murmur?
* Loud systolic murmur present along what?
* Enhanced with what? Why?

A
  • Crescendo-decrescendo sounding type murmur – gets louder when blood first rushes out then gets softer.
  • Loud systolic murmur present along left sternal border, may also have what feels like two pulses -caused when the mitral valve is pulled alongside the outflow tract causing obstruction during contraction.
  • Enhanced with Amyl Nitrate, vasodilator – decreases the afterload which increases the septal hypertrophy obstruction and murmur becomes louder.
38
Q

Hypertrophic Cardiomyopathy: Symptoms and Signs
* Murmur decreases with what? Why?
* Murmur increases with what? Why?

A
  • Murmur decreases with squatting or handgrips– increases preload and increases venous return, increasing the preload in the ventricle decreases the septal hypertrophy obstruction and the murmur becomes softer.
  • Murmur increases with Valsalva and rapid standing – we increase intrathoracic pressure which reduces preload andreduces the left ventricular volume which increases the obstruction and the murmur intensity.
39
Q

Hypertrophic Cardiomyopathy
* What is shown on ECG and Chest x-ray?

A

Majority will have ECG abnormalities; LVH, prominent Q waves, left atrial enlargement, left axis deviation, ST elevation or depression, possible T-wave inversions.

40
Q

Hypertrophic Cardiomyopathy: Dx Studies
* What is gold stand? What does it show?

A

Echo is gold standard: LVH, asymmetrical septal wall thickness and EF greater than 60%
* 1stdegree family members should be screened

41
Q

Hypertrophic Cardiomyopathy
* Why use doppler?
* Why use cardiac MRI?
* What else could be useful?

A
  • Doppler – used to establish outflow obstruction and peak gradients
  • Cardiac MRI – great for identifying hypertrophy.
  • CT and PET may be useful
42
Q

Hypertrophic Cardiomyopathy: Txt
* What activity can you not do?
* What should be the FIRST drug in sx individuals?
* Why use CCB?
* What is contraindicated?

A
  • No competitive sports or strenuous exercise without treatment or a plan of care.
  • Beta-blockers should be the initial drug in symptomatic individuals – will assist with diastolic filling of the stiff left ventricle.
  • Calcium channel blockers, especially Verapamil have been effective – improves diastolic function but may cause hypotension as well.
  • Digoxin is contraindicated -may increase force of contraction and makeoutflow obstruction worse
43
Q

Hypertrophic Cardiomyopathy: txt
* If in atrial fibrillation, treat with what?
* What about fluid?
* What can be done with unresponsive to medical therapy?
* Nonsurgical sepal ablation by what?
* Those at high risk for sudden death are treated with what?

A
  • If in atrial fibrillation, treat with antiarrhythmics or radiofrequency ablation.
  • Stay hydrated as dehydration can make symptoms worse.
  • Surgical myomectomy (cutting extra muscle) for those unresponsive to medical therapy.
  • Nonsurgical sepal ablation by injection of alcohol into septal branches.
  • Those at high risk for sudden death are treated with an implantable cardioverter-defibrillator.
44
Q

Hypertrophic Cardiomyopathy
* What is the prognosis?

A

Sudden death, especially during exercise may be the initial event – increased size leads to reduced oxygen delivery and ischemia which leads to fatal arrythmias.

45
Q

Hypertrophic Cardiomyopathy: What is the highest risk patients? (5)

A
  • Personal history of serious ventricular arrythmias or survival of a sudden cardiac even
  • Family history of sudden death
  • Unexplained syncope
  • Documented nonsustained ventricular tachycardia
  • Maximal LV wall thickness of 30 mm or more
46
Q

Stress Cardiomyopathy: Essentials of Dx
* Occurs after what?
* What happens with heart and pulmonary?
* Predominately affects who?

A
  • Occurs after a major catecholamine discharge
  • Acute chest pain or shortness of breath
  • Predominately affects postmenopausal women whohave experienced severe, unexpected emotional stress in the prior 1 to 5days.

“Broken Heart Syndrome”
described first in Japan

47
Q

Stress Cardiomyopathy
* Presents as what
* What imaging?
* What is the recovery?

A
  • Presents as an acute anterior MI, but coronaries normal at cardiac catheterization
  • Imaging reveals left ventricular ballooning due to anteroseptal stunning of the myocardium
  • Most patients recover completely.

“Broken Heart Syndrome”
described first in Japan

48
Q

Stress Cardiomyopathy
* Also referred to as what? What does that result in?
* Key feature is what?

A
  • Also referred to as tako-tsubo syndrome, resulting shape of the LV acutely suggests a rounded ampulla form similar to a Japanese octopus pot.
  • Key feature is that the myocardial stunning that occurs does not follow the pattern suggestive of coronary ischemia.
49
Q

Stress Cardiomyopathy
* Most occur from what?

A
  • Most occur from a prior stressful event, either emotional or physical including hypoglycemia, lightning strikes, during alcohol withdrawal and following emotional stress (broken heart syndrome).
50
Q

Stress Cardiomyopathy
* Both circulating epinephrine and norepinephrine released leads to what?
* Leads to what?

A
  • Both circulating epinephrine and norepinephrine released leads to myocardial damage through multiple mechanisms.
  • Leads to spasms and increased cardiac workload.

“Broken Heart Syndrome” described first in Japan

51
Q

Stress Cardiomyopathy
* What are the sxs?

A
  • Symptoms are similar to any acute coronary syndrome.
  • Typical angina and dyspnea and usually present.
  • Syncope is rare and arrythmias are not uncommon.
52
Q

Stress Cardiomyopathy
* What is shown on ECG?

A
  • ECG reveals ST-segment elevation as well as deep anterior T-wave inversion
  • Dramatic T-wave inversion gradually resolves with time
53
Q

Stress Cardiomyopathy
What is shown on chest radiograph?

A

Either normal or may show pulmonary congestion
* Although there is not cardiomegaly present in this image, it is used to show example of the pulmonary congestion that you would see on x-ray.

54
Q

Stress Cardiomyopathy
* What does Echo show?
* Urgent cardiac catheterization reveals what?
* Initial cardiac enzymes are what?

A
  • Echocardiogram reveals LV wall thickness that is normal.
  • Urgent cardiac catheterization reveals normal coronary vessels.
  • Initial cardiac enzymes are positive but taper quickly.
55
Q

Stress Cardiomyopathy
* What is the txt?

A
  • Immediate therapy is similar to any acute MI.
  • Most patients received ASA, beta-blockers, and ACE inhibitors until the LV function recovers.
  • Consideration for potential protective role for anticoagulation with possibly Warfarin due to changesin structural of the left ventricle that can lead to thrombus formation.
56
Q

Stress Cardiomyopathy: Prognosis
* Generally good unless there is a serious complication such as what?
* Recovery?
* Studies have found that generally occurs with who? What are the triggers?

A
57
Q

Restrictive Cardiomyopathy: Essentials of diagnosis
* What dominates?
* What is present?
* What is the MCC?

A
  • Right heart failure tends to dominate over left heart failure.
  • Pulmonary hypertension is present.
  • Amyloidosis is the most common cause.
58
Q

Restrictive Cardiomyopathy: Essentials of diagnosis
* How do you dx?
* What can also be a part of the dx?
* This is a condition develops when?

A
  • An echo is key to diagnosis.
  • Myocardial biopsy can also be a part of the diagnosis.
  • This is a condition that develops over years.

Pump strength normal, but relaxation impaired

59
Q

Restrictive Cardiomyopathy: Pathology
* What happens to the myocardium?
* When blood fills the chambers, what happens?
* What happens to the blood?
* Less filling, a form of diastolic heart failure but with what?
* On echo, it may show what?

A
60
Q

Restrictive Cardiomyopathy
* What are the causes?

A
61
Q

Restrictive Cardiomyopathy
* What are the sxs?

A
62
Q

Constrictive Pericarditis
* What is it? What does it lead to?
* What cannot expand? What does it cause?
* What leads to systemic back up of blood flow?

A
63
Q

Constrictive Pericarditis
* What is the cause?

A
  • Cause is idiopathic in origin, likely infectious in nature, common in regions with TB and is potentially reversible. Likely related to chest radiotherapy.
64
Q

Constrictive Pericarditis
* What is sign is present? What is the cause?
* Kussmaul’s sign canbe seen in both?

A
  • Kussmaul’s sign – paradoxical rise in JVP on inspiration is seen – right ventricle is not as complaint, so you get abackup of blood.Pericardium is noncompliant and results in failedredistribution of increased systemic venous return – pressure in right atrium rises much more than in the pleural pressure causing inspiratory distention of neck veins.
  • Kussmaul’s sign canbe seen in both constrictive pericarditis and restrictive cardiomyopathy.
65
Q

What does the chest x-ray and CT of chest show?

A

calcified constrictive pericarditis

66
Q

Restrictive Cardiomyopathy: Dx
* What does the CXR?
* What does an echo show?
* What Endomyocardial biopsy for?

A

CXR
* Cardiomegaly or mild to moderate enlarged cardiac silhouette

Echo will showa reduced diastolic filling, when the heart relaxes to fill with blood

Endomyocardial biopsy
* Differentiate restrictive disease from other forms of cardiomyopathies

67
Q

Restrictive Cardiomyopathy
* What are some other dx studies?

A
  • Cardiac MRI
  • BNP – elevated.
  • ECG: Low-amplitude QRS complex due to restrictive ventricular contraction
68
Q

Restrictive cardiomyopathy vs Constrictive pericarditis
* The single distinctive feature differentiating constrictive pericarditis from restrictive cardiomyopathy what?
* In constrictive pericarditis the pericardiumis almost always what?
* ID what?
* What is the test of choice?

A
  • The single distinctive feature differentiating constrictive pericarditis from restrictive cardiomyopathy is anatomic, not physiologic.
  • In constrictive pericarditis the pericardiumis almost always thickened and motion of the heart within the pericardium isconstrained.
  • Identifying the thickness of the pericardium is crucial in separating the difference.
  • Test of choice would be a cardiac MRI.
69
Q

Restrictive Cardiomyopathy
* Little useful therapy is available for what?
* Mainstay is what?
* What can slow HR and improve filling?
* What can be helpful in sarcoidosis?

A
  • Little useful therapy is available for either the causative conditions or the restrictive cardiomyopathy itself.
  • Mainstay is diuretics but excessive diuresis can produce worsening kidney dysfunction.
  • Beta-blockers help slow heart rate and improve filing.
  • Corticosteroids may be helpful in sarcoidosis.
70
Q

Restrictive Cardiomyopathy txt
* Amyloidosis depends on what?
* What is needed?
* What is the prognosis

A
  • Amyloidosis depends on type.
  • Anticoagulation needed due to increased risk of thromboembolism.
  • Prognosis – once symptomatic, life span typically 1-3 years with optimal control
71
Q
A

Clinical Medicine 3 (27 decks)

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