CV lecture - Pathophysiology of cardiomyopathies


Click on the questions to see the answer! Questions made from our lectures . Let me know of any mistakes

Question 1 - What is SV dependent on?

1. EDV (preload)
2. Resistance to ejection of blood (afterload)
3. Contractility

Question 2 - What is starlings law?

The greater the end diastolic pressure (up to a point) the greater the contraction of the ventricle.


Question 3 -What valve closes as pressure in the left ventricle drops below the pressure in the aorta?

Aortic valve.


Question 4 - True or false the pressure in the left atrium is greater than the pressure in the pulmonary veins?

Question 5 - What is the result of increased LA pressure?

LA pressure up = Pulmonary
Capillary pressure (PCWP) up

• Interstitial edema
• Vascular redistribution
• Alveolar edema
• (PND, and orthopnea, and SOBOE)

Question 6 - What is the result of increased RA pressure?

- As the RA pressure rises, the downstream leg vein pressure rises, thus,the hydrostatic force to “push” fluid
into the interstitium and overwhelm the capacity of the lymphatics to remove excess fluid.

- Results in peripheral edema

- Increased fluid in the portal veins results in ascites

- PND and orthopnea

Question 7 - What are heart filling pressures?

Left and right atrial pressures.


Question 8 - Why are heart failure patients with cool wet hands doing worse then patients with warm dry hands?

Poor cardiac output leads to the cool hands.

The wettness is due to increased sympathetic stimulation.

That's bad mmmmm-kay

Question 9 - How does an S3 sound compare to an S4?



It can be thought of as a sound which is generated when the ventricle is forced to dilate beyond its normal range because the atrium has overloaded volume. An S3 is usually heard best with the bell of the stethoscope placed at the apex while the patient is in the left lateral decubitus position. The presence of an S3 is usually normal in children and young adults, but pathologic in those over the age of 40.


The late stage of diastole is marked by atrial contraction, or kick, where the final 20% of the atrial output is delivered to the ventricles. If the ventricle is stiff and non-compliant, as in ventricular hypertrophy due to long-standing hypertension, the pressure wave generated as the atria contract produces an S4. It is heard best with the bell of the stethoscope at the apex.


Question 10 - How does the body respond to low CO?

- Decreased renal perfusion leads to activation of RAAS

- Sympathetic nervous system activation (nor-epineferine)

– Other neurohormones (BNP)


Question 11 - True or false, if you have an MI that leads to heart failure it is not considered a cardiomyopathy?



Question 12 - Name the 4 types of cardiomyopathy?

1. Dilated
2. Hypertrophic
3. Restrictive
4. Arrhythmogenic right ventricular

Question 13 - What is the difference between eccentric and concentric hypertrophy?

Eccentric = chamber radius is increased and the wall thickness is increased moderately

concentric = chamber radius may not change, the wall thickness greatly increases


Question 14 - What is the pathology in idiopathic dilated cardiomyopathy?

- Four chamber dilation

- Mild to moderate ventricular hypertrophy

- Interstitial fibrosis and myocyte hypertrophy

- "functional" atrioventricular regurgitation is common

- Normal coronary arteries


Question 15 - What does "functional" atrioventricular regurgitation mean?

Functional mitral regurgitation (MR) is an important component of the pathophysiology of dilated cardiomyopathy and congestive heart failure (CHF), and is characterized by the absence of structural abnormalities of the mitral valve leaflets, chordae, and papillary muscles. The most common secondary cause of functional MR is dilated cardiomyopathy (idiopathic or ischemic) where the pathophysiologic mechanisms of MR are multi factorial: changes in the size, shape, and function of the left ventricle (LV) and left atrium; dilatation and dysfunction of the mitral valve annulus; and mechanical LV desynchronization.

reference article/504561

S. Serge Barold *, I. Eli Ovsyshcher †

From the *University of South Florida College of Medicine, Tampa, Florida and †Faculty Health Sciences, Ben Gurion University of the Negev, Beer Sheva, Israel

Question 16 - What are some of the possible clinical presentations of Dilated cardiomyopathy?

- Heart failure symptoms 75%-85%
- Anginal chest pain 8%-20%
- Emboli (systemic or pulmonary) 1%-4%
- Syncope <1%
- Sudden cardiac death <1%


Question 17 - What is pulsus alternans? Is it a positive or negative prognostic sign?

Pressure Alternans is a sign of a failing ventricle. It can be seen in Left Ventricular pressure tracing or arterial waveform (shown above) where it represents severe left ventricular dysfunction. In severe Right ventricular dysfunction, Pulsus or Pressure Alternans can be seen in the Right ventricular pressure tracing recorded from a Swan-Ganz catheter.

Notice the beat-to-beat variation in the pressure tracing. Pulsus Alternans is felt to be a manifestation of decreased myocardial contractility. Decreased contractility is attributed to deletion of the number of myocardial cells contracting on alternate beats. Another mechanism which may be involved (to a lesser extent) in creating this effect is an alteration in diastolic volume leading to beat-to-beat variation in preload.


Question 19 - Patients with hypertrophic cardiomyopathy can have a high ejection fraction, so what is the problem?

- Diastolic dysfunction

- Arrhythmias

- Ischemia

- MR

- LVOT obstruction


Question 20 - What is the most common cause of hypertrophic cardiomyopathy?


• Familial in ~ 55% of cases with
autosomal dominant transmission
• Mutations in one of 4 genes encoding
proteins of cardiac sarcomere
account for majority of familial cases
• Most mutations novel (not useful for
screening yet)


Question 21 - What is the cause of obstruction in hypertrophic cardiomyopathy?


Question 22 - What causes the diastolic dysfunction in HCM?

- Diastolic Dysfunction due to

• Increased LV cavity stiffness
- Hypertrophy
- Fibrosis
- Fibrillar disarray

• Impaired Relaxation
- Ischemia
- Abnormal Ca metabolism
- Abnormal loading


Question 23 - What are the physical exam findings of HCM?

Bisferens pulse (“spike and dome”)
murmur of outflow obstruction (crescendo/decrescendo)
Mitral regurgitation

Question 24 - How can you determine if a murmur is caused by HOCM or AS?

Mummur of HOCM vs. AS

Valsalva (↓preload, ↓ afterload)
Squatting (↑ preload, ↑ afterload)
Standing (↓preload, ↓ afterload)

- Smaller LV volume brings septum
closer to anterior MV leaflet: more
obstruction and louder murmur.

- Larger LV volume separates upper
septum from anterior MV leaflet: less
obstruction and softer murmur.


Question 25 - What are two ways to treat HCM?

- Myomyectomy

- Alcohol septal ablation


Question 26 - Compare and contrast DCM HCM and restrictive myopathies physical findings.?


- Decreased C.O.

- Pulmonary venous congestion:

- Cardiac:
laterally displaced apex
S3, mitral regurgitation murmur

- Systemic congestion
↑ JVD,↑ liver, ascites, peripheral edema

-Bisferens pulse (“spike and dome”)

- murmur of outflow obstruction (crescendo/decrescendo)

- Mitral regurgitation

Symptoms of right and left heart failure

Jugular Venous Pulse
– prominent x and y descents