Congestive Heart Failure (CHF)

by Carlo Raj, MD

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    We will take a look at the myocardium. With the myocardium, it is the fact that we are working with the middle part of the heart. If it is endocardium, then you are thinking more along the lines of valvular heart disease perhaps. It is exactly what you are doing. So let's take a look at the myocardium and the categories of pathologies that come under or affect the myocardium. We will take a look at CHF, congestive heart failure. You know this as being end-stage heart disease. So, anything that causes damage to the myocardium from dilated cardiomyopathy to hypertrophic cardiomyopathy to restrictive cardiomyopathy and so forth, eventually if there is enough death that is taking place in the myocardium, are you not going to result in CHF? The most common cause of CHF is going to be ischemic. So, if your patient has something like an ST elevation in leads V1, V2, and V3, and then you know there is a transmural myocardial infarction affecting which coronary artery? The left anterior descending and at some point later on down the road, your patient may develop congestive heart failure. You see my point. So ischemia would be a very common cause or actually it is the most common cause of CHF. CHF final and common pathway of myocardial disease. Now the way that we will approach this is dilated cardiomyopathy and hypertrophic cardiomyopathy would be relatively common at least in developed countries. Is that clear? You want to think that a dilated cardiomyopathy as being end-stage heart disease just like you have cirrhosis being end-stage liver disease. Listen to what I am saying. I am drawing a lot of parallels here and I will keep doing this for you so that you don't waste as much time memorizing details...

    About the Lecture

    The lecture Congestive Heart Failure (CHF) by Carlo Raj, MD is from the course Congestive Heart Failure. It contains the following chapters:

    • Pathogenesis and Etiologies
    • Definition
    • Systolic Disfunction
    • Diastolic Disfunction
    • Signs & Symptoms
    • Diagnosis & Treatment
    • Medications

    Included Quiz Questions

    1. Chagas.
    2. Valvular heart disease
    3. Sarcoidosis
    4. Rheumatic heart disease
    5. Alcohol
    1. Ischemic heart disease
    2. Rheumatic fever
    3. Mitral valve prolapse
    4. Hemochromatosis
    5. Coxsackie virus.
    1. Staphylococcus infection
    2. Aschoff bodies
    3. Valvular insufficiencies
    4. Pericarditis
    5. Myocarditis
    1. Cirrhosis
    2. Asthma
    3. Diabetic neuropathy
    4. Hematuria
    5. Hemorrhagic stroke
    1. Alcohol
    2. Sarcoidosis
    3. Hemochromatosis
    4. Amyloidosis
    5. Endomyocardial fibrosis
    1. Stroke volume of 95 mL and End Diastolic Volume of 144 mL.
    2. Eccentric hypertrophy of left ventricle.
    3. Laterally displaced point of maximal impulse.
    4. Difficult contraction of the heart.
    5. Ejection fraction of 30%
    1. Associated with eccentric hypertrophy of left ventricle.
    2. Difficulty filling the left ventricle.
    3. Decreased chamber size.
    4. Associated with pressure overload.
    5. Preserved ejection fraction early in the disease process.
    1. Left heart failure.
    2. Cor pulmonale.
    3. Primary lung disease.
    4. Coronary artery disease affecting the right coronary artery.
    5. Congenital heart disease.
    1. Negative inotropy.
    2. Positive inotropy.
    3. Negative chronotropy.
    4. Positive chronotropy.
    5. Negative dromotropy.
    1. Decreased end diastolic volume.
    2. Increased pressure of the heart.
    3. Decreased venous return.
    4. Decreased ejection fraction.
    5. Decreased stroke volume.
    1. Decreased effective circulating volume.
    2. Decreased venous return.
    3. Aldosterone receptor activation.
    4. Aortic arch baroreceptor activation.
    5. Increased hydrostatic pressure.
    1. The fluid has an abnormally high protein content.
    2. It is associated with transudate fluid.
    3. Right sided heart failure is associated with elevated jugular venous distention.
    4. Left sided heart failure leads to pulmonary edema.
    5. It is the result of increased hydrostatic pressure.
    1. Digoxin
    2. Metoprolol
    3. Furosemide
    4. Verapamil
    5. Enalapril
    1. Diuretics
    2. Digoxin
    3. Beta blockers
    4. Calcium channel blockers
    5. Nitrates
    1. Left ventricular filling defect
    2. Right ventricular filling defect
    3. Loss of atrial kick
    4. Pump defect
    5. Deficient preload
    1. Isovolumetric relaxation
    2. Isovolumetric contraction
    3. Passive filling
    4. Rapid filling
    5. Ejection
    1. a wave
    2. p wave
    3. v wave
    4. qrs complex
    5. y descent
    1. Positive jVD
    2. Orthopnea
    3. Pulmonary rales
    4. Paroxysmal nocturnal dyspnea
    5. Foam Cells
    1. Hemosiderin laden macrophages
    2. LDL laden macrophages
    3. Cholesterol laden macrophages
    4. Coal laden macrophages
    5. none of the above
    1. Class III
    2. Class I
    3. Class II
    4. Class IV
    5. Not enough information
    1. T-tenting on EKG.
    2. Suppress tachycardia in hypoglycemic diabetic patients.
    3. Bronchospasm.
    4. Heart block.
    5. Hypotension.
    1. Dry cough
    2. Angioedema
    3. Hyperkalemia
    4. hypotension
    5. T-tenting on EKG
    1. Diabetes
    2. Acute renal failure
    3. History of angioedema
    4. African Americans
    5. Hypertrophic Obstructive Cardiomyopathy
    1. Spirinolactone
    2. Metoprolol
    3. Lisinopril
    4. Isosorbide mononitrate
    5. Losartan
    1. Nitrates increase venous return.
    2. Nitrates decrease preload.
    3. Nitrates cause arterial vasodilation.
    4. Nitrates cause venodilation.
    5. Nitrates decrease total peripheral resistance.

    Author of lecture Congestive Heart Failure (CHF)

     Carlo Raj, MD

    Carlo Raj, MD

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    Great talk but what about management of dilated & hypertrophic cardiomyopathy
    By Hamed S. on 17. February 2017 for Congestive Heart Failure (CHF)

    Really great talks and focus on the underlying pathophysiology. However, it would have been good to cover the management of dilated and hypertrophic cardiomyopathy which differs somewhat to dilated cardiomyopathy