gnur 293 Heart failure

c. pulmonary edema

.

Explain why left ventricular failure leads to right ventricular failure. Explain why right ventricular failure leads to left ventricular failure.

Certain conditions initially cause left side heart failure for example a left ventricular MI, systemic hypertension. Other conditions can initially cause right side heart failure for example right ventricular MI, pulmonary embolism, pulmonic valve stenosis, pulmonary hypertension. However uncorrected left side failure results in right side failure and vice versa resulting in bi-ventricular failure

Diastolic Heart failure

Diastolic heart failure is caused by abnormal diastolic function with preserved ejection fraction and is caused by impaired ventricular relaxation which is an active process requiring ATP, or by ventricular compliance in other words increased stiffness of the ventricle.

f. CNS alterations such as confusion and impaired memory-

may be related to other heart failure symptom and chronically low CO

d. paroxysmal nocturnal dyspnea (PND)-

patient with heart failure assumes supine position

ventricular compliance

Intrinsic property of chamber that decribes its pressure-volume relationship during filling Compliance= Change in Volume/ Change in Pressure

end systolic volume (ESV)

is the volume of blood in a ventricle at the end of contraction, or systole, and the beginning of filling, or diastole. ESV is the lowest volume of blood in the ventricle at any point in the cardiac cycle. The main factors that affect the end-systolic volume are afterload and the contractility of the heart.

end diastolic volume (EDV)

volume of blood in the ventricles at the end of diastole, at the end of the filling period. factor that contributes to cardiac preload

cardiac index

(CI) is sometimes used instead of cardiac output bc the cardiac output varies in people i. =Cardiac output divided by body surface area

Explain the pathophysiological basis for the following clinical manifestations of heart failure: a. Tachycardia

- HR increase to compensate for the decrease in SV (CO= SVx HR)

Preload

- the ventricular wall tension at the end of diastole - the stretch just before contraction, end-diastolic volume/pressure

Afterload-

- the ventricular wall tension during contraction, the resistance that must be overcome for ejection

h. Cough

Cardiac asthma, ACE inhibtors

6. What is ventricular remodeling? What are the pathophysiological mechanisms involved in ventricular remodeling?

a. Progressive change is heart size & structure b. Results from overactivation of neurhormonal systems and cardiac inflammation c. Involves myocytes (cardiac muscle cells) which undergo hypertrophy & cell death due to apoptosis & necrosis d. Involves non-myocytes in the extracellular matrix including fibroblasts & endothelial cells e. Results in loss of ventricular function f. Pathophysiological mechanisms i. SNS & RAAS in Ventricular Remodeling ii. g. Signal Transduction Involved in Ventricular Remodeling

Systolic heart failure

a. Systolic heart failure is caused by conditions that impair ventricular contractile function resulting in a decreased ejection fraction. 5. Explain why left ventricular failure leads to right ventricular failure. Explain why right ventricular failure leads to left ventricular failure. a. Certain conditions initially cause left side heart failure for example a left ventricular MI, systemic hypertension. Other conditions can initially cause right side heart failure for example right ventricular MI, pulmonary embolism, pulmonic valve stenosis, pulmonary hypertension. However uncorrected left side failure results in right side failure and vice versa resulting in bi-ventricular failure

Explain the causes of systolic dysfunction and the causes of diastolic dysfunction that lead to heart failure. Why is the ejection fraction normal or near normal in diastolic heart failure and decreased in systolic heart failure?

b. Systolic Heart Failure (Reduced Ejection Fraction): HFrEF i. Inability of the ventricle to contract normally caused by conditions such as: 1. Decreased cardiac contractility (e.g. MI, dilated cardiomyopathy, drug-induced) 2. Cardiac pressure overload (e.g. hypertension, aortic stenosis, coarctation of the aorta) 3. Cardiac volume overload (e.g. aortic or mitral regurgitation, left-to-right intracardiac shunt, fluid overload)

g. Decreased clearance of medications-

chronic hepatomegaly, liver dysfunction

Why is an elevated serum level of B-type natriuretic peptide (BNP) used as an indicator of heart failure?

i. Brain natriuretic peptide (BNP) is produced and released in response to pressure and volume overload of the cardiac chambers. This occurs in both systolic and diastolic heart failure. BNP causes arterial and venous dilation, natriuresis, and suppression of the renin-angiotensin-aldosterone system and the sympathetic nervous system. BNP inhibits myocardial fibrosis and hypertrophy and enhances diastolic function. ii. Serum levels of BNP can be measured to help with determining the diagnosis, prognosis and response to treatment in heart failure. Recently, BNP levels have been found to be predictive of cardiovascular morbidity even in individuals without heart failure.

c. myocardial hypertrophy

i. Capillary growth does not keep pace with muscle growth ii. Growth of myofibrils is greater than that of mitochondria resulting in inadequate ATP production iii. Increase amount of collagen surrounding heart cells increasing the diffusion distance for oxygen d. Compensatory mechanisms initially can be beneficial to survival and help maintain the cardiac output. However when they are sustained for a long period of time they actually contribute to the worsening of cardiac function and contribute to the progression of heart failure

d. Increased Blood Volume

i. Excessive fluid administration ii. Renal dysfunction

10. Explain the factors that can trigger symptoms of heart failure in a person who was previously in a state of compensated heart failure. a. Compliance Issues

i. Failure to follow nutrition plan ii. Failure to take medications as prescribed

b. Increased Metabolic Demands

i. Fever ii. Infection iii. Pregnancy iv. Hyperthyroidism v. Anemia

c. Diastolic Heart Failure (Normal Ejection Fraction): HFnlEF

i. Impaired ventricular filling or relaxation caused by abnormalities that increase the resistance to the inflow of blood into the ventricle, such as: 1. Restrictive cardiomyopathy 2. Pericardial tamponade 3. Cardiac hypertrophy 4. Cardiac hypoxia

f. Conditions that Impair Myocardial Contractility

i. Negative inotropic medications ii. Myocardial ischemia or infarction

b. tachycardia

i. SNS stimulation of HR 1. Initially an increase in HR can maintain CO: CO = SV x HR 2. Very rapid heart rates: a. Increase myocardial oxygen demands b. Decrease the time available for ventricular filling c. Shorten the period of disatole & therefore decrease coronary blood flow 3. ATP is required for both muscle contraction and muscle relaxation therefore oxygen requirements of the heart increase with increase of HR 4. Tachycardia Results in decreased left ventricular perfusion(blood flow)

c. Dysrhythmias

i. Tachycardia ii. Bradycardia

e. Increased Afterload

i. Worsening systemic hypertension ii. Pulmonary hypertension iii. Pulmonary embolism

What are the beneficial effects of Nesiritide, which is a recombinant form of BNP, when used to treat heart failure?

i. a human B-type natriuretic peptide (hBNP), is an effective agent for improving hemodynamic profiles and symptoms of disease in individuals with acute severe decompensated CHF. ii. 1. Indicated for the treatment of decompensated heart failure 2. Beneifts a. Decreases the levels of a variety of neurotransmitters or hormones that have been found to be detrimental in heart failure b. Promotes vasodilatation which decreases the afterload on the heart c. Decreases pulmonary congestion which can improve the ability to breathe more easily, reducing dyspnea

Explain why the following mechanisms can initially help compensate for a cardiovascular disorder but eventually contribute to the development of heart failure: Frank-Starling (length-tension) mechanism

ii. It involves an increase in length of cardiac muscle fibers which then allows them to generate more tension (a more forceful contraction)

e. jugular venous distention (JVD)-

increased central venous pressure caused by increase in venous BV

ejection fraction-

the fraction of EDV ejected from the ventricle during systolic contraction EF= SV/ EDV

stroke volume (SV)

volume of blood ejected from the ventricle during on contraction,systole (EDV-ESV

cardiac output (CO)

volume of blood ejected from ventricle per minute (SV x HR)

b. peripheral edema-

water and sodium retention, increase in blood volume and venous hydrostatic pressure- more fluid in subcutaneous tissue - decrease amounts of albumin by altered liver function