E3. Heart failure Flashcards
Define congestive heart failure.
It is a complex neuroendocrine syndrome in which endogenous compensatory mechanisms that provide effective short-term circulatory support contribute to progressive cardiac dysfunction and death.
What are the clinical signs of left-sided heart failure?( Two causes, many signs)
–pale mucous membranes, prolonged capillary refill time, tachycardia, weak pulse, lethargy, depression, weakness, exercise intolerance, prerenal azotemia. (due to decreased forward stroke volume results in hypotension)
– pulmonary edema, coughing, dyspnea (difficulty breathing), orthopena (difficulty breathing when lying down), tachypnea, exercise intolerance and cyanosis. (due to high end diastolic pressure and resultant high pressure in the pulmonary vein)
What are the clinical signs of right-sided heart failure? (5)T
– Distention of the jugular and peripheral veins, ascites, hepatomegaly and splenomegaly, pleural effusion, peripheral edema (rare). (Due to high end diastolic pressure in the right ventricle causing increased pressure in the anterior and posterior vena cava)
What is the difference between heart failure and heart disease?
Heart disease is when you have signs like murmurs, arrhythmias, and cardiac abnormalities. Heart failure is when these signs have become so severe that it affects the heart to the point where it can no longer properly function.
What is the normal physiological response to decreased cardiac output?(Short-term, e.g. exercise/standing)
– The baroreceptors sense a decrease in blood pressure and then activate the sympathetic nervous system.
– increase in contractility of the heart (positive inotropy)
– increase heart rate (positive chronotropy)
– Venoconstriction and arterioconstriction redirects blood flow to vital centers. A
What is the normal physiological response to decreased cardiac output? (Long-term, e.g. hemorrhage)
What does angiotensin II do in this response?
What does aldosterone to in this response?
– Short-Term mechanisms occur, along with the following:(Decreased renal blood flow results in activation of the renin-angiotensin-aldosterone system (RAAS)which increases the Venous return to heart). This all causes the myocardial fibers stretch, enhancing myocontractility and cardiac output (Frank Starling relationship)
Angiotensin II:
–causes peripheral vasoconstriction in veins and arteries
– venoconstriction
– Arterio-constricting effects of angiotensin II increase peripheral
resistance and help to maintain blood pressure
Aldosterone:
–Sodium and water retention at the kidneys; increases blood volume
What are two examples of a heart dysfunction (heart disease) that can lead to heart failure?
Dilated cardiomyopathy (pump failure) and chronic valve disease.
What happens in dilated cardiomyopathy to cause heart failure?
The ventricular walls become thinner causing the force in systole to be decreased. This results in a lowered a cardiac output.
What happens in chronic valve disease to cause heart failure?
The mitral valves are thickened and contracted which results in a mitral regurgitation. As the left ventricle contracts up to 70% of the stroke volume can recover through the damaged mitral valve into the left atrium thus decreasing cardiac output.
Why can dilated cardiomyopathy and chronic valve disease lead to heart failure?
Because they are both features in an abnormal heart. So when the sympathetic nervous system is activated to correct this they don’t respond normally. The increased peripheral resistance caused by the sympathetic nervous system will lead to decreased blood flow and signs of hypotension in the abnormal heart.
What type of levels are elevated in people and dogs in heart failure? What type of relationship to these levels have with survival?
Norepinephrine levels are elevated, and they have an inverse relationship with survival time (The higher the norepinephrine level, the shorter the survival time).
What is cardiac hypertrophy?
o A response to chronically increased tension on myocardial fibers and angiotensin II
o Supports heart function, but only slows the progression to failure
o Pathologic remodeling
What is Eccentric Hypertrophy?
o Caused by chronic increased diastolic pressure (volume overload)
o Characterized by cells elongating by the addition of sarcomeres in series, resulting in a larger ventricle
with an increased chamber size with walls of normal thickness
o Result: normal contractility, but the end diastolic volume is increased to accommodate the larger
volume of blood that needs to be ejected in order to maintain blood pressure and forward stroke
volume
o Increased ventricular volume then raises afterload—the resistance is going to be greater when the
ventricle is trying to eject blood
o Eccentric hypertrophy in the atria increases compliance and helps to prevent increases in atrial
pressure, leading to increased venous pressure and edema.
What is Concentric Hypertrophy?
o Occurs when there is increased systolic ventricular pressure (pressure overload)
o Aortic stenosis or systemic hypertensions
o The sarcomeres replicate side-by-side/parallel, resulting in wider cells and a thicker, stiffer/less
distensible ventricular wall, which is less able to dilate in diastole
o Decreased filling in diastole, which leads to increased preload, which can result in edema
o Increased wall thickness = increased MVO2, resulting in anaerobic metabolism if CO and oxygen supply
to the heart is not increased
o Hypoxia decreases heart muscle contraction efficiency, promoting arrhythmias
What are the signs of heart failure?
Signs of congestion, low output/forward heart failure (weakness and syncope), severely decreased blood flow(Cardiogenic shock).
