Flashcards in Congestive Heart Failure (CHF) Deck (47)
Generally describe the condition of CHF
The heart is unable to pump blood at the rate sufficient to meet the metabolic demands of the tissues or can only do so at an elevated filling pressures.
How can CHF occur?
Most often insidiously via chronic work overload (i.e. HTN or valvular diseases) or ischemic myocardial disease (following MI). Can also happen acutely via fluid overload, acute valvular dysfunction or a large MI.
What is the concept of the Frank-Sterling mechanism and how does this explain why during CHF the body tries to compensate with more fluid retention?
Frank sterling mechanism states (in this case it applies to myocytes) that when a muscle is stretched (up to a point) with increased volume, more of the sarcomeres become involved and cross-bridges, and therefore the heart will contract with more force, and the body accomplishes this by having more fluid retention to increase pre-load.
What is "ventricular remodeling?"
Molecular, cellular and structural changes of the heart, such as cardiac hypertrophy.
How does the body attempt to compensate for CHF in terms of neuroendocrine?
NorEpi is released by adrenergic nerves (to increase heart rate and contractility, and vascular resistance), activation of the RAS system and release of atrial natriuretic peptide (the latter two adjust filling volumes and pressures).
Most frequent cause of heart failure?
Systolic dysfunction, progressive deterioration of contractile function of the heart, due to ischemic injure, pressure/volume overload or dilated cardiomyopathy.
What is "diastolic dysfunction?"
Ventricles fails to fill appropriately during diastole, i.e. massive left ventricular hypertrophy, fibrosis, amyloid deposition, or constrictive pericarditis.
What are two causes of cardiac hypertrophy?
Increased mechanical work due to pressure/volume overload, or activation of ß adrenergic receptors.
Histologically how do hypertrophied myocytes look?
Large nucleus w/ increased mitochondria, the nucleus is larger due to more DNA but no division.
What is "pressure overload hypertrophy" and what causes it?
Increase of ventricle size due to concentric bands of muscle being made and increased thickness, this happens in response to HTN or valvular disease which would increase the pressure in the ventricles.
How do volume overload hypertrophy differ from pressure overload?
Characterized by ventricular dilation due to myocytes growing in series rather than increase in ventricular muscle thickness where myocytes increases in cross sectional area. In fact the wall can be thicker, thinner or normal in ventricular hypertrophy thus we must measure heart weight rather than heart thickness.
Why is ventricular hypertrophy a bad thing, shouldnt a larger heart be more powerful?
Increased size doesn't correlate with increased capillary supply, so basically we have a bigger mass that needs more nutrients but the same amount of supply that it had when the heart was much smaller --> muscles get exhausted and increased possibilities of ischemia.
How is fibrosis involved in hypertrophy?
Along with hypertrophy, fibrosis is accompanied.
What happens at a genetic level with prolonged hemodynamic overload?
Shift in genetic expression to that seen in fetal cardiac development (where we have fetal forms of ß myosin heavy chains).
How is gene expression appeared to be altered?
Changes in the expression of miRNA (non coding RNA that inhibit the expression of certain proteins in mRNA).
Which miRNA is associated with cardiac hypertrophy? Prevention of cardiac hypertrophy?
downregulation of miR-208 and upregulation of miR-195 = cardiac hypertrophy. Overexpression of miR-195 will lead to hypertrophy, overexpression of miR-208 is protective.
What kind of cardiac hypertrophy is associated with aerobic exercise?
Volume overload hypertrophy w/ increased capillary supply, aka physiologic hypertrophy. This is also accompanied by descreased HR and BP.
Is weight lifting good for the heart?
Evidently not... it is associated with pressure-overload hypertrophy and thus deleterous effects.
What is "forward failure" and "backwards failure?"
The inability of the heart to deliver enough blood to cause tissue perfusion is forward failure, and the pooling of blood in the venous system is called backwards failure (which can cause pulmonary/peripheral edema).
What are the 4 main causes of left sided heart failure? What do these generally have in common?
Ischemic heart disease, HTN, aortic and mitral valve disease and myocardial diseases. Generally occurs from pulmonary circulation congestion, stasis of blood in left chamber, and hypoperfusion of tissues leading to organ dysfunction.
How does the atria suffer from impaired ventricular function?
Causes dilation of the left atria and increases risk of a fib, resulting in stasis of blood esp in the atrial appendage.
What is a common site of thrombus formation in the atria if blood is static?
The atrial appendage.
What causes the Kerley B lines noted in the chest x-rays?
Caused by perivascular and interstitial edema esp in the interlobar septa --> creates an image of the kerley B lines in chest x ray, which are horizontal lines seen at the base of the lungs.
What are "heart failure cells" and what do they indicate?
These are hemosiderin laden macrophages; RBC seems into the pulmonary edema fluid and macrophages eat them, but store the hemoglobin in the form of hemosiderin. This indicates previous episodes of pulmonary edema if seen.
What are clinical manifestations of left sided heart failure?
Cough and dyspnea (first in exercise and later at rest) seen initially, and later as disease progresses to more pulmonary edema pt's get orthopnea and paroxymal nocternal dyspnea
What is "paroxymal nocternal dyspnea?"
Dyspnea so bad that it feels like suffocation that occurs at night.
What causes thrombus and thromboembolic strokes risk in CHF?
LV dysfunction often leads to a fib which causes stasis of blood --> thrombus --> increased risk of strokes and thromboembolic events.
Why does CHF activate RAS? Why is this a problem?
Less renal perfusion due to decreased stroke volume from the heart, which induces an activation of renin and the RAS cascade, increase fluid retention and contribute to/exacerbate pleural edema.
Besides activating the RAS pathway, what else does CHF cause the kidney to do?
If hypoperfusion of the kidney is severe enough, it will lead to pre-renal azotemia.
How is the brain affected by left sided heart failure?
In severe cases pts get cerebral hypoxia which gives rise to hypoxic encephalopathy, and this can progress into stupor or coma.
Left sided heart failure can be divided into systolic and diastolic failure, what are they?
Systolic failure is caused by whatever damage that produces decreased cardiac output by the LV. Diastolic failure is when cardiac output is ok at rest, but the LV is very stiff so the heart is unable to accomidate for exercise because LV will be unable to fill up and thus pump out sufficient blood.
What is "flash pulmonary edema"?
In diastolic failure where the LV is quite stiff, any increase in LV backs blood up in the LA and into the pulmonary circuit --> rapid pulmonary edema onset, emergency.
Who are more prone for diastolic failure?
Women over the age of 65, reason for female unknown.
What causes diastolic failure?
HTN, DM, obesity, bilateral renal artery stenosis, fibrosis, restrictive cardiomypoathies and pericarditis. Also the heart stiffens with age naturally anyway.
What is the most common cause of right sided heart failure?
Left sided heart failure which puts more strain on the right side, and eventually that also fails, thus everything that causes LS HF also causes RS HF.
What is "Cor Pulmonale?"
RS HF unassociated with the left side, this is due to parenchymal diseases of the lungs, or secondary to disorders that messes with pulmonary vasculature, pulmonary embolus, chronic causes of hypoxia. All of this has pulmonary HTN in common.
What is a common feature of all the etiologies that causes right sided HF?
Pulmonary HTN as a result of Right side of the heart dilation and hypertrophy.
How does right sided heart failure differ from the left?
Pulmonary congestion is minimal, but the engorgement of systemic and portal venous system is pronounced.
How can RS heart failure lead to "Nutmeg Liver?"
Fluid will back up in the portal and hepatic vessels from the lungs, causing congestion around the central veins of hepatic lobules making the center red-brown and the periphery more pale and fatty --> produces the nutmeg like appearance.
What is cardiac sclerosis and cardiac cirrhosis?
In the case of RS HF esp in conjunction with LS HF, central areas of the liver becomes fibrotic causing the sclerosis, and in extreme cases the cardiac cirrhosis.
What is pulmonary edema and pleural effusions associated with?
Left sided heart failure, LSHF.
What are consequences of intense pleural edema?
There can be so much fluid that corresponding lung fails to inflate, causing atelactesis. Fluid can also seep into the peritoneal space and produce ascites.
What kind of edema is the hallmark of RS HF?
Edema of the peripheral and dependent portions of the body (ankle and periorbital edema). If hospitalized bedridden pt, presacral edema might predominate. Anasarca can also occur.
What are pedal, periorbital, presacral and generalized edema (anasarca) associated with?
Right Sided heart failure RSHF.
What are clinical features of RSHF?
HSM, peripheral and periorbital edema, pleural effussions and ascites.
Which sided heart failure affects the kidneys more?
Right sided, leading to more fluid retention and azotemia than LSHF.