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| Question | Answer |
|---|---|
| In heart failure, the sympathetic nervous system (SNS) is chronically activated as a compensatory mechanism to | maintain blood pressure and cardiac output. While beneficial initially, sustained sympathetic stimulation leads to harmful, maladaptive effects, including cardiomyocyte apoptosis, fibrosis, and increased arrhythmia risk. |
| SNS activation causes chronic stimulation of B-adrenergic receptors caused by | arterial underfilling and hypoperfusion |
| Sustained SNS stimulation and renal hypoperfusion causes the activation of this system | The RASS System which stands for Renin-Angiotensin-Aldosterone-System |
| Initial activation of SNS and RAAS alters | pre- load, ventricular contractility and heart rate to maintain cardiac output |
| Chronic elevation of SNS and RAAS can cause | cardiac myocyte apoptosis, hypertrophy, fibrosis and myocardial necrosis |
| After about 12 hours SNS activation | Long range control of BP and volume managements kicks in when the RAAS activates |
| Angiotensinogen is continuously produced by the liver and | released into the blood stream where it comes in contact with renin |
| In response to stress, this is released by the kidneys | Renin |
| When renin from the kidneys meets with Angiotensinogen from the liver it forms | Angiotensin I |
| When angiotensin I enters the lungs it comes in contact with | Angiotensin Converting Enzyme which then turns Angiotensin I into Angiotensin II |
| Angiotensin II causes | Vasoconstriction |
| Vasoconstriction caused by Angiotensin II causes | tightening of blood vessels which pushes more blood to the heart, lungs and brain |
| Angiotensin II travels to the adrenal glands and tells the kidneys to make | Aldosterone |
| Aldosterone is responsible for | regulating blood pressure, blood volume and electrolytes by telling the kidneys to retain salt and water and excrete potassium which increases blood volume and blood pressure |
| The hormone aldosterone is released by the adrenal glands and controlled by RAAS when the body | experiences a drop in pressure or volume |
| too much aldosterone can cause | too much sodium retention contributing to myocardial fibrosis of the failing heart |
| SNS activation causes an increase in these three catecholamines | epinephrine, norepinephrine and dopamine |
| vasopressin, also known as ADH or antidiuretic hormone is released from the pituitary gland in response to | arterial underfilling, hypovolemia, plasma osmolality (dehydration, hyperglycemia, Diabetes Insipidus) |
| In RAAS, the myocardial oxygen demand is | increased as the heart rate rises causing the heart to work harder |
| Vascular resistance and afterload INCREASE in response to | Angiotensin II |
| Brain Natriuretic Peptides rise in response to the | stretching of the left ventricle caused by increased afterload and increased vascular resistance |
| these two things perpetuate an elevated heart rate | SNS activation and release of catecholamines Epinephrine, Norepinephrine and dopamine |
| BNP less than 100 | low likelihood of fluid retention as a source of dyspnea |
| BNP 100-300 | suggests heart failure but not definitive |
| BNP >400 | indicates mild heart failure |
| BNP >600 | indicates moderate heart failure |
| BNP>900 | indicates severe heart failure |
| NT-Pro BNP > 125 pg/ml | suspected heart failure |
| BNP levels may be higher in these 3 groups | women, older individuals and individuals with impaired kidney function |
| BNP may be falsely lower in | obese individuals |
Created by:
DMolinary