Transcript
When a pt is suffering major blood loss the body will have a ?(decrease) in blood volume it causes a ? in blood pressure (BP). The Baroreceptors in the carotid arteries, aortic arch and the kidneys are stimulated. The Baroreceptors send the info to the cardiac center of the medulla oblongata, which is then stimulated. When this happens the SNS is stimulated to release the neurotransmitter, Norepinephrine. Norepinephrine binds to the adrenal medulla to stimulate the release of 2 hormones, Norepinephrine (Norepi) and Epinephrine (Epi). Norepi & Epi will now control the heart rate, peripheral resistance, stroke volume and blood volume. HEART RATE Norepi & Epi bind to Beta receptors on the K+ (potassium) funny leak gates on the sinoatrial (SA) node of the heart, causing the K+ funny leak gates to close more times per minute, which increases (?) the heart rate (HR). More blood is being pumped into the arteries per minute which is an ? in cardiac output (CO). CO is ml ejected from ventricle/min. (CO=HRxSV). By ? CO there is more blood in the arteries causing a rise in BP (BP=COxPR). Peripheral Resistance (PR) is the friction of the blood against the walls of the artery. Norepi &Epi bind to alpha receptors on the smooth muscles surrounding the arteries. Calcium (Ca+2) gates on the sarcoplasmic reticulum open. Muscle contraction causes the artery to vasoconstrict down to half its original diameter causing PR to ? 4x. ? PR causes and ? in BP (BP=PRxCO) Stroke Volume (SV) is the mL of blood that is ejected from the ventricles per beat. SV ? when end diastolic volume (EDV) ? and end systolic volume (ESV) ?. EDV is the Vol of blood in the ventricle at the end of diastole. Norepi &Epi bind to receptors on smooth, cardiac & skeletal muscles. These muscles contract down on the veins which cause the blood to move towards the heart. ? venous return causes an ? in EDV. A rise in EDV cause SV to rise (SV=EDV-ESV). By ? SV there is an ? in CO (CO=SVxHR). An ? in CO causes BP to rise (BP=COxPR). There are 2 ways to ? ESV. 1st Norepi &Epi bind to receptors on the myocardial membrane causing CA2+ gates on the membrane along with the sarcoplasmic reticulum to open. Excess Ca2+ enters the cell causing more actin & myosin to bind. This ?force of contraction. ? ESV equals ? SV (SV=EDV-ESV). By ? SV there is an ? in CO (CO=SVxHR). An ? in CO causes BP to rise (BP=COxPR). 2nd way to ? ESV is Frank Starling Law. When VR is ? the ventricular muscle of the heart stretches. This allows Actin and Myosin to align better to ? contractility. The ? in contractility causes a ? in ESV. The ? in ESV causes an ? in SV (SV=EDV-ESV). The ? in SV causes an ? in CO (CO=SVxHR). The ? in CO causes an ? in BP (BP=COxPR). Blood Volume Norepi &Epi bind to Juxtaglomerular cells in the kidneys. The JG cells secrete the hormone Renin. Renin interacts with Angiotensinogen, a hormone secreted by the liver. After their interaction, Renin converts Angiotensinogen, which is inactive, to become active and turn into Angiotensin I. The Angiotensin Converting Enzyme (Ace) converts Angiotensin I into a stronger hormone called Angiotensin II. Angiotensin II can do two different tasks. 1st, Angiotensin is a very potent vasoconstrictor that causes an ? in PR, which causes ? in BP (BP=PRxCO). 2nd it binds to the Adrenal cortex and stimulates the release of the hormone Aldosterone. Aldosterone binds to the kidneys to ? sodium (Na+) reabsorption. The high concentration of Na+ stimulates the movement of water from the intracellular fluid and extracellular fluid. The water moves by osmosis into the blood stream. This causes and ? in blood volume which causes an ? BP. Also, the high concentration of Na+ stimulates neurons, called the Osmoreceptors, in the Hypothalamus. Osmoreceptors stimulate an unquenchable thirst. With the intake of fluids there is an ? in the blood volume and this causes an ? in BP. Osmoreceptors also stimulate the posterior pituitary gland to release a hormone called Anti-Diuretic Hormone (ADH). ADH affects the kidneys by ? water reabsorption. This causes the urine output to ? and the blood volume is maintained. Blood Viscosity is the thickness of blood. A ? in blood volume causes a ? in the # of red blood cells (RBC). ? RBC causes a ? in oxygen (O2) saturation (sat). Chemoreceptors in the kidneys will be stimulated by low O2 sat. The kidneys secrete a hormone called Erythropoietin that binds to the red bone marrow stimulating an ? in Erythropoiesis. The ? in the # of RBC causes blood viscosity to ?, which causes a ? in PR. ? in PR causes an ? in BP. (BP=PRxCO)
