Before exam on Tuesday Flashcards
Ways in which the endothelium prevents clotting
- Prevents the collagen from coming into contract with the platelets
- Produces prostacyclin and nitric oxide. This stop other platelets from binding on to other platelets which are bound to the collagen.
- Produces tissue factors pathway inhibitors which stop thrombin production.
- Expresses thrombomodulin and heparin which inactivate thrombin.
- Secretes tissue plasminogen activator which converts to plasmin and digests clots.
How do baroreflexes work ?
In the short term this is done through baroreflexes. Baroreflexes are found in the aortic arch and carotid sinus. They are stretch reflexes, then there is an increase is MAP they are stretched and send signals to the brain. Aortic signals are sent via the vagus nerve and carotid sinus signals are sent through the glossopharyngeal nerve. The signal is processed in the brain and assed to the parasympathetic signals in the vagus nerve which act on the SA node and decrease the heart rate. If there is a decrease in MAP then the brain sends signals to the SA node through the sympathetic nerves to increase the HR. Sympathetic nerves cause increased stoke volume and blood vessel constriction.
Describe the 3 ways in which the kidneys control blood pressure
- Sympathetic nerves act on the juxtaglomerular apparatus and induce the secretion of Renin from juxtaglomerular cells in the kidneys. Renin is converted to inactive angiotensinogen and then into angiotensin I. The angiotensin converting enzyme (ACE) then converts angiotensin I to Angiotensin II. Angiotensin II stimulates the release of aldosterone from the adrenal cortex which increase Na2+ reabsorption in the loop of Henle and therefore blood pressure. Angiotensin II also simulates the release of ADH from the pituitary glands which increases water permeability and therefore increases blood pressure. Angiotensin II is also a vasoconstrictor which increase TPR increasing blood pressure. This pathways is generally called the renin angiotensin aldosterone system.
- The antidiuretic factor (ADH) is produced by the hypothalamus and released from the posterior pituitary gland. The release of ADH is triggered by a number of things including, a decreased blood volume, increases osmolarity, increased interstitial fluid and presence of circulating angiotensin II. ADH increases the water permeability of the collecting duct, reducing diuresis (urine excretion) and increasing plasma volume. ADH also causes vasoconstriction which also increased MAP.
- The atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) are produced and released from the myocardial cells in the atria and venticules respectively. If there is an increase in MAP there will be increased tension in the ventricles which triggers the secretion of ANP and BNP. These hormones increase excretion of Na+, inhibit renin release and act on medullary CV centres to reduce BP.
Describe the BP during and after the Valsalva manoeuvre
- The manoeuvre starts and it causes an increase in pressure within the thorax which moves through the system causes an increase in pressure in the blood vessels.
- This loss of pressure gradient means blood cannot move in the veins very easily and so blood pressure starts to decrease as CO decreases and causes MAP to decrease
- Drop in BP is detected by the baroreceptors and they increase the HR, cause vasoconstriction to increase TPR and will increase CO. This creates a small increase in BP.
- The manoeuvre stops causing a big drop in the pressure through the system.
- The venous return returns to normal increasing preload and CO and BP
- There is a return to normal within the system
When CO decreases what happens to MAP?
Decreases too
What are the local methods of blood flow control ?
- Decrease in perfusion causes a increase in blood flow when molecules are released from the endothelium and cause vasodilation. This is known as autoregulation and occurs in the kidneys, heart and brain.
- Supply/demand mismatch causes increased blood flow when molecules are released from the endothelium and cause vasodilation. This is called active hyperaemia.
- Injury response
- Occlusion of a vessel causes an increase in flow. This is called resistant hyperaemia.
What are the systemic methods of blood flow control ?
Sympathetic nerves release noradrenaline which acts on the A1 receptors in the blood vessels causes vasoconstriction and the B2 receptors of the heart causing vasodilation.
Adrenal medulla releases adrenaline which acts on the same receptors.
What are the 5 methods of venous return ?
Pressure falls as you move through the vascular tree. There is a small drop in pressure between the arteries, a large drop into the arterioles and it then continues to fall until it is back in the heart. The pressure different through the system is what drives the movement on blood.
Gravity pulls blood downwards.
The skeletal muscle pump increases the movement of venous blood back to the heart. It occurs where there is a rhythmic contraction of skeletal muscles in the legs i.e. when you are exercising. A lack of skeletal muscle pump use can cause a DVT.
The respiratory pump also increases venous return. An increase in respiratory rate and depth increases venous return and EDV. This is because inspiration causes a decrease in alveolar pressure adding to the pressure gradient and pulling blood up towards the lungs.
The venomotor tone is the contraction of the smooth muscle which surrounds the veins and venules. This increases capacitance and EDV.
cardiac output =
heart rate x stroke volume
Where do the three standard limb leads run from and to ?
SLL I LA to RA
SLL II LL to RA
SLL III LL to LA
Stages of the cardiac cycle
Late diastole. Here there is no contraction occurring and the ventricles are filling passively.
Atrial systole. Here the atrial contract forcing a small amount of blood into the already fairly full ventricles.
Isovolumic ventricular contraction. The ventricles start to contract, this increase the pressure in the ventricles. The ventricular pressure surpasses the atrial pressure and so the AV valves (i.e. the mitral and tricuspid valves) close but dose not create enough pressure to open the semilunar valves.
Ventricular ejection. Ventricular pressure surpasses the artery pressure and so the semilunar valves open. Blood is ejected.
Isovolumic ventricular relaxation. The ventricles relax and blood flowback into the cusps of the semilunar valves and close them.
What is the effect of the physical forces during inspiration and expiration ?
On inspiration they open the airways
On expiration they close the airways
4 Laws that are important in respiration
- Boyles law states that the pressure exerted by a gas is inversely proportional to its volume P a 1/V).
- Daltons law states that the total pressure of a gas mixture is the sum of the pressures of the individual gases.
- Charles Law states that the volume occupied by a gas is directly related to the absolute temperature (v a T). This doesn’t matter so much in the body as the body temp is ruffly constant.
- Henry’s law states that the amount of gas dissolved in a liquid is determined by the pressure of the gas and it’s solubility in the liquid.
Table or partial pressures
PaO2 Arterial oxygen 100 13.3 PaCO2 Arterial carbon dioxide 40 5.3 PAO2 Alveolar oxygen 100 13.3 PACO2 Alveolar carbon dioxide 40 5.3 PVO2 Venous oxygen 40 5.3 PVCO2 Venous carbon dioxide 46 6.2
What is the spirometry look like for normal, obstructive and restrictive conditions ?
Normal FEV1 4l FVC 5l
Restrictive FEV1 2.8 FVC 3.1
Obstructive FEV1 1.3 FVC 3.1
Draw the compliance graphs for a restrictive and an obstructive lung disease
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Describe how CO2 is transported in the blood
When CO2 molecules diffuse from the tissues into the blood, 7% remains dissolved in plasma and erythrocytes, 23% combines in the erythrocytes with deoxyhemoglobin to form carbamino compounds, and 70% combines in the erythrocytes with water to form carbonic acid, which then dissociates to yield bicarbonate and H+ ions. Most of the bicarbonate then moves out of the erythrocytes into the plasma in exchange for Cl- ions & the excess H+ ions bind to deoxyhemoglobin. The reverse occurs in the pulmonary capillaries and CO2 moves down its concentration gradient from blood to alveoli.
What 4 factors can change the oxygen delivery to tissue ?
Decrease pH
increase temp
Increase CO2
Increase [DPG]
Types of hypoxia
- Hypoxaemic Hypoxia: most common cause of hypoxia. Reduction in O2 diffusion at lungs either due to decreased PO2atmos or tissue pathology.
- Anaemic Hypoxia: Reduction in O2 carrying capacity of blood due to anaemia (red blood cell loss/iron deficiency).
- Stagnant Hypoxia: Heart disease results in inefficient pumping of blood to lungs/around the body
- Histotoxic Hypoxia: poisoning prevents cells utilising oxygen delivered to them e.g. carbon monoxide/cyanide
- Metabolic Hypoxia: oxygen delivery to the tissues does not meet increased oxygen demand by cells.
How do central chemoreceptors work ?
Central. Found in the medulla. They are responsible for the primary ventilatory drive. They respond to H+ (PCO2) in the cerebrospinal fluid around the brain. An increase in PCO2 in the blood causes an increase in CO2 in the cerebrospinal fluid which reacts to form H+ which then stimulate the central chemoreceptors which in tern stimulates the respiratory control centres in the medulla and increase the rate and depth of breathing. Increase in ventilation means carbon dioxide is breathed out and the stimulus is removed slowing down respiration. They cant respond to an increase in H+ in the blood because the blood brain barrier prevents H+ from crossing but allows CO2 to cross. We are very sensitive to PCO2 because it is toxic to cells if it builds up. People with chronic lung disease PCO2 can become chronically elevated which means that the brain becomes desensitised to elevated PCO2 and therefore the peripheral chemoreceptors are relied on. This is known as hypoxic drive.
How do peripheral chemoreceptors work ?
Peripheral. Found in the carotid and aortic bodies. They are the secondary ventilatory drive. They respond primarily to PO2 and plasma [H+]. A significant fall in the partial pressure (100mmHg down to 60) of oxygen cause a increase in ventilation. Note that peripheral chemoreceptors only respond to partial pressure not total oxygen content.
