Weeks 1-3:Cardiovascular

Transcription

1 Weeks 1-3:Cardiovascular Cardiac Output The total volume of blood ejected from the ventricles in one minute is known as the cardiac output. Heart Rate (HR) X Stroke Volume (SV) = Cardiac Output Normal cardiac output = 5litres Cardiac output measurement This measurement is expressed as litres per minute and is calculated by multiplying the stroke volume by the number of contractions per minute (heart rate). In a healthy individual at rest, each ventricle ejects approximately 70mL with each contraction (stroke volume), at an approximate heart rate of 75bpm, giving a cardiac output of 70 x 75, which is approximately 5,250mL/min or 5.25L/min. Stroke Volume Is the amount of blood pumped out of the ventricle per beat Blood pressure (BP) The pressure of the blood in the circulatory system, often measured for diagnosis since it is closely related to the force and rate of the heartbeat and the diameter and elasticity of the arterial walls. As you age pressures elevate (systolic markedly increases). Cardiac Output (CO) X Systemic Vascular Resistance (SVR) = BP Systolic pressure = pressure in your blood vessels when your heart beats. Diastolic pressure = pressure in your blood vessels when your heart rests between beats. Mean arterial pressure (MAP) = defined as the average pressure in a pts arteries during one cardiac cycle. It is a better indicator of perfusion to vital organs than systolic BP. Average MAP is approx mmhg. Trending BP overtime with diastole increasing Change in a cardiac output (?SV may be decreased) the diastolic pressure increases to maintain the perfusing pressure. Thus, maintaining the MAP to perfuse vital organs, ensuring CO and SV are efficient from the ventricle. Trending BP with diastole decreasing Vasodilating effect. Thus, HR will increase to achieve increased CO (filling the space). Case study Impaired ventricle function during procedure AF increase in HR resulting in AF (arrhythmia) due to reduced CO as the pts BP could not compensate as it was beta blocked (causing pts body to go into an arrhythmia).

2 Physiological compensation Reserve Mechanisms of the heart Compensation mechanisms to meet changing demands. 1. Increasing HR to increase cardiac output 2. Dilation to create muscle stretch and more effective contraction 3. Hypertrophy of myocytes over time to generate more force 4. Increasing stroke volume by increasing venous return and increased contractility Baroreceptors are special receptors that detect changes in your blood pressure. Important baroreceptors are found in the aorta and the carotid sinus. If the BP within the aorta or carotid sinus increases, the walls of the arteries stretch and stimulate increased activity within the baroreceptors. Renin angiotensin aldosterone system (RAAS) Hormone system that regulates blood pressure and fluid balance. Decreased blood flow detected (Change in cardiac output) = activation of the RAAS system. Angiotensin II important actions Stimulation of aldosterone release from adrenal cortex Vasoconstriction of renal and other systemic vessels Enhanced tubuloglomerular feedback makes macula densa more sensitive Enhance Na-H exchanger and Na channel function to promote Na re-absorption

3 CNS control of breathing Cerebral medulla Located at the base of the brain above the spinal cord Determines rate, rhythm and depth of breathing O2 and CO2 receptors (medulla, carotid and aortic arch) Lung stretch and irritant (receptors) Fever/pain/anxiety Can also be impaired by opioids/benzodiazepines, anaesthetic, stroke, sleep apnoea, spinal cord injury and phrenic nerve injury. Chest wall and diaphragm mechanics Lungs need to be able to expand and relax through passive recoil. Action of breathing in and out is due to changes in pressure within the thorax in comparison with the outside (external respiration). When we inhale the intercostal muscles (between the ribs) and diaphragm contract to expand the chest cavity, the diaphragm flattens and moves downwards and the intercostal muscles move the rib cage upwards and out. This increase in size decreases the internal air pressure and so air from the outside (at a now higher pressure than inside the thorax) rushes into the lungs to equalise the pressures. When we exhale the diaphragm and intercostal muscles relax and return to their resting positions, this reduces the size of the thoracic cavity thereby increasing the pressure and forcing air out of the lungs. Pulmonary circulation The lungs are in series with the left and right heart. An important consequence of this arrangement is that blood flow through the lungs must equal blood flow through the rest of the body. This makes the lungs and effective organ for gas exchange, filtering and metabolism. This arrangement also permits the pressures of the pulmonary and the systemic circulation systems to differ due to in part to the presence of the cardiac valves. Pulmonary arteries carry de-oxygenated blood. Pulmonary veins carry oxygenated blood. Pressures in the pulmonary circulatory system Pulmonary blood pressure is normally a lot lower than systemic blood pressure. Normal pulmonary artery pressure is 8-20 mm Hg at rest. If the pressure in the pulmonary artery is greater than 25 mmhg at rest or 30 mmhg during physical activity, it is abnormally high and is called pulmonary hypertension. Pulmonary Blood flow resistance Hypoxic vasoconstriction is by far the most important modulator of smooth muscle tone in

4 the pulmonary arterioles is the partial pressure of O2 in the alveolus (PAO2). Interestingly, the smooth muscle of the pulmonary arterioles responds in an opposite manner than does smooth muscle systemic arterioles. This improves matching of blood flow for ventilation as if an area of the lung is poor ventilated the PAO2 in that region decreases. Resulting in constriction = decrease in blood flow to the area. Blood does not go to alveoli that is under oxygenated or under ventilated as it cannot diffuse across and become oxygenated. Chronic hypoxic vasoconstriction Pulmonary Hypertension The increased resistance in the pulmonary vascular system increased work (afterload) for the right ventricle which in turn causes right ventricular hypertrophy. A hypertrophied right ventricle is more subject to failure than a normal right ventricle. Prolonged increased tone of smooth muscle in the pulmonary arterioles leads to irreversible hypertrophy of the smooth muscle. At this point, making pulmonary hypertension irreversible. Correcting pulmonary hypertension = Nitric Oxide (NO) The nitric oxide counteracts hypoxic-induced vasoconstriction Metabolic function of the lung The type-2 alveolar cells make pulmonary surfactant. Pulmonary surfactant is essential for normal compliance of the lung. (easily open and normal ventilator conditions) In the lung, converting enzyme, converts inactive Angiotensin I to active Angiotensin II. Converting enzyme also converts bradykinin to an inactive metabolite. The lung makes immunoglobin A, which provides a defence mechanism against pulmonary infections. The upper airway secretes mucus which is essential for removal of inhaled particles The lung removes serotonin from the blood; some of this serotonin may be transferred to platelets. Prostaglandin E2 is a smooth muscle relaxant keeping the ductus arteriosus open during foetal life. The elevation of pulmonary and systemic PO2 which occurs when newborn begins to breathe causes contraction of the smooth muscle of the ductus arteriosus causing the ductus to close. If the ductus fails to close, inhibitors of prostaglandin synthesis (indomethacin) can be administered to facilitate closure of the ductus. (NEONATE RELATED) Oxygen and carbon dioxide transport Oxygen is bound to Hb (98.5%) and 1.5% in plasma. Capillaries transporting O2 and dissolving from Hb (diffusion)

5 Respiratory acidosis is caused by CO2 retention. If carbon dioxide accumulates it will react with water in the body to produce carbonic acid which ionises to hydrogen ions and bicarbonate ions. Accumulation of hydrogen ions causes a low blood ph, this can result in respiratory acidosis. In a spontaneously breathing pt, this occurs due to hypoventilation either from shallow breaths and/or a low RR. Respiratory causes: Chronic bronchitis, asthma, severe pneumonia, airway obstruction, airway swelling and foreign body airway obstruction (food, vomit etc). Non-respiratory causes: Head injuries/brain tumours, neuromuscular diseases, drugs, anaesthetics, sedatives and cardiac/respiratory arrest. Symptoms: Slow or difficult breathing, Headache, Drowsiness, Restlessness, Tremor, Confusion, Tachycardia, Changes in blood pressure, Swelling of the blood vessels in the eyes and Cyanosis. Counteract: This situation can be compensated by the kidneys increasing production of bicarbonate ions which are alkaline and therefore act as a buffer to neutralise the acidic effects of the excess carbon dioxide. Note: The body has substantial control over acid-base balance by altering alveolar ventilation and the elimination of CO2 through the lungs. The elimination of acid through the lungs is 100% more efficient than the elimination of acid through the kidneys. Respiratory alkalosis occurs when a pt hyperventilates and alveolar ventilation is increased as a result of large frequent breaths; CO2 decreases (due to excessive exhalation of CO2) in arterial blood, causing a decrease in hydrogen ions resulting in a rise in ph. Causes: pulmonary disease, stroke, severe anxiety (leading to hyperventilation) and high altitudes. Symptoms: dizziness, light-headedness and numbness of hands and feet. treatment: aims to elevate CO2 making the blood more acidic Metabolic Acidosis Defined by an arterial ph of less than 7.35 with a serum bicarbonate ion concentration of less than 22mmol/L (acceptable range is 22-26mmol/L). Distinguish between respiratory acidosis and alkalosis PaCO2 normal range is Value above = Acidosis Value below = Alkalosis Causes: severe diarrhoea, excessive production of acids, as in diabetic ketoacidosis, failure of the kidneys to excrete hydrogen ions and poor perfusion (induced by shock). Symptoms: most are attributed to cause of the acidosis however; Tachypnoea, Confusion, Lethargy, Depression of consciousness (which can lead to coma), Cardiac arrthymias, Severe metabolic acidosis can lead to shock or death may occur. Counteract: Depending on the severity of the episode, hyperventilation may help to elevate the blood ph and hence make the blood less acidic by exhaling excess carbon dioxide. Treatment: In a situation of acute metabolic acidosis, the main focus is the correction of the underlying cause, therefore it is best to avoid giving bicarbonate, even if the ph is below 7.1, as this can lead to metabolic alkalosis. When the underlying illness is treated the body will

6 Cardiogenic Shock Cardiac failure reduction in CO due to impaired ability to pump (cardiac contractility) Cause AMI (manifests when 40% or more of the left ventricle is ischaemic) Cardiac surgery Cardiac contusion/trauma Valve disease Cardiomyopathy Myocarditis Poisoning/drug overdose Signs low cardiac output (cardiac index <2.1 L/min/m2) hypotension severe pulmonary congestion high central vascular filling pressures (pulmonary artery occlusion pressure >18mmHg) Treatment optimise oxygen supply and demand (patient positioning, administer O2, CPAP/BiPAP and limit physical activity) Preload reduction relieves pulmonary congestion reducing myocardial workload and improves contractility which in part is impaired by overstretched ventricles. (patient positioning, IV diuretics, glyceryl trinitrate infusions, ultrafiltration and respiratory support) Inotropic therapy promotes myocardial contractility to improve cardiac output and BP. (dobutamine, dopamine, adrenaline, noradrenaline, vasopressin etc.) pg.694 Afterload control (with caution of not inducing further hypotension) oral ACE inhibitors should be introduced after stabilisation of cardiogenic shock