Cardiovascular Flashcards
(42 cards)
Describe the central neural control of the cardiovascular system reflexes
Cortical influences- emotion
Complex reflex patterns originate in nuclei in the brain- exercise, feeding/satiety, alerting, thermoregulation, reproduction
Simple reflexes originate from the medulla
Reflexes also influence catecholamines, vasopressin, renin I angiotensin system
Describe the autonomic supply of the CVS
Rostral ventrolateral medulla (RVLM)- nucleus, organotopically organised- descending excitatory activity to T1➡ L1-2- increases HR via beta1 receptors, stimulates adrenaline secretion, and vasoconstriction
Vagus- decreases HR via muscarinic receptors
Describe the baroreceptor reflex pathway
Decrease ABP, decrease baroreceptors firing
Input from CN 9&10 to nucleus tractus solitarius
➡ inhibit nucleus ambiguus less
➡ inhibit RVLM less
Increase HR and vasoconstriction
➡ inhibit SON and PVN➡ inhibit pituitary less➡ ADH release
What are the functions of the baroreceptor reflex
Continuously buffers changes in ABP
Increase during exercise, coughs, sneezes
Decrease during standing up, dehydration or haemorrhage , digestion, thermoregulation in high temperature
Describe the atrial stretch receptor reflex
Decrease blood volume- decrease afferent activity to NTS➡ paraventricular nuclei➡ increase sympathetic activity to kidney via a pathway that by bypasses RVLM and via renal nerves from the RVLM➡ increases renal vasoconstriction➡ decrease GFR➡ renin➡ angiotensin➡ ADH➡ increase blood volume
Describe the 2 main mechanisms that regulate the respiratory influence on the heart
Central nervous mechanisms- central insoiratory drive (CID) excites the phrenic nerve and inhibits the nucleus ambiguus decreasing vagus influence in the heart increasing HR
Reflex from pulmonary stretch receptors- inspiration➡ pulmonary stretch receptors➡ NTS➡ inhibit nucleus ambiguus➡ decrease vagus➡ increase HR
Briefly describe the two reflexes from peripheral chemoreceptor stimulation?
From hypoxia
When respiration cannot increase- primary cardiovascular reflex response to chemoreceptor stimulation dominates to decrease HR, vasoconstriction (except brain) to conserve oxygen
When respiration can increase- effects of increase respiration increases HR
When might someone get systemic hypoxia when respiration cannot increase?
Under muscle relaxant- ventilated at a constant rate and depth
High spinal transection
Long dive underwater
Fetus in utero
Severe respiratory disease
Superimposed upon local effects of hypoxia- decrease HR and contractility, cerebral, muscle and coronary vasodilation, pulmonary basic instruction (pulmonary oedema, right ventricular failure, systemic oedema)
When might someone get systemic hypoxia when respiration can increase?
Hypoxia atmosphere
High altitude
Less severe respiratory disease
Increase in respiration and heart rate plus vasocontriction in GIT, kidney, helps to restore PaO2 so systemic tisdures do not become as hypoxic and pulmonary vasoconstriction is less severe
Describe the diving reflex
Reflex evoked by trigeminal receptors
Cold water on face/nose
Inhibition of central inspiratory neurones➡ expiratory apnoea and decrease HR, vasoconstriction
O2 conserving
Clinically receptors stimulated by sinus washing, irritant vapours, intubation, lumps of food in the pharynx
Describe the changes in oxygen consumption in dynamic exercise
Requires an increase in ventilation and cardiac input
O2 consumption is graded with work load up to a maximum the anaerobic threshold
Recovery after exercise to repay the oxygen debt
Describe the change in cardiac output with dynamic exercise
Heart rate increases in a graded manner with graded dynamic exercise up to a max ~220 beats/min minus age
Increase SV is dependent on contractility and venous return which is greater when supine with the skeletal muscle pump and respiratory pump
Greater proportion of output goes to skeletal and cardiac muscles at the expense of the viscera- muscle contraction interferes with vasodilation
Describe the local effects of exercising muscles on the cardiovascular and respiratory system
Exercise hyperaemia- local vasodilation
K, P, adenosine released by muscle into interstitial space
Graded with exercise intensity
PGI2, NO from endothelium
Causes relaxation of vascular smooth muscle
Counteracted by mechanical influence of contracting muscles
What is the exercise reflex?
K, P and adenosine released stimulate metaboreceptors
Joint receptors are also stimulated in dynamic exercise
Reflex tachycardia
Metaboreceptors➡️ medulla ➡️subthalamic locomotor region (hypothalamus) the exercise integrating area
Increase motor activity to diaphragm and intercostal muscles to increase respiration, increase sympathetic and decrease parasympathetic to the heart
Increase sympathetic noradrenergic activity- Reflex vasoconstriction in GIT, kidney, skin and all skeletal muscles
Via connections with central respiratory neurones, cardiac vagal motor neurones and RVLM to sympathetic pre-ganglionic neurones
Describe the central command involved in dynamic exercise
Subthalamic locomotor region (SLR) in the hypothalamus
Exercise integrating area received inputs from the cortex
Result in increase respiration, HR CO and vasoconstriction in GIT
Also increase set point of baroreceptors
Describe static exercise
Metabolites get trapped in the contracted muscle and cause greater stimulation of metaboreceptors
Exercise reflex is greater of a given work load than during dynamic exercise
Large increase in ABP
Exercise hyperaemia occurs after static exercise
Time limited- fatigue occurs relatively quickly
Oxygen delivery is limited
Carries cardiovascular risk
Describe hypoxia due to altitude in humans
Tolerant until 60mmHg or 8kPa of oxygen in blood- when desaturation starts
Symptoms start to appear when blood is less than 90% saturated eg. Loss of visual acuity then postural stability iand recall and reaction time decreases under 80%
What are the acute responses to altitude?
Low PO2 stimulates peripheral chemoreceptors leading to ventilation (which is opposed to varying degrees by hypoxia depressing respiratory centres
Hyperventilation causes a fall in PaCO2➡ hypocapnia and rise ikn pH (respiratory alkalosis)➡ inhibition of peripheral and central chemoreceptors➡ slight fall in total ventilation- reduces the response too hypoxia
Fall in CO2 also means that oxygen delivery to tissues is not as efficient as Hb affinity for ocyhgen increases
Loss of CO2 can also cause Cheyne-Stokes respiration while asleep
However hyper ventilation is necessary to reduce the risk of severe hypoxia by decreasing the space taken up by CO2 in the alveoli and keeps the partial pressure of the gases as high as possible for effective diffusion
Describe the cardiovascular response to altitude
Tachycardia caused by hyperventilation by action on the nucleus ambiguus
Reduce peripheral resistance raises tissue perfusion
Cerebral blood flow- vasoconstriction due to the altitude induced hyperventilation- very response I’ve to CO2 but not O2- severe hypoxia leads to vssodilation
Pulmonary circulation- hypoxic vasoconstriction helps V/Q- promotes blood flow to the best alveoli
What is mountain sickness?
Headache above 2500m plus: dizziness, irritability, vomiting, nausea, sweating, breathlessness, insomnia, fatigue
Thought to be caused by cerebral oedema- hypoxia dilation increases cerebral capillary filtration pressure and hypoxia induced increased permeability
Pulmonary oedema- uneven hypoxia vasoconstriction of pulmonary vessels leading to pulmonary hypertension, increased capillary permeability- protein leakage
Treated by supplementary oxygen and reducing altitude
What are chronic responses to high altitude?
Adaptive and alcclimatization
Body compensates for low PO2 and improve O2 delivery to tissues
Hyperventilation increases again as the altered pH is restored (HCO3 moves away from the CSF to resdtore cerebral pH and metabolic compensation for respiratory alkalosis decreased HCO3 reabsorption and H secretion) which leads to 2,3 DPG production to decrease O2 binding affinity, and peripheral chemoreceptor sensitivity increases
Also the O2 carrying capacity in blood is increased by increased EPO, increased RBC count and Hb conc
More pulmonary capillaries open
HR increases but SV decreases so CO is restored
Angiogenesis, increased cytochrome oxidase, increased myoglobin content in sketal muscle in tissues
Describe calcium channel blockers as vasodilators
Stop influx of calcium to the smooth muscle cell of the vessel and initiating contraction
Dihydropyridine (DHPs) eg. Nifidipine, nimodipine
L-type channel blockers
Used in angina for coronary vessel walls and systemic vessels (more constriction in veins)
Peripheral vascular disease- Raynaud’s sydrome- extreme basic instruction in extremities
May have use for improved cerebral function after a stroke or in dementia
Side effects- flushing and decreased GIT activity
Describe K channel blockers as vasodilators
Open K channels to allow K efflux and causing the hyperpolarisation of the cell
Eg. Minoxidil, cromakalim
Work by ATP-modukated K channels (K(ATP))
Primarily arterial effects to reduce total peripheral resistance
Used in severe hypertension only as there are more side effects- headache/flushing, tachycardia, oedema
Describe organic nitrates as vasodilators
Eg glyceryl trinitrate (GTN)
Work by releasing NO to upregulate guanylyl cyclase
Used in angina, coronary vessels and systemic circulation (more constriction in arterioles)
Side effects- excess vasodilation- hypotension, refelkx tachycardia, headache
Administered sublingually or transdermally for prophylaxis
Other egs. Isosorbide mono/dinitrate
Amyl nitrate (Poppers)- tolerance
Sodium nitroprusside- NO release to increase cA/GMP- used in hypertensive emergencies
