From digestion to transport
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Transcript of From digestion to transport
From digestion to transport
The transport system
Link to presentation used in class (supplemented by additional slides…)
• Stephen Taylor transport presentation
Syllabus details relating to BLOOD
• 6.2.6 State that blood is composed of plasma, erythrocytes, leucocytes (phagocytes and lymphocytes) and platelets
• 6.2.7 State that the following are transported by the blood: nutrients, oxygen, carbon dioxide, hormones, antibodies, urea and heat
Contents of blood
Cells and fragments found in blood
All cellular components originate from haemopoetic stem cells in the bone marrow
The ‘cells’and fragments of blood
Lymphocytes
Phagocytes – macrophage…
Phagocytes: neutrophils
The heart and how it works
Mammalian 4-chambered hearts develop from 3-chambered hearts
The cardiovascular system is a double circulation
The cardiovascular system is a double circulation
The CVS is a double circulation (3)
Systemic circulation
The systemic circulation
The pulmonary circulation
The pulmonary circulation
6.2.1: Draw a heart, labelling the 4 chambers, associated blood
vessels, valves and route of blood through the heart
Let’s draw a heart!
• Drawing a heart...
Control of the cardiac cycle
• control of the cardiac cycle• conducrtion system of the heart
Explain the basic cardiac cycle…
• Animation 1• slightly more detailed cardiac cycle
Control of heart rate
In order to understand control of heart rate, we need to understand WHY heart rate might
increase or decrease….Give me some reasons why heart rate might
increase or decrease?
The sino-atrial node is the major pacemaker of the heart
Heart rate and force of contraction are controlled by the medulla (brainstem)
• Cardio-accelerator centre – cardiac nerve: increases heart rate (epinephrine)• Cardio-inhibotory
centre – vagus nerve – decreases heart rate (Ach)
The medulla responds to many factors
An increase in carbon dioxide tension in the
blood is sensed by chemoreceptors in the
heart and carotid artery, and sent to the medulla
for processing…
The sino-atrial node is affected by both sympathetic (adrenaline/noradrenaline) and parasympathetic (Ach) fibres
Cardiac output
• Cardiac output = volume of blood pumped by the heart in L/minute.
• Cardiac output is is the product of HEART RATE (BEATS/MINUTE) and STROKE VOLUME (ML/BEAT)
• CO can be increased by means of increasing heart rate OR stroke volume
Tissue oxygen delivery:‘the bottom line’
• depends on cardiac output (cardiac function and forward flow) and arterial oxygen content (CaO2)
• Oxygen delivery (DO2) = cardiac output multiplied by the oxygen content of blood
DO2= CO X [Hb] X SpO2 X 1.34(each 1 g of haemoglobin can carry 1.34 g of oxygen)
Myocardial perfusion
myocardial perfusion occurs during diastole
• A high heart rate means less time for diastolic filling and myocardial perfusion
• A high heart rate increases myocardial work and increases myocardial oxygen requirement: the heart has to work harder’
Cardiac Output(intrinsic ability of heart)
Heart RateStroke Volume
(volume ejected/contraction)
Preload
ContractilityAfterload
Fluid Therapy
Venous blood volume
Sympathomimetics Depressant drugs
vasopressors
(-) DrugsHypothermia Vagal stim. Symp stim
(+)Anticholinergics Symp stimHyperthermia
Total peripheral resistance is resistance to blood flow
provided by the vascular bed• determined principally by
vascular tone • also affected by blood
viscosity and ventricular wall tension
arterial blood pressure is the PRODUCT of CO and total peripheral resistance
• If CO remains the same and afterload then BP rises
• If CO remains unaltered and afterload (e.g. acepromazine) then BP falls
Heart rate may affect cardiac output during anaesthesia
Heart rate can be influenced by MOST anaesthetic drugs:
• opioids• α2 agonists• inhalants• ACh inhibitors (anticholinergics)• barbiturates• ketamine
severe bradycardia (not compensated by changes in stroke volume) or severe tachycardia will reduce cardiac output
Severe tachycardia decreases cardiac output
• decreased preload (most of filling occurs in first half of diastole)
• decreased stroke volume
• decreased myocardial oxygenation potential (coronary arteries fill in diastole)
Catecholamine receptorsReceptor Location Principal effect
α1Smooth muscle - most vascular
arteriolessphincters of bladder and GIT
iris dilator
peripheral vasoconstriction
α2pre-synaptic sympathetic neuronsmultiple post-synaptic locations
Pre-synaptic inhibition of neurotransmitter release,
reduced sympathetic outflow
β1heart musclesalivary glands
fat tissue
cardiac – increased rate and force of contraction
β2bronchioles of lung, heart,
arterioles of skeletal muscles, brain and lungs
bladder wallGI tract
bronchodilationskeletal muscle vasodilation
cardiac effects