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