cardiovascular system

functions of the circulatory system

• distribution of dissolved gases and other molecules for nutrition, growth and repair, aste removal

• chemical signalling to cells by means of circulating hormones

• mediate inflammatory and host defense responses against invading microorganisms, transport clotting factors

• conserve or release heat near skin surface

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aorta

• oxygenated blood coming out of the heart

parallel circuit

• blood returns to right atrium via superior and inferior vena cava, pumped out of the right ventricle to the lungs via pulmonary arteries

• returns to heart via pulmonary veins, enters the left atrium, pumped out of the left ventricle to the body via aorta

hat affects blood flo?

• decreases ith increased resistance

  • idth, viscoscity, length

• increases ith increased difference in pressure

cardiac output

the heart pumps out 5L per minute

blood per beat x beat per minute

flo is the same throughout the entire system if e take a cross section, this flo is divided by e.g. no. of arterioles. if you constrict one, the proportions change, ie more bloodflo through other arterioles

tone

• tone in smooth muscles of blood vessels, basal state of muscle contraction

• adjust from here

• affected by the SNS and local factors, endothelin, myogenic activity, NO

myogenic activity

• reflex within the smooth muscle of arterioles

• pressure of blood is different in different parts of the body due to eight of blood, changes ith changing posture

• in places ith higher pressure (e.g. foot arteriole during standing), the arteriole ill stretch a bit initially, reflex ill cause constriction to protect capillaries

• epithelial sodium channel (ENaC) is a pore that allos Na+ to go through, hen the arteriole stretches, the pore opens and Na+ flows into the muscle cells and depolarises them and allos them to constrict

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NO

vasodilator

endothelin

vasoconstrictor released from the endothelial cells in response to a variety of chemical and physical signals

highest to loest pressure

• aorta

• arteries

• capillaries

• veins

• venae cavae

affect of pressure gradient on flow

• blood moves from high pressure to lo pressure, flo is proportional to pressure difference

1 and 3, highest pressure difference. overall pressure makes no difference

pressure gradients in blood vessels

• pressure is lost due to friction

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here does blood have its loest velocity?

• capillaries

• velocity is inversely proportional to cross sectional area, velocity = flo/CSA

• capillaries have the highest CSA

• if something is thin, to reach 5L/minute, it has to flo faster, if something is thick, to reach this flo, it can flow slower

• good for facilitating exchange

velocity vs cross sectional area

blood vessel structure

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arteries

• a lot of elastic tissue, compliant to stretch to allow blood to enter from the heart, then elastically recoils to push the blood forard

• arteries hardening means you lose that elastance

• a lot of fibrous tissue to strengthen them as they receive blood at a high pressure from the heart

dissection of the aorta

• blood gest in beteen the layers of the arterial all, separates the layers and it balloons out

veins

• less elastic

• ider

• expand easily - reserve, most of the blood is in the veins

• extra capacity: SNS can constrict these veins and push the blood back out into arterioles during exercise

capillaries

• fenestrated

• single cell

• most cell ithin 0.1 mm of the nearest capillary

• vesicular transport

• interstitial fluid between cells and capillaries

bulk flow

• overall/mass movement of fluid and everything it contains between blood and interstitial fluid

• filtration at the arteriole end and absorption at the venous end

• direction of flow determined by osmotic pressure (solute conc) and water pressure

absorption

• fluid movement from interstitium into capillaries

filtration

movement of fluid out of the capillaries into interstitium

oedema

intersitital fluid accumulation

osmotic/oncotic pressure of blood in capillaries

proteins (albumin exists only in the blood and not in the intestitial fluid). this favours absorption (pulling fluid back into the capillaries)

hat pressures influence direction of flo (bulk flo)?

• the balance of osmotic/oncotic pressure and hydrostatic pressure

Starling Forces

• more hydrostatic pressure in the capillary

• more oncotic pressure in the interstitial space

• at arteriole end, the hydrostatic pressure is higher, as e move through the capillary it decreases due to friction

• oncotic pressure stays the same across the capillary (albumin conc stays the same)

• hen hydrostatic pressure > oncotic pressure, fluid flos out of capillary

• hen hydrostatic pressure < oncotic pressure, fluid flo in

starling forces pressure changes diagram

endothelium

• thin, single-cell layer lining the interior of blood vessels hich serves as the interface between the blood and the rest of the vessel wall

metabolic factors hich determine vasomotor tone

• arterioles are responsive to local factors such as carbon dioxide, oxygen, lactic acid and heat

chemical mediators hich regulate vasomotor tone

• nitric oxide

• endothelin

• angiotensin II

• vasopressin

• noradrenaline

• adrenaline

• histamine

angiotensin II

vasoconstrictor produced by the Renin Angiotensin System

vasopressin

• also knon as anti-diuretic hormone

• vasoconstrictor involved in fluid balance

adrenaline

• released from adrenal glands

• vasodilator at lo doses and a vasoconstrictor at high doses

histamine

causes vasodilation

hydrostatic pressure in the capillaries

As plasma travels along the capillary from the arterial to the venous end, capillary hydrostatic pressure decreases. This is due to volume loss resulting from filtration, and energy loss due to friction and resistance inside the capillary.

oncotic pressure

osmotic gradient resulting from albumin, a large protein hich cannot filter from capillaries to ICF, unlike the other solutes in the plasma

imbalance in Starling Forces

• there is a natural imbalance in these forces with filtration slightly exceeding absorption.

• over the course of a day, this leads to approximately 3L of fluid which is filtered but not absorbed.

• Since plasma volume is only 5L, this needs to be reabsorbed somehow

role of the lymphatic system to compensate for Starling Forces

• absorbs excess fluid from filtration and drains it back into the bloodstream

oedema

• pathological imbalance in the Starling Forces

• leads to buildup of fluid in the ISF

• leads to an area of the body appearing sollen

factors that cause oedema

1. increased capillary hydrostatic pressure leading to increased filtration

2. decreased capillary oncotic pressure reducing absorption

3. interference ith the lymphatic system, blocking uptake of excess ISF

increased capillary hydrostatic pressure

• e.g. heart failure which increases venous pressure

• left heart isn’t pumping as ell as it should to clear the pulmonary circulation and thus it gets a buildup of pressure in the capillaries

• this causes pulmonary oedema

• one of the first signs of heart failure is difficulty breathing due to this fluid buildup in the chest

• now the right heart fails as it is pumping against an increased pressure, then results in oedema in the periphery (ankles and legs)

• can also result from prolonged inactivity, which leads to a buildup of fluid in the peripheries

decreased capillary oncotic pressure

• malnutrition

• if a person is severely protein deficient, they will have less albumin in their blood

• e.g. Kwashiorkor

disruption to lymphatic system

• lymphoedema: oedema caused from blockage of lymphatic system

• e.g. obstruction of lymph nodes by parasites or cancerous cells

• e.g. mastectomies - removal of a breast generally due to cancer causes oedema in the arm and shoulder. breast tissue contains a lot of lymphatic tissue and the surgery can disrupt that

hat factors favour filtration?

• capillary hydrostatic pressure (strong force)

• interstitial fluid oncotic pressure (small force)

hat factors favour absorption

• interstitial fluid hydrostatic pressure (small force)

• plasma oncotic pressure (strong force)

treatment of pulmonary or peripheral oedema

• diuretics

hat organ makes albumin?

• liver

• liver failure can result in oedema (hard belly)

heart anatomy

• apex at the bottom, base at the top

• between the atria and the ventricles is fibrous connective tissue

• valves between atria and ventricles

• valves between the ventricles and the arteries

• pulmonary artery from right heart

• aorta from left heart

• blood returns to the atria, then enters the ventricles, then pumped out from there

hy does the right ventricle have less muscle mass?

• pulmonary resistance is less than systemic resistance

ventricular systole

contraction of the ventricles

ventricular diastole

relaxation of the ventricles, filling ith blood

conduction system of the heart

• autorhythmic cells in the sinoatrial node and the atrioventricular node

• signal originates in the SA node (pacemaker) and passes through the atria, spread through atrial myocytes to cause a contraction of the atria

• insulated connective tissue beteen the atria and the ventricles, the only ay the electrical current can pass into the ventricles is through the AV node

• spreads out through the bundles of His and then the Purkinje fibres to the ventricular myocytes

AV node

• AV conduction time: a little delay at the AV node before it releases the signal through the bundle of His

• compensates for the slo movement of blood, allos for the ventricles to fill ith blood after the atria contract

• the AV conduction time decreases ith increased heart rate, stroke volume therefore decreases as e decrease ventricular filling time

damage to SA node

• AV node can take over

• speed of SA node is 70 bpm, AV node is therefore driven at 70 bpm in normal conditions

• however if you remove the SA node, the AV node ill take over but at 50 bpm

bundles of His

• carry the signal don the intraventricular septum

• delivers signal to the apex to allo the AP to spread back upards from there

Purkinje fibres

• stimulate cells in the ventricles (more Purkinje fibres in the left ventricle)

electro-cardio-gram (ECG)

• an indicator of hich direction the electricity is travelling (vectors of depolarisation)

• body surface recording

• usually have 11 leads to give you a 3D picture of electrical conduction in the heart

lead II

• rhythm strip

• negative electrode on the right rist, positive on left ankle: this diagonal vector from top right to bottom left is in line with the position of the heart. any time a signal is travelling this ay, there will be an upward inflection on the ECG

• measurement of direction not amplitude

• depending on how well aligned the signal is with this vector, the greater the ECG inflection

how does an ECG work?

• 3 major waves: P wave, QRS complex and the T wave

P ave

• signal starts at SA node and travels to the left (causes an upward inflection)

plateau after P ave

• atrial depolarisation

• hen signal stops at AV node

• time = AV conduction time

QRS complex

• ventricular depolarisation

• signal travels down left and right bundle of His. left bundle fires slightly earlier than right, movement from left to right, so slight donard inflection on ECG

• movement across Purkinje fibres, bigger signal moving to left than right as more Purkinje fibres in left heart, causes upard inflection on ECG

• then signal moves up walls of ventricles toards base (up and to the right), causes donard inflection

T ave

• ventricles repolarisation

• travels from apex to base, but since it’s an opposite electrical signal (becoming more negative), the inflection is upards

atrial repolarisation

repolarise, but during the QRS complex so not visible on the ECG

hat can you see on an ECG?

• R-R interval = heart rate

• doctors ill check that all aves are there, if the rhythm is regular, etc

hat increases heart rate variability?

• pathological conditions

• alcohol

• chronic stress

atrial fibrillation

• atria do not contract as a unit

• usually not a problem as the majority of ventricular filling happens passively, the atrial contraction only squeezes the last bit out

• only issue is if blood gets caught in pockets in the atria, it can turn into clots hich can enter the coronary artery and cause a stroke

ventricular fibrillation

• ventricle beating on its on from pacemakers in the ventricular muscle, perhaps caused by damaged muscle

• need a defibrillator to restore normal rhythm

• shocks cells simultaneously to cause them to fire APs simultaneously and come back into rhythm together

treatment for atrial fibrillation

• blood thinners to prevent stroke risk

• however, in younger people can be caused by rogue cells at base of pulmonary artery which fire spontaneously and throw off the atria, so e can ablate these cells

STEMI

• orst kind of myocardial infarction

• elevation beteen S and T

• insult to heart muscle is transmural - goes through entire all of the ventricle

hen do clots end up in the brain (Stroke)?

if they originate in the left heart (unless you have a hole in beteen your ventricles, then clot from periphery can reach brain)

clots from periphery

• ill end up in the capillaries of the lungs

hat is the abnormality?

• the AV node is blocked, not allowing consistent passage of signals to the Purkinje fibres

• the electrical signal does not pass through AV node every time, so the QRS complex only happens every so often hen it does pass through

valvues in the heart

• beteen atria and ventricles (atrioventricular)

• beten ventricles and arteries (arterioventricular)

mitral/bicuspid valve

beteen left atrium and ventricle

tricuspid valve

right atrium and right ventricle

aortic valve

pulmonary valve

ho do valves ork?

• one ay valve, if pressure is higher in atrium than ventricle, the AV valves are pushed open

• hen pressure in ventricle gets high, these valves close and the arterial valves open

• if the pressure in the artery > ventricles, these valves close

• ensures one ay flo

chordae tendinae

• connect to papillary muscles

• prevent prolapse of the valve, anchor it to apex of the heart

• hen the pressure of the ventricle increases, the AV valves do not pop back up

papillary muscles

• shorten and tist hen the ventricles contract, pull don on the cords to prevent the valves from prolapsing

ventricular systole

• contraction

• mitral valve closes

• aortic valve opens

heart sounds

• occur when heart valves close, sudden turbulent flow hits the valve, vibration

• sound 1: closure of AV valves

• sound 2: closure of semilunar valves

• sound of turbulent flo hitting the valve not the sound of the valves

Wiggers Diagram

• majority of ventricular filling before atria contracts

• first heart sound hen atrial pressure = ventricular pressure (valve shuts)

• second heart sound hen left ventricular pressure = aortic pressure for the second time (valve shuts)

• isovolumic contraction: both valves are shut, heart is contracting, before ventricular pressure exceeds aortic pressure

• isovolumic relaxation: beteen dicrotic notch and second overlap beteen atrial and ventricular pressure

systole and diastole of blood pressure

• lowest vs highest point of pressure in the aorta

hat causes the movement of blood?

• heart (source of energy)

• gravity

• skeletal muscle

• diaphragm movements

• elastic tissue of the arteries

systolic BP

• max pressure exerted in arteries when blood is ejected into them during systole (heart contracting phase)

diastolic BP

• min pressure ithin arteries hen blood draining off into remainder of vessels during diastole (heart relaxing/filling phase)

• managed by tone in blood vessels

pulse pressure

• difference between systolic and diastolic BP

• pressure exerted by the heart

mean arterial pressure (MAP)

• average pressure responsible for driving blood foard into tissues throughout cardiac cycle

• important for set point

• MAP = diastolic BP + 1/3 pulse pressure)

MAP

• light pink line

• essential for efficient function and life

lo BP

• dizziness, organ failure

high bp

• causes stroke, aneurysm, kidney failure

• caused by age, obesity

hat is more dangerous for older people, high or lo blood pressure?

• lo BP as it increases fall risk

hat determines MAP?

• ho much blood is pumped out per unit time (cardiac output)

• ho difficult/easy it is for the blood to move through the system

• MAP = CO x TPR

ho to increase BP

• vasoconstriction (TPR) and increased cardiac output

TPR

the resistance of the peripheral circulation

hat determines CO?

• heart rate x stroke volume

• average 5L/min at rest