Cardiovascular Flashcards
(22 cards)
Close circulatory system
- heart
- blood vessels
- pressure
- pumping
- transport
Fluid in the circulatory system (blood) is separated from the interstitial fluid
Require a pump - heat:
The heart
Spit into two: the lungs (pulmonary circuit) and the rest of the body (systemic system)
- veins carry blood to the heart
- arteries carry blood away from the heart
Duel pump: one for deoxygenated (right) and one for oxygenated (left)
Had 4 chambers:
- 2 atria: receives blood and pumped it to the ventricles
- 2 ventricles: pumping blood on, into the arteries
Made of cardiac muscle (myocardium)
Left ventricles muscle thicker then right (needs to pump blood around the whole body).
Pathway of blood
In series
- right ventricle
- pulmonary artery
- pulmonary circuit
- pulmonary veins
- left atrium
- left ventricle
- aorta
- systemic circuit
- venae cava
- right atrium
- right ventricle
Parallel flow within the circuits
Blood travels through the aorta and the arteries branch off to reach only one organ at a time, so each organ gets oxygenated blood and nutrients
The live gets blood that comes from the digestive track to filter the content
Hear valves
Atrio-ventriclar valves - stop back flow of blood
- Right: tricuspid valve
- Left: bicuspid valve a.k.a mitral
Semilunar valves - prevent back flow from the artery into the ventricle
- right: pulmonary artery valve
- left: aortic valve
Cardiac muscle tissue
Strong pumping action - which must never cease.
Cell are smaller than cells of skeletal muscle and show branching and are interconnected - intercalated disks to allow ions to flow form one cell to the next, so can contract together as a unit.
Desmosomes - resist the stress of contraction so they don’t rip apart
Electrical activity of the heart
Self-excitable tissue:
- auto-rhythmic cells (pacemaker cells): about 1% of cardiac cells (other 99% contractile cells).
SA and SV nodes: pacemaker potentials.
Rhythmicity
SA node (sinoatrial node):
- kicks off the electrical activity in the atria
- sends signals to the second node.
Second node- AV node (atrio-ventricular node): helps with distribution of the excitation.
Conditions fibres:
- Bundle of His
- Purkije fibres
Cardiac cycle
Systole: contraction
Diastole: relaxation
4 phases of cardiac cycle:
- Ventricular filling: when pressure in the atria is higher then the ventricles, the AV valve opens.
- passive phase: no atria or ventricular contraction, blood is just trickling in with pressure gradient
- active phase: atria contract and push blood into the ventricles.
- Isovolumetric ventricular contraction: ventricles contract - increases pressure. AV and semilunar valves closed. No blood entering or exiting the ventricles.
- Ventricular ejection: as the pressure in the ventricles is greater then the pressure in the arteries the semilunar valve opens and blood get ejected into the arteries.
- Isovolumetric ventricular relaxation: ventricles relax which decreases the pressure. The AV and semilunar valves close. No blood entering or exiting the ventricles
Arteries and veins
Thick muscular walls, smooth muscle.
Splitting up in to smaller and small arteries then arterioles then network of capillaries (very thin walls, only one cell thick. Rings of smooth muscle regulate blood flow). Then venules then bigger and bigger veins. Less muscle than arteries.
Veins have valves to prevent back flow due to less blood pressure
Atherosclerosis - build up of fat in arteries - can for a blood clot.
Liquid tissue: the blood
Cells, nutrients and proteins transported in plasma.
O2 CO2 Amino acids Glucose and other sugars Vitamins Lipids Hormones, ions, fibrinogen, proteins (e.g enzymes, antibodies) Various breakdown products, especially urea (nitrogenous waste).
Red blood cells
Erythrocytes
No nucleus
Contain haemoglobin
Made in the bone marrow of big bones and are stimulated by a hormone called erythropoietin (EPO) - produced by the kidneys in response to low oxygen levels in blood.
Haemoglobin carriers oxygen - needs to interact with an iron ion
ECG: electro cardiogram
P = little spike: atrial depolarisation (electrical activity kicking off in the atrium).
R = big spike: Q R S is de-polarisation in the ventricle (electrical activity in the ventricle muscle cells).
T =medium spike: ventricular re-polarisation (resetting the electrical potential)
R-R = full cycle
A-T = estimate of duration of ventricular contraction
Pressure flow and cardiac output
Flow will proceed through the path of least resistance
Left and right side contract together. Heart rate (HR) is the beats per minute and influence cardiac output (measured in litres per minute).
Another influence is how much blood is pumped through by each contraction: stroke volume (SV).
For each contraction, a certain amount is ejected: cardiac output
HR * SV = CO
For each ventricle:
EDV (end diastolic volume) - ESV (end sistolic volume) = SV (stroke volume).
Control of cardiac output
Not caused y central nervous system, but it can still regulate rate and force of cardiac contractions.
Cardiac output under controlled of:
- neural control
- hormonal control
Both of these are known as extrinsic controls (from outside the heart).
- heart rate is increased by sympathetic nervous activity, or by adrenaline (and noradrenaline)
- heart rate is decreased by parasympathetic (day to day) nervous activity
- heart rate can be affected by hormones e.f adrenaline (epinephrine), similar to effects of sympathetic nervous system stimulation.
Factors influencing cardiac outputs: heart rate and stroke volume
Stroke volume affected by:
Ventricular contractions
- increase contractility - increase stroke volume
- sympathetic NS connects with ventricular myocardium - increase in ventricular contractility
- adrenaline can also stimulate increased ventricular contractility
EDV (end diastolic volume) Starling’s law of the heart:
- the more ventricles fill with blood, the more they contract (intrinsic control)
- EDV sometimes called ‘pre-load’ as it puts a load on the myocardium prior to contraction
Afterload:
-ventricles contract - pushing against arterial pressure (afterload).
Blood pressure - physics
- liquid in pipes
- pressure gradient (delta P). Heart site of highest pressure. Arterial walls stretch and recoil. Pulse. As blood vessels get smaller, resistance increases. Flow is inversely proportional to resistance.
- resistance (R): Poiseuille’s law - length viscosity and radii. Has to be flat and laminar flow. Controlled by vasoconstriction and vasodilation.
- depends on: length, diameter, bends of pipe, viscosity of liquid
MAP mean arteriole pressure = SP + (2* DP) / 3
Controls of regulation of blood pressure
Oscillation during each cardiac cycle
Smooth muscle in arterial walls - nervous and hormonal responses can cause vasoconstriction or vasodilation - diameter change - (TPR)
Often coupled to changes in cardiac output
Local signals for vasoconstriction and vasodilation
Nitric oxide (NO) gas: major vasodilation inducer (also known as EDRF).
Endothelin (polypeptide): vasoconstriction inducer
Baroreceptors
Convey information about:
- MAP
- pulse pressure
- change in pressure over time.
Located at strategic points:
- aortic arch
- sinuses of carotid arteries (neck).
When pressure drops it sends signals to hypothalamus, adrenal medulla and kidneys
Hormonal effects
Adrenaline: alpha and beta. Low levels only bind beta receptors.
- in most tissue: mostly alpha receptors on blood vessels - vasoconstriction
- in heart and skeletal muscle: beta - vasodilation
ANP (atrial natriuretic peptide) - prompts sodium loss in the urine, water follows by osmosis, less stretch in the atria. Made and stored in the heart.
ADH (anti-diuretic hormone) - against losing a lot of water. Pituitary. Reabsorb water
RAAS (rennin-aldosterone-angiotensin system. Renin is an enzyme. Angiotensinoven large molecules circulates in the blood (inactive). If pressure drop, kidneys release renin. Renin in the blood chops off bit of angiotensin and product called angiotensin 1.
Conversation of angiotensin 1 to 2 by ACE (found in lining of blood vessels). Angiotensin 2 causes vasoconstriction and activation of aldosterone (from adrenal gland), which makes the kidneys retain more salts and water. It make you thirsty.
Hypertension
Optimum range is higher
Stiff arterial walls - less sensitive
Treatment is ACE inhibitors
