Cardiovascular Flashcards
Why do we need a CVS?
Pump blood through lungs & carry oxygen, Transport nutrients to muscles & organs, Circulates hormones & immune mediators, Connection to lymphatic system, Human Reproduction, Temperature Regulation
Fick’s Law (of Diffusion)
The time needed to diffuse a given distance is proportional to the square of the distance. t ∝ d²
Deoxygenated Blood Circulation
Blood returns to the heart, from the veins, via the right atrium and is pumped through the lungs by the right ventricle.
Oxygenated Blood Circulation
Blood returns to the heart, from the lungs, via the left atrium and is pumped through the body by the left ventricle.
Pulmonary Circuit
The pathway of deoxygenated blood through the heart, to the lungs.
Systemic Circuit
The pathway of oxygenated blood, out from the heart, towards the rest of the body.
Vein
A blood vessel that carries blood to the heart, from other parts of the body.
Artery
A thick blood vessel that carries blood from the heart to other parts of the body.
Systole
The contraction or period of contraction, of the heart, in which blood is forced into the aorta and pulmonary artery.
Diastole
The phase in which the heart relaxes, between contractions; specifically the period when two ventricles are dilated, by the blood flowing into them.
What drives blood flow?
Output of blood at high pressure creates a pressure difference with the distant blood vessels. The Pressure difference drives blood flow.
Typical Resting Blood Pressure
120/80 mmHg
Cardiac Output
The volume of blood expelled/ejected by either ventricle of the heart, per unit of time (per min). (usually refers to the left ventricle output)
Cardiac Output = Heart Rate x Stroke Volume
Maximum Heart Rate
220 - Age
How do you control blood flow?
Controlling the resistance of the vessels gives some control of blood flow.
Blood Flow
Blood flow = (Pa - Pv) / Resistance (increased resistance = lower blood flow)
Blood flow is…
1) Proportional to pressure across blood vessel
2) Inversely proportional to resistance of blood vessel
Difference in pressure of the Systemic and Pulmonary Systems
High pressure for systemic circulation, to pump blood around the body. Low pressure for the pulmonary circulation system to allow gas exchange.
4 main functional groups of blood vessels
Arteries, Arterioles, Veins & Venules, Capillaries
Arteries
Elastic vessels: Accommodate stroke volume convert ejection into continuous flow
Arterioles
Resistance vessels: Control arterial BP and regulate local blood flow
Veins & Venules
Capacitance Vessels: Control filling pressure of the heart and provide a reservoir of blood
Capillaries
Exchange Vessels: Nutrient Delivery to cells tissue water and lymph formation removal of metabolic waste
Clinical Significance of Cardiac Output
Myocardium (muscular tissue of the heart) & brain are relatively under perfused. This creates potential clinical problems e.g. Angina, MI, stroke triggered by relatively moderate fall in perfusion. Cardiac Output and blood flow needs to be carefully controlled.
Where is the main drop of pressure in the pressure profile of circulation?
Arterioles, just before the capillaries. This drop in pressure and then the continuous fall in pressure creates a pressure difference. That is what actually drives the flow.
Why does blood slow down in capillaries?
The total cross-sectional area increases, due to the increase in the number of capillaries. This slows down the blood, because the flow is the same, therefore, the velocity will be inversely proportional to the total cross-sectional area.
How do you calculate blood velocity?
blood flow / TOTAL cross-sectional area
What is the advantage of blood flow being slower in capillaries?
It allows gaseous/nutrient exchange to occur.
Where is the greatest volume of blood located, when distributed?
Systematic Veins and venules serve as a reservoir, holding 65% of volume.
Structure of Blood Vessel Walls
Sympathetic nerves in the tunica adventitia release noradrenaline, which stimulates α1 receptors leading to vasoconstriction.
Endothelium releases nitric oxide which relaxes the vessels leading to vasoconstriction.
Sinoatrial Node
A group of cells located in the wall of the right atrium.
Ability to spontaneously produce an action potential, that travels through the heart vis the electrical conduction system. Sets the rhythm of the heart and so it is known as the heart’s natural pacemaker. The rate of action potential production (and therefore the heart rate) is influenced by nerves that supply it.
Atrioventricular Node
Part of the electrical conduction system of the heart. Electrically connects the right atrium and the right ventricle, delaying impulses that atria have time to eject their blood into ventricles before ventricular contraction.
What is the resting potential of the cell?
Resting negative voltage in the cell interior, as compared to the cell exterior. It ranges from -40mV to -80mV.
Depolarisation
The reduction of the membrane’s resting potential, so that it becomes more positive and less negative.
Repolarisation
A change to the membrane’s potential, after depolarisation, so that it returns to its resting potential.
P wave
Atrial depolarisation and contraction
PR Segment
AV Nodal delay
QRS Complex
Ventricular depolarisation contraction (atria repolarising simultaneously)
ST Segment
Ventricles contracting and emptying
T Wave
Ventricular Repolarisation
TP interval
Ventricles are relaxing and filling
Cardiac Diastole
All chambers are relaxed and blood flows into the heart
Atrial Systole, Ventricular Diastole
Atria Contract, pushing blood into relaxed ventricles.
Ventricular Systole, Atrial Diastole
After the atria relax, ventricles contract, pushing blood out of the heart.
Lub
Closure of tricuspid/mitral valves at the beginning of the ventricular systole
Dub
Closure of aortic/pulmonary valves (semilunar valves) at end of ventricular systole
Blood Flow Equation
Blood Flow (CO) = Blood Pressure/ Total Peripheral Resistance
Heart Rate & Contractility
SA Node pacemaker also sympathetic and parasympathetic nerves control heart rate. The strength of the contraction is due to sympathetic nerves and circulating adrenaline increasing intracellular calcium.
Preload
Stretching of heart at rest, increases stroke volume, due to Starling’s Law
Afterload
Opposes ejection, reduces stroke volume, due to Laplace’s Law
Starling’s Law
Energy of contraction of cardiac muscle is relative to the muscle fibre length at rest.
Greater stretch of ventricle in diastole( blood entering), then greater energy of contraction and greater stroke volume achieved in systole.
Central venous Pressure
mmHg end diastole pressure or filling pressure
Molecular Basis SL- Unstretched Fibre
Overlapping actin/myosin, Mechanical inference, Less Cross-bridge formation available for contraction
Molecular Basis SL- Stretched Fibre
Less Overlapping actin/myosin, less mechanical inference - potential for more cross-bridge formation, increased sensitivity to Ca2+ ions
Effects of Starling’s Law
Balances outputs of the right ventricle and left ventricle!!!
Fall in cardiac output during a drop in blood volume or vasodilation( e.g. haemorrhage, sepsis)
Restores cardiac output in response to intravenous fluid transfusions.
Responsible for fall in cardiac output during orthostasis (standing for a long time) leading to postural hypotension & dizziness as blood pools in legs.
Contributes to increased stroke volume & cardiac output during upright exercise.
Afterload (explained)
Afterload opposes the contraction that ejects blood from the heart and is determined by wall stress directed through the heart wall. Stress through the wall of the heart prevents muscle contraction.
Laplace’s Law
Describes parameters that determine afterload. Wall tension (T), pressure (P) and radius (r) in a chamber
T∝Pr
Wall stress equation linked to LL
S (Wall stress)= T (wall tension)/ w (wall thickness)
S= Pr/ 2w
How do you increase afterload?
Increasing pressure and radius
How do you decrease afterload?
Increasing wall thickness
Why does radius affect wall stress/afterload?
Small ventricle radius •Greater wall curvature •More wall stress directed towards centre of chamber •Less afterload •Better ejection Larger ventricle radius •Less wall curvature •More wall stress directed through heart wall •More afterload •Less ejection Huge theoretical radius •Negligible wall curvature •Virtually all stress directed through wall
Importance of LL
Opposes Starlings Law at rest, Facilitates ejection during contraction, Contributes to a failing heart at rest and during contraction
