CO and blood pressure (wk7) Flashcards
Describe the basics of cardiac output
-What is it and what does it depend on?
- Cardiac output is the volume of blood that is pumped out by the heart every minute.
- The correct abbreviation for cardiac output is (Q with a dot above)
- Cardiac output is measured in ml or l, so the units are ml.min-1 of l.min-1
- Cardiac output depends on heart rate (beats per minute) and stroke volume (volume of blood ejected per meat in ml or l).
- Cardiac output is calculated from: cardiac output = heart rate x stroke volume
Cardiac output
-Abbreviation, units and typical values
-Complete table from 07/11
Control of HR
-The role of the autonomic system and hormones
- Parasympathetic nerve endings (known as vagus nerve) secrete the neurotransmitter acetylcholine, which slows heart rate. Parasympathetic stimulation is concentrated to the atria, at the SA and AV nodes. The parasympathetic stimulation slows down the heart rate and releases acetylcholine to do this.
- Sympathetic fibres (known as cardiac nerves) supply the SA and AV nodes, and increase HR by releasing norepinephrine. It releases norepinephrine on beta receptors which stimulate the SA and AV nodes which increases the HR
- Circulating epinephrine also triggers an increase in heart rate but lags behind neural stimulation.
Control of HR
-Pacemaker cell changes
-Pacemaker cell changes -> The threshold potential line is a drifting line which is different from the flat line in other cells. This means that there will always be an eventual stimulation. There are fewer stimulation on the above graph which shoes the slower heart rate.
Control of HR
-Pacemaker cell changes + parasympathetic and sympathetic stimulation
- Parasympathetic stimulation of the SA node cells cause their membranes to become more hyperpolarised, and the depolarising drift to become slower. As a result the SA node rhythm becomes slower and heart rate decreases.
- Sympathetic stimulation of the SA node cells cause their membranes to become more depolarised, and the depolarising drift to become faster. As a result the SA node rhythm becomes faster and heart rate increases. It also: shortens the AV node delay, shortens myocyte action potential and increases speed of relaxation
Control of stroke volume
-Length-tension relationship in cardiac muscle
Stroke volume is regulated by 2 opposing factors: The force by which the muscle cells contract and, The arterial pressure against which they have to eject the blood. In turn, the force of contraction is regulated by 2 processes: The length-tension properties of cardiac muscle cells, and The effects of hormonal influence on the contractility of cardiac muscle.
Control of stoke volume
-The greater the stretch of the cardiac muscle fibres, the greater the force of the contraction. The length-tension relationship is the relationship between end-diastolic volume and stroke volume, which is controlled by Starling’s Law. End-diastolic volume can be increased by greater filling of the heart (venous return). This leads to greater stroke volume because stretching cardiac muscle fibres causes them to contract more forcefully. The more blood that returns to the heart, the more forceful the contraction
Control of stroke volume
-Contractility of cardiac muscle
Sympathetic nerve activity (epinephrine) and circulating epinephrine increase the force of contraction, or contractility. Under conditions that increase contractility, cardiac muscle will contract more forcefully for a given amount of stretch
Complete the summary of mechanisms that regulate cardiac output
-From 07/11
Blood pressure
-Profile across the CV system
- Blood pressure is the driving force for flow in the CV system (pressure gradient between arteries and veins) and it must be maintained at all times.
- Blood pressure must be regulated so that it is high enough to create flow, but not too high to put excessive stress on the CV system.
- Blood pressure in the arteries is pulsatile, reflecting the pressure oscillations in the heart during the cardiac cycle, and it is continuous in the veins, reflecting the loss of forward energy mainly due to friction.
Blood pressure across the CV system
-Maintenance of forward movement during the entire heart cycle
Blood pressure is highest close to the heart and it declines as blood moves further away from it. The elastic properties of the walls of major arteries ensure that blood keeps moving forward even when the heart is in diastole and it does not exert pressure on the blood.
Measurements of blood pressure
-Techniques and methodology
-> Direct cannulation 18th century, direct cannulation 21st century + cuff and stethoscope, automated wrist cuff monitor, beat to beat blood pressure monitor and automated arm cuff monitor
Measurements of blood pressure
-Sound of the heart
-We are listening to the vessels not the heart. The sounds can be heard when the pressure is between the systolic and diastolic pressure – when the arteries are open for only part of the heart. No matter the technique used to measure blood pressure, the principle remains the same and it depends on sounds produced by arteries as they open and close when they are occluded by a cuff.
Mean arterial blood pressure (MABP)
-Basics
Mean arterial pressure (MAP) is calculated from the values of systolic and diastolic blood pressure, but it is not an average of 2. Diastole lasts almost twice as long as systole does and MAP is closer to the diastolic blood pressure value. It has to be closer to diastole than systole. MAP is calculated from: MAP = diastolic + (systolic-diastolic / 3).
MABP
-‘Normal’ values
So-called normal blood pressure is 120mmHg for systolic and 80 mmHg for diastolic blood pressure and 93mmHg for mean arterial pressure. These numbers are commonly presented as 120/80. 120/80 would be accurate enough if we were all young adults of average build. Blood pressure has a lot of variability between groups, but also within groups depending on conditions.
