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Clinical Science Applied to Nursing
Blood Pressure Clinical Science Applied to Nursing Copyright CSAN 2011 Cardiff University
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Why is theory and practice of Blood Pressure important?
How can we relate it to clinical practice?
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ARTERIAL BLOOD PRESSURE-
Too low a value of arterial blood pressure hypotension blood flow to the tissues will be reduced (for example to the brain and induce a faint Too high a value of arterial blood pressure hypertension this may cause excessive capillary pressures and damage e.g heart (myocardial infarction) kidneys, brain (stroke) and eyes
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Effects of High Blood Pressure on Your Body
Food for thought Artery Damage
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Effects of High Blood Pressure on Body
Food for thought Effects of High Blood Pressure on Body Hardening of the arteries Stroke Heart attack Kidney damage Blindness
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Blood Pressure and Pregnancy
Food for thought Blood Pressure and Pregnancy Gestational hypertension The effects of high blood pressure for mother and foetus can be dangerous. High blood pressure can: harm the mother's kidneys and other organs cause low birth weight and early delivery Some mothers can develops preeclampsia which can threaten the lives of both the mother and the foetus
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Blood Pressure and Children
Food for thought Blood Pressure and Children One in three children in Wales are above a healthy weight (WAG, 2010) The Health Behaviour in School-Aged Children (HBSC) Survey found that among 13-year-olds 22% of boys and 17% of girls are classed as overweight, and 4% of boys and 2% of girls classed as obese Obese children have approximately a 3-fold higher risk for hypertension than non obese children (Sorof and Daniels, 2002). Hypertension in childhood is due to renal causes and only occasionally drug treatment (eg steroids)
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Food for thought An adult’s blood pressure is considered high when the readings are greater than 140 mm Hg systolic or 90 mm Hg diastolic (BHS, 2004) Non-modifiable Risk Factors: Age male sex family history Primary cause of raised cholesterol (genetic) diabetes mellitus (autoimmune) Modifiable Risk Factors Excess alcohol (43 units/day) Excess salt intake Lack of exercise Environmental stress smoking Overweight (obesity) Type II -Diabetes (Type II can often coexists with obesity, dyslipidaemia, hypertension)
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Learning Outcomes Define blood pressure
State why its important to study normal mechanism of blood pressure – for example what is the effect of hypertension State the function of blood pressure Explain how blood pressure is commonly measured Name factors that influence blood pressure. Define cardiac output and state how it is calculated Discuss the factors that are involved in cardiac output Describe the main control mechanism for regulation of the blood pressure
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What is Blood Pressure The blood pressure is the force that causes blood to flow through the arteries, capillaries, and finally veins back to the heart
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What is Blood Pressure? Blood pressure is the amount of force exerted by the blood against the walls of the blood vessel Arterial Blood pressure Blood must circulate through the body and organs to maintain life E.G. To carry oxygen and nutrients to the cells To remove waste products from the cells The Heart is the pump that circulates the blood Pressure difference in the vascular system ensures that blood flows around the body That is why pressure varies in arteries, veins and capillaries
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Arterial Blood Pressure
Expressed as systolic/diastolic Adult Normal – 120/80 mmHg High – 140/90 mmHg Systolic pressure (top number) Pressure generated during ventricular contraction Diastolic pressure Pressure during cardiac relaxation
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Blood Pressure Each blood vessel has a blood pressure value – e.g. arterial blood pressure 120 mm Hg systolic Capillary blood pressure averages 25 mm Hg The pressures in the pulmonary system are much lower than systemic circulation Blood flows from an area of high to an area of low blood pressure - there must be a difference in pressure for the blood to flow.
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Blood Pressure Pulse Pressure (PP) Mean Arterial Pressure (MAP)
Difference between systolic and diastolic PP = systolic - diastolic Mean Arterial Pressure (MAP) Average pressure in arteries MAP = diastolic + 1/3 (systolic – diastolic)
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Blood Pressure is generated by Ventricular Contraction
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Blood pressure Blood pressure is different in blood vessels and varies from minute to minute dependant on factors such as stress
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Blood Pressure A blood pressure reading consists of two numbers:
Systolic pressure - the first, highest number Indicates pressure when the ventricles contract to push blood out to the body Diastolic pressure- the second, lower number Indicates when the heart relaxes between beats
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How can we measure Blood Pressure?
Blood Pressure can be measured in two ways: Indirectly, using a sphygmomanometer and ausculating (listening) with a stethoscope, the sounds you hear are called Korotkoff sounds Directly, using an arterial cannula (only used in Critical Care Areas, Operating Theatres). (l00k up this reference: British Hypertension Society )
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Measuring BLOOD PRESSURE
External blood pressure measurements: We apply a cuff to the arm & apply pressure to the cuff to form a constricting band around the arm and around internal arteries. The pressure in the cuff is initially above Blood pressure in the arteries– as the cuff pressure falls, it ‘meets’ the blood pressure & 1st Korotkof sound is heard. When the cuff pressure falls below the blood pressure, the Korotkof sound disappears
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Blood Pressure
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Making sense of what we hear
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Function of blood pressure
Systemic BP maintains the essential flow of substances into and out of organs
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Function of blood pressure
Systemic blood pressure maintains the essential flow of the substance into and out of the organs Control of blood pressure especially to the vital organs is essential for the maintenance of homeostasis Control of BP is essential for the maintenance of homeostasis
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Blood flow through the vessels
vessels is directly proportional to the difference in pressure between the ends of the tube
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Healthy young adults: Resting
Arterial Blood Pressure the driving force for blood in the circulatory system Healthy young adults: Resting Systolic pressure = 120 mmHg Diastolic is about 80 mmHg Healthy children values vary (see Whaley & Wong 2000): Rough Guide Systolic pressure 1 –7years: age in years + 90: 8-18 (2 x age in years) + 83 & Diastolic pressure: 1-5 years 56mmHg, 6-8years: age in years + 52
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Blood Pressure measurement in adult
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Blood Pressure in Pregnancy
Blood pressure during pregnancy is checked at every antenatal appointment Blood pressure change a little over whole pregnancy. This is perfectly normal. The pregnancy hormone progesterone relaxes the walls of blood vessels. This causes blood pressure fall during first and second trimesters This lower blood pressure may cause a woman to faint if they stand for too long or when getting up too quickly Blood pressure is at its lowest between 18 and 20 weeks of pregnancy In that period a woman will have produced an extra 1 to 2.5 litres of blood, which your heart has to pump around your body Blood pressure returns to its pre-pregnancy levels in the last few weeks before baby is born.
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What are the reasons for monitoring BP during Pregnancy
May help to identify: High blood Pressure Pre-eclampsia, gestational hypertension Blood pressure change in pregnancy? The effects of high blood pressure range from mild to severe. High blood pressure can: In the most serious cases, the mother develops preeclampsia which can threaten the lives of both the mother and the foetus.
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Factors to consider when taking BP measurements
Cold Exposure Bowel/Bladder Distension Caffeine Physical Activity Stress
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Making sense of what we hear
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Factors which influence BP
Cardiac output (and venous return) Blood volume and viscosity Peripheral resistance Elasticity of the blood vessels
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Factors influencing blood pressure
Blood Pressure = Blood Volume × Peripheral Resistance Cardiac Output = circulating blood volume Cardiac Output = Heart Rate × Stroke Volume Cardiac output affects circulating blood volume. * Any increase in circulating blood volume * will cause a corresponding increase in cardiac output. * The increased cardiac output * will increase blood volume * causing an increase in the blood pressure. As cardiac output is determined by multiplying the heart rate times the stroke volume, * any increase in either of them * * will increase cardiac output * and effect an increase in blood pressure. * For instance, an increased heart rate due to the release of epinephrine by the adrenal glands into the blood during an emergency, * will increase blood pressure. *
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Factors which influence blood pressure
Cardiac output (CO) Total Peripheral Resistance (TPR) Or BP = CO x TPR
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Cardiac output Cardiac Output = Heart Rate x Stroke Volume l/min bpm mL In a healthy adult this is 70 bpm x 75mL= 5L/min
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Terms, Definitions & Units
BP = CO x TPR Cardiac Output (CO) - the amount of blood pumped by a ventricle per minute. Units may be in Liters per minute Heart Rate (HR)- number of cardiac cycles per minute. Normal beat per minute Stroke Volume – (mls) amount of blood pumped out of a ventricle each beat. Average resting stroke volume = 70 ml. Cardiac output * refers to the amount of blood pumped by a single ventricle per minute. It may be reported in milliliters or Liters per minute. Heart rate * is the number of cardiac cycles per minute. The average heart rate for adult males is from beats/minute. The average heart rate for adult females varies from 72-80/minute. Stroke volume * refers to the amount of blood pumped out of a ventricle with each beat (contraction). The average stroke volume for an adult is around 70 ml. Knowing the heart rate and the stroke volume, one can calculate the cardiac output by simply multiplying the two. For instance, if the heart rate is 70/minute and the stroke volume is 70 ml, what would be the cardiac output? 70/minute x 70ml = 4,900 ml (4.9 L.) *
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Factors that influence cardiac output
Stroke volume – the amount of blood ejected from each ventricle at each heartbeat. Heart Rate – regulated by the autonomic nervous system (ANS) Increased heart rate caused by the release of epinephrine into blood by the adrenal glands = increased cardiac output, which increases circulating blood volume, to increase blood pressure.
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Stroke Volume Preload Afterload Contractility
Stroke volume is determined by three factors: Preload Afterload Contractility
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Preload Blood volume Venous return The vasomotor tone
- related to the volume of blood in the ventricle at the end of diastole: - End Diastolic Volume Factors affecting preload are: Blood volume Venous return The vasomotor tone
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Factors Aiding Venous Return
Venous blood pressure alone is too low to promote adequate blood return and is aided by the: Respiratory “pump” – pressure changes created during breathing suck blood toward the heart by squeezing local veins Muscular “pump” – contraction of skeletal muscles moves blood toward heart Valves prevent backflow during venous return
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Preload: Factors which influence Venous return to the heart
Muscle pump Respiratory Pump Valves in the vein
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Afterload Described as the resistance against which the ventricle must work. Whilst Preload is a major determinant of myocardial contractile power Afterload is mainly mechanical factor that affects performance
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Total Peripheral Resistance (TPR)
Peripheral Vascular Resistance resistance exerted by the action of the walls of the resistance vessels impeding blood flow most resistance is provided systemically by the arterioles,and small and medium sized arteries – exert a powerful influence in the control of blood pressure.
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Factors which influence TPR
The length of the vessel the blood The diameter of the lumen of the vessel The viscosity of the blood
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Pulse and Mean Arterial Pressures
Mean arterial pressure (MAP) = Diastolic + 1/3 pulse pressure MAP is considered to be the perfusion pressure seen by organs in the body. It is believed that a MAP that is greater than 60 mm Hg is enough to sustain the organs of the average person. MAP is normally between 70 to 110 mm Hg If the MAP falls significantly below this number for an appreciable time, the end organ will not get enough blood flow, and will become ischaemic The difference between the systolic and diastolic pressure is known as pulse pressure Pulse pressure = Systolic–Diastolic
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Control of Blood Pressure
Short term control - mainly involves: First Response by: Autonomic Nervous System. The receptors which monitors changes in BP are: Baroreceptor reflex Chemoreceptor reflex Circulating hormones (They are Responsible for maintaining BP homeostasis) Second or Indirect Adaptive Response by : Renin-angiotensin Mechanism Long term control involves regulation of Blood Pressure by the kidneys.
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MECHANISMS OF B/P CONTROL
Higher brain stimulus Baroreceptors Chemoreceptors
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Control of Blood Pressure
Short term control - mainly involves: Baroreceptor reflex Chemoreceptor reflex Circulating hormones Long term control involves regulation Of blood Pressure by the kidneys.
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Control of the Heart
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Vasoconstrictors and Vasodilators
Epinephrine and Norepinephrine Angiotensin II Vasopressin Vasodilators EDRF (NO) endothelium derived relaxing factor- is produced and released by the endothelium to promote smooth muscle relaxation
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Cardiovascular centers of the brainstem
Medulla oblongata is essential to Cardiovascular centers.
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Second or Indirect Adaptive Response by Renin-angiotensin Mechanism
When BP Renin is released by the kidney into the blood Renin stimulates Angiotensinogen (in lungs) to convert to Angiotensin I (mild constrictive hormone) Angiotensin I is then converted by (ACE) Angiotensin Converting Enzyme to Angiotensin II When Angiotensin II causes 1 Vasoconstriction 2. Release of aldosterone from the adrenal cortex. Prevents excretion of Na+ water in kidneys reduce water loss from circulation and this increases Blood Volume which in turn increases Blood Pressure
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Homeostatic Blood Pressure Regulation Mechanisms
Baroreceptors * in aortic arch & carotid sinuses: sensitive to changes in blood pressure. Reflex Centers in Medulla Cardioacceleratory - increases heart rate Cardioinhibitory - decreases heart rate Vasomotor - changes diameter of vessels BP* - Stimulates Cardioinhibitory center to heart rate & Vasomotor center to diameter. Homeostatic mechanisms for the regulation of blood pressure include the following reflex centers in the medulla oblongata: * * the Cardioacceleratory center, which increases heart rate, * the Cardioinhibitory center, which decreases heart rate, and * the vasomotor center in the aortic arch and the carotid sinuses, which can change the diameter of the arteries and arterioles causing vasoconstriction or vasodilation. In addition to the reflex centers in the medulla, there are peripheral baroreceptors * in the walls of the aortic arch , the carotid sinuses and nearly every other elastic artery in the heck and thorax which are sensitive to changes in blood pressure. * * A sudden increase in blood pressure * will cause the Cardioinhibitory center * to decrease heart rate * and will stimulate the vasomotor center * to increase the diameter of arterioles, thus reducing the blood pressure. * A sudden drop in blood pressure noted by the baroreceptors * will stimulate the Cardioacceleratory center to increase heart rate * while stimulating the vasomotor center to decrease * the diameter of arterioles to increase blood pressure. * BP* - Stimulates Cardioacceleratory center to heart rate & Vasomotor center to diameter.
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Anti Diuretic Hormone (ADH)
Released from Posterior Pituitary gland in response to low blood volume and low BP conserves body water by reducing the loss of water in urine vasoconstriction of mainly Splanchnic circulation & fluid retention WHAT is the Splanchnic circulation?
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Atrial Natriuretic Peptide (ANP)-
released from the atria by large atrial stretch Produces diuretic responses from kidney, also vasodilation and decrease in renin release.
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Fluid Exchange 85% of fluid that leaves blood is returned at venous end What about the other 15%?
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References Fox S. (2009) Human Physiology, (11th Ed), McGraw-
Hill International Edition Saladin K. (2010) Anatomy & Physiology, (5th Ed) McGraw-Hill International Edition Sorof J and Daniels S (2002), Hypertension. 2002;40:441 Useful website:
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