This document discusses hypertension and factors involved in regulating blood pressure. It defines hypertension as a condition that mainly affects cerebral, coronary, and renal vessels, and can lead to organ failure. During hypertensive emergencies, a quick rise in blood pressure can cause acute organ dysfunction such as aortic dissection or renal failure. Blood pressure is regulated by components of the cardiovascular system including the heart, sympathetic nervous system, kidneys, baroreceptors, and renin-angiotensin-aldosterone system. Genetic mutations can also impact blood pressure by altering activity within these regulatory pathways.
Gas exchange between the alveoli and the pulmonary capillary blood occurs by diffusion, as will be discussed in the next chapter. Diffusion of oxygen and carbon dioxide occurs passively, according to their concentration differences across the alveolar-capillary barrier. These concentration differences must be maintained by ventilation of the alveoli and perfusion of the pulmonary capillaries.
Alveolar ventilation brings oxygen into the lung and removes carbon dioxide from it. Similarly, the mixed venous blood brings carbon dioxide into the lung and takes up alveolar oxygen. The alveolar Image not available. and Image not available. are thus determined by the relationship between alveolar ventilation and pulmonary capillary perfusion. Alterations in the ratio of ventilation to perfusion, called the Image not available., will result in changes in the alveolar Image not available. and Image not available., as well as in gas delivery to or removal from the lung.
Alveolar ventilation is normally about 4 to 6 L/min and pulmonary blood flow (which is equal to cardiac output) has a similar range, and so the Image not available. for the whole lung is in the range of 0.8 to 1.2. Image not available. However, ventilation and perfusion must be matched on the alveolar-capillary level, and the Image not available. for the whole lung is really of interest only as an approximation of the situation in all the alveolar-capillary units of the lung. For instance, suppose that all 5 L/min of the cardiac output went to the left lung and all 5 L/min of alveolar ventilation went to the right lung. The whole lung Image not available. would be 1.0, but there would be no gas exchange because there could be no gas diffusion between the ventilated alveoli and the perfused pulmonary capillaries.
Oxygen is delivered to the alveolus by alveolar ventilation, is removed from the alveolus as it diffuses into the pulmonary capillary blood, and is carried away by blood flow. Similarly, carbon dioxide is delivered to the alveolus in the mixed venous blood and diffuses into the alveolus in the pulmonary capillary. The carbon dioxide is removed from the alveolus by alveolar ventilation. As will be discussed in Chapter 6, at resting cardiac outputs the diffusion of both oxygen and carbon dioxide is normally limited by pulmonary perfusion. Thus, the alveolar partial pressures of both oxygen and carbon dioxide are determined by the Image not available. If the Image not available. in an alveolar-capillary unit increases, the delivery of oxygen relative to its removal will increase, as will the removal ...
Gas exchange between the alveoli and the pulmonary capillary blood occurs by diffusion, as will be discussed in the next chapter. Diffusion of oxygen and carbon dioxide occurs passively, according to their concentration differences across the alveolar-capillary barrier. These concentration differences must be maintained by ventilation of the alveoli and perfusion of the pulmonary capillaries.
Alveolar ventilation brings oxygen into the lung and removes carbon dioxide from it. Similarly, the mixed venous blood brings carbon dioxide into the lung and takes up alveolar oxygen. The alveolar Image not available. and Image not available. are thus determined by the relationship between alveolar ventilation and pulmonary capillary perfusion. Alterations in the ratio of ventilation to perfusion, called the Image not available., will result in changes in the alveolar Image not available. and Image not available., as well as in gas delivery to or removal from the lung.
Alveolar ventilation is normally about 4 to 6 L/min and pulmonary blood flow (which is equal to cardiac output) has a similar range, and so the Image not available. for the whole lung is in the range of 0.8 to 1.2. Image not available. However, ventilation and perfusion must be matched on the alveolar-capillary level, and the Image not available. for the whole lung is really of interest only as an approximation of the situation in all the alveolar-capillary units of the lung. For instance, suppose that all 5 L/min of the cardiac output went to the left lung and all 5 L/min of alveolar ventilation went to the right lung. The whole lung Image not available. would be 1.0, but there would be no gas exchange because there could be no gas diffusion between the ventilated alveoli and the perfused pulmonary capillaries.
Oxygen is delivered to the alveolus by alveolar ventilation, is removed from the alveolus as it diffuses into the pulmonary capillary blood, and is carried away by blood flow. Similarly, carbon dioxide is delivered to the alveolus in the mixed venous blood and diffuses into the alveolus in the pulmonary capillary. The carbon dioxide is removed from the alveolus by alveolar ventilation. As will be discussed in Chapter 6, at resting cardiac outputs the diffusion of both oxygen and carbon dioxide is normally limited by pulmonary perfusion. Thus, the alveolar partial pressures of both oxygen and carbon dioxide are determined by the Image not available. If the Image not available. in an alveolar-capillary unit increases, the delivery of oxygen relative to its removal will increase, as will the removal ...
Properties of cm, plateau potential & pacemaker by Pandian M this PPT for I ...Pandian M
Describe the properties of cardiac muscle including its morphology, electrical, mechanical and metabolic functionsSLOs: After attending lecture & studying the assigned materials, the student will: 1.Describe the general features of cardiac muscle.2.Discuss the light and electron microscopic appearance of cardiac muscle, characteristic features of sarcotubular system.3.Enlist the electrical properties of heart muscle.4.Explain the phases of cardiac muscle action potential5.Explain the nodal action potential.6.Differentiate between cardiac muscle A.P. and nodal A.P., effect of nervous innervation and ions on AP.7.Enumerate and explain the mechanical properties of heart muscle, metabolic functions, characteristic features.
Properties of cm, plateau potential & pacemaker by Pandian M this PPT for I ...Pandian M
Describe the properties of cardiac muscle including its morphology, electrical, mechanical and metabolic functionsSLOs: After attending lecture & studying the assigned materials, the student will: 1.Describe the general features of cardiac muscle.2.Discuss the light and electron microscopic appearance of cardiac muscle, characteristic features of sarcotubular system.3.Enlist the electrical properties of heart muscle.4.Explain the phases of cardiac muscle action potential5.Explain the nodal action potential.6.Differentiate between cardiac muscle A.P. and nodal A.P., effect of nervous innervation and ions on AP.7.Enumerate and explain the mechanical properties of heart muscle, metabolic functions, characteristic features.
Cardiovascular System + Key Terms + Disease AreaNouman Minhas
Comprehensive presentation on Cardiovascular system.
It covers the Anatomy and Physiology of CV system.
It covers the Related Terms i.e Cardiac Output etc
It covers major diseases related to CV systems .
.............YOU will FIND it USEFUL...................
Prepared by Marta R. Gerasymchuk, MD, PhD, Associate professor of pathophysiology department of Ivano-Frankivsk NAtional Medical University, Ukraine
combine lecture
ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
Report Back from SGO 2024: What’s the Latest in Cervical Cancer?bkling
Are you curious about what’s new in cervical cancer research or unsure what the findings mean? Join Dr. Emily Ko, a gynecologic oncologist at Penn Medicine, to learn about the latest updates from the Society of Gynecologic Oncology (SGO) 2024 Annual Meeting on Women’s Cancer. Dr. Ko will discuss what the research presented at the conference means for you and answer your questions about the new developments.
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
Recomendações da OMS sobre cuidados maternos e neonatais para uma experiência pós-natal positiva.
Em consonância com os ODS – Objetivos do Desenvolvimento Sustentável e a Estratégia Global para a Saúde das Mulheres, Crianças e Adolescentes, e aplicando uma abordagem baseada nos direitos humanos, os esforços de cuidados pós-natais devem expandir-se para além da cobertura e da simples sobrevivência, de modo a incluir cuidados de qualidade.
Estas diretrizes visam melhorar a qualidade dos cuidados pós-natais essenciais e de rotina prestados às mulheres e aos recém-nascidos, com o objetivo final de melhorar a saúde e o bem-estar materno e neonatal.
Uma “experiência pós-natal positiva” é um resultado importante para todas as mulheres que dão à luz e para os seus recém-nascidos, estabelecendo as bases para a melhoria da saúde e do bem-estar a curto e longo prazo. Uma experiência pós-natal positiva é definida como aquela em que as mulheres, pessoas que gestam, os recém-nascidos, os casais, os pais, os cuidadores e as famílias recebem informação consistente, garantia e apoio de profissionais de saúde motivados; e onde um sistema de saúde flexível e com recursos reconheça as necessidades das mulheres e dos bebês e respeite o seu contexto cultural.
Estas diretrizes consolidadas apresentam algumas recomendações novas e já bem fundamentadas sobre cuidados pós-natais de rotina para mulheres e neonatos que recebem cuidados no pós-parto em unidades de saúde ou na comunidade, independentemente dos recursos disponíveis.
É fornecido um conjunto abrangente de recomendações para cuidados durante o período puerperal, com ênfase nos cuidados essenciais que todas as mulheres e recém-nascidos devem receber, e com a devida atenção à qualidade dos cuidados; isto é, a entrega e a experiência do cuidado recebido. Estas diretrizes atualizam e ampliam as recomendações da OMS de 2014 sobre cuidados pós-natais da mãe e do recém-nascido e complementam as atuais diretrizes da OMS sobre a gestão de complicações pós-natais.
O estabelecimento da amamentação e o manejo das principais intercorrências é contemplada.
Recomendamos muito.
Vamos discutir essas recomendações no nosso curso de pós-graduação em Aleitamento no Instituto Ciclos.
Esta publicação só está disponível em inglês até o momento.
Prof. Marcus Renato de Carvalho
www.agostodourado.com
Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...VarunMahajani
Disruption of blood supply to lung alveoli due to blockage of one or more pulmonary blood vessels is called as Pulmonary thromboembolism. In this presentation we will discuss its causes, types and its management in depth.
New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
Couples presenting to the infertility clinic- Do they really have infertility...Sujoy Dasgupta
Dr Sujoy Dasgupta presented the study on "Couples presenting to the infertility clinic- Do they really have infertility? – The unexplored stories of non-consummation" in the 13th Congress of the Asia Pacific Initiative on Reproduction (ASPIRE 2024) at Manila on 24 May, 2024.
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Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
Explore natural remedies for syphilis treatment in Singapore. Discover alternative therapies, herbal remedies, and lifestyle changes that may complement conventional treatments. Learn about holistic approaches to managing syphilis symptoms and supporting overall health.
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
2. ActualityActuality
Arterial hypertension is a very commonArterial hypertension is a very common
condition. Cerebral, coronary and renal vesselscondition. Cerebral, coronary and renal vessels
are mainly affected byare mainly affected by the deleterious effect ofthe deleterious effect of
this condition, and both acute and chronic organthis condition, and both acute and chronic organ
failure may ensue.failure may ensue.
Exacerbation of underlyingExacerbation of underlying pathophysiologicpathophysiologic
conditions or new precipitating factors can leadconditions or new precipitating factors can lead
to hypertensive crisis, either urgencies orto hypertensive crisis, either urgencies or
emergencies.emergencies.
During hypertensive emergencies, a quick raiseDuring hypertensive emergencies, a quick raise
in arterial pressure may lead to acute andin arterial pressure may lead to acute and
significant organ dysfunction,significant organ dysfunction, such as aorticsuch as aortic
dissection, acute myocardial infarction,dissection, acute myocardial infarction,
intracranial bleeding or acute renal failure.intracranial bleeding or acute renal failure.
PerioperativePerioperative hypertension often takes thehypertension often takes the
shape of a crisis and it can be related toshape of a crisis and it can be related to
hypothermia, pain, neuro-hormonal response tohypothermia, pain, neuro-hormonal response to
surgical trauma or antihypertensive drugssurgical trauma or antihypertensive drugs
withdrawal.withdrawal.
3. CONTENTCONTENT
• 1. Factors which predetermine the level of blood pressure for a1. Factors which predetermine the level of blood pressure for a
man, basal tone of vessels.man, basal tone of vessels.
• 2. Pressor and depressor systems of organism, their description.2. Pressor and depressor systems of organism, their description.
• 3. Arterial hypertensions: kinds, classification. Degrees of high3. Arterial hypertensions: kinds, classification. Degrees of high
arterial pressure.arterial pressure.
• 4. Nephrogenic hypertensions: reasons, kinds, pathogenesis.4. Nephrogenic hypertensions: reasons, kinds, pathogenesis.
• 5. Etiology and pathogenesis of endocrinal hypertension.5. Etiology and pathogenesis of endocrinal hypertension.
• 6. A role of the sympathetic nervous system in pathogenesis of6. A role of the sympathetic nervous system in pathogenesis of
nerogenic hypertension.nerogenic hypertension.
• 7. Salt hypertension: etiology, mechanisms of development.7. Salt hypertension: etiology, mechanisms of development.
• 8. Etiology and pathogenesis of essential hypertension.8. Etiology and pathogenesis of essential hypertension.
• 9. Complication of essential hypertension.9. Complication of essential hypertension.
• 10. Reasons and mechanisms of arterial hypotension.10. Reasons and mechanisms of arterial hypotension.
4. Determinants of Blood Pressure
• Components of B/P
– Pressure of blood against the walls of
the arteries
– The elasticity of the artery walls
– The volume and thickness of the blood
5. • Systolic Blood Pressure (SBP) pressure measured in brachial
artery during systole (ventricular emptying and ventricular
contraction period)
• Diastolic Blood Pressure (DBP) pressure measured in brachial
artery during diastole (ventricular filling and ventricular
relaxation)
• Mean Arterial Pressure (MAP) "average" pressure throughout the
cardiac cycle against the walls of the proximal systemic
arteries (aorta)
• estimated as: .33(SBP - DBP) + DBP
• Total Peripheral Resistance (TPR) - the sum of all forces that
oppose blood flow
• length of vasculature (L)
• blood viscosity (V)
• vessel radius (r)
Definitions
TPR = ( 8 ) ( V ) ( L )
( p ) ( r 4
)
6. Physiological factors affecting Arterial Blood pressurePhysiological factors affecting Arterial Blood pressure
AgeAge::
New born: 80/40 mmHgNew born: 80/40 mmHg
4 years: 100/65 mmHg.4 years: 100/65 mmHg.
Adults: 120/80 mmHgAdults: 120/80 mmHg
After that: Gradually increase due to increase elasticity of arteries.After that: Gradually increase due to increase elasticity of arteries.
SexSex::
Children: have equal Blood pressure.Children: have equal Blood pressure.
Adults before 45 years: male more than female.Adults before 45 years: male more than female.
Adults after 45 years: the diastolic B.P. is more in female than males.Adults after 45 years: the diastolic B.P. is more in female than males.
RaceRace:: ABP in oriental is less than in European and American.ABP in oriental is less than in European and American.
GravityGravity:: B.P. in upper parts of the body is more than the lower partsB.P. in upper parts of the body is more than the lower parts
especially during standing.especially during standing.
Meals:Meals: Digestion increases the arterial blood pressure.Digestion increases the arterial blood pressure.
Emotions and exerciseEmotions and exercise:: increase the arterial blood pressure.increase the arterial blood pressure.
SleepSleep:: Deep quiet sleep decrease A.B.P., while sleep with dreamsDeep quiet sleep decrease A.B.P., while sleep with dreams
increase A.B.P.increase A.B.P.
7. Measurements of Blood PressureMeasurements of Blood Pressure
1- Direct Method1- Direct Method
The most accurate means for measuring bloodThe most accurate means for measuring blood
pressure is directly within an artery (intra-arterial)pressure is directly within an artery (intra-arterial)
using a catheter.using a catheter.
But because this method is invasive, it is neitherBut because this method is invasive, it is neither
practical nor appropriate for repeated measurementspractical nor appropriate for repeated measurements
in non-hospital settings, or for large-scale publicin non-hospital settings, or for large-scale public
health screenings.health screenings.
2- The mercury-filled sphygmomanometer2- The mercury-filled sphygmomanometer
The usual method of measurement, therefore, is aThe usual method of measurement, therefore, is a
noninvasive means that uses a sphygmomanometer,noninvasive means that uses a sphygmomanometer,
which includes either a column of mercury orwhich includes either a column of mercury or
pressure-registering gauge.pressure-registering gauge.
8. Cardiovascular Hemodynamic Basics
Flow (Q)
Pressure (MAP) P aorta – P vena cava
= =
Resistance (TPR) (8) (V) (L)
(p) (r 4
)
Flow (Q) = () (Pa – Pv) (r 4
)
(8) (V) (L)
V = viscosity of fluid (blood) flowing through the pipe
L = length of pipe (blood vessel)
r = radius of the pipe (blood vessel)
Pa = aortic pressure
Pv = venous pressure
Normally Resting Q is
about 5 - 6 liters / minute
BP = CO x PRBP = CO x PR
9. RA
RV
LUNGS LA
LV
AORTA
ARTERIOLES
SYSTEMIC
ARTERIES
VEINS
(CAPACITANCE VESSELS)
(100)
(92)
(40)
low compliance
13% of blood volume
high compliance
64% of blood volume
PO2 = 40 PCO2 = 46
(0)
(2)
PO2 = 100
PCO2 = 40
PO2 = 160
PCO2 = .3
CAPILLARY
BEDS
7% of blood volume
9% of blood volume
(7)
(13) (3)
Ohms Law: Flow (Q) = upstream pressure – downstream pressure
resistance
Systemic Circulation = 100 mmHg – 0 mmHg = 100 ml / sec = 6 liters / min
Flow (Q) 1 mmHg sec / ml
The “Closed” Cardiovascular
Hemodynamic System
Mean arterial pressures in red
(20)
10. Blood Pressure RegulationBlood Pressure Regulation
Systemic arterial pressure is a function ofSystemic arterial pressure is a function of
stroke volume, heart rate, and totalstroke volume, heart rate, and total
peripheral resistanceperipheral resistance
The major organs involved in regulation ofThe major organs involved in regulation of
blood pressure are the heart (HR & SV),blood pressure are the heart (HR & SV),
the SNS (TPR-total peripheral resistance),the SNS (TPR-total peripheral resistance),
and the kidneys (ECF – extracellular fluidand the kidneys (ECF – extracellular fluid
volume & secretion of renin).volume & secretion of renin).
(Wynne, Woo, & Olyaei, 2007, p. 1093)(Wynne, Woo, & Olyaei, 2007, p. 1093)
12. Regulative systemsRegulative systems
Sympathetic Nervous SystemSympathetic Nervous System
BaroreceptorsBaroreceptors
– Nerve cells in carotid artery & aortic archNerve cells in carotid artery & aortic arch
– Maintain BP during normal activitiesMaintain BP during normal activities
– React to increases & decreases in BPReact to increases & decreases in BP
BP – impulse to brain to inhibit SNS; HR &BP – impulse to brain to inhibit SNS; HR &
force of contraction; vasodilation of arteriolesforce of contraction; vasodilation of arterioles
BP – activates SNS; vasoconstriction ofBP – activates SNS; vasoconstriction of
arterioles; HR & heart contractilityarterioles; HR & heart contractility
1. Barroreceptors of aorta arch and sinus caroticus
14. Increased BP send inhibitory
impulse to sympathetic
vasomotor center in
brainstem;
In long-standing
hypertension, baroreceptors
adjust to elevated BP and
reads it as normal; doesn’t
make adjustments; also
becomes less responsive in
some older adults
15. On standing up venous return fallsOn standing up venous return falls
Cardiac output diminishesCardiac output diminishes
Arterial blood pressure is reducedArterial blood pressure is reduced
Baroreceptor afferent firing reducedBaroreceptor afferent firing reduced
Medullary centres inhibition reducedMedullary centres inhibition reduced
THE BARORECEPTOR REFLEX - AN EXAMPLETHE BARORECEPTOR REFLEX - AN EXAMPLE
CORRECTION OF POSTURAL HYPOTENSIONCORRECTION OF POSTURAL HYPOTENSION
Effect of gravity onEffect of gravity on
venous returnvenous return
Preload diminishedPreload diminished
- Starling’s Law- Starling’s Law
Subject possibly feels faintSubject possibly feels faint
as cerebral flow is reducedas cerebral flow is reduced
Due to reduced arterial B.P.Due to reduced arterial B.P.
VasoconstrictionVasoconstriction
TachycardiaTachycardia
Raised stroke workRaised stroke work
Tend to
restore
arterial
blood
pressure
Increased sympathetic tone toIncreased sympathetic tone to
arteriolesarterioles
Reduced vagal tone to s.a.Reduced vagal tone to s.a.
nodenode
Increased myocardial sympathetic toneIncreased myocardial sympathetic tone
16. Sympatetic activitySympatetic activity
Increase BP
Increases
heart rate
and
contractility
Increase
cardiac
output
Vasoconstriction
increasing
peripheral
vascular
resistances
Increases
sodium and
water
reabsorption
Increases
vascular tone at
precapillary
level
Induces
vascular
remodelling
Increase
diastolic
pressure
Chronic
Ischemia
and AMI
Increased left
ventricular
hypertrofy and
oxygen
consumption
17.
18. Blood pressure regulation by the renin-angiotensin systemBlood pressure regulation by the renin-angiotensin system
and the central roles of sodium metabolism in specificand the central roles of sodium metabolism in specific
causes of inherited and acquired forms of hypertension.causes of inherited and acquired forms of hypertension.
Components of theComponents of the
systemic renin-angiotensinsystemic renin-angiotensin
system are shown in black.system are shown in black.
Genetic disorders thatGenetic disorders that
affect blood pressure byaffect blood pressure by
altering activity of thisaltering activity of this
pathway are indicated inpathway are indicated in
red;red; arrowsarrows indicate sitesindicate sites
in the pathway altered byin the pathway altered by
mutation. Genes that aremutation. Genes that are
mutated in these disordersmutated in these disorders
are indicated inare indicated in
parentheses. Acquiredparentheses. Acquired
disorders that alter blooddisorders that alter blood
pressure through effectspressure through effects
on thison this pathway arepathway are
indicated in blue.indicated in blue.
(From Lifton RP, et al:
Molecular genetics of
human blood pressure
variation. Science 272:676,
1996.)
19.
20. Increase BPIncrease BP
Renin
Angiotensin II
AldosteroneAldosterone
VasoconstrictionVasoconstriction
on systemic andon systemic and
renal vasselsrenal vassels
Left ventricularLeft ventricular
hypertrophyhypertrophy
andand
myocardialmyocardial
ischemiaischemia
Increase leftIncrease left
ventricularventricular
wallwall
tensiontension
Alteration of renalAlteration of renal
arterial andarterial and
capillarycapillary
vessels’ wallvessels’ wall
Glomeruar ischemia,Glomeruar ischemia,
parenchymal damage,parenchymal damage,
proteinuria, end-stageproteinuria, end-stage
renal failurerenal failure
ADHADH
Sodium andSodium and
water renalwater renal
retentionretention
HHypervolemiaypervolemia
Effect of renin-angiotensin systemEffect of renin-angiotensin system
on cardiovascular homeostasison cardiovascular homeostasis
2.2. ReninRenin––angiotensinangiotensin systemsystem
21. Mutations altering blood pressure in humans.Mutations altering blood pressure in humans.
A diagram of a nephron, the filtering unit of the kidney, is shown. The molecular pathways mediating NaCl reabsorption in
individual renal cells in the thick ascending limb of the loop of Henle (TAL), distal convoluted tubule (DCT), and the cortical
collecting tubule (CCT) are indicated, along with the pathway of the renin-angiotensin system, the major regulator of renal
salt reabsorption. Single gene defects that manifest as inherited diseases affecting these pathways are indicated, with
hypertensive disorders in red and hypotensive disorders in blue. Abbreviations: Al, angiotensin I; ACE, angiotensin
converting enzyme; All, angiotensin II; MR, mineralocorticoid receptor; GRA, glucocorticoid-remediable aldosteronism;
PHA1, pseudohypoaldosteronism, type 1; AME, apparent mineralocorticoid excess; 11b-HSD2, 11b-hydroxysteroid
dehydrogenase-2; and DOC, deoxycorticosterone. (From Lifton RP, et al: Molecular mechanisms of human hypertension.
Cell 104:545, 2001.)
22. Regulative systems
3. Renin–angiotensin-aldosteron system
Renin Actination of
suprarenal glangs
(cortical layer)
Na reabsorbtion
in kidney increase
Angiotensin 2
Aldosteron
excretion
Na concentration in
blood increase,
blood osmotic
pressure increase
Move of extravascular
fluid inside the
vessels
Increase of circulative
blood volume
(CBV)
CО increase
23. Mechanism of Action of AldosteroneMechanism of Action of Aldosterone
Increases CO by increasing blood volume
.
24. BP Regulation: EndotheliumBP Regulation: Endothelium
Nitric oxideNitric oxide is secreted by endothelial cellsis secreted by endothelial cells
which results in relaxation of blood vesselswhich results in relaxation of blood vessels
It also produces local vasodilators, suchIt also produces local vasodilators, such
asas prostacylcinprostacylcin andand endothelium-derivedendothelium-derived
hyperpolarizing factorhyperpolarizing factor
EndothelinEndothelin is an extremely potentis an extremely potent
vasoconstrictor and also stimulatesvasoconstrictor and also stimulates
vascular smooth muscle growthvascular smooth muscle growth
(Wynne, Woo, & Olyaei, 2007, p. 1094)(Wynne, Woo, & Olyaei, 2007, p. 1094)
26. Hypertension:Hypertension: DefinitionDefinition
Persistent elevation ofPersistent elevation of
Systolic bloodSystolic blood pressurepressure ≥140 mm Hg≥140 mm Hg
oror
Diastolic blood pressureDiastolic blood pressure ≥90 mm Hg≥90 mm Hg
Worldwide an estimatedWorldwide an estimated 1 billion1 billion peoplepeople
have hypertension; about 1 in 3have hypertension; about 1 in 3
Americans affectedAmericans affected
Direct relationship between hypertensionDirect relationship between hypertension
and cardiovascular disease (CVD)and cardiovascular disease (CVD)
31. Risk Factors forRisk Factors for -- Primary HypertensionPrimary Hypertension
Age (>55)
Alcohol
Cigarette smoking
Diabetes mellitus
Elevated serum lipids
Excess dietary sodium
Gender
– SBP rises with age Alcohol – excessive use strongly correlated
to hypertension
– Smoking – increases risk for CV disease ; vasoconstriction
– Diabetes – along with hypertension greater risk for target organ
disease and usually more severe
– Hyperlipidemia elevated in people with hypertension; increases
risk of atherosclerosis
– Some pts Na sensitive Males have higher rates of hypertension
<55 and increased in women>55
32. Risk Factors forRisk Factors for
Primary HypertensionPrimary Hypertension
Family historyFamily history
ObesityObesity
EthnicityEthnicity
Sedentary lifestyleSedentary lifestyle
StressStress
33. Primary HypertensionPrimary Hypertension
Water and sodium retentionWater and sodium retention
• AA high sodium intake may resulthigh sodium intake may result
in water retentionin water retention
• Some people are Na sensitiveSome people are Na sensitive
(about 20%) ; not everyone(about 20%) ; not everyone
with high salt diet developswith high salt diet develops
hypertensionhypertension
34. Pathophysiology ofPathophysiology of
Primary HypertensionPrimary Hypertension
Water and sodium retentionWater and sodium retention
Certain demographics areCertain demographics are
associated with “saltassociated with “salt
sensitivity”sensitivity”
ObesityObesity
Increasing ageIncreasing age
African American ethnicityAfrican American ethnicity
People with diabetes, renalPeople with diabetes, renal
diseasedisease
35. Pathophysiology ofPathophysiology of
Primary HypertensionPrimary Hypertension
• Stress and increased SNS activityStress and increased SNS activity
– Produces increased vasoconstrictionProduces increased vasoconstriction
– ↑↑ HRHR
– ↑↑ Renin releaseRenin release
– Angiotensin II causes direct arteriolarAngiotensin II causes direct arteriolar
constriction, promotes vascularconstriction, promotes vascular
hypertrophy and induces aldosteronehypertrophy and induces aldosterone
secretionsecretion
36. Pathophysiology ofPathophysiology of
Primary HypertensionPrimary Hypertension
Insulin resistance & hyperinsulinemia
High insulin concentration
stimulates SNS activity and impairs
nitric oxide–mediated vasodilation
Not present in secondary
hypertension and don’t improve
when hypertension is treated
37. Risk factors and aetiological influences in hypertensionRisk factors and aetiological influences in hypertension
Risk factor or aetiologicalRisk factor or aetiological
influenceinfluence
Possible rationale and commentPossible rationale and comment
MajorMajor
Family historyFamily history Inherited tendency – probably polygenicInherited tendency – probably polygenic
Dietary Na highDietary Na high Fluid retention; vascular wall oedema; ion pump defectFluid retention; vascular wall oedema; ion pump defect
ObesityObesity Possible artefact of measurement (problem with arm cuff)?Possible artefact of measurement (problem with arm cuff)?
Greater perfusion demands of increased body massGreater perfusion demands of increased body mass
Reducing weight can reverse borderline HPTReducing weight can reverse borderline HPT
AlcoholAlcohol Unknown mechanism; possibly 30% of HPT related to alcohol abuseUnknown mechanism; possibly 30% of HPT related to alcohol abuse
Sedentary lifeSedentary life Unknown mechanism; regular exercise lowers BPUnknown mechanism; regular exercise lowers BP
Renal diseaseRenal disease Overt or occult renal disease often implicated: cause or effect?Overt or occult renal disease often implicated: cause or effect?
MinorMinor
AgeAge
Stress or type A personalityStress or type A personality Overactive sympathetic nervous system → vasoconstriction and/or raised COOveractive sympathetic nervous system → vasoconstriction and/or raised CO
Difficult to quantify; effect may have been exaggeratedDifficult to quantify; effect may have been exaggerated
DietaryDietary
Ca, K, Mg ↓Ca, K, Mg ↓
Saturated fatSaturated fat
Animal productsAnimal products
Some evidence,Some evidence,
May induce vasoconstriction via endothelial interactionsespecially for KMay induce vasoconstriction via endothelial interactionsespecially for K
Vegetarians may have lower BPVegetarians may have lower BP
Glucose intoleranceGlucose intolerance Complex interaction between insulin resistance, hyperlipidaemia and HPTComplex interaction between insulin resistance, hyperlipidaemia and HPT
RaceRace Increased average BP in urban Blacks: response to stress or dietary salt?Increased average BP in urban Blacks: response to stress or dietary salt?
SmokingSmoking NoNo sustained effect on BP itself but greatly exacerbates atheroscleroticsustained effect on BP itself but greatly exacerbates atherosclerotic
complicationscomplications
BP, blood pressure; Ca, calcium; CO, cardiac output; HPT, hypertension; K, potassium; Mg, magnesium; Na, sodium.BP, blood pressure; Ca, calcium; CO, cardiac output; HPT, hypertension; K, potassium; Mg, magnesium; Na, sodium.
38. HypertensionHypertension
Clinical ManifestationsClinical Manifestations
Referred to as the “silent killer”Referred to as the “silent killer”
Frequently asymptomatic until targetFrequently asymptomatic until target
organ disease occursorgan disease occurs
Or recognized on routine screeningOr recognized on routine screening
40. Target Organ DamageTarget Organ Damage
Caused by damage to the body’s blood vesselsCaused by damage to the body’s blood vessels
which particularly affect the following organs:which particularly affect the following organs:
Blood VesselsBlood Vessels
HeartHeart
KidneysKidneys
BrainBrain
EyesEyes
42. Hypertension-Hypertension-ComplicationsComplications
• Cerebrovascular diseaseCerebrovascular disease
– Stroke
• Peripheral vascular diseasePeripheral vascular disease
• Nephrosclerosis
• Retinal damageRetinal damage
• AtherosclerosisAtherosclerosis most common cause of cerebrovascular disease;
hypertension major risk factor for cerebral atherosclerosis and stroke
• AtherosclerosisAtherosclerosis in peripheral blood vessels too; can lead to PVD, aortic
aneurysm, aortic dissection
• Hypertension one of leading causes of end-stage renal disease, esp. in
African-Americans; some degree of renal dysfunction usual in person with
even mild BP elevations
• RetinaRetina is only place blood vessels can be directly visualized; if see damage
there then indicates damage in brain, heart, & kidney too; Can cause
blurring, retinal hemorrhage and blindness
44. Wong, T. Y. et al. N Engl J Med 2004;351:2310-2317
Examples of Mild Hypertensive Retinopathy
AV nicking
Focal
narrowing
AV nicking
Copper
wiring
45. Secondary HypertensionSecondary Hypertension
►It is caused by another diseaseIt is caused by another disease
process such as:process such as:
►Renal FailureRenal Failure
►Diabetes MellitusDiabetes Mellitus
►Cushing’s SyndromeCushing’s Syndrome
►Primary AldosteronismPrimary Aldosteronism
►Coarctation of the AortaCoarctation of the Aorta
►PheochromocytomaPheochromocytoma
►Sleep ApneaSleep Apnea
46.
47. Secondary hypertension representSecondary hypertension represent
symptoms of such diseasessymptoms of such diseases
• 1. Diseases of kidneys: glomerulonephritis (14 %),
pielonephritis, interstitial nephritis due to abusing
analgetics, hereditary nephritis (syndrome Alport’s),
polycytosis kidney.
• 2. Stenosis of renal artery (1 %). Hypertension arises not in
each stenosis. The most often reason of stenosis, caused
atherosclerotic platelits(at 70-80 of %), which damage
usually proximal third of renal artery on the one hand.
Other reason of stenosis with hypertension its
fibromuscular hyperplasia of an average third of renal
artery. It, as a rule, double-side and more often happens at
the women. The mechanism of hypertension in stenosis of
renal artery – hyperproduction of renin.
48. Secondary hypertension representSecondary hypertension represent
symptoms of such diseasessymptoms of such diseases
• 3. Primary aldosteronism (Cоnn syndrome)3. Primary aldosteronism (Cоnn syndrome) – in 1 %– in 1 %
of cases. The reasons – unilateral adenomaof cases. The reasons – unilateral adenoma
glomerular zone adrenal glands or double-sideglomerular zone adrenal glands or double-side
diffuse hyperplasia of adrenal glands.diffuse hyperplasia of adrenal glands.
• 4. Paraganglioma (1 %)4. Paraganglioma (1 %) – tumour from chromaffin– tumour from chromaffin
cells of medullarcells of medullar layer adrenal glands or sympatheticlayer adrenal glands or sympathetic
nerves, as a rule –nerves, as a rule – benighnbenighn. In paraganglioma is. In paraganglioma is
increased both cardiac output, and peripheralincreased both cardiac output, and peripheral
resistance.resistance.
• 5. Coarctation of the aorta is an anatomic defect5. Coarctation of the aorta is an anatomic defect, in, in
which aorta in pectoral or abdominal department iswhich aorta in pectoral or abdominal department is
narrowed to such extend, that it represents seriousnarrowed to such extend, that it represents serious
barrier for blood circulation. In all vessels, whichbarrier for blood circulation. In all vessels, which
depart from the aorta proximal of narrowing, thedepart from the aorta proximal of narrowing, the
resistance increases and is increased arterialresistance increases and is increased arterial
pressure.pressure.
49. Pheochromocytoma
• A pheochromocytoma is a tumor of chromaffin tissue, which containsA pheochromocytoma is a tumor of chromaffin tissue, which contains
sympathetic nerve cells.sympathetic nerve cells.
• The tumor is most commonly located in the adrenal medulla but canThe tumor is most commonly located in the adrenal medulla but can
arise in other sites, such as sympathetic ganglia, where there isarise in other sites, such as sympathetic ganglia, where there is
chromaffin tissuechromaffin tissue. Although only 0.1% to 0.5% of persons with. Although only 0.1% to 0.5% of persons with
hypertension have an underlying pheochromocytoma, the disorder canhypertension have an underlying pheochromocytoma, the disorder can
cause serious hypertensive crises.cause serious hypertensive crises.
• Eight percent to 10% of the tumors are malignant.Eight percent to 10% of the tumors are malignant.
• Like adrenal medullary cells, the tumor cells of a pheochromocytomaLike adrenal medullary cells, the tumor cells of a pheochromocytoma
produce and secrete the catecholaminesproduce and secrete the catecholamines epinephrine andepinephrine and
norepinephrine.norepinephrine.
• TheThe hypertensionhypertension that develops is the result of a massive release ofthat develops is the result of a massive release of
these catecholamines. Their release may be paroxysmal, rather thanthese catecholamines. Their release may be paroxysmal, rather than
continuous, causing periodic episodes of headache, excessivecontinuous, causing periodic episodes of headache, excessive
sweating, and palpitations.sweating, and palpitations.
• HeadacheHeadache is the most common symptom and can be quite severe.is the most common symptom and can be quite severe.
Nervousness, tremor, facial pallor, weakness, fatigue, and weight lossNervousness, tremor, facial pallor, weakness, fatigue, and weight loss
occur less frequently. Marked variability in blood pressure betweenoccur less frequently. Marked variability in blood pressure between
episodes is typical.episodes is typical.
• Some persons with pheochromocytoma have paroxysmal episodes ofSome persons with pheochromocytoma have paroxysmal episodes of
hypertension, sometimes to dangerously high levels; others may havehypertension, sometimes to dangerously high levels; others may have
sustained hypertension; and some may even be normotensive.sustained hypertension; and some may even be normotensive.
50. Peripheral Arterial DiseasePeripheral Arterial Disease
(PAD)(PAD)
§ PAD is equivalent in risk to ischemic heart disease.PAD is equivalent in risk to ischemic heart disease.
§ Any class of drugs can be used in most PAD patients.Any class of drugs can be used in most PAD patients.
§ Other risk factors should be managed aggressively.Other risk factors should be managed aggressively.
§ Aspirin should be used.Aspirin should be used.
51. Hypertension in OlderHypertension in Older
PersonsPersons
§ More than two-thirds of people over 65 have HTN.More than two-thirds of people over 65 have HTN.
§ This population has the lowest rates of BP control.This population has the lowest rates of BP control.
§ Treatment, including those who with isolated systolic HTN,Treatment, including those who with isolated systolic HTN,
should follow same principles outlined for general care ofshould follow same principles outlined for general care of
HTN.HTN.
§ Lower initial drug doses may be indicated to avoid symptoms;Lower initial drug doses may be indicated to avoid symptoms;
standard doses and multiple drugs will be needed to reach BPstandard doses and multiple drugs will be needed to reach BP
targets.targets.
52. Postural HypotensionPostural Hypotension
§ Decrease in standing SBP >10 mmHg, when associatedDecrease in standing SBP >10 mmHg, when associated
with dizziness/fainting, more frequent in older SBPwith dizziness/fainting, more frequent in older SBP
patients with diabetes, taking diuretics, venodilators, andpatients with diabetes, taking diuretics, venodilators, and
some psychotropic drugs.some psychotropic drugs.
§ BP in these individuals should be monitored in the uprightBP in these individuals should be monitored in the upright
position.position.
§ Avoid volume depletion and excessively rapid doseAvoid volume depletion and excessively rapid dose
titration of drugs.titration of drugs.
53. Hypertension in WomenHypertension in Women
Hypertensive disorders complicate 6% to 8% ofHypertensive disorders complicate 6% to 8% of
pregnancies.pregnancies.
They are the second leading cause, after embolism, ofThey are the second leading cause, after embolism, of
maternal mortality in the United States, accounting formaternal mortality in the United States, accounting for
almost 15% of such deaths.almost 15% of such deaths.
Hypertensive disorders also contribute to stillbirths andHypertensive disorders also contribute to stillbirths and
neonatal morbidity and mortality.neonatal morbidity and mortality.
The incidence of hypertensive disorders of pregnancyThe incidence of hypertensive disorders of pregnancy
increases with maternal age and is more common inincreases with maternal age and is more common in
African-American women.African-American women.
54. Classification of High Blood Pressure inClassification of High Blood Pressure in
PregnancyPregnancy
Classification Description
GestationalGestational
hypertensionhypertension
Blood pressure elevation, without proteinuria, that isBlood pressure elevation, without proteinuria, that is
detected for the first time during midpregnancy anddetected for the first time during midpregnancy and
returns to normal by 12 weeks postpartum.returns to normal by 12 weeks postpartum.
ChronicChronic
hypertensionhypertension
Blood pressure ≥140 mm Hg systolic or ≥90 mm HgBlood pressure ≥140 mm Hg systolic or ≥90 mm Hg
diastolic that is present and observable before the 20thdiastolic that is present and observable before the 20th
week of pregnancy. Hypertension that is diagnosed forweek of pregnancy. Hypertension that is diagnosed for
the first time during pregnancy and does not resolvethe first time during pregnancy and does not resolve
after pregnancy also is classified as chronicafter pregnancy also is classified as chronic
hypertension.hypertension.
Preeclampsia-Preeclampsia-
eclampsiaeclampsia
Pregnancy-specific syndrome of blood pressure elevationPregnancy-specific syndrome of blood pressure elevation
(blood pressure >140 mm Hg systolic or >90 mm Hg(blood pressure >140 mm Hg systolic or >90 mm Hg
diastolic) that occurs after the first 20 weeks ofdiastolic) that occurs after the first 20 weeks of
pregnancy and is accompanied by proteinuria (urinarypregnancy and is accompanied by proteinuria (urinary
excretion of 0.3 g protein in a 24-hour specimen).excretion of 0.3 g protein in a 24-hour specimen).
PreeclampsiaPreeclampsia
superimposedsuperimposed
on chronicon chronic
hypertensionhypertension
Chronic hypertension (blood pressure ≥140 mm Hg systolicChronic hypertension (blood pressure ≥140 mm Hg systolic
or ≥90 mm Hg diastolic prior to 20th week ofor ≥90 mm Hg diastolic prior to 20th week of
pregnancy) with superimposed proteinuria and with orpregnancy) with superimposed proteinuria and with or
without signs of the preeclampsia syndromewithout signs of the preeclampsia syndrome
55.
56. 1st period
functional violations
(heart hypertrophy)
2d period
Pathological changes in arteries and arterioles (dystrophy):
- Arterioles sclerosis
- Arteriole’s wall infiltration by plasma (leads to dystrophy)
- Arterioles necrosis (hypertonic crisis arises in clinic)
- Vein’s wall thickening
Arterial hypertension after-effects
57. 33dd periodperiod
Secondary changes in organs and systemsSecondary changes in organs and systems
KidneyKidney
((nephrosclerosisnephrosclerosis andand chronicchronic
kidneykidney insufficiencyinsufficiency))
KidneyKidney
((nephrosclerosisnephrosclerosis andand chronicchronic
kidneykidney insufficiencyinsufficiency))
CNSCNS
–– brain hypoxiabrain hypoxia
–– neurons destructionneurons destruction
–– apoplexyapoplexy ((because vessels destruction and rupturebecause vessels destruction and rupture
leads toleads to brain hemorrhagesbrain hemorrhages and brainand brain
destructiondestruction))
CNSCNS
–– brain hypoxiabrain hypoxia
–– neurons destructionneurons destruction
–– apoplexyapoplexy ((because vessels destruction and rupturebecause vessels destruction and rupture
leads toleads to brain hemorrhagesbrain hemorrhages and brainand brain
destructiondestruction))
HeartHeart
Decompensate heart failureDecompensate heart failure
HeartHeart
Decompensate heart failureDecompensate heart failure
Organs of visionOrgans of vision
- retinopathyretinopathy ((retina’sretina’s vessels injuryvessels injury))
- hemorrhages and separation (exfoliation) ofhemorrhages and separation (exfoliation) of
retinaretina,, that leads to blindnessthat leads to blindness
Organs of visionOrgans of vision
- retinopathyretinopathy ((retina’sretina’s vessels injuryvessels injury))
- hemorrhages and separation (exfoliation) ofhemorrhages and separation (exfoliation) of
retinaretina,, that leads to blindnessthat leads to blindness
Endocrine systemEndocrine system
Glands atrophy and sclerosisGlands atrophy and sclerosis
Endocrine systemEndocrine system
Glands atrophy and sclerosisGlands atrophy and sclerosis
Arterial hypertension after-effectsArterial hypertension after-effects
58.
59. Hypertensive crisisHypertensive crisis
DefinitionDefinition
Severe elevation in BP ( >220/120 mmHg)Severe elevation in BP ( >220/120 mmHg)
Sub classified into emergency and urgencySub classified into emergency and urgency
Hypertensive emergencyHypertensive emergency
Require an immediate reduction in BP ( 1 hr )Require an immediate reduction in BP ( 1 hr )
Rx IV therapy and in ICURx IV therapy and in ICU
Hypertensive urgencyHypertensive urgency
No evidence of progressive end-organ injuryNo evidence of progressive end-organ injury
Require only gradual reduction in BP in 24-48 hrRequire only gradual reduction in BP in 24-48 hr
60. Laboratory TestsLaboratory Tests
§ Routine Tests
• Electrocardiogram
• Urinalysis
• Blood glucose, and hematocrit
• Serum potassium, creatinine, or the corresponding estimated
GFR, and calcium
• Lipid profile, after 9- to 12-hour fast, that includes high-
density and low-density lipoprotein cholesterol, and
triglycerides
§ Optional tests
• Measurement of urinary albumin excretion or
albumin/creatinine ratio
§ More extensive testing for identifiable causes is not generally
indicated unless BP control is not achieved
61. Collaborative CareCollaborative Care
Lifestyle ModificationsLifestyle Modifications
Wt. reduction
10 kg (22 lb) loss; SBP by 5-20 mm Hg
DASH eating plan (dietary approaches to stop
hypertension)
Na reduction
<2.4 g of sodium/day
Moderate alcohol intake
Men: 2 drinks/day or less
Women: 1 drink/day or less
62. Collaborative CareCollaborative Care
Lifestyle ModificationsLifestyle Modifications
Physical activity:Physical activity:
– Regular physical (aerobic) activity,Regular physical (aerobic) activity,
– At least 30 min, most days of weekAt least 30 min, most days of week
Avoidance of tobacco productsAvoidance of tobacco products
Stress managementStress management
63. ExperimentalExperimental models of arterialmodels of arterial
hypertensionhypertension..
Models confirming a role of the nervous factor in increase ofModels confirming a role of the nervous factor in increase of
arterial pressure:arterial pressure:
1.1. Arterial hypertension owing to an irritation ofArterial hypertension owing to an irritation of
hypothalamus nucleuseshypothalamus nucleuses. The irritation of a back nucleus. The irritation of a back nucleus
frequently resultsfrequently results toto hypertension, connected with increasehypertension, connected with increase
of cardiac output. The irritation of a central nucleus causesof cardiac output. The irritation of a central nucleus causes
hyperensionhyperension due todue to of peripheral resistance increase.of peripheral resistance increase.
Electricity stimulation ventro-medial nucleus givesElectricity stimulation ventro-medial nucleus gives
hypertension, which depends from simultaneoushypertension, which depends from simultaneouslyly increaseincrease
of cardiac output and peripheral resistance.of cardiac output and peripheral resistance.
2.2. Arterial hypertension from double-side damage nucleusArterial hypertension from double-side damage nucleus
tractus solitarii totractus solitarii to medullamedulla oblongoblongataata of rats, where areof rats, where are
located primary synapsis of sinuaorticus baroreceptors.located primary synapsis of sinuaorticus baroreceptors.
Arterial pressure is increased immediately without changeArterial pressure is increased immediately without change
of frequency of cardiac rof frequency of cardiac rateate. The reason of hypertension is. The reason of hypertension is
the sharp increase of peripheral resistancethe sharp increase of peripheral resistance
3.3. Reflexogenic hypertensionReflexogenic hypertension,, inin dogs and rabbits adogs and rabbits affterffter
section depressor nerve Ludvig-Cion or sinus nerves Heringsection depressor nerve Ludvig-Cion or sinus nerves Hering
..
64. ExperimentalExperimental models of arterial hypertensionmodels of arterial hypertension..
Models, which confirm participation renals factor in occurrence andModels, which confirm participation renals factor in occurrence and
stabilization of arterial hypertension:stabilization of arterial hypertension:
1.1. Vasorenal hypertensionVasorenal hypertension, which is caused by narrowing renals arteries., which is caused by narrowing renals arteries.
Conditions of reproduction: а) arteries should be narrowed only partially,Conditions of reproduction: а) arteries should be narrowed only partially,
instead of are blocked completely;instead of are blocked completely; bb) the narrowing should be double-) the narrowing should be double-
side; c) the variant is possible(probable): narrowing arteries of one kidneyside; c) the variant is possible(probable): narrowing arteries of one kidney
plusplus removalremoval of the other kidney.of the other kidney.
2.2. Renoprival hypertensionRenoprival hypertension it arises afterit arises after removelremovel both kidneys andboth kidneys and spendingspending
ofof animal on dialysisanimal on dialysis..
Models confirming a role of adrenal glands in fixing arterialModels confirming a role of adrenal glands in fixing arterial
hypertension:hypertension:
1.1. Mineral-corticoids hypertensionMineral-corticoids hypertension –– in the casein the case ofof longlong introduction ofintroduction of
aldosteron with simultaneousaldosteron with simultaneouslyly purpose of solution NaCl instead of water.purpose of solution NaCl instead of water.
2.2. Salty hypertensionSalty hypertension. Sodium chlorids in a fair quantity even without. Sodium chlorids in a fair quantity even without
additional hormonal effects is capable to cause hypertension.additional hormonal effects is capable to cause hypertension.
Model confirming role of the hereditary factor in etiology ofModel confirming role of the hereditary factor in etiology of
hypertonic disease.hypertonic disease.
Exists genetic (spontaneous) hypertension in rats.Exists genetic (spontaneous) hypertension in rats. InIn the animal withthe animal with
spontaneous hypertension is revealed higher, than in normal animals,spontaneous hypertension is revealed higher, than in normal animals,
permeability ions channels in membranes smoothmusclepermeability ions channels in membranes smoothmuscle cellscells of arteries.of arteries.
These membrane defects can have some significance in increase ofThese membrane defects can have some significance in increase of
arteries tonus and regulation of volume extracellular liquid. They can bearteries tonus and regulation of volume extracellular liquid. They can be
considered as one of the factors pathogenesis hypertonic disease.considered as one of the factors pathogenesis hypertonic disease.
65. ReferencesReferences
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Wilkins), Trade paperback (2003)Wilkins), Trade paperback (2003) // Carol Mattson Porth, Kathryn J. Gaspard. –ChapterCarol Mattson Porth, Kathryn J. Gaspard. –Chapter
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6.6. SilbernaglSilbernagl S.S. Color Atlas of PathophysiologyColor Atlas of Pathophysiology / S./ S. SilbernaglSilbernagl, F., F. LangLang //// ThiemeThieme..
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7.7. Corwin Elizabeth J. Handbook of Pathophysiology / Corwin Elizabeth J. – 3th edition.Corwin Elizabeth J. Handbook of Pathophysiology / Corwin Elizabeth J. – 3th edition.
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427, 431–435.427, 431–435.
8.8. Copstead Lee-Ellen C. Pathophysiology / Lee-Ellen C. Copstead, Jacquelyn L.Copstead Lee-Ellen C. Pathophysiology / Lee-Ellen C. Copstead, Jacquelyn L.
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9.9. Robbins and Cotran Pathologic Basis of DiseaseRobbins and Cotran Pathologic Basis of Disease 88th edition./ Kumar, Abbas, Fautoth edition./ Kumar, Abbas, Fauto. –. –
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9.9. American Heart Association WebsiteAmerican Heart Association Website
Editor's Notes
The systolic blood pressure reflects the rhythmic ejection of blood into the aorta (Fig. 1). As blood is ejected into the aorta, it stretches the vessel wall and produces a rise in aortic pressure. The extent to which the systolic pressure rises or falls with each cardiac cycle is determined by the amount of blood ejected into the aorta with each heart beat (i.e., stroke volume), the velocity of ejection, and the elastic properties of the aorta. Systolic pressure increases when there is a rapid ejection of a large stroke volume or when the stroke volume is ejected into a rigid aorta. The elastic walls of the aorta normally stretch to accommodate the varying amounts of blood that are ejected into the aorta; this prevents the pressure from rising excessively during systole and maintains the pressure during diastole. In some elderly persons, the elastic fibers of the aorta lose some of their elasticity, and the aorta becomes more rigid. When this occurs, the aorta is less able to stretch and buffer the pressure that is generated as blood is ejected into the aorta, resulting in an elevated systolic pressure.
Diastolic Blood Pressure
The diastolic blood pressure is maintained by the energy that has been stored in the elastic walls of the aorta during systole. The level at which the diastolic pressure is maintained depends on the elastic properties of the aorta and large arteries and their ability to stretch and store energy, the resistance of the arterioles that control the outflow of blood into the microcirculation, and the competency of the aortic valve. The small diameter of the arterioles contributes to their effectiveness as resistance vessels because it takes more force to push blood through a smaller vessel than a larger vessel. When there is an increase in peripheral vascular resistance, as with sympathetic stimulation, diastolic blood pressure rises. Closure of the aortic valve at the onset of diastole is essential to the maintenance of the diastolic pressure. When there is incomplete closure of the aortic valve, as in aortic regurgitation, the diastolic pressure drops as blood flows backward into the left ventricle, rather than moving forward into the arterial system.
Pulse Pressure
The pulse pressure is the difference between the systolic and diastolic pressures. It reflects the pulsatile nature of arterial blood flow and is an important component of blood pressure. During the rapid ejection period of ventricular systole, the volume of blood that is ejected into the aorta exceeds the amount that exits the arterial system. The pulse pressure reflects this difference. The pulse pressure rises when additional amounts of blood are ejected into the arterial circulation, and it falls when the resistance to outflow is decreased. In hypovolemic shock, the pulse pressure declines because of a decrease in stroke volume and systolic pressure. This occurs despite an increase in peripheral vascular resistance, which maintains the diastolic pressure.
Mean Arterial Pressure
The mean arterial blood pressure represents the average blood pressure in the systemic circulation. The mean arterial pressure can be estimated by adding one third of the pulse pressure to the diastolic pressure (i.e., diastolic blood pressure + pulse pressure/3). Hemodynamic monitoring equipment in intensive and coronary care units measures or computes mean arterial pressure automatically. Because it is a good indicator of tissue perfusion, the mean arterial pressure often is monitored, along with systolic and diastolic blood pressures, in critically ill patients.
Sympathetic Nervous System (4 Points)
1. both cardiac output and TPR increased with SNS tone
2. level of efferent SNS tone is set in CNS by medullary vasomotor center. stimulation of alpha2 adrenergic receptors in medulla lowers SNS tone and BP.
3. inhibition of ganglionic transmission or NE release from post-ganglionic nerve fiber can reduce CO and TPR.
4. alpha1 or beta1 adrenergic receptor blockade can reduce TPR and CO respectively.
Blood Pressure – influenced by 3 major factors
Total peripheral resistance
Baroreceptor (BR) and CNS Influences
u BP r u BR firing rate r vasodilation r d BP
d BP r d BR firing rate r u sympathetics r u BP
Chemoreceptor influences
dO2, u CO2, d pH r CNS stim. r vasoconstriction
Circulating catecholamine influences
E and NE have varying effects on TP
E and NE usually activate a receptors r u TPR
Fight or flight response
Q
Blood Volume
Renin – Angiotensin system
Sympathetic Activity
Noradrenaline and adrenaline, either from sympathetic neurons or epirenal medullar cells, interact with peripheral smooth cell-μ1 adrenergic receptors increasing vascular tone at pre-capillary level. They also increase heart rate and contractility through interaction with cardiac-β1 adrenergic receptors. The net effect of sympathetic stimulation is an increase in CO. Chronic adrenergic stimulation induces vascular remodelling and smooth muscular cells proliferation, thus increasing diastolic pressure, while arterial vessels thicken and stiffen due to lipid, calcium and collagen accumulation and deposition in vascular walls.
Moreover, chronically increased vascular tone leads to increased myocardial mass (e.g., left ventricular hypertrophy) and oxygen consumption, which in turn can lead to chronic ischemia or acute myocardial infarction. At renal level, increased sympathetic activity enhances sodium and water retention, further contributing to maintain elevated blood pressure.
Short-Term Regulation
The mechanisms for short-term regulation of blood pressure, those occurring over minutes or hours, are intended to correct temporary imbalances in blood pressure, such as occur during physical exercise and changes in body position. These mechanisms also are responsible for maintenance of blood pressure at survival levels during life-threatening situations. The short-term regulation of blood pressure relies mainly on neural and hormonal mechanisms, the most rapid of which are the neural mechanisms.
The renin-angiotensin-aldosterone system plays a central role in blood pressure regulation. Renin is an enzyme that is synthesized, stored, and released by the kidneys in response to an increase in sympathetic nervous system activity or a decrease in blood pressure, extracellular fluid volume, or extracellular sodium concentration. Most of the renin that is released leaves the kidney and enters the bloodstream, where it acts enzymatically to convert an inactive circulating plasma protein called angiotensinogen to angiotensin I (Fig. 5). Angiotensin I travels to the small blood vessels of the lung, where it is converted to angiotensin II by the angiotensin-converting enzyme that is present in the endothelium of the lung vessels. Although angiotensin II has a half-life of several minutes, renin persists in the circulation for 30 minutes to 1 hour and continues to cause production of angiotensin II during this time.
Angiotensin II functions in both the short-term and longterm regulation of blood pressure. It is a strong vasoconstrictor, particularly of arterioles and to a lesser extent of veins. The vasoconstrictor response produces an increase in peripheral vascular resistance (and blood pressure) and functions in the shortterm regulation of blood pressure. A second major function of angiotensin II, stimulation of aldosterone secretion from the adrenal gland, contributes to the long-term regulation of blood pressure by increasing salt and water retention by the kidney. It also acts directly on the kidney to decrease the elimination of salt and water.
From lecture Doctor of medicine, professor Khara Mariya Romanivna
Hypertension as a diagnosis is considered when the average of TWO or more consecutive clinical visits documents a DBP of 90 mmHg or greater or a SBP of 140 mmHg or greater.
Elevated SBP is the main contributor of target organ damage.
Age/ Loss of arterial elasticity, &gt;65 years, increased collagen content, increased vascular resistance
heredity-, Close relatives
Sex/Race- men (female &gt;55 yrs), African-Americans
Obesity- central abdominal obesity- increases cardiac workload and strains the vessels
Stimulants- Smoking/caffeine-vasoconstrictors
Sodium- water retention causes volume expansion/ decreases effects of certain B/P meds
Hyperlipidemia- plaque in the vessels
Diabetes- elevated glucose, insulin, and lipoprotein metabolism
Socioeconomic-lower and less educated
Renin is an enzyme released by the kidney to help control the body&apos;s sodium-potassium balance, fluid volume, and blood pressure.
Description
When the kidneys release the enzyme renin in response to certain conditions (high blood potassium, low blood sodium, decreased blood volume), it is the first step in what is called the renin-angiotensin-aldosterone cycle. This cycle includes the conversion of angiotensinogen to angiotensin I, which in turn is converted to angiotensin II, in the lung. Angiotensin II is a powerful blood vessel constrictor, and its action stimulates the release of aldosterone from an area of the adrenal glands called the adrenal cortex. Together, angiotensin and aldosterone increase the blood volume, the blood pressure, and the blood sodium to re-establish the body&apos;s sodium-potassium and fluid volume balance. Primary aldosteronism, the symptoms of which include hypertension and low blood potassium (hypokalemia), is considered &quot;low-renin aldosteronism.&quot;
Figure 1. Examples of Mild Hypertensive Retinopathy. Panel A shows arteriovenous nicking (black arrow) and focal narrowing (white arrow). Panel B shows arteriovenous nicking (black arrows) and widening or accentuation (&quot;copper wiring&quot;) of the central light reflex of the arterioles (white arrows).
Causes of Secondary Hypertension
Autonomic hyperactivity (spinal cord injury, Guillain-Barre syndrome, diabetes mellitus)
• Intracranial hypertension and brain edema
• Pheochromocytoma
• Tumors secreting renin or aldosterone
• Eclampsia and preeclampsia
• Vasculitis and scleroderma
• Parenchymal renal disease (e.g., acute glomerulonephritis)
• Renal vascular disease (e.g., renal artery stenosis or thrombosis)
• Drugs (e.g., cocaine, amphetamine, phencyclidine)
• Drug interaction (e.g., monoamine oxydase inhibitor with tyramine, tryciclics antidepressants or sympathomimetics)
• Abrupt withdrawal of anti-hypertensive drugs (e.g., clonidine)
• Alcohol withdrawal
Gestational Hypertension. Gestational hypertension represents a blood pressure elevation without proteinuria that is detected for the first time after midpregnancy. It includes women with preeclampsia syndrome who have not yet manifested proteinuria, as well as women who do not have the syndrome. The final determination that a woman does not have the preeclampsia syndrome is made only postpartum. If preeclampsia has not developed and blood pressure has returned to normal by 12 weeks postpartum, the condition is considered to be gestational hypertension. If blood pressure elevation persists, a diagnosis of chronic hypertension is made.
Preeclampsia-Eclampsia. Preeclampsia-eclampsia is a pregnancyspecific syndrome. It is defined as an elevation in blood pressure and proteinuria developing after the 20th week of gestation. It is defined as an elevation in blood pressure (systolic &gt;140 or diastolic &gt;90 mm Hg) and proteinuria (≥0.3 g/24 hours) developing after the 20th week of gestation. The presence of systolic pressure ≥160 mm Hg, diastolic pressure ≥110 mm Hg; proteinuria (≥2.0 g/24 h); increased serum creatinine (&gt;1.2 mg); platelet counts &lt;100,000 cells/mm; elevated liver enzymes; persistent headache or cerebral or visual disturbances; and persistent epigastric pain serve to reinforce the diagnosis. Preeclampsia may occur in women who already are hypertensive, in which case the prognosis for the mother and fetus tends occurence, in a woman with preeclampsia, of seizures that cannot be attributed to other causes.
Preeclampsia occurs primarily during first pregnancies and during subsequent pregnancies in women with multiple fetuses, diabetes mellitus, or coexisting renal disease. It is associated with a condition called a hydatidiform mole (i.e., abnormal pregnancy caused by a pathologic ovum, resulting in a mass of cysts). Women with chronic hypertension who become pregnant have an increased risk of preeclampsia and adverse neonatal outcomes, particularly when associated with proteinuria early in pregnancy.
Pregnancy-induced hypertension is thought to involve a decrease in placental blood flow, leading to the release of toxic mediators that alter the function of endothelial cells in blood vessels throughout the body, including those of the kidney, brain, liver, and heart. The endothelial changes result in signs and symptoms of preeclampsia and, in more severe cases, of intravascular clotting and hypoperfusion of vital organs. There is risk for development of disseminated intravascular coagulation, cerebral hemorrhage, hepatic failure, and acute renal failure. Thrombocytopenia is the most common hematologic complication of preeclampsia. Platelet counts of less than below 100,000/mm3 signal serious disease. The cause of thrombocytopenia has been ascribed to platelet deposition at the site of endothelial injury. The renal changes that occur with preeclampsia include a decrease in glomerular filtration rate and renal blood flow. Sodium excretion may be impaired, although this is variable. Edema may or may not be present. Some of the most severe forms of preeclampsia occur in the absence of edema. Even when there is extensive edema, the plasma volume usually is lower than that seen in normal pregnancy. Liver damage, when it occurs, may range from mild hepatocellular necrosis with elevation of liver enzymes to the more ominous hemolysis, elevated liver function tests, and low platelet count (HELLP) syndrome that is associated with significant maternal mortality. Eclampsia, the convulsive stage of preeclampsia, is a significant cause of maternal mortality. The pathogenesis of eclampsia remains unclear and has been attributed to both increased coagulability and fibrin deposition in the cerebral vessels.
From lecture Doctor of medicine, professor Khara Mariya Romanivna
From lecture Doctor of medicine, professor Khara Mariya Romanivna