cardiovascular system disorders 2€™s pathophysiology: concepts of altered health states from...

Cardiovascular System Disorders 2

Lecture 20

Pathology and Clinical

Science 1 (BIOC211)

Department of BioscienceText Reference:

Porth’s Pathophysiology: Concepts of Altered Health States

Sheila C. Grossman & Carol Mattson Porth.

Ninth Edition.

Copyright © 2014 Lippincott, Williams & Wilkins Publishers, Inc.

© endeavour.edu.au

© Endeavour College of Natural Health endeavour.edu.au 2

Session Learning Outcomes

The aim of this session is to :

o Comprehend the pathophysiology of atherosclerosis

o Identify the risk factors and understand how to prevent

the atherosclerosis and Coronary Heart Disease (CHD)

o Describe the clinical features, investigations and

management of CHDs.


ATHEROSCLEROSIS

Introduction

oMay manifest as CAD (angina, MI,

sudden death), cerebrovascular

disease (stroke and TIA) or peripheral

vascular disease (claudication and

limb ischemia)


ATHEROSCLEROSIS

o Complex inflammatory process.

o Vascular endothelium is critical for maintaining

vascular integrity & homeostasis

o Atherogenesis thought to be triggered by initial

endothelial injury or dysfunction:

• Mechanical shear stresses

• Biochemical abnormalities

• Immunological factors

• Inflammation

• Genetic alteration


RISK FACTORSTraditional Risk Factors

• Age

– Increases with age

• Gender

– M > F (premenopausal)

– M = F (postmenopausal)

• Family History

– Other risk factors can be familial

– ? independent

• Smoking

– Proportional to quantity

– Decrease in risk (almost to normal) after 10yrs abstinence


RISK FACTORSo Diet and Obesity

• High fat, low antioxidants

o Hypertension

• Systolic & diastolic

o Hyperlipidaemia

– High LDL

– Low HDL

– Decreased cholesterol = reduced progression +

regression of coronary artery disease (CAD)

– Lipid lowering Rx = decreased mortality

o Diabetes mellitus

• Also magnifies the effect of other risk factors


LIPID TRANSPORT Schematic

representation

of the

exogenous and

endogenous

pathways for

triglyceride and

cholesterol

transport.

From Porth’s Pathophysiology: Concepts of Altered Health States. (9th ed., p. 744), by


Philadelphia, U.S.A. Walters Kluwer Health - Lippincott, Williams & Wilkins


RISK FACTORSNewer risk factors

o Sedentary life style

• Lack of exercise

o Psychological well-being

• Work stress, lack of social support, depression & personality

o Alcohol

o Genetic factors

o Lipoprotein (a)

o Coagulation factors

• Serum fibrinogen, homocysteine

o C-reactive protein (CRP)


RISK FACTOR MANAGEMENT

o Primary prevention

• modification of risk factors that reduce the development of coronary atheroma

o Secondary prevention

• modification of risk factors that slow the progression of established disease

o Smoking

• ↓ amount

• complete cessation

o Hypertension

• Control HT



oLipids

• any decrease is beneficial

• Lipid lowering agents (statins)

oExercise



o Weight

• Maintain ideal body weight

o Diabetes Mellitus (DM)

• Optimise BGL

o Diet

• Reduce saturated fat

• Increase vegetables + grains

• Fish, lean meat

• Limit take-away, snack food, cakes etc

• Avoid high cholesterol foods + offal


DEVELOPMENT OF

ATHEROSCLEROSIS

o Follows endothelial dysfunction

o Accumulation of oxidized lipoproteins

o Lipoproteins are taken up by macrophages

o Macrophages become lipid-laden foam cells

o Fatty streaks appear & progress

o Plaque formation

o Cytokine release further damages endothelium


DEVELOPMENT OF ATHEROSCLEROSIS

From Porth’s Pathophysiology: Concepts of Altered Health States. (9th ed., p. 750),

by Sheila C. Grossman & Carol Mattson Porth.


Endothelial Cell Injury Migration of Inflammatory

Cells



Lipid Accumulation &

Smooth Muscle Cell

ProliferationPlaque Structure

From Porth’s Pathophysiology: Concepts of Altered Health States. (9th ed., p. 751),

by Sheila C. Grossman & Carol Mattson Porth.




Porth’s Pathophysiology: Concepts of Altered Health States




© Endeavour College of Natural Health endeavour.edu.au


From Pathology. (2nd ed., p. 161), by A. Stevens & J. Lowe. 2000, London. Mosby,

Harcourt Publishers Ltd.

© Endeavour College of Natural Health endeavour.edu.au

ATHEROSCLEROSIS

http://www.portalesmedicos.com/imagenes/publicaciones_10/1009_modelo_animal_arterio

sclerosis/arteria_coronaria_aterosclerosis.jpg


DEVELOPMENT OF

ATHEROSCLEROSIS

oCollagen produced by smooth muscle cells = advanced/raised fibrolipidplaque

oAdvanced plaque can grow slowly (encroaching on lumen) or become unstable (thrombosis with obstruction = complicated plaque)


DEVELOPMENT OF

ATHEROSCLEROSIS

o Plaque thrombosis caused by:

• Superficial endothelial injury exposing connective tissue

with platelet adhesion = superficial thrombus

• Deep endothelial fissuring of advanced plaque allowing

blood to enter inside the plaque (highly thrombogenic

environment) = thrombus within plaque

o 50% reduction in luminal diameter results in

haemodynamically significant stenosis

• Smaller distal arteries/arterioles become maximally

dilated

• Any increase in myocardial demand = ischaemia


COMPLICATIONS

From Pathophysiology for the Health Professions (2nd ed., p. 274), by B Gould, 2002. Philadelphia. W B Saunders Company.


ATHEROSCLEROSIS

From Porth’s Pathophysiology: Concepts of Altered Health States.

(9th ed., p. 747), by Sheila C. Grossman & Carol Mattson Porth.

Philadelphia, U.S.A. Walters Kluwer Health - Lippincott, Williams &

Wilkins


CORONARY HEART DISEASE

CHD is the most common form of heart disease

o Epidemiology

• Single most important cause of

premature death in Europe, South

America, Australia and New Zealand

• In UK 1 in 3 men and 1 in 4 women die

from CHD


CORONARY HEART DISEASE

CAD results in variety of clinical situations

• Stable angina pectoris (AP)

• Unstable AP (UAP)

• Myocardial Infarction (MI) = advanced plaque with total occlusive thrombus

• Heart failure

• Arrhythmia

• Sudden death


STABLE ANGINA

Angina Pectoris

Symptom complex of chest pain, discomfort due to transient myocardial ischaemia

o Causes

• Coronary atheroma is the most common cause

• Aortic valve disease

• Hypertrophic cardiomyopathy


STABLE ANGINA

Clinical features

• Central chest pain, discomfort or

breathlessness precipitated by exertion

or stress

• Promptly relieved by rest

Investigation

• Resting ECG, exercise ECG

• Coronary arteriography


STABLE ANGINA

Management

• Careful assessment

• Risk factors management

• Control symptoms

– Antiplatelet therapy - Low dose aspirin

– Antianginal drugs – nitrates, beta-blockers

– Percutaneous coronary interventions (PCI) - Stents

– Percutaneous trans-coronary arteriogram (PTCA)

– Coronary artery bypass graph (CABG)

Prognosis

• Depends on number of diseased vessels, degree of left ventricular dysfunction

• Single vessel and good LV function ( 5 yr survival > 90%)


BALLOONING – STENTS – BYPASS

Stent insertion

Bypass Graft





ANGIOPLASTY

http://www.vascular.co.nz/angioplastyrev%20copy.jpg


UNSTABLE ANGINA

Characterised by new onset or rapidly worsening angina, angina on minimal exertion or angina at

rest

Diagnosis

• Evaluation of ECG

• Biochemical markers for cardiac damage

Management

• Admission to hospital due to risk of myocardial infarction (MI)

• Bed rest, antiplatelet therapy

• Same as for stable angina


ANGINA

PAIN





MYOCARDIAL INFARCTION

Definition

o Result of sudden decrease or interruption to arterial blood flow to the myocardium

Pathophysiology

o Coronary atheroma with plaque rupture + superimposed thrombus

o Myocardial necrosis = permanent myocardial damage

Causes

o Atheroma (predominantly) as above



Clinical Features

o Key CF= chest pain

• severe, constant pain, unrelieved with

rest/nitrates

o Nausea/vomiting/sweating/breathlessness

o Anxiety and fear of impending death

o Collapse and syncope

o Sudden death



Investigations

o ECG

o Biochemical markers – Creatine Kinase (CK); Troponin

o Chest X ray

o Echocardiography

Treatment

o Immediate access to medical care and defibrillation facility

o Emergency Rx (aspirin, thrombolysis, pain relief (morphine)

o CCU, bed rest

o Identify & Correct Risk Factors

o Subsequent Medical Rx – aspirin, B-blockers, ACEI, statins)

o Ongoing assessment


MYOCARDIAL INFARCTIONComplications

• Arrhythmias

• Post infarct ischaemia

• Acute circulatory failure

• Mechanical complications

–Papillary muscle damage – valve lesions

–Rupture of interventricular septum – VSD

–Rupture of ventricle

• Embolism

• Heart failure

• Ventricular aneurysm



Prognosis

o Mortality 25% without medical care

o 50% of death from MI occur within 24 hrs

o 40% die within 1 month

o Those survive an acute attack – 5 yr survival 75%

Differential Diagnosis

o As by main symptoms

o Cardio/pulmonary (CP) (CVS vs. other)

o MI vs. Upper abdominal pathologies


Readings and ResourcesResources:

o Set Textbooks:

Colledge, N.R., Walker, B.R. & Ralston S.H. (2014). Davidson’s Principles and Practice of Medicine, (22nd ed.). Edinburgh.

Churchill Livingstone.

Grossman, S.C. & Porth, C.M. (2014). Porth’s Pathophysiology: concepts of altered health states, (9th ed.). Philadelphia,

U.S.A. Walters Kluwer Health - Lippincott, Williams & Wilkins.

o Additional textbooks:

Davies, A. & Moores, C. (2010). The respiratory system: basic science and clinical conditions, (2nd ed.). Edinburgh. Churchill,

Livingstone, Elsevier.

Field, M., Pollock, C., Harris, D. (2010). Systems of the Body: The Renal System; Basic Science and Clinical Conditions. (2nd

ed.). United Kingdom: Churchill Livingstone.

Jamison, J.R. (2006) Differential Diagnosis for Primary Care: a handbook for health care practitioners. (2nd ed.). Edinburgh.

Churchill Livingstone.

Lee, G. & Bishop, P. (2013). Microbiology and Infection Control for Health Professionals, (5th ed.). Frenchs Forest, NSW.

Pearson Education.

McCance, K.L. & Huether, S.E. (2014). Pathophysiology: the biological basis for disease in adults and children, (7th ed.). St.

Louis, MO. Elsevier.

Murphy, K. (2011). Janeway’s immunobiology, (8th ed.). New York. Garland Science.

Noble, A., Johnson, R. & Bass, P. (2010). The cardiovascular system: basic science and clinical conditions, (2nd ed.).

Edinburgh. Churchill, Livingstone, Elsevier.

Pagana, K.D. & Pagana, T.J. (2013). Mosby’s diagnostic and laboratory test reference, (11th ed.). St. Louis, MO. Elsevier.

Smith, M.E. & Morton, D.G. (2010). The digestive system: basic science and clinical conditions, (2nd ed.). Edinburgh.

Churchill, Livingstone, Elsevier.

VanMeter, K.C. & Hubert, R. (2014). Gould’s pathophysiology for health professions, (5th ed.). St. Louis, MO. Elsevier.


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