Week 5 Module 1 - Disorders of Blood Pressure, Heart Failure, Circulatory Shock

FOCUS

Blood pressure

volume ejected by blood on walls of arteries

Adequate perfusion of body tissue depends on

Pumping ability of heart, transport of blood through vessels, sufficient blood to fill circulatory system, tissues ability to extract and use oxygen and nutrients

BP determined by

volume ejected by heart into arteries, elastance of walls of arteries, rate at which blood flows out of arteries

BP approximated by

flow or CO and systemic vascular resistance or svr

Systolic pressure

pressure while heart is contracting, normal is less than 120 mmhg

Diastolic pressure

pressure while heart is relaxing, normal is less than 80 mmhg

Pulse pressure

Difference between systolic and diastolic

MAP (mean arterial pressure)

Average pressure in arterial system during ventricular contraction and relaxation

Ideal BP

adequately perfuses all various organ systems without causing damage

RAAS system and low bp

Kidneys release renin, initiating cascade resulting in angiotensin II for vasoconstriction and aldosterone for sodium and water retention to increase blood volume and bp

Antidiuretic hormone and low bp

Released by hypothalamus to increase water reabsorption in kidneys to increase blood volume and bp

Hypertension

BP is permanently higher than normal, systolic 140 mmhg or more, diastolic is 90 mmhg or more

Aetiology of primary hypertension

Heterogenous disorder with various overlapping factors

Pathogenesis of primary hypertension

interaction of genetic and environmental factors, altered structure and function of cv system and kidneys, gradually over years

Primary hypertension

High BP in which secondary causes are not known

Primary hypertension unmodifiable risk factors

Age, family history, race, sex (male)

Primary hypertension modifiable risk factors

high salt diet, excess alcohol, obesity, physical inactivity, lower SES

Pathphysiology of primary hypertension

Obscure, rarely single clear reason, vessel wall inflammation and loss of vessel integrity

Aetiology of secondary hypertension

Result of underlying condition

Pathyphysiology of secondary hypertension

Renovascular hypertension, primary aldosteronism, obstructive sleep apnoea, alcoholism, prescription or over the counter medications

Clinical manifestations of hypertension

Waking or frequent headaches, blurred vision, confusion, fatigue, dizziness or unsteadiness in gait, nocturia, dependent oedema, muscle weakness or cramps, arrhythmias, sweating

Hypertension-mediated organ damage (HMOD) in heart

Left ventricular hypertrophy and left atrial dilation, atrial fibrillation, valvular heart disease

Hypertension-mediated organ damage (HMOD) in vasculature

Peripheral, aortic disease - aneurysm or dissection

Hypertension-mediated organ damage (HMOD) in brain

Dementia and cognitive impairment

Hypotension

decrease in systemic BP below accepted low values, systolic less than 90 mmhg or diastolic less than 60 mmhg

Clinically significant hypotension

Drop of equal to or more than 20/10 mmhg from baseline

Aetiology of hypotension - decreased volume

Decrease venous return = decreased preload = decrease co = decrease bp

Aetiology of hypotension - decreased co

decreased contractility or decreased hr = decreased stroke volume = decreased bp

Aetiology of hypotension - decreased svr

pathological vasodilation = blood pooling in periphery = decreased bp

Aetiology of hypotension - autonomic / neurogenic

failure of baroreceptor reflex or loss of sympathetic tone

Hypotension pathogenesis - decreased cardiac output

Any condition that impairs myocardial contractility, reduced reload or affected heart rate

Hypotension pathogenesis - Reduced systemic vascular resistance (SVR)

Vasodilation decreases svr and causes a drop in bp, caused by autonomic dysfunction or distributive shock = excessive vasodilation due to release of inflammatory mediators

Hypotension pathogenesis - impaired baroreceptor reflex

Autonomic neuropathy, prolonged bed rest, neurodegenerative disease

Hypotension pathogenesis - fluid and electrolyte imbalance

Hypovolaemia due to dehydration, haemorrhage or excessive diuresis, electrolyte imbalances worsen hypotension

Hypotension pathogenesis - endocrine dysregulation

Adrenal insufficiency, hypothyroidism decreases cardiac contractility and heart rate

Hypotension pathogenesis - autonomic nervous system dysfunction

Inadequate beta compensation leads to hypotension

Clinical manifestations of hypotension - symptoms

dizziness or light-headedness, lack of concentration, blurred vision, nausea, rapid shallow breathing, fatigue, thirst, palpitations, tremor, anxiety

Clinical manifestations of hypotension - signs

Altered BP, tachycardia, pallor cold clammy skin, weak thready pulse, prolonged capillary refill, confusion, fainting

Mechanisms that regulate arterial pressure

baroreceptor reflex, ADH, RAAS

Baroreceptors

Mechanoreceptors that relay info in autonomic nervous system

High pressure baroreceptors

Carotid sinuses and aortic arch

Low pressure baroreceptors

Atria, ventricles, pulmonary vasculature

Baroreceptors A-fibres

Large, myelinated, dynamic changes

Baroreceptors C-fibres

Smaller, unmyelinated, steady baseline BP control

Baroreceptor reflex (neural control - short term)

Utilises high pressure sensors in carotid sinuses and aortic arch to signal to medulla

Clinical diagnosis of heart failure

Symptoms caused by impaired ability of one or both ventricles to pump at normal pressure, structural or functional

Aetiology of heart failure

Myocardial or valvular heart disease, congenital heart defects, constrictive pericarditis, acute mi, hypertension

Pathophysiology of heart failure

Depressed ventricular contractility caused by underlying cardiac disease triggers neurohormonal activation, compensatory response involving key systems help maintain bp and vital organ perfusion

Clinical manifestations of heart failure

Short of breath, fatigue, swollen ankles, loss of appetite, coughing, dizziness, abnormal breathing, sleep disturbance

Heart failure with reduced ejection fraction (HFrEF)

Left ventricular ejection fraction is less than 40 percent

Haemodynamic changes of HFrEF

Decrease contractility, decreased stroke volume, increased preload, increased afterload, increased left ventricle end diastolic pressure

Neurohormonal activation of HFrEF

SNS increases norepinephrine, raas causes sodium and water retention

Ventricular remodelling of HFrEF

Eccentric hypertrophy, cellular changes, shape changes

Heart failure with reduced ejection fraction common causes

coronary heart disease, previous mi, hypertension

Heart failure with reduced ejection fraction leads to

Poor cardiac output, activates neurohormonal responses that long term can be either maladaptive or ineffectual

Heart failure with preserved ejection fraction (HFpEF)

Left ventricular ejection fraction greater than 50 percent

Diastolic dysfunction with HFpEF

Slowed relaxation, stiff ventricle, atrial dependence

Haemodynamic abnormalities with HFpEF

Increased left ventricle diastolic pressure at rest and during exercise, increased left atrial and pulmonary venous pressure, reduced left ventricle distensibility shifts pressure volume curve upward

Structural remodelling with HFpEF

Concentric hypertrophy, increased wall thickness, fibrosis stiffens heart and impairs relaxation

Right heart and pulmonary circulation with HFpEF

Majority experience pulmonary hypertension, chronically elevated left atrial pressure transmitted to pulmonary circulation, right ventricle dysfunction due to chronic afterload

Pathophysiology of Heart failure with preserved ejection fraction

Highly heterogenous disease, echocardiography, myocardial stiffening, reduced left ventricular compliance, impaired relaxation

Aetiology of Heart failure with preserved ejection fraction

Hypertension, ischaemic heart disease, diabetes, valvular heart disease

Class 1 HF severity

patients with heart disease without resulting limitation of physical activity, physical activity does not cause symptoms

Class 2 HF severity

Patients with heart disease resulting in slight limitation of physical activity, symptoms develop with ordinary activity but not at rest

Class 3 HF severity

Patients with heart disease resulting in marked limitation of physical activity, symptoms develop with less than ordinary physical activity but not at rest

Class 4 HF severity

Patients with heart disease resulting in inability to carry on physical activity without discomfort, symptoms may occur at rest

Common manifestations of heart failure

Dyspnoea on exertion, orthopnoea, fatigue, limited exercise tolerance, cyanosis, cachexia and malnutrition, distention of jugular veins, fluid retention and oedema

Shock definition

State of cellular and tissue hypoxia due to either reduced oxygen delivery, increased oxygen consumption, inadequate oxygen utilisation or a combination

Pathogenesis of shock

Collapse of systemic arterial blood pressure, blood flow does not meet energy demands and is diverted from most tissue and organs to supply vital organs causing cellular hypoxia

Results of shock

Renal failure, gastric ulcers, intestinal infarction, sloughing of skin

Types of shock - sepsis (distributive)

Infections or pancreatitis

Types of shock - neurogenic (distributive)

Interruption of autonomic pathways causing decreased vascular resistance and altered vagal tone

Types of shock - anaphylactic (distributive)

Widespread allergic reaction

Types of shock - cardiogenic

Problems affecting pumping of heart - cardiomyopathic, arrhythmic, mechanical

Types of shock - hypovolaemic

direct loss of effective circulating blood volume - haemorrhagic such as trauma, non haemorrhagic such as burns or vomiting

Types of shock - obstructive

Pulmonary vasculature or mechanical

Common manifestations of shock

Anxiety, altered mental state, hypotension, rapid weak and thready pulse, cool clammy skin, rapid shallow breaths, hypothermia, thirst, fatigue, distracted look in eyes often with dilated pupils

Treatment of shock

Airway and breathing, treat underlying cause of shock, specific therapies refined, response to therapy monitored