Cardiovascular Disorders Flashcards
Haemodynamic, Vascular, Heart Disorders
Oedema: Aetiology and Pathophysiology
Oedema results from changes in capillary pressures.
the selectively permeable capillary walls balance hydrostatic and osmotic pressure
-Hydrostatic pressure: pushes fluid into the tissues
Osmotic pressure: pushes fluid back into capillaries
Chemical mediators in injuries can increase capillary permeability
High blood pressure or venous blockages can raise Hydrostatic Pressure -> oedema
Lymphatic system obstructions post surgery -> lymphoedema
if there isn’t enough proteins in the capillary bed and if the kidneys excrete the proteins into the urine, it can decrease osmotic pressure –> oedema
Oedema: Epidemiology and Clinical Manifestations
Epidemiology:
exact prevalence (commonness and frequency) of Oedema is unknown
influenced by factors such as pregnancy, heart failure, kidney, or liver diseases, deep vein thrombosis, and certain medications
Clinical Manifestations:
weight gain, swelling, or puffiness
can be localised or systemic
Severe Oedema may threaten life, particularly in vital organs
Oedema: Diagnosis and Management
Diagnosis:
medical history, physical exams, tests e.g. X-rays and blood analysis
Management:
depends on Oedema location
e.g. leg elevations, compressions stockings, albumin, and diuretics are effective for limb oedema
e.g. specific management protocols for abdominal, brain and lung oedema
Hypertension: Background
is high blood pressure - a major cause CV Disease and stroke
Normal BP: 120/80 mmHg
Hypertension: 140/90 mmHg or higher
Young people: higher diastolic pressure
Older people: higher systolic pressure
often Asymptomatic, leading to underdiagnosis, known as the ‘silent killer’
Hypertension: Causes and Pathophysiology
Essential Hypertension: no known causes
Secondary Hypertension: from other conditions
Pregnancy can instigate Hypertension
involves vessel inflammation and muscle hypertrophy
Some theories include SNS imbalance, RAAS overactivity, metabolic syndrome (especially insulin resistance)
Hypertension: Epidemiology, risk factors and Management
Epidemiology and Risk Factors:
Higher prevalence in males and older individuals
influenced by obesity, diet, alcohol use, and nicotine
Management:
Regular monitoring for diagnosis
Lifestyle modifications (diet, exercise, stress reduction) and medications like diuretics and beta blockers
Circulatory Shock
Acute condition with significant hemodynamic alterations
leads to poor tissue perfusion and impaired cellular metabolism
Types of Circulatory Shock
cardiogenic (heart cannot pump enough blood to meet the body’s needs)
neurogenic (HR, BP and temp become unstable due to nervous system damage after a spinal cord injury)
anaphylactic (results from severe allergic reaction)
hypovolemic (when fluid or blood volume is lost drastically)
septic (when your blood pressure drops to a dangerously low level after an infection)
Circulatory Shock: Pathophysiology and phases of shock
due to Inadequate tissue perfusion and oxygen delivery
contains compensated (body can fix poor tissue perfusion) and non-compensated (body can no longer fix poor tissue perfusion) phases
Circulatory Shock: Clinical manifestations, diagnosis and management
symptoms include changes in BP, HR and consciousness
Treatment varies by type, often focusing on oxygenation and underlying causes
Peripheral Arterial Disease: Causes and Pathophysiology
reduced blood flow to limbs causing ischemia (reduced blood flow) and necrosis
imbalance in vasoconstriction and vasodilation regulation
Peripheral Arterial Disease: Clinical manifestations, diagnosis and management
Key symptom is claudication (muscle pain caused by little or lack of blood flow) and atherosclerosis (gradual) and embolism (sudden)
Diagnosis: doppler studies, angiography, or venography,
Management: aims to maintain or improve circulation, using surgical techniques and medications (e.g. aspirin - NSAID and clopidogrel - anti-platelet medication - to prevent blood clots)
Aneurysms: Causes and pathophysiology
changes in blood vessel walls leading to potential rupture due to abnormal bulging/dilation
often linked to atherosclerosis (thickening or hardening of arteries)
Types include:
True - vessel breaks
Dissecting - tear in vessel
False aneurysm - vessel leaks
Aneurysms: Clinical manifestations, diagnosis and management
is asymptomatic until rupture
Management: through surgery to prevent growth or rupture
Deep Vein Thrombosis (Thrombophlebitis and phlebothrombosis): causes and pathophysiology
Deep Vein Thrombosis is clot formation in deep veins
conditions related to inappropriate blood clot formation
Thrombophlebitis involves clot formation with venous wall inflammation
Phlebothrombosis involves blood clot formation but no inflammation