How the CVS fails Flashcards
Stroke
Rapid loss of brain function due to loss of perfusion to parts of the brain
Cerebrovascular accident
Haemorrhagic stroke
Cerebral blood vessel rupture
Ischaemic stroke
Cerbebral blood vessel blockage
Causes of BV burst
Stresses
- high pressure
- large diameter/ high wall tension
- low elasticity/ low compliance
- turbulent flow
Damage
- trauma
- atherosclerosis
- diabetes
Vessel wall tension
Tension in a cylinder is the force trying to rip the wall apart
Proportional to P x radius
Larger the vessel, greater the wall tension
Compliance
The change in volume caused by a change in pressure
Causes of turbulent flow
Junctions Mixing Obstacles - atherosclerosis - endothelial damage
Endothelium activities (6)
Blood vessel tone: local control of perfusion, vasodilation
Fluid filtration: blood brain barrier, CSF, kidney, GI secretions
Haemostasis: esp fibrinolysis
White cell recruitment: atherosclerosis
Angiogenesis
Hormone trafficking
Transcytosis
The transport of molecules across the cytoplasm, especially the epithelium
Acute myocardial infacrtion
Region of heart tissue is dead or dying
Usually caused by blocked coronary artery
Reduces the capacity of the heart to pump
Atherosclerosis
A disease process resulting in furring of the arteries
Asymptomatic but can lead to other disorders
Coronary artery disease
A disease process resulting in obstruction of the arteries supplying heart tissue
Angina or asymptomatic
Primary causes is atherosclerosis
Treatment for coronary artery disease
Drugs for hyperlipidaemia, angina or hypertension
Stenting or surgically replacing clogged vessels
Plaque rupture
When the fibrous cap of a plaque bursts open
Can cause a thrombus or and embolism
MI: sympathetic activity
Sympathetic nervous system releases adrenaline and noradrenaline
- response to pain and haemodynamic abnormalities
In heart failure leads to:
- increased HR
- increased contractility
- increased PR
- increased risk of arrhythmia
Forces on H2O in capillaries
Arterial end:
- low osmotic pressure
- high hydrostatic pressure
- net movement into lymphatic system
Venous end
- high osmotic pressure
- low hydrostatic pressure
- net movement into capillaries
Pulmonary oedema
Fluid accumulation in lungs so impaired gas exchange as O2 diffusion is lengthened
Caused by left heart failure
Symptoms:
- dyspnoea, orthopnoea
- hypoxia
Ascites
Accumulation of fluid in the peritoneal cavity
Many causes including heart failure
Peripheral oedema
Swelling of tissues, esp ankles
Many causes, esp chronic low output heart failure
Compensation
Maintaining homeostasis of a physiological function despite stresses or malfunctions
Decompensated heart failure
Medical emergency
The failure of the heart to maintain adequate blood circulation after long standing vascular disease
Respiratory distress
Kidneys increase plasma volume to compensate for poor perfusion of renal tissue, leads to fluid overload
Cardiac remodelling
Growth of cardiac muscle
Caused by injury:
- MI
- hypertension
- valve disease
Results in hypertrophy or dilation
Ventricular hypertrophy
Response to work
Athlete’s heart
Eccentric: dilate due too volume overload
Concentric: thicken due to pressure overload
Antidiuretic hormone
Also called vasopressin Causes kidneys to reabsorb more water Decreases diuresis From posterior pituitary Peptide
Aldosterone
Causes kidneys to reabsorb more NaCl
Directly decreases natriuresis which decreases diuresis
From adrenal cortex
Steroid
Natriuresis
Loss of sodium to the urin
Diuresis
Loss of water to the urine
Angiotensin II
Increases pressure
Vasoconstriction
Increased fluid retention
- increases aldosterone secretion by adrenal cortex
- increases ADH secretion by posterior pituitary
Contributes to ventricular hypertrophy and remodelling
Angiotensin I
Precursor of angiotensin II
Decapeptide
Angiotensin converting enzyme
The enzyme that converts inactive Ang I into vasoactive Ang II
Secreted by the kidneys and lungs
Renin- angiotensin- aldosterone system
Angiotensinogen converted to Ang I with renin enzyme
Ang I converted to Ang II with ACE
ACE causes an increase in aldosterone secretion by adrenal cortex
Thiazide and thiazide like diuretics
E.g. indapamide
Blocks reabsorption at the distal convoluted tube
Loop diuretics
E.g. furosemide
Blocks reabsorption in the thick loop
K+ sparing diuretics
E.g. spironolactone
Inhibits aldosterone receptors in cortical collecting duct
Chronic low output heart failure
Cardiac output is low, usually due to accumulated damage to the heart
Chronic condition with poor 5 year survival rate
Left heart failure
Respiratory symptoms
Right heart pumps into lungs but left atrium is too full
Increased hydrostatic pressure in pulmonary circulation
Right heart failure
Systemic symptoms
Increased central venous pressure
Can lead to peripheral oedema
Heart failure symptoms and signs
Fatigue especially during exertion Peripheral oedema Dyspnoea - orthopnoea - paroxysmal nocturnal dyspnoea
Cardiogenic shock
Critically low perfusion due to low cardiac output
Medical emergency
Progresses by positive feeback
Chronic heart failure treatments
ACE inhibitors
Diuretics
Beta blockers
Fluid overload
Pathological state where there is too much fluid in the blood Symptoms: - peripheral oedema - ascites - pulmonary dyspnoea - increased central venous pressure