How the CVS can fail Flashcards
Vessel wall tension
The amount of pressure applied on the walls of a blood vessel.
The greater the radius of the vessel, the more tension is being applied.
Tension= pressure x radius of vessel
Compliance
The change in volume in a vessel/ chamber, caused by change in pressure (stretchiness)
The higher the compliance, the stretchier the vessel.
Veins have a higher compliance than arteries.
Vascular compliance decreases with age due to calcification, disease.
Turbulent blood flow
Flow of blood occurs in ‘eddies’.
This is occurs when blood: Is at high speed Is branching Has low viscosity Is mixed
Laminar blood flow
Straight, uninterrupted blood flow. Flow of blood is slower closer to the vascular walls.
Due to sheer force, laminar flow is atheroprotective.
Reasons for blood vessel damage
Trauma- especially iatrogenic interventions, like percutaneous coronary intervention (PCI)
Atherosclerosis
Diabetes
Plaque rupture
In an atheroma- occurs when the fibrous cap bursts open.
This causes the content of the atheroma to leak out to the lumen of the vessel.
This triggers an immune response and can form a thrombus which is deadly. Can cause ischemia and hypoxia.
Stroke
Rapid loss of brain function due to loss of perfusion to the brain
Haemorrhagic- cerebral blood vessel rupture (internal bleeding).
Cause- Stress, trauma, atherosclerosis, diabetes.
Ischaemic- Blockage of the cerebral vessel. Symptoms: FAST Face Arms Speech Time
Blood vessel stresses
High blood pressure
Large diameter= more tension
Low compliance, less response to change in volume.
Turbulent flow
Atherosclerosis
Hardening of a blood vessel wall due to fat deposits made from hyperlipidaemia
Coronary heart disease
Obstruction of the coronary arteries.
Possible causes:
Atherosclerosis (mainly)
Coronary vasospasm (rapid contraction of vessels)
Symptoms:
Can be asymptomatic
Angina
Dyspnea
Treatment:
Placing stents to widen arteries
Medication
Replacing vessels with synthetic/ grafts
Acute myocardial infarction
Dying/dead myocardial tissue due to ischaemia.
Reduces contractility of the heart and its overall function.
Symptoms:
Most of the time, severe chest pain will be felt (spreading down the arm)
Some pains symptoms are atypical (no in normal places)
Functions of the endothelium in blood vessels.
- Blood vessel tone.
Releases NO which causes vasodilation. Controls perfusion at local factors. - Filtration.
Filters blood/ fluid. Such as; glomerulus, blood brain barrier. - Haemostasis: formation of blood clot.
Secrete cytokines to facilitate this process. - Angiogenesis
- Transcytosis of hormones- movement of hormones across cells
- Recruitment of WBCs in inflammation
Compensation heart failure
Occurs when stress is placed on the heart but the body tries to combat this through homeostatic means - increasing cardiac output
- Increased function of kidneys: increasing blood volume
- Increased sympathetic activity; Higher HR, release of adrenaline and noradrenaline, increased peripheral resistance.
Decompensation heart failure
Failure to maintain sufficient circulation despite compensatory means.
Usually a consequence of other conditions/ diseases: Vascular diseases Valvular dysfunction Myocardial infarction Pneumonia Arthythmias
Consequences:
- Poor perfusion in tissues
- Respiratory distress
- Jugular venous tension
Treatment of decompensation cardiac failure
Medication:
Nitroglycerin- blood vessel dilation= increased blood flow
Furosemide- diuretic= decreased blood volume, decreases BP
Intervention:
Non-invasive positive pressure ventilation (NIPPV)- supplying gases and pressure support through a mask.
Peripheral oedema
Occurs when arterial pressure is too high, hydrostatic pressure in capillaries too high. Forces fluid to stay out of vessels.
Causes swelling in tissue.
Sympathetic activity during myocardial infarction
In response to pain and changes in blood volume- noradrenaline and adrenaline are released.
Allows compensatory mechanism:
Increased heart rate
Increase contractility of the heart
Increased peripheral resistance
HOWEVER- increases tendency to have arrhythmias
Pulmonary oedema
Build up of fluid in the lungs due to left heart failure.
Left heart is unable to pump enough blood and is too full. This increase hydrostatic pressure in the veins due to blood damming.
Increased hydrostatic pressure in pulmonary circulation causes excess fluid to leave vessels in the lungs.
Consequences:
Impairs gaseous exchange by making diffusion of O2 longer (travel across liquid)—-> dyspnea, orthopnea, hypoxia.
Cardiac remodelling
Change to the ventricular muscle in response to injury, due to changes in preload/afterload. Includes change in: Size Shape Function
Ventricular hypertrophy
Type of cardiac remodelling that causes the cardiomyocytes to enlarge in response to injury.
Eccentric HT: dilation of ventricle- increases volume in ventricle
Concentric HT: thicken of muscular wall- increases pressure
Chronic low output heart failure
Low cardiac output due to accumulated heart damaged.
Symptoms include:
Swelling of ankles
Ascites (swelling of the abdominal cavity)
Angiotensin II
A peptide hormone that causes vasoconstriction, thus increasing blood pressure.
Mainly produced in the lung through angiotensin converting enzyme (ACE), converting it from angiotensin I.
Angiotensin II also helps to increase blood volume by stimulating the secretion of aldosterone and ADH.
Also involved in ventricular hypertrophy and remodelling.
Aldosterone
Corticosteroid hormone, secreted by the adrenal cortex.
Acts on the kidneys to reabsorb more NaCl, which causes further absorption of water.
This increases blood pressure and decreases diuresis.
ADH
Antidiuretic (peptide) hormone: released from the pituitary gland.
Stimulates the reabsorption of water at the collecting duct in the kidneys.
This increases blood pressure and decreases diuresis.
Thiazide drugs
Diuretics that blocks the reabsorption of water at the distal convoluted tube. This increases diuresis and blood pressure
Example: Indapamide
Loop diuretics
Blocks reabsorption of water at the loop of Henle.
This increases diuresis and decreases blood pressure.
Example; furosemide
Potassium sparing diuretics
Inhibits the binding of aldosterone to its receptors in the cortical collecting duct.
This increases diuresis and decreases blood pressure.
Example: spironolactone
Indapamide
THIAZIDE diuretic used to treat high blood pressure.
Furosemide
LOOP diuretic drug used to treat high BP.
Spironolactone
K+ sparing diuretic used to treat high BP.
Angiotensin II synthesis
- Angiotensinogen is made in the liver.
- Enzyme renin is made in the kidneys.
- Stimulates the production of angiotensin I
- Angiotensin I is converted to II in the lungs using ACE.
Symptoms and treatment of heart failure
Fatigue
Peripheral oedema
Paroxysmal nocturnal dyspnea ( breathlessness at night)
Orthopnea
Treatment:
ACE inhibitors- decreased blood pressure
Diuretics- also increase BP
Beta blockers- increase CO, blood flow.
Cardiogenic shock
Low perfusion in tissue due to low cardiac output.
Occurs when systolic pressure is <90 mm Hg in most cases
