Blood pressure & CVS disease continuum Flashcards
Blood pressure
- Pressure exerted on the walls blood vessel
- Pressure is essential to perfuse all the cells of the entire body
- Systemic: systole/diastole 120/80 mmHg
- Pulmonary: 25/8 mmHg
- Venous: 6-8 mmHg
Calculate BP
Cardiac x Peripheral Resistance
Cardiac output
Heart rate x Stroke volume
Normotension
Autoregulation
- Change in blood flow detected by local receptor in microprofusion (Tissue fluid formation)
- Involentary vary depending on metabolic need
Normotension
Neural
- Nerve that releases sympathetic and parasympathetic activity modulate BP
- Short-term regulation of blood pressure
- Responses to transient changes in arterial pressure, via baroreflex mechanisms
Blood viscosity effect on blood pressure
- Causing polycythaemia causes too much red blood cells
- Impacting the blood flow and vascular resistance
Hormonal
- Long term regulation of blood pressure e.g. ADH in kidney
Neural regulation
Aortic arch
Baroreceptors in the aorta
Neural regulation
Carotid sinus
Baroreceptors in the carotid artery (more than one)
Neural regulation
Vagus nerve
Connects the Baroreceptors to the vasomotor control in brain stem (informs the pressure and regulate heart)
Neural regulation
glossopharyngeal nerve
Connect the Carotid Sinus to the vasomotor centre (regulate short term blood pressure) e.g. stress
trigger ehen there is low CO2 and O2
Neural response to high blood pressure
- Baroreceptors sense the high pressure and they start firing signals to the cardiovascular centres in the brain
- Vagal innovation causes the supression of the heart rate via the sypathetic nervous system
- Vaodialation occours in the vasomotor cells to decrease blood pressure
- Noradrenaline decreases the heart rate and the heart contraction
- Cause decrease in cardiac output decrease
Neural response to low blood pressure
- Decrease in arterial blood pressure which is dectected by the baroreceptors that supresses its firing rate
- Signal is transmitted to cardiovasular centre which increases sympathetic cardiac activity
- Causes the release of adrenaline increase heart contraction and cardiac output
- Supression of vagal activity therefore vasoconstriction occours which causes sympathetic vasomotor activity
Hormonal regulation
Renin-Angiotensin-Aldosterone System (RAAS)
Low blood pressure
- Causes renal Hypoperfusion due to low pressure this stimulates granular cells that stimulates the release of Renin (enzyme)
- The liver releases angiotensinogen in the circulatory systen is converted by the Renin into Angiotensin I
- The lungs then secreates Angiotensin converting enzyme (ACE) to convert Angiotensin I to Angiotensin II
- Stimulation of aldersterone from adrenal cortex this increases sodium reabsorbtion
Angiotensin II
low BP
- Peptide hormone that acts as a vasoconstricter of smooth muscle
- This increases the pressure and peripheral
- Stimulates hormones the Aldosterone
Aldosterone
Low BP
- Increases sodium reabsorbtion so electrolytes are not lost via Na/K+ pump
- Osmotic pressure increases as water moves in due to decrease in water potential
- Invascular volume increased via supiror and inferior vena cava (venus return
- Increease cardiac output and peripheral resistance
Hormonal regulation
Renin-angiotensin-aldosterone system (RAAS)
High blood pressure
- Causes renal Hyperperfusion due to high pressure this stimulates granular cells that supresses the release of Renin (enzyme)
- Causes vasodialation more blood flow reducing the peripheral resistance
- No aldersterone so decrease in Sodium absorbtion
- More sodium excreated in urine with water reduce intervasular volume so decrease in venous return and cardiac output
Antidiuretic hormone
- Secreated by Hypothalamus & transported to prosterior pituitary
- Stimulates kidneys to reabsorb more water as lumen becomes permeable to water
- Prevent loss of fluids in the urine increasing fluid levels resore blood volume and pressure
Atrial Natriuretic Hormone
- Secreated by cells in the atria of the heart
- Natriuretic hormones are antagonists to angiotensin II
- preventing aldosterone release helps loss of sodium and water from the kidneys.
- Suppress renin, aldosterone, and ADH production and release.
- Blood volume and blood pressure drop restore blood volume
Adrenaline/Nor-adrenaline
- Released in the adrenal medulla
- Extends the body’s sympathetic nervous system
- Increase heart rate and force of contraction
- Vasoconstriction and moblisation of liver
Erythropoietin
- Decrease in blood flow and oxygen levels decrease (hypoxia)
- EPO released by the kidneys which stimulates production of erythrocytes in bone marrow its a vasoconstrictor
- Increase viscosity resistance and pressure
- Decrease in oxygen
Exercise and blood pressure
- The contraction of the muscle can regulate vascular homeostasis
Decrease in stroke volume
Hypovolmia
Low Blood pressure
- Blood loss haemorrage
- Dehydration
- Diarrhoea
- Heavy burns loosing body fluids
Decrease Cardiac output
Structural dysfunctions
Low Blood pressure
- Valve disease isn’t shutting properly or is kept open
- Ischemia - low nutrient supply tissue tire easier
Decreased Heart rate
Arrythmias
Low Blood pressure
- Sinus bradycardia
- AV nde block
- Ventricular fibrillation - involentary not coordinated by cardiac myocytes
Hypotension
Systematic vasodialation
Low Blood pressure
- Sepsis
- Autonomic dysfunction
- Neurogenic diseases - lack of development of vasodialation decreased periphral restriction
Peripheral resistance
Obstruction
Low Blood pressure
- Pulmonary embolism - reduce pulmonary supply causes obstruction and reduced blood flow
Hypertension
Sodium homeostasis
High Blood pressure
- Renal disease
- Nephropathy - aging population looses nefron so renal recognition of signal from the heart
- Reduced nephron number
- GFR
- Poor venous return and poor cardiac output
Increase cardiac output
Hormonal imbalence
High blood pressure
- Renin - too much means that there would be large increase
- Angiotensin II
- Aldosterone
- Erythropoietin
- Adrenaline/Noradrenaline
Increase in hypertension
Systematic vasoconstriction
- Stress
- Autonomic dysfunction
Increase in hypertension
Structural dysfuntion
- Obesity - poorly regulated lipid and carbohydrate metabolism high adiposity
- Endothelial dysfunction - altered cell membrane cause artery and venous issue
- Venous constriction