Cardiovascular system Flashcards
Blood pressure formulas
CO = HR x SV
Heart rate = balance of sympathetic and parasympathetic influence on SA node, influenced by hormones ~70
Stroke volume = amount of venous return: end-diastolic vol - end-systolic vol ~70
Increases with sympathetic activity
Most affected by blood volume
Short-term: osmotic pressure in capillaries
Long-term: conc of salt-water balance
Cardiac output = ~5000cm3
MAP = TPR x CO
Total peripheral resistance proportional to viscosity of blood and diameter of blood vessels
Blood viscosity - no. of RBCs
Arteriolar radius - sympathetic activity, skeletal muscle activity (local) action of vasoconstrictors (extrinsic)
Blood pressure regulation
When blood pressure is low
1) Baroreceptors (baroreflex)
Firing rate decreases
Sends a signal to cardiovascular control centre
Increases sympathetic nervous activity, decrease parasympathetic activity
HR and SV increase
CO and TPR increase
When blood pressure is high
2) Stretch receptors
Aortic arch and carotid sinus receptors detect change in stretch
release ANP and BNP (atrial natriuretic peptide and brain natriuretic peptide)
ANP –> excrete water BNP –> excrete salt => decrease blood pressure
Also decreases renin release
3) ONLY FOR LOW BP. RAAS renin-angiotensin aldosterone system
Receptors detect changes in renal perfusion (concentration of Na and Cl in renal filtrate)
Kidneys release renin (from the granular cells in the JGA)
Renin increases Na reabsorption from DCT and CT, also increasing water retention
Renin converts angiotensinogen to active state angiotensin I.
Angiotensin I is converted to angiotensin II by ACE (angiotensin converting enzyme)
Angiotensin II:
Is a potent vasoconstrictor
Increases SNS
Triggers release of aldosterone from the adrenal gland, which increases Na reabsorption which increases water reabsorption too since salt follows water.
Triggers release of vasopressin/anti-diuretic hormone ADH from the posterior pituitary gland which increases water reabsorption
By increasing number of aquaporins in the walls of collecting ducts
Orthostatic intolerance
- what is it
- what does it cause and its effects
- how do you respond pre-syncope and syncope
A form of low blood pressure arising from changes in posture → standing upright from a supine position
Blood pooling in legs
Insufficient cerebral blood flow
Low oxygen perfusion in brain
Syncope:
A transient loss of consciousness due to lack of blood perfusion (ischemia) which leads to lack of oxygen in tissues (hypoxia)
Returns individual to supine position allowing even distribution of blood
Pre-syncope symptoms
Dizziness, nausea, pallor, sweating, tinnitus
Response:
Pre-syncope
Stop dental procedure
If in chair, lie back to horizontal position; if not, ask to lie down on floor
Raise patient’s legs above heart
Measure heart rate
May ask to wiggle toes and drink water
Syncope
Stop dental procedure
If in chair, lie back to horizontal position
Raise patient’s legs above heart
Measure blood pressure and heart rate
Consciousness usually returns rapidly but if not
Call 000/activate emergency protocol
Lie patient in recovery position on side.
DRSABCD - danger response send for help , airway breathing cpr defibrillator.
Blood clotting
Haemostasis
1) Vascular spasm
Myogenic response: Blood vessel immediately constricts in response to vessel damage, reducing blood flow to site of wound and thus blood loss
Also causes the endothelial lining of the vessel walls adjacent to the break to adhere together, further reducing blood flow
2) Formation of platelet plug
Injured vessel endothelial cells release von Willebrand factor which attracts intial platelets to site by chemotaxis
Platelets adhere to the exposed connective tissue layer of the injured endothelium and are activated by the collagen
From alpha storage granules, platelets release platelet factors: ATP, ADP, thromboxane 2
ADP causes platelets to become sticky and adhere to each other
Thromboxane 2 causes aggregation of more platelets
Meanwhile, non-injured vessel releases nitric oxide and prostacyclin which inhibits platelets from adhering to intact endothelium, this confines the clot to the injury site.
3) Blood coagulation i.e. clotting
Platelet plug releases plasma clotting factors which activates other factors in the blood, starting a clotting cascade
Which ends in prothrombin being converted to active enzyme thrombin
Thrombin converts fibrinogen to fibrin which cross-links to form an insoluble polymer over the wound, forming a clot above the platelet plug
4) Clot retraction and dissolution
Platelets trapped within the fibrin meshwork contract, pulling the edges of the damaged vessel closer together
Platelets secrete factors which promote fibroblasts invasion into the network, which forms scar tissue and starts healing process
Plasmin, a fibrinolytic enzyme, begins to dissolve the clot
Macrophages clear away debris by phagocytosis
Specialisations of the heart
Cardiac muscle
- Involuntary, connected to autonomic nervous system, rhythmic contractions
- Cardiomyocytes and cardiocytes that make up the myocardium:
- Branched cells, mono or binucleated in the central of cells
- Intercalated discs
- Contain desmosomes, gap junctions and fascia adherens: basically ZA but for cardiac muscle.
- Ribbon-like intercellular junctions in the transversal sections of intercalated discs, where anchor actin filaments attach thin filaments in the sarcomeres to cell membrane
- Desmosomes: keep cells connected when they contract
- Gap junctions: provide direct contact between cells, allowing electrical communication → waves of depolarisation spread rapidly through heart
Conduction of signals through cardiac muscle
- PQRST cycle
- How is action potential initiated
Cardiac muscle conduction
AP is initiated at the SA (sinoatrial) node
AP spreads through both atria by interatrial and internodal pathways, atria contract
At AV (atrioventricular) node, signal passes to the AV bundle/bundle of His, which conduct the signal to the apex of the heart
Signal is passed to Purkinje fibres which spread it throughout ventricular myocardium
→ 5) Calcium-induced calcium release (CICR) occurs as depolarised T-tubules release Ca2+ from the sarcoplasmic reticulum.
6) Ca binds to troponin on actin filament, troponin binds to tropomyosin forming troponin-tropomyosin complex which moves aside to expose cross-bridge binding site on actin, myosin filament binds and slides over actin filament → muscle contraction
PQRST cycle
P wave = Atrial depolarisation
PR = AV nodal delay
Prevents ventricles from contracting earlier/at the same time as atria → prevents backflow of blood while valve is open
QRS = depolarisation of ventricles, and atria repolarising simultaneously, valves close.
S → T = ventricles are contracting and emptying - systole
T = repolarisation of ventricles
TP = ventricles relax and fill - diastole
Action Potential initiation by Pacemaker cells
1) Na funny channels (I-f) open simultaneously, allowing Na+ to flow into cell causing a slow, gradual depolarisation, while K+ channels close to reduce outflow of K+.
2) Transient T-type Ca channels open, continuing the slow depolarisation.
The slow depolarisation = pacemaker potential
3) When threshold is reached (-40mV), Long lasting L-type Ca channels open, allowing Ca2+ to flow out of cell, causing a rapid depolarisation - rising phase
4) When +10mV is reached, K+ channels, Na+, and Both T and L Ca2+ channels open, causing repolarisation - falling phase. Positive charges leave the cell, restoring membrane potential
→ known as the refractory potential, usually occurs with diastole
