Cardiology Flashcards
What are the 5 layers of the heart?
Outside the heart
Fibrous pericardium
Serous pericardium- parietal
Pericardial fluid
(on the heart)
Serous pericardium- visceral (epicardium)
Myocardium
Endocardium
How long is systole and diastole?
Systole- 0.3 seconds
Diastole- 0.5 seconds
During ejection, what proportion of blood is released from the ventricles?
2/3 of ventricular volume is ejected
Diastasis
The stage of diastole where the initial passive filling of the ventricles have slowed (before the atria contracts to complete active filling)
Stages of the cardiac cycle
Filling phase (passive filling followed by contraction of the atria for active filing after diastasis), isovolumetric contraction, outflow phase, isovolumetric relaxation
How many percent of ventricular refill is passive?
80% passive, 20% due to atrial contraction
What is the P wave on an ECG and how long does it take?
Atrial depolarisation/atrial systole
0.08-0.1s
What is the PR interval on an ECG and how long does it take?
Time between atrial depolarisation and ventricular depolarisation (Time taken for atria to depolarise and electrical activation to get to the AVN)
0.12-0.2
Prolonged PR interval- possibility of first degree heart block
What is the QRS complex on an ECG and how long does it take?
Ventricular depolarisation (hidden atrial repolarisation)
0.06-0.1s (less than 0.12s)
Prolonged QRS could be due to bundle branch block (M shape right bundle block, W/V left bundle block)
What is the ST segment?
Interval between ventricular depolarisation and repolarisation
ST elevation- indication of Myocardial infarction
Intrinsic autoregulation
Intrinsic autoregulation: A local mechanism of blood flow control that is driven by the metabolic needs of tissues and organs.
Some examples include
Active hyperemia- local vasodilation when there is increased metabolic activity to increase blood flow to organs that have increased metabolic demands.
Release of nitric oxide by endothelial cells cause vasodilation
Myogenic autoregulation
Myogenic autoregulation (contraction): A local mechanism of blood flow control that relies on the ability of blood vessels to constrict or dilate in response to changes in intravascular pressure.
When blood pressure is increased, stretching the vascular smooth muscle, the muscle automatically constricts until the diameter is normalised or slightly reduced. (vice versa, when the smooth muscle isn’t getting stretched as much due to low blood pressure, the muscle relaxes and dilates in response.- increases blood flow) – in order to maintain constant blood flow
This is to maintain blood flow
What is active and reactive hyperemia?
Active- a metabolic response due to an increase in physical activity for example- exercise for example
Reactive- during occlusion of tissue, less or no blood flows, after occlusion is removed, there is increased blood flow to the tissue
What are peripheral chemoreceptors?
What is their strongest stimulus?
They are receptors located in the Aortic bodies (aortic arch) and carotid bodies (carotid sinus)
They respond to changes in partial pressure of CO2, O2 and pH although the STRONGEST STIMULUS is a reduction in oxygen (when partial pressure of oxygen is less than 60%).
How do peripheral chemoreceptors work when there is decreased O2, decreased pH and increased CO2?
Glossopharyngeal and vagus nerve brings signals from the peripheral chemoreceptors in the carotid and aortic bodies to the Dorsal respiratory group, stimulating the VRG –> which increases inspiratory signals, increasing the frequency of action potentials travelling along the phrenic and intercostal nerves (C3-5, T1-11) –> increasing the frequency of contractions of the external intercostals and diaphragm, thus increasing respiration rate and ventilation, more CO2 expelled and more O2 inspired.
What are baroreceptors?
They are receptors found in the carotid sinus and aortic arch that function as arterial blood pressure sensors.
How do baroreceptors act when blood pressure is low?
Decreased bp –> less stretch of the walls of the carotid sinus and aortic arch –> baroreceptors fire less frequently –> decreased signals to the cardiovascular centre (pressor region) in the brain stem by CN9 and CN10 –> sympathetic nervous system is stimulated and parasympathetic nervous system is inhibited –> arterioles constrict which increases total peripheral resistance, increasing bp.
Also,
- Cardioacceleratory centre triggers release of noradrenaline, increasing heart rate, cardiac ouput and bp
- Cardiac decelerator centre is deactivated, reducing parasympathetic effect on the heart, increasing heart rate, cardiac ouput and bp
constriction of veins, higher EDV, increased preload, increased sarcomere stretch, increased contractility, increased CO, increased BP
How do baroreceptors act when bp is high?
Increased bp –> increased baroreceptors firing due to more stretch in walls of aortic arch and carotid sinus –> more signals to the cardiovascular centre (depressor region) by CN9 and 10 –> sympathetic nervous system inhibited, parasympathetic stimulated -> arterioles dilate (vasomotor centre) –> tpr decreases –> bp decreases
There is also increased dilation of veins which decreases venous return and TPR thus reducing bp
Where are cardipulmonary baroreceptors located?
Atria, ventricles and pulmonary arteries. They respond to blood volume and act to regulate blood pressure.
What are central chemoreceptors?
They are receptors located in the medulla which sense (small) changes in partial pressure of carbon dioxide or pH of the cerebral spinal fluid.
How do central chemoreceptors respond to high CO2 levels, and low pH?
High CO2 levels lead to low pH level in the CSF (due to CO2+H2O-> H2CO3 -> H+ + HCO3-
High CO2 leads to Low pH (high protons) which stimulates the central chemoreceptors which in turn stimulate the DRG and pneumotaxic centre –> inspiratory signals are sent to the ventral grey horn –> increasing impulses along the intercostal and phrenic nerves –> more frequent contractions of muscles, increased ventilation –> decreased CO2, increase pH levels.
What is Cardiac output and what is its equation?
The volume of blood each ventricle pumps as a function of time (litres per minute)
Cardiac output = HR x SV
Blood pressure equation
BP = CO x TPR
What is pulse pressure and what is its equation?
The force the heart generates each time it contracts
PP = Systolic - diastolic pressure
Mean arterial pressure equation
MAP = Diastolic pressure + ⅓ PP
What is stroke volume and what is its equation?
The volume of blood ejected from each ventricle during systole
SV = EDV-ESV
Starling’s law of the heart
Increased end diastolic volume causing increased myocyte stretch leads to an increased contraction of the heart during systole
What is preload?
The volume of blood present in the left ventricle before contraction occurs. (amount of myocyte stretch)
What is afterload?
The pressure that the left ventricle must overcome to eject blood during systole
How does a dilation of arteries affect afterload?
It decreases it. Dilation of arteries results in decreased pressure in the aorta and pulmonary trunk, so less pressure is needed to eject blood from the ventricles.
What is poiseuille’s law?
Q (flow) = pi x Pressure x r^4 / 8 x length x viscosity
Flow equation
Pressure/resistance
What are some local responses that lead to vasodilation and vasoconstriction?
Vasodilators- hypoxia, decreased pH/increased CO2/increased H+, NO and prostacyclin (secreted by healthy endothelium)
Vasocontrictors- endothelin 1(injured endothelium)
What are some hormones responsible for vasodilation and vasoconstriction?
Vasodilation- Ach at M2 receptors, Atrial natriuretic peptide
Vasocontrictors- angiotensin 2, ADH, noradrenaline
Difference between central and peripheral chemoreceptors
Central - responds to changes in PaCO2, located in the medulla, slower
Peripheral- responds to changes in O2 mainly (pH and CO2 at a smaller proportion), located in aortic and carotid bodies, faster
Why is a hypoxic drive bad?
In people with COPD where their levels of CO2 are chronically high, their drive becomes hypoxic and they mainly rely on their peripheral chemoreceptors for breathing. Meaning that they only breath in response to low oxygen levels.
It is bad to give someone with a hypoxic drive large amounts of oxygen as peripheral chemoreceptors would decrease respiration, possibly leading to respiratory arrest.
What is total peripheral resistance?
It is the total peripheral systemic resistance that are mainly due to arterioles.
What is contractility?
The force of contraction of the heart
What is compliance?
How easily the heart chamber expands when filled with blood
What are the neurotransmitters and receptors responsible for parasympathetic and sympathetic stimulation of the heart?
Acetylcholine at M2 receptors
Noradrenaline at B1 adrenergic receptors
Differences between elastic and muscular arteries
Muscular arteries contain more smooth muscle cells in the tunica media
Elastic arteries contain more elastic tissue in the tunica media
Muscular arteries are found further away from the heart (radial, ulnar arteries)
Elastic arteries are those nearest to the heart (aorta and pulmonary arteries)
Elastic arteries have larger lumens than muscular arteries
(Elastic arteries need to withstand greater pressures of blood)
What are arterioles?
Arteries with 3 or less layers in the tunica media, they are the point where arteries transition towards capillaries.
They are the site of highest TPR.
How many percent of blood in the body do veins hold?
70%
3 ways which veins return blood to the heart
Skeletal muscle contraction (during exercise)
Respiratory pump- muscles need blood (intercostal muscles, lungs)
Peristalsis (smooth muscle contraction in GI tract)- needs blood
Describe blood flow in capillaries and some characteristics of capillaries
Slow blood flow for increased nutrient exchange
Continuous(fully intact endothelium and basement membrane) and fenestrated capillaries (endothelial gaps)
Discontinuous (huge endothelial gaps and incomplete basement membrane) - allows Red blood cells to pass through
What is normal blood pressure measurement?
120/80 mmHg
120 systolic
80 diastolic
What is the difference between pulmonary and systemic blood vessels?
Hypoxic conditions cause pulmonary vessels to vasoconstrict (diverting blood to areas with more oxygen) - oxygen causes vasodilation
Hypoxic conditions cause systemic vessels to vasodilate (allowing more oxygen to reach those sites)
Pulmonary vessels are thin walled
Systemic vessels are thick walled
Pulmonary- 25/8mmHg
Systemic- 120/80mmHg
Life span of erythrocytes
What stimulates red blood cell production? Where is it produced?
120 days
Erythropoietin- produced by the kidney
What is an immature red blood cell called
Reticulocyte
Life span of white blood cells
What stimulates white blood cell production? Where is it produced?
6-10 hours
Granulocyte colony stimulating factor synthesised in the bone marrow
Life span of platelets
What stimulates platelet production? Where is it produced?
7-10 days
Thrombopoietin - liver
How many constituents of blood are there and what makes up these ‘phases’
The cellular component (45%)- composed of red blood cells, white blood cells and platelets. (< 2% white blood cells and platelets so about 43% RBC)
The fluid component (55%)- composed of plasma
How many litres of blood does the average adult human have?
5 litres
What is the normal haematocrit of the body?
Haematocrit is the measure of the proportion of red blood cells in the body, normal value is 0.45
What is serum?
Plasma without clotting factors
What is the precursor of all blood vessels?
Haematocytoblast
What are the precursors of platelets, granulocytes, lymphocytes, monocytes, red blood cells?
Platelet- megakaryocyte - megakaryoblast
Granulocytes - myeloblast
Lymphocytes- lymphoblast
Monocyte- monoblast
Red blood cell- proerythroblast
What are the granulocytes and agranulocytes
Granulocytes- neutrophil, basophil and eosinophil
Agranulocytes- Lymphocyte and monocyte
Function and appearance of neutrophils
Key mediators in inflammatory response, phagocytosis
Multi-lobed nucleus
Function and appearance of monocytes
Immature cells which can become macrophages and antigen presenting cells
kidney bean (reniform) nucleus
Function and appearance of eosinophils
First acting cells in parasitic response. Antagonistic to basophils by decreasing histamine responses. They decrease allergic responses.
Antihistamine binds competitively to IgE receptors (to histamine)
Pink granules- bi lobed nucleus
Function and appearance of basophils
Basophils (mast cells in tissues)
Histamine producing cells which bind to IgE receptors, increasing allergic response.
Dark blue granules
bi lobed nucleus
Function and appearance of lymphocytes
Cell mediated and innate immunity (Adaptive immune response)
Little cytoplasm
Mostly nucleus- round big nucleus
What process do megakaryocytes undergo to become platelets?
Endomitosis (DNA doubles, cell doesn’t divide)
What happens to the smooth muscle upon injury to a blood vessel?
What are the mechanisms of contraction (what causes it to contract)
- It contracts to limit blood loss
- When endothelial cells are injured, they secrete endothelin- 1 which binds to a receptor causing vasoconstriction.
Explain the process of injury and platelet plug formation (4 steps)
Vascular spasm
When a blood vessel is damaged, via neural control and endothelin-1 released by endothelial cells, they undergo vasoconstriction → vasoconstriction of the blood vessels temporarily slows down blood flow in the affected area and decreases the diameter of blood vessels to prevent blood loss.
Platelet plug formation (platelet adhesion)
When a vessel is injured, the endothelium is disrupted and collagen fibres are exposed. (an injured endothelium means that nitric oxide and prostacyclin (PGI2) which inhibit platelet activation are now inhibited- usually released by the endothelium) → The platelets adhere to the collagen fibres via an intermediary called von willebrand factor (secreted by injured endothelial cells) - This is done via glycoprotein 1B on the platelet surface membrane.
Platelet activation
Binding of platelets to collagen fibres triggers the release of the contents of their secretory vessels via exocytosis. One of these contents include platelet dense granules → ADP released from these granules act on P2Y1 and P2Y12 receptors on the platelets causing platelet amplification (at the site of injury)
—– Platelet activation also induces the synthesis of thromboxane A2 which cause vasoconstriction and stimulates further platelet activation
Platelet aggregation
Platelet activation increases the expression of glycoprotein 2b/3a receptors on platelets which allow for platelet aggregation (via fibrinogen- forms bridges between platelets via binding to the glycoprotein 2b/3a receptors), Forming the platelet plug
Explain the intrinsic pathway of the coagulation cascade
Coagulation cascade- the transformation of blood into a solid gel called a thrombus which consists mainly of fibrin
Intrinsic pathway
Factor 12 is activated to factor 12a when it comes into contacts with exposed collagen fibres. (contact activation)
Factor 12a catalyses the activation of factor 11 to factor 11a, (thrombin also contributes to the activation of factor 11)
Factor 11a catalyses the activation of factor 9 to factor 9a. (needs calcium)
Factor 9a interacts with factor 8a and calcium to form a complex that activates factor 10 to factor 10a. (factor 8 is activated by thrombin)
Factor 10a reacts with factor 5 and calcium in order to convert prothrombin- factor 2 to thrombin- factor 2a (factor 5 is activated by thrombin)
Thrombin has a few functions:
It is an enzyme which converts soluble fibrinogen to insoluble fibrin which secures the blood clot. (Factor 1 to factor 1a)
It can turn blood from liquid to a jelly like substance so as to slow down the flow of blood to prevent loss of blood.
It activates factor 13 to become factor 13a which crosslinks the fibrin strands to create a mesh that overlies the platelets to prevent the platelet plug from dislodging and causing an embolism.
Thrombin also contributes to the activation of factors 5, 8 and 11
Where are clotting factors made?
The liver
Which are the vitamin k dependent clotting factors?
X, IX, VII, II
What is the difference between a homologous and autologous blood transfusion?
Homologous- usually emergency transfusion where someone collects and infuses the blood of a compatible donor into himself/herself
Autologous- The collection and re-infusion of a patient’s own blood or blood components. (relieves pressure on community blood supply)
Explain the extrinsic pathway of the coagulation cascade. Is the extrinsic or intrinsic pathway faster?
The extrinsic pathway is faster than the intrinsic pathway.
Extrinsic pathway
When there is tissue damage, our tissue releases a protein called tissue factor (factor 3) - (located outside the endothelium)
Factor 3 binds to and activates factor 7, converting it to factor 7a.
The complex of factor 7a and factor 3, and calcium catalyse the activation of factor 10 to factor 10a.
This complex also catalyses the activation of factor 9 (which in turn activates factor 10 even more)
So the clotting cascade can be initiated by either activation of factor 12 or the generation of factor 3 (tissue factor)
Describe what happens after the coagulation cascade has occurred and (platelets have contracted to pull the endothelial lining closer together along with regenerated a new endothelial lining)
Fibrinolysis. Tissue plasminogen activator found on endothelial cells activates plasminogen to plasmin.
Plasmin degrades the fibrin mesh (releasing fibrinogen and d-dimer) → this is why in deep vein thrombosis, where a blood clot is formed, there will be elevated d dimers.
The circulating fragments are cleared by proteases
Name 2 things secreted by endothelial cells
Nitric oxide and prostacyclin (PGI2) - used to inhibit platelet and keep it inactive
What is von Willebrand’s factor? What would a lack of this result in?
A protein required for platelets to adhere to damaged blood vessels (exposed collagen fibres) to help blood clot
A lack of von Willebrand’s factor would result in platelet dysfunction and it would take longer for bleeding to stop. (longer prothrombin time)
Why is the liver important in clotting?
Most clotting factors are synthesised in the liver (except clotting factors 3, 4, and 8)
The liver also produces bile salts which are required for the absorption of vitamin K which is required to produce certain clotting factors.
What is universal acceptor and universal donor? (blood group)
How does a positive and a negative affect it?
AB+= universal acceptor
O- = universal donor
+ can’t donate to -
- can donate to +
ABO- carbohydrate antigens that can’t cross the placenta
What is Rhesus D?
Peptide antigen - can cross placenta
If you have the Rhesus D antigen, you produce anti-D antibodies. (no immune response to rhesus D antigens)
What happens if a non rhesus D mother has kids with the rhesus D antigen?
1st child- there is no immune response- however, the mother’s body starts to make Rhesus D antibodies (and becomes sensitised)
2nd child- with the already present anti-D antibodies, there will be a rapid immune response - can result in anaemia and death
What are the phases of action potential in the cardiac myocyte?
Phase 4- resting membrane potential (-90mv)
When threshold potential is reached,
Phase 0- depolarisation, massive influx of Na
At +20mv,
Phase 1 - partial repolarisation, sodium channels close and there is a transient efflux of K+
Phase 2- plateau, L type Ca2+ channels open, balancing the efflux of K+
Phase 3- repolarisation –> More K+ channels open (rectifying channels), L type Ca2+ channels close
THERE IS NO HYPERPOLARISATION in myogenic contractile cell- it is generated by the sinoatrial node
What is the function of troponin and what are its 3 binding sites?
Troponin- A protein that changes shape when calcium binds to it, pushing tropomyosin to expose the myosin binding sites on actin, thus enabling contraction to occur.
Troponin T- Binds troponin and tropomyosin
Troponin I- Inhibits actin and myosin interaction
Troponin C- Binding site for Ca2+ that helps initiate contraction
Absolute refractory period
No action potentials can be generated regardless the strength of the stimulus (sodium channels inactivated)
Relative refractory period
An action potential can be generated with a strong enough stimulus (sodium channels slowly coming out of inactivation)
Describe nodal cell action potential
How is depolarisation spread from the right to left atrium?
Resting membrane potential-> -60mv
Threshold-> -40mv
1) Leaky sodium channels allow a slow inflow of sodium ions into the cell
2) T-type calcium channels open (-55mv), calcium ions enter and threshold potential is reached.
3) At -40mv, L-type voltage gated calcium channels open, further depolarising the cell (+10mv),
4) K+ channels open and there is an efflux of K+
ESSENTIALLY, intercalated discs allow action potentials to spread from one myocyte to the next.
Depolarisation is spread to the left atrium via Bachmann’s bundle.
What is the T wave on an ECG?
Ventricular repolarisation
How long is a big square and small square in an ECG
big- 200ms
small- 4ms
What are the unipolar leads, bipolar leads and chest leads
Unipolar- aVR, aVL, aVF
Bipolar- I, II, III
Chest- V1,2,3,4,5,6
Key things to remember for Leads of ECG
I- Right hand to left hand
II - Right hand to left leg
III - Left hand to left leg
Right hand - always negative
Left leg- always positive
aVR- is the negative one
Which are your inferior, lateral, septal and anterior leads?
Lateral- I, V5, V6, aVL
Septal- V1, V2
Anterior- V3, V4
Inferior- II, III, aVF
What does the Right coronary artery supply?
SAN, AVN, Right atrium, right ventricle, part of left ventricle, posterior interventricular septum
What does the right marginal artery supply?
Inferior body of the heart. Right ventricle and apex of the heart
What does the posterior interventricular artery supply?
Right and left ventricle
What does the left coronary artery
Left atrium and ventricle, interventricular septum, part of right ventricle
What does the left anterior descending artery supply
right ventricle and left ventricle
What does the left marginal artery supply
Left ventricle
What does the circumflex artery supply?
Left atrium and ventricle (part of the right ventricle)
What arises from the ectoderm?
Ectoderm
H- Hair and nails
E- Epidermis
N- nervous system- brain, spinal cord, nerves, neural crest cells
S- Sense organs- Eyes, ears and nose
(pineal gland)
What arises from the mesoderm?
Mesoderm
M- Muscles (Skeletal, smooth and cardiac- CVR system)
A- Adrenal cortex
C- Connective tissue (bone, cartilage, blood, lymph)
R- Renal system
U- Uritogenital system (gonads)
What arises from the endoderm?
Endoderm
E- epithelial lining of the gut - respiratory tube
E- Endocrine organs (liver, pancreas),
G- Gallbladder
What is Cushing’s triad/phenomenon?
Three primary signs that often indicate an increase in intracranial pressure
Decreased pulse
Increased systolic bp
Decreased respiration
Function of pericardial fluid
Fluid in the pericardial space that reduces friction between the parietal and visceral layer during heart contractions
What is basal metabolic rate and what are some factors that affect it?
BMR- the amount of energy needed to keep the body alive in the resting state.
Increases with: High BMI, hyperthyroidism, fever, low ambient temperature
Decreases with: age, females are less metabolically active, starvation, hypothyroidism
Function of trabeculae carneae
They increase the contractility of the heart
Difference between endothelial, mesothelial and epithelial cells
Mesothelial - Lines serous cavities of the body (peritoneum, pericardium and pleura)
They secrete serous fluid which lubricates the serous membranes to reduce friction between organs and surrounding structures
Endothelial- Lines the interior surface of blood vessels
Regulates blood flow, controls the passage of molecules in and out of blood vessels (participates in immune responses)
Epithelial- Found throughout the body, lining various internal and external surfaces
Serve as protective barriers. Have specialised functions depending on their location (absorption, secretion, etc)
