Cardio Flashcards
What is haematocrit
the percentage of blood volume occupied by red blood cells
what causes a high haematocrit - i.e. Polycythaemia?
Excessive production of RBCs and dehydration (which reduces plasma volume)
what causes low haematocrit?
anaemeia
sites of haemolysis
spleen, bone marrow, lymphnodes
which leukocytes are the most abundant
neutrophils
neutrophils - function and appearance
phagocytosis - they are the first line of defence during acute inflammationthey have multi lobed nuclei with relatively translucent cytoplasm
function of basophils + appearance
responsible for anaphylaxis - produces histamine| multi lobed and has so many purple/bluey granules you can barely see the nucleus
eosinophils - function and appearance
Combats parasitic infection and neutralises histamine.| Double lobed nucleus with bright pink eosinophilic granules.
what do monocytes differentiate into? and where? give some specific exampleswhat is their function? what do they look like?
they are monocytes in blood and differentiate into macrophages in tissue.Examples: microglial cells (CNS), Kupffer cells (Liver), tissue macrophages, alveolar macrophagesFunction is phagocytosis of foreign materialLarge, fine white granule-looking-things, kidney shaped nucleus, kinda wobbly round the edges
Name the 3 types of lymphocytes and give some extra info e.g site of production and function.
T cells: progenitors originate in bone marrow but they migrate to and mature in thymus - have many functions but naive t cells identify specific antigens; helper t cells help activate other immune cells, produce cytokines and help B cells with antibody production; cytotoxic cells kill cells by releasing cytotoxic granules; there are also memory t cellsB cells: originate and mature in bone marrow - plasma cells produce antibodies and memory cells remain in case of reinfectionBoth have large round nucleus and are agranularNatural killer cells - kill virus infected cellsHas large round nucleus but is granulated
platelets: structure, function, production
structure: anucleate and discoid - becomes spiculated (spikey) with pseudopodia (temporary protrusions) when activatedfunction: produce platelet plug along with clotting factors for haemostasisproduced as fragments of cytoplasmic material derived from megakaryocytes and modulated by thrombopoeitin
haemostasis? primary? secondary?
Haemostasis is the process to prevent and stop bleeding.Primary involves platelet plugs and the 3 As after vessel injury: Adhesion, Activation, AggregationSecondary: coagulation cascade and fibrin clot formation
What happens when vessel injury occurs?
Endothelial wall becomes exposedSmooth muscle contracts to limit blood lossMechanisms of contraction:- Endothelin release- Nervous stimulation
what happens in the adhesion phase of primary haemostasis?
Subendothelial collagen becomes exposed| Platelets bind to collagen via vWF (von Willebrandβs factor) using their receptor GP1B
what happens in the activation phase of primary haemostasis?
Once bound to the subendothelium, platelets change shapePlatelets release alpha and electron dense granules, to escalate haemostasis processAlpha:vWF, Thromboxane A2, fibrinogen and fibrin-stabilizing factorElectron-dense:ADP, Ca2+, Serotonin
Aggregation
Lots of platelets binding to each other using GP2b/3a receptors and fibrinogen - forms platelet plug
The important parts of the coagulation cascade
Prothrombin (II) -> Thrombin (IIa) (catalysed by Xa and/or Va)Thrombin converts Fibrinogen (I) -> Fibrin (Ia)Fibrin is stablised by Fibrin-stabilising factor (XIIIa)this causes a cross-linked fibrin clot to be formedfactor IV (Ca2+) is also important
Which factors in the coagulation cascade are Vitamin-K dependant?
X (precursor to what activates thrombin), IX, VII, II (Prothrombin)Remember 1972
fibrinolytic pathway
plasminogen -> plasmin which then mediates fibrin -> fibrin degradation products (important in PE and DVT - D-Dimer??)can be inhibited by thrombin activatable fibrinolysis inhibitor
types of blood transfusion.
homologous (emergency transfusion from other person - have to test safety, recipient serum mixed with donor blood to check for reaction)autologous (self-transfusion)
blood types? how are they classified? presence of antigens and antibodies?
classified by presence of specific antigens and antibodiesA - A antigens and Anti-B antibodiesB - B antigens and Anti-A antibodiesAB - A and B antigens but NO antibodies (universal recipient)O - NO antigens but has anti-A and anti-B antibodies (universal donor)focus on antibodies for recipients, and antigens for donor suitability
Rhesus factor (D protein presence)
Rh+: - contains D-antigen (most immunogenic), no antibodies- can receive from both Rh+ and Rhβ only donates to Rh+Rh-:- contains no antigens, and anti-D antibodies- can donate to both Rh- and Rh+- only receives from Rh-the antibodies are not naturally occuring unlike anti-a and -b. anti-d will only be made if RH- blood comes into contact with Rh+ blood
formation of primitive heart tube
during week 3/4 the visceral mesoderm forms 2 heart tubes which then fuse. There is some craniocaudal folding which makes it look kinda like a funky shrimp. It has 5 divisions.
divisions of heart tube
truncus arteriosus: ascending aorta and pulmonary trunkbulbus cordis: smooth outflow portion of ventriclesprimitive ventricle: majority of the ventriclesprimitive atrium: both auricular appendages, all of left atrium, anterior portion of right atriumsinus venosus: smooth part of right atria where VC connects, the Vena Cava, coronory sinus
septation
(formation of atrial septum - occurs after looping of heart tube to make something kinda c shaped and more like a heart)1. septum primum starts developing from top - the open part is foramen primum2. septum primum has a bit at top and a bit in middle - top hole is foramen secundum, below is foramen primum3. septum primum is only at top and bottom with septum secundum forming at the top on right side of primitive heart - foramen primum completely closed4. septum secundem is at top and bottom now but the top part is partially going over the foramen secundum (in between the two bits of septum primum) - the part between the 2 parts of septum secundum that blood can actually flow through is the foramen ovale5. foramen ovale closes
aortic arches - time period, names , what they form
weeks 4-6symmetrical, sprouts from aortic sac - 6 of them (but 6th one is actually pulmonary arteries from the pulmonary trunk)I - maxillaryII - stapedialIII - common carotids and proximal part of internal carotids (distal part made from extensions of dorsal aortae)IV - aortic arch and right subclavian (both sides join with 7th intersegmental)V - regresses completelyVI - pulmonary arteries and ductus arteriosus on left 7th segmental arteries (not an aortic arch) form the left subclavian and part of right subclavian
extra embryology facts
Heart appears in 3rd week (starts beating ~day 23)Constriction of ductus arteriosus > ligamentum arteriosum 10-15 hours after birthObstetrical climbing = constriction of umbilical vein > ligamentum teresIncrease L atrial pressure & decreased R atrial pressure due to first breath causes foramen ovale to close > fossa ovalisDuctus venosus constricts > ligamentum venosum shortly after birth
membrane potential definition
the difference in electrical potential between the interior and exterior of a celle.g. if inside is +1 and outside is 0 the membrane potential is +1if inside is 0 and outside is +1 the membrane potential is -1
membrane potential of cardiac myocyte at rest
-90mV| more positive outside cells
is a cardiac action potential longer or shorter than in skeletal muscle
cardiac action potential is around x100 linger than in skeletal muscles. Voltage gated Ca2+ channels open more slowly and stay open longer than Na+ channels (sometimes called L-type Ca2+ channels i.e. long lasting or dihydropyridine - target of amlodipine treatment - antihypertensive)skeletal muscle action potential is a spike, cardiac myocyte action potential is more like a wiggly water slide that peaks lower and slightly after the skeletal action potential
action potential/cardiac cycle phases
phase 4: resting phase - -90mV. SAN generates an action potential which causes depolarisation. If it reaches the threshold, phase 0 starts.phase 0: depolarisation - threshold (-60mV) reached and Na+ channels open.phase 1: partial repolarisation - at +30mV Na+ channels close and there is transient K+ channels open allowing K+ out of the cellsphase 2: plateau - L-type Ca2+ channels open to allow an influx of Ca2+ into the cell to balance the efflux of K+phase 3: repolarisation - Ca2+ channels close allowing repolarisationthere is a bit of overshoot and over polarisation which is when the refractory periods happenphase 4: resting
In what phase of the cardiac cycle does contraction occur?
phase 2 - contraction occurs when there is a calcium influx
refractory periods
absolute refractory period - when the cell is completely unexcitable (longer for myocytes than skeletal muscle)relative refractory period - when the cell can be depolarised by a greater than usual stimulus
where is the sinoatrial node located? what does it do? what is it modulated by?
in the right atrium - it is the primary pacemaker (rate of discharge: 60-100/min) - vagus stimulation decreases rate, noradrenaline from sympathetic nerves increases rate
pacemaker potential
There is no resting baseline line in normal depol/repol. No plateauing. Phase 4 equivalent - prepotential: slow influx of Na+ through HCN channels (hyperpolarisation activated cyclic nuclotide gated channels - permeable to K+) - slow depol from -60mV to -40mVPhase 0 equivalent - depolarisation: influx of Ca2+ through voltage-gated t type channels (specifically found in heart condutive cells) - -40mV -> +10mVPhase 3 equivalent - repolarisation: Ca2+ channels close and voltage-gated K+ channels open - +10mV -> -60mV (at which point f type Na+ channels open again - they open at most negative membrane potential)
which cells act as pacemakers in heart - what do they do
pacemakers are responsible for automacity of heart. Nodal cells generate the pacemaking potential (1%?)
sympathetic stimulation of pacemaker potential
- noradrenaline binds to beta-1 receptors - increases Ca2+ channels opening - faster depol- steeper phase 0 - increased heart rate and force of contraction
parasympathetic (vagal) simulation of pacemaker potential
- Ach activates K+ channels - hyperpolarises membrane - takes longer to reach treshold potential- reduces influx of clacium so slower depolarisation (shallower slope of phase 0)- decreases heart rate
excitation-contraction coupling
Wave of depolarization (AP) spreads into myocytes via T tubules.L-type Ca2+ channels open π‘ͺ Ca2+ enters the muscle cellCa2+ binds to Ryanodine Receptor π‘ͺ release of more Ca2+ from Sarcoplasmic Reticulum (Ca2+ induced Ca2+ release.)Ca2+ binds with Troponin which uncovers active site on tropomyosinCross-bridge cycling = Muscle contraction
What causes contraction in excitation-contraction coupling?
The presence of Ca2+ in the cytosol. Force of contraction is directly proportional to cytosolic Ca2+ levels.drugs and chemicals that increase cardiac contractility (like adrenaline, Digoxine, cardiac glycosides) are increasing the levels of cytosolic Ca2+
Electrode and lead (for ECG) definitions
Electrode is the object placed on the body to pick up electrical signalsA lead is a specific plane in which you are observing the heart
shapes of ECG graphs
+ve going to a positive electrode = curve goes up+ve to -ve electrode = curve goes down (as in it is inverted/peaking underneath the baseline instead of above it)-ve to +ve electrode = curve goes downif the charge is going at an angle and so only part of the vectored charge is picked up (e.g. like how a thrown ball has a horizontal and vertical part that combines to form the final vectored trajectory) - then the curve will just be shorter but the same width and shape
list all the ECG leads
6 limb leads:I - goes from right arm (-ve) to left arm (+ve) - bipolar - (the leaving part is always negative and receiving part is positive) II - from right arm (-ve) to left leg (+ve) - bipolarIII - left arm (-ve) to leg (+ve) - bipolaraVR - right shoulder - unipolaraVL - left shoulder - unipolaravF - left ankle - unipolar6 chest leads:Lead V1 β 4th IC space to right of sternal borderLead V2 β 4th IC space to the left of sternal borderLead V3 β midway between V2 and V4Lead V4 β 5th IC space, mid-clavicular lineLead V5 β anterior axillary line at same level as V4Lead V6 β midaxillary line at same level as V4 and V5
Key parts of ECG:
P wave - atrial repolarization. QRS - ventricular depolarisation. T wave - ventricular repolarization. PR segment - delay in AVN ST segment - plateau phase of ventricular repolarization.PR interval - atrioventricular conduction time - this is when atrial systole happensQT interval - Total ventricular contraction during systole.
What is a segment in ECG
A period of isoelectric neutrality
What is an interval in ECG
A region including magnitude
what is the ejection fraction
the proportion of the EDV that is pumped out the LV per beat, SV/EDV, provides an indication of the contractility of the heart
what percentage of blood passively fills the lungs?
70-80% - during diastole - helps equalise pressure
what is the atrial booster?
atrial systole - it pushes the remaining blood into the ventricle - PR interval donβt forget that this is an important part of ventricular diastole
what percentage of blood ejected during maximal ejection?
65-75% of blood in the ventricles (then reduced ejection happens)
What can passive ventricular filling be split into
rapid inflow - to equalise pressure - most of the blood entres herediastasis - the slow ventricular filling that occurs afterwrds when pressure is nearly equalised
what factors affect stroke volume?
preload, afterload, contractility, (heart rate?)
what occurs during the Frank-Starling curve (in the heart)?
- Increased stretch opens stretch-sensitive calcium channels= increased cytosolic calcium π‘Ί increased force of contraction2. Stretch enhances affinity of troponin C for calcium π‘Ί increased force of contractionAfter maximum stretch reached:Little overlap between actin and myosin π‘Ί lots of unbound myosin heads π‘Ί decreased force of contraction π‘Ί decreased stroke volue (curve starts going down)
factors that affect preload?
venous return, heart rate, ventricular compliance, atrial contractility, valvular resistance
inotropy meaning
relates to force of contraction
chronotropy meaning
relates to heart rate
what happens in increased contractility?
+ve inotropy -> Increases Force of Contraction π‘ͺ increases SV
what are some positive inotropic agents?
Sympathethic nervous systemHormones: adrenaline, thyroxineDrugs: e.g. Digoxin
decreased contractility
-ve inotropy -> decreased force of contraction -> decreased SV
negative inotropic agents?
Parasympathetic nervous system, Drugs: e.g. Ξ²-blockers
factors affecting afterload
valvular diseases, TPR, Aortic pressureSVR/TPR: mainly determined by radius of vesselsVasodilation π‘ͺ Decreased resistance π‘ͺ decreased afterloadVasoconstriction π‘ͺ Increased resistance π‘ͺ increased afterloadAortic pressure:Increased aortic pressure = increased LV pressure (hypertension) π‘ͺ increased afterloadDecreased aortic pressure = decreased LV pressure (hypotension) π‘ͺ decreased afterloadValvular diseases:Mitral valve regurgitation π‘ͺ decreased LV wall stress π‘ͺ decreased afterloadAortic stenosis π‘ͺ Increased LV pressure π‘ͺ Increased afterload
afterload definition
ventricular wall stress during sytole
blood pressure definition
the pressure exerted by blood on a given vessel surface area
pressure equation
ΞP = Pi β Pf Pi = MAP (mean arterial pressure)Pf = CVP (venous pressure)or ΞP = Q x TPR
systolic pressure definition
point when LV pressure during ejection = aortic pressure during ejection
diastolic pressure
Pressure caused by recoiling of arteries during diastole
pulse pressure equation
PP = SP - DP
Mean arterial pressure equation
MAP = 1/3(PP) + DP or MAP = DP + 1/3(SP - DP)MAP = CO x TPR
blood flow definition
The volume of blood that flows through the systemic circulation per unit of time(it is equal to cardiac output)
velocity of blood flow equation
V = Q/A
Types of blood flow
Laminar:Smooth, streamlined flowTurbulent:Disruption to laminar flow (e.g. decrease in vessel diameter)Produces Korotkoff sounds
what affects viscosity of blood
haematocrit:anaemia = decreased viscositypolycythaemia = increased viscosity
resistance equation
8nl/pi r^4
Poisueilleβs equation (this thing seems to change depending on what source I look at so just use whateverβs in the question)
change in pressure combined with resistanceQ = (Pi - Pf)pi r^4 / 8nl
what mainly determines resistance in a healthy individual
vessel radius
what is blood volume controlled by
RAAS - renin-angiotensin-aldosterone system
Intrinsic control of BP
Myogenic autoregulationSelf regulation of arterioles based on stretch experienced - if pressure increased in an arteriole, it would constrict to decrease flow and so pressure Local mediatorsHormones, nerves, local autocrine and paracrine agents.
local vasoconstrictors of arterioles
Endothelin-1, internal pressure
local vasodilators of arterioles
ProstacyclinHypoxia (only in systemic circulation)Tissue factor NO/EDRF (endothelium derived relaxing factors - one of which is nitrc oxide)H+/K+/Ca2+AdenosineBradykinin
Extrinsic control of BP
Humoral factorsBaroreceptors Neural control
Circulating hormonal factors - vasoconstriction and vasodilation
Vasoconstrictors - adrenaline (ALPHA adrenergic receptors), angiotensin II, ADHVasodilators - Atrial Natriuretic Peptide, adrenaline (BETA 2 adrenergic receptors)
Baroreceptors - function, location, nerves involved
Pressure receptors that control short term change in BP.Found in carotid sinus and aortic arch
afferent neurons from CN IX and CN X (glossopharyngeal and vagus) travel to medulla oblongata.efferent neurons (SNS/PSNS) travel to heart and vessels
How do baroreceptors work? give an example
They are constantly firing and if BP drops then they decrease their discharge rate.e.g. in a haemorrhage - BP dropssends signals to medulla which acts through nts and vmc (vasomotor centre) to:
Increase sympathetic activity Raise HR (and CO) Increase contractility (and CO)Cause arteriolar vasoconstriction due to innervation and raised angiotensin II (increased TPR)
Decrease parasympathetic activity Raise HR (and CO)
which nerves involved with baroreceptor reflex
vagus (recieves input from aortic arch) and glossopharyngeal
What is a universal plasma donor?2-What ion is responsible for the major depolarization in nodal cells?3- What is serum?4-What enzyme is responsible for clot breakdown?5-Which of the following clotting factors are not vitamin K dependent? a) X b) II c) IV d) VII6-Which protein can be measure in the blood as a sign for myocardial infarctions?7-Which type of vessel is responsible for the total peripheral resistance for the systemic circulation?8-Which cranial nerve receives input from aortic arch baroreceptors?9-Which of these is not a factor of cardiac preload? a) Venous return b) Atrial contractility c) TPR d) Heart Rate10-Which ECG event corresponds to atrial systole?
1-Type AB+2-Calcium3-Blood plasma without clotting factors4-Plasmin5-C6-Trop T7-Arterioles8-CN X9-C10-PR interval
Where do the SA and AV nodes lie
SA node - upper wall of right atrium| AV - bottom of right atrium on the septum
What does right coronary artery supply
Right atrium and part of ventricle| SA node in 60% of people and AV node in 90% of people
what does right marginal artery supply
right ventricle| apex
What does posterior intraventricular artery supply
part of right and left ventriclesposterior 1/3 of IVSAV node (PIV always supplys AV node so AV node proportions mirror PIV proportions in the population)
What does left coronory artery supply
left atrium and ventricleIVS and part of right ventricle (from LAD)at least some part of the AV bundlesSA node in 40% of people, AV node in 30% of people
what does left anterior descending supply
left and right venricles (anterior aspect)| anterior 2/3 of IVS
what does left marginal supply
left ventricle
what does circumflex artery supply
left atrium and ventricle
percentages of population that has right-, left- and co-dominent coronary circulation
70%, 10%, 20% respectivelyso 90% of population have PIV coming from RCA and 30% has PIV from LCA
where is the apex of the heart/mitral valve sound found?
left midclavicular line - 5th intercostal space
where do you hear aortic valve sound, pulmonary valve sound and tricuspid valve sound
aortic - 2nd intercostal space - right sternal borderpulmonary - 2nd intercostal space - left sternal bordertricuspid - 5th intercostal space - right sternal border
Phrenic nerve: roots, modality of innervation, what it innervates, path through thorax
C3, 4, 5Motor and sensorydiaphragmRight Phrenic nerve;Descends ANTERIORLY (phrenic, front) along R lung rootTravels along pericardium of R atriumPasses through diaphragm at IVC opening (T8)
Left Phrenic nerveDescends ANTERIOR to L lung rootCrosses aortic arch, bypasses vagus nerveTravels along pericardium of L ventriclePasses through diaphragm separately
Vagus nerve: roots, modality of innervation, what it innervates, path through thorax
CN10motor and sensory; parasympathetic and sympatheticParasympathetic to ALL orgens of thorax and abdomen - gives of superior laryngeal branch to supply thyroid, and recurrent laryngeal loops around aorta or subclavian to supply larynxPasses behind nerve roots, passes through diaphragm at T10
what type of artery is the aorta?
elastic artery
why are arterioles the main source of TPR? (aka why donβt other vessels contribute as much to TPR?)
The media of large arteries are more elastic than the smaller arteries, which have more muscleCapillaries are fenestrated (have holes) so things can easily flow in/out Capillaries also have pericytes which are involved in the regulation of blood flow
Layers of artery wall (and arterioles), from lumen out
Endothelium, basement membrane, intima, internal elastic lamina, media, external elastic lamina, adventitiaarterioles are the same but without the external elastic lamina
Layers of vein wall and venule, lumen out
Endothelium, basement membrane, intima, media, adventitiasame for venule
why are veins capacitence vessels?
they hold up to 70% of blood volume - normally
pulmonary circulation pressure
20/8
systemic circulation pressure
120/80
average cardiac output
~5-6L
average stroke volume
~70mL
average heart rate
60-100 beats per minute
average end diastolic volume
~130ml
average ejection fraction
65%
average end systolic volume
~50ml
Factors affecting cardiac output
Anything that affects stroke volume or heart rateAge, Gender, Pregnancy, Exercise, Emotions, Posture, Sweating(AG PEEPS)
What does the Frank Starling law dictate about force of contraction
Within PHYSIOLOGICAL LIMITS, the force of contraction is directly proportional to initial length of muscle fiber.
tamponade meaning
when pericardium fills with blood or fluid - increased pressure on heart can contract as easily
What does venous return depend on?
skeletal pump activity, ECF volume, sympathetic activity-venoconstriction
what does atrial pump activity depend on
Atrial contraction increases due to sympathetic activity
What factors affect myocardial contractility?
More ventricular muscle mass increases contractilitySympathetic stimulation increases ventricular contractility, Parasympathetic decreasesHormones- thyroxine increases left ventricle contractilityDrugs and chemicals- caffeine, digoxin (both increase)
Factors affecting heart rate
Influence mainly by autonomic activityVagal stimulation decreases HR, Sympathetic stimulation increases HR.Tachycardia does not necessarily mean a proportionate increase in CO as duration of diastole SHORTENS, meaning ventricles have less time to be filled= EDV decreases/does not increases as much AS EXPECTED. vice versa in bradycardia.
what is the reason for SA node automacity/pacemaker potentials?
spontaneos diastolic depolarisations (Phase 4) - caused by HCN Na+ channels which open when hyperpolarised
