Cardiovascular Science Flashcards
(145 cards)
1
Q
Where does the cardiac impulse usually originate?
A
Sino-atrial node
2
Q
What is autorhythmicity?
A
The ability to beat without external stimuli
3
Q
Which drug may be used in extreme bradycardia? Why?
A
Atropine - it blocks ACh receptors
4
Q
Which ions are responsible for cardiac cell depolarisation, and which for repolarisation?
A
Depolar (more +): Na+, Ca2+. Repolar (more -): K+
5
Q
In the SAN, cells are never at rest. What is the term for the ‘resting potential’?
A
Pacemaker potential
6
Q
Describe the action potential in pacemaker cells.
A
Phase 4: funny current (Na) slowly increases potential. Once a threshold is reached, transient Ca channels open, which open L-type. Ultrarapid K efflux channels open, repolarising the cell and reopening If channels.
7
Q
Describe the action potential in non-pacemaker cells.
A
- Na+ in: a stimulus (disruption of neighbouring cells’ gap junctions) increases Em and triggers fast Na+ channels, rapidly increasing Em (+60mV); at about +30, fast channels inactivate, abruptly ending phase 1
- K+ out: a brief efflux of K+ by transient K+ channels, allowing a short-lived partial repolarisation
- Ca2+ in, K+ out: these two ions ‘balance’ to produce the plateau phase, prolonging the action potential
- K+ out: activation of delayed rectifying K+ channels produces rapid repolarisation
- Em = EK+ (-90mV)
8
Q
Describe the Vaughan-Williams classification of anti-arrhythmics and how they relate to the non-pacemaker action potential.
A
- Na+ channel blockers: e.g. procainamide, lidocaine, flecainide - affects phase 0 (Na+ influx)
- Beta-blockers (e.g. propranolol) - affects phase 4 (K+ rectifier channels, prolongs refractory period)
- K+ channel blockers (e.g. amiodarone) - affects phase 3 (K+ out channels)
- Ca2+ channel blockers (e.g. verapamil, diltiazem) - affects phase 2 (plateau phase)
9
Q
Which feature of ventricular action potential is unique to the heart?
A
Plateau phase
10
Q
How does the autonomic nervous system effect the SAN action potential?
A
NA/symp increases steepness/frequency. ACh/para decreases it
11
Q
Which receptors does the autonomic nervous system act upon?
A
NA - B1, ACh - M2
12
Q
Describe briefly the G protein mechanisms of the autonomic nervous system.
A
B1/M2 -> Gs/Gi -> adenylyl cyclase catalyses ATP to cAMP (or is blocked), increasing/decreasing [cAMP]ic
13
Q
What is the chronotropic effect?
A
Slope of action potential curve. Increased chronotropicity describes increased heart rate
14
Q
What is the inotropic effect?
A
Contractility and output. Positive inotropes increase contractility.
15
Q
What is the dromotropic effect?
A
Conduction velocity; increased dromotropicity describes increased conduction through the AVN
16
Q
What is the lusotropic effect?
A
Myocardial relaxation -> duration of systole (+ decreases systole)
17
Q
Which two manoeuvres may be used to stimulate the vagus nerve and decrease heart rate?
A
Valsalva (breathing), massage of bifurcation of carotids
18
Q
What is the cardiac cycle?
A
The orderly depolarisation and repolarisation sequence of atrial and ventricular contractions/relaxations.
19
Q
What are the five stages of the cardiac cycle?
A
- Passive atrial filling
- atrial contraction; a wave on JVP
- isometric ventricular contraction (ventricular pressure < A+PA pressures),
- ventricular ejection,
- isometric ventricular relaxation
20
Q
What causes the first and second heart sound?
A
Closure of the AV then semilunar valves
21
Q
Describe the normal features of the JVP waveform, and the dicrotic notch.
A
- A wave = Atrial contraction
- C wave = Closure of the triCuspid valve
- V wave = Ventricular systole
- Aortic valve closure causes transient increase in pressure
22
Q
Describe the causes of JVP pathology.
A
- Absent A waves = Atrial fibrillation
- cannon A waves = occur when atria contract against closed valves, e.g. in complete heart block, VT, and ventricular ectopic beats
- large A waves = increased atrial pressure, e.g. in tricuspid stenosis, RVH
- large V waves = ventricular pathology, e.g. tricuspid regurgitation
23
Q
Why are cellular junctions vital in cardiac cells?
A
Enable autorhythmicity, provide low resistance, and ensure myocytes are reached.
24
Q
What is the name of the smallest functional unit of cardiac muscle?
A
Myofibril
25
What is the purpose in increased [cAMP]ic?
Opens calcium channels
26
Describe how calcium is built up in the myocyte and what its purpose is.
Calcium induced calcium release (small ic Ca opens VGICs and ryanodine channels in sarcoplasmic reticulum). Ca breaks troponin and allows myosin and actin to bind
27
Describe the Frank-Starling law.
What enters the heart must be ejected. Increase in EDV increases stroke volume increases force.
28
Describe, using the Frank-Starling law, how left ventricular hypertrophy may occur.
Chronic raised EDV increasing venous return. Sympathetic innervation only
29
What is the refractory period?
A period during which another action potential cannot be started
30
Describe why the refractory period occurs.
K+ is leaving the cell preventing depolarisation.
31
Describe the relationship between refractory period and heart rate.
Increased refractory period - decreased heart rate, and vice versa
32
During diastole, why doesn't arterial pressure fall to 0?
Due to vasomotor tone and elastic recoil
33
Describe mean arterial pressure (mAP).
* mAP is the average BP over the period of the cardiac cycle
* mAP = CO x SVR = (SV x HR) x SVR
* mAP should be ~70-105mmHg
34
What is the need to maintain a narrow range of MAP?
* < 60 to perfuse the organs (below this causes shock)
* >105 to prevent vascular damage
35
Why are we concerned primarily about arterial pressure, rather than others?
Arterioles are the primary resistance vessels (due to their ability to vasoconstrict and vasodilate)
36
Describe the auscultation of blood pressure.
* blood flow is heard when turbulent and not laminar
* BP is measured by auscultating the Korotkoff sounds; the first sound (K1) is heard when flow is initially maximally restricted (turbulent; systolic BP) and K5 when maximally relaxed (laminar; diastolic BP)
37
Name the types of short-term and long-term control of BP.
* short-term: baroreceptors (pressure), chemoreceptors (O2, CO2, pH), muscle receptors (metabolic activity), higher brain centres (temperature, exercise, emotion), and methods of extrinsic control (nervous system/ adrenaline (sympathetic-induce release from adrenal medulla); constrictors such as angiotensin II and TXA2 and dilators such as histamine, bradykinin and NO)
* both short- and long-term: ANP (atrial natriuretic peptide) is a powerful vasodilator released in response to atrial stretch; 'natriuretic' refers to Na+ excretion (H2O follows Na+, BP is decreased)
* long-term: ADH (vasopressin), RAAS system
38
Describe the RAAS system and its primary result of activation.
* Renin in kidney converts angiotensiongen to angiotensin I in liver,
* then ACE converts this to angiotensin II in the lungs. This causes vasoconstriction and Na/H2O retention, increasing BP
* aldosterone is a mineralocorticoid which also results in renal Na+/H2O retention and increased BP
39
Describe the natriuretic peptide system and its primary result of activation.
* (Pre-pro BNP -> pro-BNP ->) BNP + ANP (ventricular and atrial) decreasing renin production, causing vasodilation and increased excretion
* long-term, the 'natriuretic' refers to Na+ excretion (followed by H2O)
40
Describe the ADH/vasopressin system and its primary result of activation.
Precursor in the hypothalamus activates the posterior pituitary gland, through osmoreceptors (detecting osmolality). Activates re-absorption of water, increasing BP and ECF
41
What is the main factor affecting blood flow?
* Radius
* Poiseuille's law (blood flow, Q, is directly proportional to the radius of the vessel ^4)
* Very small alterations in radius have profound effects on resistance and blood flow (radius x2 = blood flow x16)
42
Which humoural agents cause vasodilation and which cause vasoconstriction?
* Vasodilation: nitric oxide (NO), bradykinin, and histamine
Vasoconstriction: angiotensin II, serotonin, TXA2, leukotrienes, endothelin
43
Describe the mechanism underpinning nitric oxide vasodilating the vessels.
* NO is synthesised by vascular endothelial cells and diffuses through the vascular smooth muscle cell membrane
* L-arganine -> ENOS -> NO
* Activates guanylate cyclase, generating cGMP and resulting in vasodilatation
* cGMP is broken down by phosphodiesterase (PDE); blockade of PDE-5 is the MOA of sildenafil (Viagra)
44
Describe how cerebral autoregulation protects against small changes to cerebral blood flow.
Automatic vasoconstriction/dilation to maintain pressure
45
Describe the control of venous return through the body.
* venous pressure depends on posture; when supine, all veins are abount the level of the heart and venous pressure ~0, whereas when standing venous pressure in the feet can be as high as 100mmHg
* venous return is driven by the arterial-venous pressure gradient, forcing flow to the veins from behind ('vis a tergo'). this is assisted by three pump mechanisms;
* cardiac pump: the RV 'sucks' blood from the right atrium and vena cava
* respiratory pump: inspiration results in decreased intrathoracic and increased intrabdominal pressures, augmenting the pressure gradient
* skeletal muscle pump: contraction of skeletal muscle displaces blood in the veins towards the heart
46
Describe the effects of exercise on the physiology.
Increased HR, CO, sympathetic discharge, vasoconstriction, and flow
47
What is the name of the sac surrounding the heart and its layers?
* The pericardium
* Visceral serous
* Parietal serous
* Pericardial cavity
48
Describe the branches of the coronary supply.
Left -> left marginal (and circumflex), left anterior descending (and diagonal/lateral). Right -> marginal and posterior intervascular
49
What is an auricle?
Extensions of the atria which allow extra filling
50
Describe superior vena cava vein supply.
jugular -> subclavian + brachial -> brachiocephalic -> SVC
51
Which structural landmark seperates the atria from the ventricles?
The coronary sulcus
52
Describe the venous return of the coronary blood itself.
Sinus venosus -> coronary sinus -> right atrium
53
Which congenital heart defect results in hypoxaemia?
Septal defect (hole)
54
What is the purpose of the oval fossa's crista terminalis?
It seperates smooth and rough muscle
55
Describe, anatomically, how the AV and semilunar valves differ.
Semilunar valves have pockets which collect blood and prevent backflow. AV valves have tendinous cords which connect them to papillary muscles
56
How do the papillary muscles contract simultaneously?
Moderator band connects the two valves
57
Describe the anatomical location of the thoracic duct.
Between the azygous vein and the oesophagus (a duck between two gooses)
58
Describe the boundaries and contents of the mediastinal divisions.
* superior: thoracic outlet (T1) to the transverse thoracic plane (T4-5)/sternal angle (angle of Louis). contains aortic arch and its branches, SVC and azygous arch, thoracic duct, vagus + recurrent laryngeal + phrenic nerves
* anterior: pericardium (posterior) to sternum (anterior). contains the thymus, internal thoracic arteries, and parasternal nodes
* middle: formed by the borders of the pericardial sac. contains the heart and its great vessel roots, trachea and main bronchi
* posterior: pericardium (anterior) to bodies of T5-12 (posterior). contains the oesophagus, descending thoracic aorta, vagus, splanchnic and sympathetic chains
59
Name the first branch of the aorta.
Coronary
60
Name the three branches of the aortic arch.
Brachiocephallic, left common carotid, left subclavian
61
Describe the diaphragmatic apertures.
* a series of apertures that permit passage of structures between the thoracic and abdominal cavities
* Vena caval foramen at T8
* Oesophageal hiatus at T10
* Aortic hiatus at T12
* this can be remembered by the number of letters [vena cava = 8; oesophagus = 10; aortic hiatus = 12] or I ate 10 eggs at 12
62
Describe the phrenic nerve.
* bilateral mixed nerve that originates from cervical nerves in the neck [C 3,4,5 keeps the diaphragm alive].
* it is the only source of somatic motor innervation to diaphragm. Somatic sensory to pleura and pericardium.
* right phrenic: passes anterior to the right subclavian artery, descending anteriorly along the right lung root, pierces the diaphragm at the vena caval aperture (T8) and innervates the inferior surface of the diaphragm
* left phrenic: passes anterior to the left subclavian artery, descending anteriorly to the left lung root, crosses the aortic arch bypassing the vagus, and innervates the inferior diaphragm
63
Describe the basic histology of the arteries.
* Tunica intima, inner elastic, tunica media, external elastic, tunica adventitia
* Vasa vasorum - the largest arteries are so thick nutrients cannot diffuse through the muscle
64
Name the three types of capillary.
Continuous, fenestrated, discontinuous.
65
What are the two main purposes of the lymphatic system?
Drains interstitial fluid, provides immune surviellence
66
How does interstital fluid flow?
Hydrostatic pressure, valves, compression by other structures
67
Name the three heart layers.
Pericardium, myocardium, endocardium
68
Describe the histology of the valves.
Lamina fibrosa, corda tendinae, papillary muscle
69
From which germ layer does the cardiovascular system originate?
The visceral mesoderm
70
Describe the main 'stalk' of the developing heart in the embryo.
* Sinus venosus -> atrium -> ventricle -> bulbus cordis -> truncus arteriosus
* twisting of the truncus arteriosus forms the vena cava
71
Which three embryological aortic arches are most important? What do they develop to?
III - common carotid, IV - right subclavian, VI - pulmonary artery
72
Describe venous supply of the liver in the embryo.
SVC -> vitellite veins -> ductus arteriorus -> umbilical and portal veins
73
How may the sympathetic nerve fibres reach their targets?
Same level synapse, superior synapse, inferior synapse, splanchnic (bypass), or adrenal medulla
74
Describe the full course of the vagus nerve (CN X).
* the vagus nerve is the 'wanderer', as it takes a wandering course from the skull to the abdominal cavity
* nuclei: dorsal motor (parasympathetic), nucleus ambiguus (motor), solitary (special sense), spinal trigeminal (general sense)
* intracranial: converged fibres from the four nuclei exit the medulla at the post-olivary sulcus, leaving the cranium at the jugular foramen (alongside CNs IX, XI)
* neck: travels within the carotid sheath, providing pharyngeal branches, superior laryngeal nerve, and the right recurrent laryngeal (loops under right subclavian artery)
* thorax: left vagus passes between left common carotid and left subclavian, becoming the anterior vagal trunk (which gives off the left recurrent laryngeal, looping under the aortic arch). the right vagus passes anterior to the right subclavian and becomes the posterior vagal trunk
* abdomen: both left and right (anterior and posterior trunks) enter through the oesophageal hiatus (T10), terminating as the oesophageal plexus
75
Describe the difference between somatic and visceral chest pain.
Somatic is sharp, well localised, and stabbing. Visceral is dull, aching, nauseating, and poorly localised
76
Describe the structure of a lipid.
Central - triglycerides (TAGs) and cholesterol esters. Internal/external apoproteins
77
Describe the classification and composition of lipids.
* lipid storage devices exist in four main types, according to the ratio of lipid and protein present
* chylomicron: 98% lipid, mainly triglycerides
* VLDL: very high lipid, mainly triglycerides
* LDL: high lipid, mainly cholesterol ('bad')
* HDL: 50/50 lipid/protein, mainly cholesterol ('good')
78
Describe how LDL is disposed of.
Receptors uptake in hepatocytes. Degradation into cholesterol and receptors. HMG-CoA reductase blocks this (Bad).
79
Describe the use of statins in cardiovascular disease, including the differences between primary and secondary prevention.
* statins are prescribed in three situations: familial hypercholesterolaemia, primary, and secondary prevention
* atorvastatin is the first-line agent in the Tayside Area Formulary; its maximum dose is 80mg
* familial hypercholesterolaemia: 10mg initially to achieve a reduction in 50% of LDL
* primary prevention: aims to prevent disease, all patients with a QRISK2 score >10% should be prescribed 20mg
* secondary prevention: history of disease (e.g. to prevent further episodes occurring), these patients should be prescribed 80mg
80
Name the cholesterol agents and describe their mechanisms of action.
* fibrates: upregulates LPL receptors by PPARa, decreases beta-oxidation
* bile-acid binding resins (cholestyramine): sequesters bile acids, using up cholesterol to create more bile acids
* NPC1LP inhibitor (ezetimibe): decreases dietary absorption of cholesterol by blocking the NPC1LP small intestine brush border enzyme
* nicotinic acid (niacin): a hormone sensitive lipase (HSL) inhibitor which decreases lipolysis in peripheral tissues
81
Describe the formation of atheroma.
Endothelial damage, accumulation of lipids and macrophages, migration of smooth muscle.
82
Describe how a complicated plaque is formed from a initial atheroma.
LDL oxidised in the intima - OXLDL. Monocyte uptake, macrophages, fatty streak, fibrofatty streak, complicated plaque
83
When may an atheroma become critical?
No collateral, small diameter, reduced blood flow
84
What are the four main complications of atheroma?
Arterial stenosis, arterial aneurysm, arterial dissection, thrombus/embolus
85
Which three factors are present in Virchow's Triad?
Endothelial damage, hyper-coaguability, circulatory stasis
86
What are the two main types of cardiovascular risk factor?
Behavioural and social
87
Describe the recommended exercise guidelines.
150 moderate or 75 intense during a week. [this may have been updated]
88
Why can cardiovascular disease be more dangerous in women than men?
Smaller vessels, increased stiffness (prone to fibrosis), increased incidence of erosion and microemboli.
89
Describe the trend in cardiovascular disease in women as they age.
Pre-menopause: more likely to be coronary. Post-menopause: more likely to be obstructive
90
Describe the very first steps of a clot formation.
Collagen exposure (damage) activates platelets, which releases thromboxane 2, ADP, and seretonin. This recruits further platelets and begins the clot cascade (fibrin and red blood cells)
91
Describe the intrinsic mechanism of activation of fibrin.
Factor X activated by tenase (IXa/VIIa). Xa binds to Va, forming prothrombinase. This enzyme converts factor II to IIa, thrombin, which converts fibrinogen to fibrin.
92
Describe the relationship between clot and thrombosis.
Clot is physiological (primary) haemostasis, while thrombosis is pathological (no injury)
93
Which clotting factors does vitamin K activate?
II, VII, IX, X (mnemonic: 1972)
94
Describe the cyclical nature of activation of vitamin K.
VK is oxidised (by Y-carboxylating factors II, VII, IX, X). This converts the reduced (hydroquinolone) form to oxidised (epoxide). Vitamin K reductase converts the oxidised form to a quinolone, then back to reduced.
95
Which drug targets the Vitamin K pathway and how does it do this?
Warfarin (targets vitamin K reductase)
96
Describe warfarin.
Slow acting vitamin K antagonist, used in VENOUS thrombosis. Significant risk of haemorrhage, so must be monitored by INR
97
Describe the three main differences between arterial and venous thrombi.
Arterial is white (platelets), venous red (RBCs). Arterial causes infarction, venous causes PE. Arterial treated by antiplatelets, venous by anti-coagulants
98
Describe the mechanisms of unfractionated and fractionated heparin.
* Whereas both types target and inactivate antithrombin III and therefore factor Xa, unfractionated (UFH) also targets thrombin (factor IIa); therefore UFH has a faster onset (1-2hr vs 2-6hr)
* LMWHs have the suffix '-parin' (dalteparin [Fragmin], enoxaparin)
* both UFH and LMWHs are reversed by protamine sulphate
99
List the main side effects of heparins and LMWHs.
Haemorrhage, thrombosis, osteoporosis, hypoaldesteronism, hypersensitivity
100
Describe the DOACs (direct oral anticoagulants), including their mechanism of action, time of onset, and reversal agents.
* there are three main 'types' of DOAC, which may inhibit factor Xa or IIa (thrombin)
* direct factor Xa inhibitors (drug contains 'Xa'), e.g. apixaban, rivaroxaban, edoxaban; these are reversed by andexanet alfa
* indirect factor Xa inhibitor (via antithrombin III) - fondaparinux - ~19hr and no specific reversal agent
* direct factor IIa inhibitors, e.g. dabigatran (~12hr) and bilvalirudin; reversed by idarucizumab
101
Describe the features of the coronary circulation which allow greater efficiency of the heart.
High capillary density, high basal blood flow, high oxygen extraction
102
When does most blood flow in the coronary circulation? Why?
During diastole - blood falls back down against the aortic valve, next to coronary vessels
103
Which blood vessels form the Circle of Willis? What is the circle of Willis?
Basillar and carotids - an anastomosis of the brain
104
Describe the blood-brain barrier.
Very impermeable to H+ ions due to tight cell junctions.
105
Which is the main factor in pulmonary circulation protecting against oedema?
Low BP (20-25/6-12) mmHg means absorptive forces > filtration forces
106
Describe the effect of hypoxia on the pulmonary arteries.
Vasoconstricts - diverts blood from areas of poor perfusion
107
Define stroke, the difference between a stroke and TIA, its classifications and risk factors.
* Acute onset of focal neurological symptoms and signs
* TIAs resolve on their own (vessels able to deal with small amount of clots with tPA) compared to stroke, which doesn't, and lasts much longer. ***[needs updated definition]***
* classified as either ischaemic (90%) or haemorrhagic (10%)
* RF: Hypertension (a reduction of 20 mmHg decreases risk by 20%) and smoking
108
Describe overdrive suppression.
The SA node is dominant, as it fires most often. This suppresses other (latent) pacemakers.
109
How may the heart's automacitity be altered physiologically?
Autonomic innervation
110
Describe the normal conduction of impulse through the heart.
* electrical excitation by the SAN causes atrial contraction, resulting in the P wave on ECG. note that the SAN's activity alone does not generate enough potential to be seen on the ECG; the entire atria contracting is the P wave
* the AVN is the only point at which atrial conduction is transmitted through to the ventricles. the pause in conduction is the PR interval (normally 0.12 - 0.20s)
* the bundle of His splits into left and right bundle branches; the LBB splits into anterior and posterior fascicles (as the left ventricle requires more power than the right)
* the Purkinje fibres are the terminal units of the cardiac conduction system in the ventricles
111
What is an escape beat?
* a ventricular escape beat is a self-generated electrical discharge initiated by, and causing contraction of, the ventricles
* 'Jumpstarts' the heart after a pause in electrical activity
* a ventricular escape beat indicates a failure of the electrical conduction system of the heart
112
What is an ectopic beat?
a disturbance of the cardiac rhythm resulting from beats arising from fibres otuside the SAN
113
Why do ectopic beats present with both a 'skipped' and a 'forceful' beat?
* a ventricular ectopic is a depolarisation prior to the end of diastole, meaning the ventricle is relatively underfilled
* the ectopic prolongs the refractory period, so a beat is dropped (the 'skipped' beat)
* the ventricle is then allowed to fill further than normal, meaning more blood is pumped ('forceful' beat)
114
What is responsible for EAD and DAD?
EAD - Na+ channels (phase 3). DAD - Ca2+ channels (phase 4)
115
Describe the mechanism by which re-entrant current within the AVN may cause additional depolarisation.
* AVNRT: AVN re-entry tachycardia
* within the AVN are a slow and fast pathway
* the fast pathway repolarises slower than the slow pathway (e.g., a motorboat produces more ripples in water than a rowing boat)
* conduction (slow pathway) meets a point which has just finished its refractory period (fast pathway), allowing it to become retrograde and depolarise the atria again
116
Heart block can be due to AV node block or bundle branch block. Describe the three types of AV node block
First degree - all impulses get through AV node, but delayed (prolonged PR interval). Second - Mobitz I - PR interval gradually increase until beat is missed. Mobitz II - every nth beat is missed. Third degree - complete block, nothing gets through, reliant on escape rhythm
117
Describe drug steady state block.
Class I agents dissociate in diastole - shortening diastole means they stay attached longer/permenantly, causing greater effect
118
Name the three main method of arrhythmia production
Increased automacicity (reduced threshold, increased slope in phase 4), afterdepolarisation, re-entrant current
119
Describe how varicose veins are formed.
Obstruction/valve incompetence forces blood from sapherous (deep) vein into the superficial veins
120
Name the fluid compartments within the body.
* intracellular (2/3 of total body water)
* extracellular (1/3 of total body water), formed of interstitial fluid (3/4 of ECF) and plasma fluid (1/4 of ECF)
121
Describe movement of substances and concentration of ions across the capillary wall.
* O2/CO2/non-polar molecules diffuse across.
* Na/K/glucose/amino acids etc travel through pores (*facilitated transport*, down a concentration gradient but through a transporter such as GLUT)
* Plasma protein is generally stuck.
* Na+ and Cl- are concentrated in the ECF, whereas K+ is concentrated intracellularly (meaning body fluids are neutral in charge)
122
Define the main forces across the capillary wall and how they vary going down the capillary.
* Hydrostatic pressure: the force exerted against a wall - in blood, this is the pressure exerted by blood against the walls of the blood vessel by the pumping action of the heart. Hydrostatic pressure causes movement out of the vessel.
* Oncotic pressure (colloid osmotic pressure): a constant, retention pressure produced by circulating albumin
* Arteriolar end: hydrostatic > oncotic, favouring filtration out the capillary
* Venous end: oncotic > hydrostatic, favouring reabsorption into the capillary
123
Define oedema and describe why it may be a bad thing.
* Oedema: swelling due to the expansion of interstitial fluid volumes in tissues or an organ
* Oedema increases the diffusion distance for oxygen and nutrients, as well as toxic byproducts of cellular metabolism; this compromises cellular metabolism
124
What is the equation for oxygen delivery index in consideration with managing cardiac arrest?
DO2I = CO x (1.39 x [Hb] x SaO2 + (0.003 x PaO2)
125
Which four H's may contribute to cardiac arrest?
* hypoxia: respiratory disease or obstruction, drug-related (e.g. overdose)
* hypovolaemia: e.g. UGI/LGI haemorrhage, trauma/stabbing/shooting
* hyper/hypometabolic: ketoacidosis (DKA, alcoholic), toxins (poisoning)
* hypothermia: exposure to cold
126
Which four T's may contribute to cardiac arrest?
* Thrombosis,
* tension pneumothorax,
* tamponade,
* toxins
127
Describe the foetal circulation.
* the umbilical vein carries oxygenated blood from the placenta to the IVC, mostly shunted from the liver by the ductus venosus
* the right atrium (RA) contains mixed blood (oxygenated from IVC, deoxygenated from SVC) and is at much higher pressure than the LA (little return from lungs, full of fluid)
* the foramen ovale allows relief of pressure from the RA to the LA
* ductus arteriosus: connects the outflow of the RV to the LV (pulmonary arteries to aorta)
* umbilical arteries: blood is drained from the internal iliac arteries back to the placenta
128
Describe the changes that occur to circulation after birth.
* fluid is reabsorbed from the lung alveoli, decreasing pulmonary resistance and vasoconstriction
* the need for the ductus arteriosus and umbilical arteries is eliminated. these are maintained by prostaglandins (released by the placenta in-utero) and constrict when these are reduced after birth
* increased pressure in the LA manually closes the foramen ovale
* once the placenta is delivered, the cord contracts in response to the cold extrauterine environment, increasing resistance to the placenta restricting its flow
129
In the timeline of congenital heart disease tests, what is assessed and when?
Day 1-2, murmur, abnormal pulse, cyanosis. Day 3-7, collapse, shock, cyanosis, death. Week 4-6, signs of cardiac failure
130
Describe transposition of the great arteries.
Aorta and pulmonary artery are swapped - incompatible with life unless blood is mixed (i.e. septal defect). RVH common, as right ventricle main pump.
131
Describe duct-dependant heart disease.
Where the ductus arteriosus is required to remain open - done so by prostaglandin E2.
132
What are the four defects of tetralogy of Fallot?
1. VSD, 2. Underdeveloped/stenosed pulmonary arteries, 3. aorta just above VSD, 4. right ventricle hypertrophy
133
What is the difference between cardiomyopathy and channelopathy?
Channelopathy - mutation to gene for ion channel. Cardiomyopathy - stiffening/difficulty to pump
134
What are the genetic causes of long QT syndrome?
Dominant - romano-ward. Recessive - Jervell-Lange-Nielsen
135
What are the time intervals of the QT interval required to diagnose long QT syndrome?
* male: >430ms
* female: >450 ms.
* each small box on ECG is 0.4s, meaning the normal QT interval (from beginning of QRS to end of T wave) should be ~11 small boxes
136
What are the four types of cardiomyopathy?
Dilated (flabby), hypertrophic, restrictive, arrhythmogenic right ventricular dysplasia
137
Describe the types of blood flow defect caused by each cardiomyopathy.
Dilated - HFrEF, hypertrophic/restrictive - diastolic (relaxing), ARVD - arrhythmia
138
What is amyloidosis?
Deposits of protein. Typically forms B-pleated sheets which the body can't get rid of
139
Describe the two stains shown by amyloidosis.
Stains congo red, apple green birefringence
140
Describe the two main types of pacemaker. Which is the better and why?
S-ICD, transvenous-ICD. S-ICD has better cosmetic and functional outcome
141
What types of screening should be used after a genetic defect for family members?
Cascade - one generation to another etc
142
What are the six main types of radiograph in the cardiovascular system?
CXR, angiograph, echocardiogram, MRI, CT scan, nuclear scan
143
How should the heart appear on a chest x-ray?
Less than 50% of the diameter of the thorax
144
Which radiological scan is the gold standard and why?
Cardiac MRI - excellent soft tissue visibility
145
Which imaging test should be used for the coronary arteries?
Angiography
