Cardiovascular Flashcards

Question

What is a refractory period, and what are the potential phases involved with this time?

Answer 1

Absolute refractory period- when the membrane can't be re-excited Relative refractory period- larger than normal stimulus needed for AP generation- although impaired conduction Supernormal period- get propagated AP from weaker than normal stimulus, although impaired conduction Full recovery time- may extend beyond return to Resting dependence The longer than normal refractory phase prevents tetanus of the heart

Answer 2

The duration of the AP is partly determined by the preceding diastolic interval- faster HR means a shorter AP

Answer 3

They respond due to electrical stimulation, thanks to its spread throughout the myocardium due to electrical coupling due to nexus junctions between neighbouring cells Their structure is laminar- not uniformly continuous, but continuous enough to propogate action potentials

Answer 4

Refers to the ability of cells to initiate an electrical impulse due to their own pacemaker activity. Found in SA, AV and his-purkinje network - Due to outward K and inward If (Na)- activated at negative potentials- and ICa

Answer 5

- Alter slope- change rates of inwards/outwards currents - Alter threshold potential - Alter max diastolic pressure- how far down the repolarization curve reaches

Answer 6

PNS- releases ACh to slow HR | SNS- releases noradrenaline to increase HR

Answer 7

AV node is slow, to allow atria to top up the ventricles before initiating contraction. Atria and ventricles are insulated from one another by the fibrous skeleton Bundle branches and purkinje fibres are fast

Answer 8

- SA node is normally the pacemaker due to its high intrinsic rate, and overdrive suppression of other pacemakers due to hyperpolarization - AV delay may be subject to blockage - Purkinje network is rapid to activate the whole endocardium synchronously - Velocity is proportional to the square root of the radius of the fibres - Velocity depends on the rate and amplitude of depolarization

Answer 9

An abnormal structure between the atrium and the ventricles, which allows the bypass of the AV node. It leads to re-entrant arhythmia (short interval between contractions, due to charge propagating a continuous loop between atria and ventricles.

Answer 10

- Thick muscular walls, inlet and outlet valves - Pump - 95mmHg pressure

Answer 11

- Muscular walls for control, C. T. for strength - Conduct and store large volumes of blood/distribution and tone - 85-95mmHg

Answer 12

- Smooth muscle to control diameter, little CT - Control flow to capillaries based on demand - 35-85mmHg

Answer 13

- Endothelium, no muscle or CT - Exchange - 15-35mmHg

Answer 14

Thin walled, large diameter - Collect blood - 0-15mmHg

Answer 15

- Think walled, variable structure and valves - Conduct and store blood - low

Answer 16

- Thin muscular walls - Reservoir for blood - 0-2mmHg

Answer 17

- Intima: endothelium with internal elastic lamina separating - Media: A lamellar unit alternating between smooth muscle, collagen and elastin Fenustrated elastin layers Adventitia: Vasa vasorum supply the layer, with collagen and elastin fibres

Answer 18

Intima: Endothelium with internal elastic lamina Media: Collagent and elastin fibres, but not nearly as many or as large. External elastic lamina Adventitia: Vasa vasorum, collagen and elastin fibres with nerves

Answer 19

1. Atherosclerosis: Endothelium damaged, causing increased intima thickness and accumulation of macrophages. It is most often caused by high cholesteol, and the free fat cells are digested by the macrophages, forming foam cells. The IEL breaks down, and blood clots can form and occlude 2. Aneurysm: Dissecting mainly found in thoracic and abdominal aorta, where the weakened intima causes blood to pool in the media Berry found in brain branch points, around circles of willis. These form large pods that can burst 3. Hypertension: 140/90+. Intima thickens, media thickens to maintain pressure, and IEL may duplicate. Increased by obesity, stress, salt and smoking

Answer 20

Endothelium and then IEL, with 2-3 layers of smooth muscle before a surrounding of collagen. Has a wall thickness equal to lumen diameter.

Answer 21

- Arch of the aorta - Arch of azygous vein - Trachea (may be bifurcated) - Thoracic duct (crosses behind oesophagus from RHS to LHS - Cardiac plexus - Ligamentum arteriosum - Good place for jugular venous pressure

Answer 22

External jugular (not great vein) empties into subclavian, which then combines with the internal jugular to form the brachiocephalic vein. The two combine to form the SVC. The left brachiocephalic vein is longer due to it needing to cross the midline

Answer 23

Aortal branches into brachiocephalic trunk, and then into common carotid and subclavian (same on each side.

Answer 24

- Phrenic: from C345 down the LHS and RHS of the pericardium Vagus: From CX. Right slides under subclavian artery to give off the R recurrent laryngeal nerve, while L goes under arch of aorta to give off L recurent laryngeal. They then wrap around the oesophagus to give the ant (left) and post (right) vagal plexuses

Answer 25

These control the voice- any change can be due not just to throat conditions, but also to bronchial tumor, and aortic aneurysm etc.

Answer 26

Deliver blood/fluids immediately Deliver toxic drugs without destroying the weaker peripheral veins Measure pressures in heart chambers

Answer 27

- External Jugular - Femoral - Internal Jugular - Subclavian

Answer 28

Pros - Easy to access and superficial - Less likely to cause a pneumothorax Cons - Small, difficult vein to threat (insert a tube) - Uncomfortable for the patient as it sits below their ear

Answer 29

``` Pros - Easy to access, especially during CPR - No chance of pneumothorax Cons - Increased infection risk - Increased clot risk - Reduction in mobility ```

Answer 30

``` Pros - Easy to find and threat Cons - Can be uncomfortable - Risk carotic artery- supplies the brain and can form a clot or an air embolism, resulting in stroke - Risk of Pneumothorax - Impossible during CPR ```

Answer 31

Pros - Most common long term - Comfortable - Less likely to be dislodged during CPR and intubation Cons - Risk pneumothorax/subclavian airway puncture - Impossible to apply pressure if artery punctured, as below clavicle - Risk to brachial plexus.

Answer 32

Record potential difference in different sites of the body due to electrical activity in the heart- the body is able to act as a conductor

Answer 33

P wave: atrial depolarization, small mass and hight, slow reflecting time taken- even though it has a similar timespan to ventricles, it has a smaller mass PR segment: Between P and start of QRS. Atria depolarized, isoelectric. Reflects time in AV node, bundle and bundle branches. QRS Complex: Ventricular depolarization- greater magnitude than P due to more mass, shorter than P wave relative to mass. Also includes atrial repolarization (though not visible) PR interval: Total time for wave to run from atria to ventricles ST segment- Isoelectric spot, when there is no moving wavefront. Plateau of AP in ventricles T wave: Asynchronous repolarization of ventricles, as the cells have slightly differing peak times QT interval: Reflection of ventricular action potential duration

Answer 34

When a wavefront moves within the heart, it causes a reversal of charge in the surrounding extracellular tisse. This forms a dipole, with a positive and a negative charge side by side, and moving in the direction of flow. This is represented by a vector (which is plotted on the ECG). The orientation represents the direction the dipole is travelling (relative to the ECG line), while the length represents strength.

Answer 35

- Magnitude of the change - Orientation of the dipole and the electrodes - Distance between the dipole and electrodes- potential difference is higher close in and vice versa.

Answer 36

- Q = ventricular septal depolarization - R = ventricular apex depolarizing - S = ventricular base depolarizing

Answer 37

As the ventricular depolarization runs from endocardium to epicardium, and repolarization is vice versa, we know that the AP duration of the endothelial cells is longer than those in the epicardium

Answer 38

- Assumes body is a volume conductor regardless of tissue type - A single dipole is not a good representation of a wavefront

Answer 39

``` Measures a single vector between two points. This is used in Einthoven's triangle, where leads are set on the Right arm, left arm and leg in order to string leads together in a triangle. The differences between each two-point interval can then be calculated. Lead 1 = LA-RA Lead 2 = LL - RA Lead 3 = LL - LA Therefore: I + III = II ```

Answer 40

Uses the potential of a single electrode relative to a point of reference- usually compared to zero, called the indifferent electrodes. This means that when the dipole faces the exploring electrode it is recorded as positive. It also allows crosses across the original einthoven's triangle, representing 6 leads (augmented unipolar leads)

Answer 41

An additional 6 leads are added to the augmented unipolar limb leads, allowing the coronal and horizontal planes to be recorded.

Answer 42

``` = Rate = Rhythm - P waves - PR interval - QRS complex - ST segment - T waves ```

Answer 43

``` Azygous veins Thoracic Duct Oesophagus Thoracic Aorta Nerves ```

Answer 44

They link the superior and inferior vena cavae. The RHS (azygous vein) receives systemic as well as RHS intercostal blood and drains into the SVC The accessory hemiazygous (sup) and hemiazygous (inf) veins run on the left side, draining the superior and inferior intercostals, respectively.

Answer 45

It's a large lymphatic duct running from the abdomen. It starts at the cisterna chyli, and runs anterior to the vertebrae up the midline It crosses from being more RHS to more LHS at the thoracic plane. It drains into the point where the left internal jugular and subclavian veins meet. It can get blocked at this point. It is important to check its associated nodes, as the whole body (apart from the R arm and face) drain their lymph through here

Answer 46

- It runs behind the left main bronchus and arch of the aorta - It can be constricted by the diaphragm, as well as by a large aneurism in the aorta, or a lung tumor. Upper 2/3: Supplied by branches of the thoracic aorta, azygous vein and sympathetic trunks Lower 1/3: Supplied by left gastric artery, gastric veins (to portal system) and vagus nerve

Answer 47

- Sympathetic trunks - Phrenic nerves - Vagus nerves

Answer 48

There are no valves to prevent backflow in the visceral veins so: - Caput medusae - Anal varices - Oesophageal varices

Answer 49

Narrowing of the aortic arch (a birth defect). Usually after the main 3 branches have been given off Body supplies descending aorta as bloodflow reverses through the post. intercostals- supplied by both sides of anterior intercostals instead

Answer 50

- Radial pulses and femoral pulses being out of sync between each other and the sides of the body. - Notching of the ribs on the chest X ray due to the size of the artery causing them to wear away (more pressure in other arteries)

Answer 51

It shows up as a shortened P R interval due to early conduction from atria to ventricles Also a wide QRS complex as while the conduction starts early, the conduction pathway isn't incredibly fast. Additionally, there is a delta wave between Q and R as conduction isn't as fast as usual within the ventricles

Answer 52

May be asymptomatic- although can have unexplained syncope or palpitations. Drugs control fast rhythms, or surgery can correct the false pathway

Answer 53

Long QT syndrome- an abnormally long delay between ventricular de- and re-polarization. Can be drug induced (from arrhythmia drugs) or genetic (due to ion channel mutation) Most commonly K+ delayed rectifier channel. Causes differences in refractoriness of myocytes and abnormal ventricular activation (possibly followed by arrhythmia and fibrillation) Assoc. with syncope and sudden death Treated with arrhythmia prevention and termination

Answer 54

- AV/bundle branch blocks- will see long PR intervels - Heart and lung structure- will see large deflections on the EKG - Potassium disturbance: Hyperkalemia leads to faster repolarization and high peaked T waves. Hypokalemia opposite

Answer 55

- Ischaemia: T wave affected - Injury- ST segment - Infarction- QRS complex

Answer 56

- Tall peaked T waves over leads facing damaged area - ST segment elevation (hours later) - reduced R wave amplitude - T wave inversion (days later) - Pathological Q waves (usually only residual signs of MI) - ST segment returns to normal (days later) - T waves return to normal (weeks) Reciprocal changes may be seen in leads facing opposite the infarction

Answer 57

Not specific to MI- but earliest signs of acute MI. Lasts 5-30 mins after onset. Same mechanism as hyperkalaemia due to K+ leakage from damaged myocytes

Answer 58

ST Segment elevation- though mechanism depends on current of injury. Systolic injury current: Ischaemic zone incompletely depolarized, so AP is different between two areas- the net current between leads is not 0 during this time Diastolic injury current: Ischaemic zone is less repolarized than healthy zone so resting RMP is higher- so the ST elevation is also at this level.

Answer 59

- Results in electrically inactive tissue forming a 'window' through which activity is reduced or absent (or, in opposite electrodes, amplified). This results in reduced R wave height and QS complexes (no R wave)

Answer 60

Changes are variable and sometimes absent - Abnormal activation distorts EKG - 12 lead EKG can't show basal/pst. RV walls well

Answer 61

- Atherosclerosis affects medium and large arteries, appearing as focal plaque thickenings. Arteriosclerosis is a general term for arterial hardening

Answer 62

Contains blood, selective transport into tissues, clotting and blood pressure control.

Answer 63

Hyperlipidaemia Cigarette smoking Hypertension Diabetes mellitus Advanced age- lesions can be seen in all ages, but only present when progressed Metabolic syndrome- fat stored in unsuited organs, increased insulin resistance, altered inflammatory predispositions

Answer 64

High levels of HDL fats (transport saturated fats away from vessel walls) Moderate alcohol consumption Cardiovascular fitness

Answer 65

1. endothelial cell injury- caused by haemodynamic force of blood (high BP), chemical insults (smoking, lipids) or cytokines Leads to altered permeability (and lipid infiltration), leukocyte adhesion and thrombosis activation 2, Chronic inflammation- leukocytes migrate into plaque - Neutrophils arrive early, then monocytes enter and take up oxidised lipoproteins, forming foam cells. When these die they release their contents, promoting necrosis, cholesterol crystals/clefts, and calcification. - Mast cells promote leukocyte & smth muscle movement into plaque, and degrade HDL - Smooth muscle cells activated by macrophages, platelets and endothelial cells. Migrate to TI, producing cytokines and attracting leukocytes. - Lipoproteins become oxidised, attracting monocytes and stimulating cytokines

Answer 66

Fibrous cap- with smooth muscle, macrophages, foam cells, fibres- fibroblasts secrete fibres to stabilize the atheroma Necrotic center- cell debris, cholesterol crystals, foam cells, calcium

Answer 67

- Often silent until sudden symtoms. Once the plaque has grown, it can cause aneurysm and rupture due to wall weakening, occlusion by a thrombus due to plaque rupture/erosion/haemorrhage/mural thrombosis, or critical stenosis by progressive plaque growth This commonly results in myocardial infarction, peripheral vascular disease, and CVD

Answer 68

Entry into the vulnerable phase- thin/no fibrous cap, high lipid content and widespread inflammation

Answer 69

- Myogenic - Striated - Electrically coupled using nexus junctions - Oxidative in metabolism - Action potentials trigger CICR

Answer 70

Forms the permeability barrier between intra- and extra-cellular contents. Continuous with the T tubules. Outer surface known as glycocaly

Answer 71

- Invaginations of the sarcolemma, rich in L type Ca2+ channels (DHPRs)

Answer 72

- They have 3 differentiations in their connection between cells: - Nexus junctions - Fascia adherens junctions - Desmosomes (macula adherens)

Answer 73

- It's an intracellular, Ca2+ storing membrane bound structure. It includes junctional couplings with T tubules and with external sarcolemma. Induces calcium induced calcium release due to RyR receptors opening and releasing Ca2+ when stimulated by Ca2+ Re-takes Ca2+ due to SERCA channels. Also rich in calsequestrin, which buffers Ca2+ and helps return it to the SR by binding to Ca2+ and reducing the gradient for the pump to work again

Answer 74

- Mostly vascular - Some ground substance - Few connective tissue and empty space - A little collagen

Answer 75

1. AP spreads across the SL and T tubules 2. Voltage causes DHPRs to open 3. Influx of Ca2+ causes RyRs to open and release even more Ca2+ 4. Ca2+ binds TnC and allows crossbridges and contraction 5. Additionally, Ca2+ is sensed by the mitochondria, and stimulates it to produce ATP

Answer 76

Process by which electrical changes at surface membrane lead to changes in intracellular Ca2+ levels, which in turn causes contraction

Answer 77

They are channels which are activated by voltage >-40mV and catecholamines to carry Ca2+ into the cell, contributing to the plateau They trigger EC coupling, and are inhibited by the trigger of CICR, as well as by dihydropyridines, Mg2+ and low plasma Ca2+ content

Answer 78

Occurs when Ca2+ leaks from the SR, making the whole cell Ca2+ transient. The amplitude and duration of these Ca2+ 'sparks' determines the body's response to this (ie contraction or not)

Answer 79

1. A low capacity, high affinity pump may be used- Ca2+ ATPase. This only contributes a little 2. An ATP independent pump driven by the steep Na+ concentration across the sarcolemma. Although this operates in both directions- stimulated by low intracellular Na+ as well as high intracellular Ca2+ and negative membrane potential. This is also maintained by the 3Na+/2K+ pump. Na+ also has spots of hot and cold concentration along the SR, driving its movement Important as Ca2+ in via DHPRs must be removed to maintain balance pH is also kept in balance by Na+/H+ exchangers 3. Majority is simply returned to the SR by SERCA transporters

Answer 80

Arterioles (2-3 smth muscle) lead to terminal arterioles (1 layer smth muscle) lead to metarteriole (incomplete smth muscle) and into capillaries. These are opened/closed by precapillary sphincters so when the body is hot/parasymp these are open and allow the capillary network to become more perfused. If wanting to direct the blood straight past the capillary bed, a thoroughfare channel connecting arterioles with venules is used. Another type of channel can have no capillaries arising from it, termed Arteriovenous anastomoses. This can allow AV shunting. If it is closed however, it forces blood through the capillaries

Answer 81

Continuous capillaries: May have closed intercellular clefts (tight junctions form a complete seal- eg. BBB) or open intercellular clefts (eg. muscle, lungs. Allows H2O, ions, other small molecules, but not plasma proteins) Fenestrated capillaries: May have closed perforations (like glycocalyx, eg. in intestine) or open perforations (as in glomeruli) Sinusoids- wide bore capillaries with large gaps allowing whole molecules and cells through. Eg. spleen due to RBC production/cleaning, and liver where endothelium is interspersed with kupffer cells.

Answer 82

Postcapillary venules: drain capillary beds. No smooth muscle but often pericytes. Site of blood plasma, neutrophil, monocyte leakage during inflammation Muscular venules: Larger, up to 2 layers smooth muscle. Characterised by thin wall relative to diameter, and bulging endothelial nuclei

Answer 83

Conduct blood at low pressure, so have thin walls and large diameters All three tunics reduced, but adventitia larger and media smaller Never a well-developed IEL Valves (infoldings of intima) prevent backflow. However, when standing still, this leaks through slowly, leading to a pressure of approx. 100mmHg in the feet. Skeletal muscle movement forces blood up, back through the veins

Answer 84

The formation of a blood clot, usually in the deep veins of the lower extremity. If part of the clot breaks loose it becomes an embolus, likely to lodge in the pulmonary arterial tree. Small clots have few to no symptoms, large fatal Caused by any event slowing blood flow, increasing coagulability or damaging the endothelium

Answer 85

Superficial veins of the legs dilate enough so that valves do not meet, causing the veins to become swollen and torturous

Answer 86

Blind ended tubes, made of endothelial cells tethered to CT with anchoring filaments. When the tissue swells, the anchoring filaments drag the tube open wider. Lack basement membranes, increasing permeability - Have large gap junctions to allow passage of proteins and whole cells

Answer 87

Resemble veins, but with thinner walls and more valves Lymph propelled through by contraction of smooth muscle around the vessel (triggered by its distension) or by its compression due to surrounding tissue Most tissues (apart from CNS, cartilage, bone, placenta, cornea, teeth, thymus) contain lymphatics- these enter a lymph node containing lymphocytes etc. This means cancer is likely to establish a secondary tumor here Eventually enters the bloodstream via the thoracic duct or right lymphatic duct

Answer 88

There can be no additional recruitment of myocytes. As CO must be equal to venous return, there must be another way to modulate contraction to maintain higher CO levels.

Answer 89

Can increase heart rate, but only by 3x and with less strove volume each time (due to reduced filling time) Can increase ventricular diameter with more blood Can alter Ca2+ action with neurotransmitters or use drugs, to increase force of contraction

Answer 90

An increase in end-diastolic ventricular volume increases the stoke volume via an immediate stretch-induced increase in contractility. This is because increased myocyte length increases force generated for conc. Ca2+

Answer 91

There is an optimal myocyte length to get the maximum force of contraction. When the myocyte is too short it can't shorten enough, and when too long it can't make enough cross bridges.

Answer 92

At higher heart rates, there is a higher force produced. This is due to the reduction in time for Ca2+ extrusion. The NCX exchange is impaired, increasing the Na2+ and Ca2+ in the cell, allowing the SR to be loaded more. On subsequent contractions, more Ca2+ is available to leave the SR. Therefore, the Ca2+ transient increases In heart failure, increased heart rate leads to decreased force as Ca2+ is not taken back up into the cell, meaning Ca2+ transients remain constant in spite of HR increase

Answer 93

They stimulate adenylyl cyclase, increasing cAMP levels. This activates proteins kinases, which phosphorylate other proteins. This results in: - Decreased Ca2+ sensitivity due to troponin I phosphorylation (although this is compensated by increased Ca2+ transient) - Increased internal Ca2+ - Enhanced SR Ca2+ ATPase - Altered RyR gating

Answer 94

It depends on [Ca2+] internal and total- although in a sigmoidal, not linear, fashion. To change strength of contraction we need to change either the Ca2+ transient (amount of Ca2+) or else the sensitivity to Ca2+ (force produced at a given Ca2+ level) The Hill coefficient reflects the steepness of the curve

Answer 95

Acidity (acidic environment causes less Ca2+) Length (increased length increases Ca2+) Catecholamines (increased catecholamines decrease Ca2+) ATP (increased ATP decreases Ca2+) Caffeine (increase caffeine increases Ca2+) Inorganic phosphate (increased IOP decreases Ca2+)

Answer 96

At acidic pHs, the Na+/H+ exchanger works on removing H+ from the cell in exchange for Na+. This reduces Ca2+ transient. At high pHs, the CHE and CBE transporters load acid into the cell.

Answer 97

The myocytes are more sensitive to Ca2+, and so increase force- although they are less able to relax, and so pump less blood.

Answer 98

Immediate: Increase Ca2+ sensitivity Slow: Increased calcium transient. This means that when stimulus frequency increases, the force of contraction also increases

Answer 99

PSNS: Decreased SA node firing so decreased force SNS: Increased SA rate, resulting in increased Ca2+ influx, increased SR pump rate and decreased sensitivity of troponin to Ca2+ (to allow relaxation)

Answer 100

- Cardiotonic steroids: Increase Na+ by inhibiting their pump. This reduces Ca2+ extrusion - Bipyridines: Increase cAMP (act like B adrenergic activators) - Heart failure: Increased dimesion so decreased efficiency- most try to decrease filling pressures by giving vasodilators (NO), ACE inhibitors and diuretics

Answer 101

They promote Ca2+ extrusion by the NCX pump. causing localized and potentially cell wide depolarization. As a consequence, they may trigger random APs

Answer 102

Increased intracellular Na2+, which slows or reverses the Na+/Ca2+ exchanger- so more Ca2+ in the cell

Answer 103

Symptoms are a continuum, and are not always set out in a black and white cutoff Additionally, depending on additional risk factors, such as age, smoking, weight, blood glucose, cholesterol, the interpretation of the result is different. Ie. someone with 150/100 blood pressure may be at less risk than someone with 120/80 blood pressure who smokes.

Answer 104

Cholesterol itself is measured in total cholesterol- including both high and low density cholesterol. By itself it isn't really a useful measurement. We should be measuring the ratio of low to high density cholesterol However, the efficiacy of cholesterol lowering drugs is equatable to measuring only LDL cholesterol, as it is only this type of cholesterol that changes.

Answer 105

It starts soon after the P wave, and ventricular volume is topped up by atrial contraction (although this is not necessary at normal heart rates)

Answer 106

Onset is at R wave peak. Ventricular volume remains unchanged and first heart sound occurs. Takes place between start of systole and opening of semilunar valves

Answer 107

Semilunar valves open, with a rapid increase in aortic flow and venous and aortic pressure. Causes a rapid decrease in LV volume and atrial pressure due to the base moving to the apex and stretching the atria

Answer 108

- The runoff from the aorta to the periphery exceeds the LV output, so aortic pressure and flow drop. Aortic pressure is just greater than LV pressure so the blood keeps moving forwards. At the end of ejection, 55-75% of blood remains

Answer 109

The aortic valve closes due to pressure gradient reversal- there is a slow backflow producing an incisura (notch) in the aortic pressure curve. The second heart sound occurs due to semilunar valve closure and while volume remains the same, LV pressure falls rapidly (although aortic pressure remains high.

Answer 110

LV pressure is below LA pressure, allowing the AV valve to open and cause a rapid LV volume increase. The third heart sound is sometimes heard here

Answer 111

This is diastasis, where pressure are aqualized and there is a slow rise in atrial and venous pressures

Answer 112

a: a retrograde pulse into the jugular vein when the atria contract - c wave: early phase of ventricular systole - v wave: a gradual pressure increase during reduced ejection and isovolumic relaxation

Answer 113

Wall thickness and valve motion, as movement changes the placement of black and white strips (representing muscle and and space).

Answer 114

The right ventricle has lower pressures as it pumps through the low-resistance lungs, rather than the entire systemic circuit. The right side valves open earlier and close later than the left side valves.

Answer 115

First heart sound is due to AV valve closure, and is of low frequency. Although the two sides close asynchronously, there is normally only one sound heard The second sound is due to semilunar valve closure, and is of higher frequency. Sometimes it can be split due to aortic/pulmonary delay The third heart sound can be heard in rapid filling The fourth sound can be caused by oscillation and stretch during atrial contraction

Answer 116

- LA pressure obtained with a catheter with a balloon on the end (deflated) - RA, RV and Pulmonary artery pressures are measured the same way, with the balloon inflated. The balloon can be threaded further into the pulmonary artery until it wedges, and so the pressure here can be approximated as LA pressure

Answer 117

- The fick method: Q = O2 added to blood in lungs / venous O1-arterial O2 Q = VO2/PaO2-PvO2 - Thermodilution: A catheter is threaded through the RA and RV, with a temperature sensor in the pulmonary trunk. Cold saline is injected into the RA, and the change in temperature reaching the artery is measured. This means that there is no arterial puncture, toxicity or recirculation

Answer 118

General: R = P1-P2 / Q Total peripheral vascular resistance: TPVR = Psyst. artery - P syst. vein / ! Pulmonary vascular resistance; P (pul art) - P (LA) / Q

Answer 119

A failure of the body to maintain sympathetic activity- vagal activity increases dramatically and HR and BP decrease and fainting occurs

Answer 120

Means that you can control what is activated- ie. in disease there is increased sympathetic stimulation to the heart, muscle and kidneys,

Answer 121

The parasympathetic system begins in the brainstem and runs down through the neck or into the head to innervate. Similarly, innervation to the bladder/genitals begins in the sacrum. The sympathetic system has a trunk of ganglia, so the nerves leave the spinal cord and run into the ganglion chain, where they run up and down the body. This means that only some fibres run through the neck The parasympathetic nervous system has long preganglionic fibres and short postganglionic fibres, while the sympathetic ganglia is vice versa

Answer 122

1: Ganglion: Receptor in N2, uses ACh. Effector tissue: Muscarinic receptor, uses ACh

Answer 123

To Smooth muscle, cardiac muscle, gland: Ganglion: Uses ACh on N2 receptor. Norepinephrine to alpha.beta receptor on target cells To adrenal medulla: Chromaffin cell: ACh on N2 receptor. Epinephrine on Alpha/beta receptor on target cells

Answer 124

N receptors: N1 is skeletal muscle, N2 is in ganglia Muscarinic receptors: On parasympathetic target tissue Adrenergic receptors: Can be B1 (heart), B2 (smooth muscle relaxer), a1 (vascular smooth muscle constrictor) or a2 (inhibit neurotransmitters)

Answer 125

Neuromuscular blockers block muscular N receptors, while ganglia blockers block ganglia N receptors

Answer 126

A1- phenylephrine A2: Clanidine B1: Botutamine B2: Salbutomol

Answer 127

Targets vagal activity by increasing SA firing

Answer 128

Vagus touches SA and AV nodes | Sympathetic touches both nodes as well as some of the ventricular walls

Answer 129

It releases ACh on to muscarinic receptors, which open potassium channels and close funny and T type Ca2+ channels, resulting in hyperpolarization and reduced spontaneous depolarization

Answer 130

It releases Norepi onto B1 receptors at the SA node, activating cAMP and augmenting the funny and T type Ca2+ channels, increasing the slope and frequency of APs, increasing HR

Answer 131

It releases norepi onto B1 receptors, activating adenylate cyclase and synthesizing cAMP. This increases intracellular Ca2+ and contractility, as well as increasing the gradient for Ca2+ efflux, helping relaxation.

Answer 132

A release of norepi onto a1 receptors causes vasoconstriction- although it can be differentially mediated- some beds may be sympathetically increased while others are not.

Answer 133

(this also applies vice versa) - Increased blood pressure increases vessel stretch - Increases firing of baroreceptors in carotid arteries and aorta - CV centre in medulla oblongata decreases symp and increases parasymp - Vasodilation, decreased force of contraction and decreased HR - Decreased TPVR and CO - Decreased blood pressure

Answer 134

``` Carotid and aortic bodies are innervated by the sinus and aortic nerves. Stimulated by hypoxia, hypercapnia and low pH to increased ventiation and symp. activity. Central chemoreceptors (ant. medulla) respond only to hypercapnia and low pH ```

Answer 135

``` Due to the presence of water on the face in terms of cold temperature and pressure/sensation fibres. Also undertaken by peripheral chemoreceptors (after a time) Involves apnea (breath holding), brady cardia, peripheral vasoconstriction and increased BP. ```

Answer 136

Systolic pressure is the highest pressure reached Diastolic pressure is the lowest pressure reached Pulse pressure is the difference between the two Mean arterial pressure is the pressure difference multiplied by 1/3

Answer 137

Blood pressure most commonly refers to systemic arterial pressure. It is very important in calculating DALYs.

Answer 138

Ventricles only spend 1/3 of their time in systole and the other 2/3 in diastole

Answer 139

Cardiac output and total peripheral resistance

Answer 140

Short term: Heart rate, inotropic state, neural and humoral factors. Long term: RAA pathway, natiuresis, aldosterone and ANF

Answer 141

Nervous activity on receptor a (vasoconstriction) and receptor b (vasodilation) Humoral vasoconstrictors: Angiotensin and ACh Humoral vasodilators: Prostaglandins, kinins and NO Local Autoregulation

Answer 142

Stroke volume Aortic Compliance Diastolic Runoff

Answer 143

It is determined by preload, afterload, chronotropy, inotropy and exercise- systolic causes increased SV, diastolic decreased.

Answer 144

The more compliant the vessel, the smaller the pulse. This is due to the fact that systolic pressure is lower, and diastolic is relatively higher due to the lack of change. Compliance decreases with age, causing increased BP

Answer 145

If downstream resistance is low, then there will be more blood leaving any given vessel during a time period, so a lower diastolic pressure. Increasing HR reduces runoff.

Answer 146

In atherosclerosis, resistance is affected as vessels are much less compliant In a patent ductus arteriosus, blood volume is increased to make up for the decreased blood going to the lungs. This results in shunting and decreased total peripheral resistance, as well as increased blood volume and increased systemic pressure.

Answer 147

When the cuff is at higher than systolic pressure, no blood gets through, so there is no sound When the cuff is without pressure, there is completely laminar flow, and there is no sound When the cuff is between diastolic and systolic pressure, only some blood gets through, and the turbulence generates sound.

Answer 148

``` P = pgh p= density g= gravity h= distance ```

Answer 149

At the feet, the arterial pressure can be calculated by additing the arterial pressure of the heart to the hydrostatic pressure in the feet. Venous pressure can be calculated by taking the venous pressure of the heart and adding it to the hydrostatic pressure in the feet. Respectively, they result in 180mmHg arterial and 90mmHg venous In the raised hand, the arterial pressure is calculated the same way, although at this point the hydrostatic pressure is -50mmHg.

Answer 150

At the lower ends of the lower vessels, the bottom is dilated, resulting in poorer resistance and so more flow- however, this is overrided by venous pooling, reducing venous return, preload and CO At the upper end of the higher tubes, there is negative pressure, causing tubes to collapse, flow to reduce or to stop/start, and causing no pressure change, a rising blood pressure and then flow.

Answer 151

The physiological response of blood vessels to injury. It prevents leaks in injured vessels

Answer 152

Healthy: Endothelial cells switch off haemostasis by insulating tissues from blood, and producing enzymatic and chemical inhibitors (NO and PG12). They also express antithrombin orn their surfaces, which binds to and inactivates thrombin In unhealthy cells, endothelial cells promote haemostasis. When they are breached, they activate platelets and the coagulation cascade. They also produce von Willebrand factor, promoting platelet adhesion to the ECM proteins exposed, and tissue factor (thromboplastin, activating the coagulation cascade) Finally, they produce endothelin, which causes vasoconstriction.

Answer 153

They are fragments of megakaryocytes, activated by ECM proteins exposed when the endothelium is damaged. They secrete chemical signals that promote vasoconstriction and platelet aggregation. Reduced platelet numbers can result in anything from purpura (under-skin bleeding) to spontaneous haemorrhage

Answer 154

A cascade of reactions through which invert zymogens are activated. It is initiated by several stimuli including tissue factor (from damaged tissues). Penultimate step is the activation of thrombin, which then goes on to catalyze the conversion of fibrinogen to fibrin, which then forms fibrin strands. This then forms a meshwork with fused platelets to form a stable plug. As fibrin is being deposited, the fibrinolytic system is activated to disassemble it.

Answer 155

1. Initial brief period of arteriole vasoconstriction due to reflexes and local factors 2. Injury to endothelium exposes ECM, activating platelets 3. Platelets release secretory granules and come together to form a plug (primary haemostasis) 4. Tissue factor is secreted by endothelium and activates the coagulation cascade: thrombin --> fibrinogen --> fibrin (secondary haemostasis 5. Solid permanent plug 6. Counter-regulatory mechanisms limit plug to site of injury.

Answer 156

Occurs when hemostasis is activated inappropriately. A thrombus is a mass formed from blood constituents within the circulation during life. They are made of fibrin, platelets, and R/WBCs. They may form in the heart or blood vessel, and can obstruct the vessel or else break off to form an embolus and obstruct elsewhere

Answer 157

Virchow's triad: - Changes in the blood vessel wall Changes in blood flow Changes in blood constituents

Answer 158

Changes can be due to endothelial activation or injury- occurs in MI, atherosclerosis, vasculitis, as well as physical and chemical damage. Vascular transplant can also encourage it as the activate intrinsic coagulation cascades to bind pro-inflammatory cascade proteins, and activate platelets.

Answer 159

Heart/Arteries: Turbulence is an important cause, ptentiallay due to aneurysms, narrowing, infarction, heart valve disease and abnormal cardiac rhytms Veins: Stasis is the important cause, cost commonly affecting pelvic and deep/superficial leg veins. May be due to RHS heart failure, immobilization or compressed veins.

Answer 160

This can lead to increased coagulation tendency. Causes include tissue damage, as in trauma, responses from the liver via pro-inflammatory proteins and cytokines. Additionally, operations, malignancy, smoke, lipids and contraception can do the same.

Answer 161

Natural coagulants Anti-thrombins The fibrinolytic cascade limits clot size as it activates plasmin to break the clot down

Answer 162

Intravascular masses that get carried by blood flow from its original site to a different place. Theyc an be thrombi, fat, air, atheromatous debris, bone marrow and amniotic fluid They cause effects due to stenosis and occlusion. Leg and pelvic veins' clots lodge in the pulmonary artery, causing pulmonary infarction, reduced CO, RHS heart failure and death. LHS heart emboli or aortic emboli enter the arterial system and can damage the brain, spleen, kidney, gut, legs and more

Answer 163

A self-limited loss of both consciousness and postural tone. Has a rapid onset, with variable warning symptoms (malignant if no warning). Usually a prompt recovery without intervention, and is due to transient global cerebral hypoperfusion.

Answer 164

Neurally-mediated reflex syndromes Orthostatic hypotension Cardiac arrhythmias Structural cardiovascular disease

Answer 165

History- ie circumstances of current and previous events, medical history, family history. Then examination, and then tests like tilt tests, head MRI

Answer 166

- Vasovagal syncope - Carotid sinus syndrome - Situational syncope- ie. during defecation, venepuncture, pain, psych stimulus etc. Due to a physiological reflex mechanism- Inhibition of heart rate (after a slight rise) and vasodepression (drop in BP) Treated with drug strategies

Answer 167

Can be due to drug action- like diuretics and vasodilators - Primary autonomic failure- multiple system atrophy, parkinson's, POTS - Secondary autonomic failure- diabetes, alcohol, amyloid. Treated with patient education and injury avoidance, as well as hydration, tilt training, wearing of support hose, drug therapy and pacing

Answer 168

Potentially life-threatening- appropriate to initiate assessment and treatment promptly. Most commonly not cardiac, but bradycardia is most common of cardiac syncope types. Bradyarrhythmias show AV block, and potential accompaniment by vasodilation Tachyarrhythmias show atrial fibrillation with a rapid ventricular rate, and paroxysms of supraventricular/ventricular tachycardia as well as torsade de pointes.

Answer 169

At the middle of the T wave upstroke, or during repolarization in the myocyte action potential. This can result in changed repolarization, with ectopic action potentials being able to be generated. (hyperpolarization zone?)

Answer 170

The awareness of a heart rate or rhythm change- usually transient and benign, often nocturnal or during rest, with exertional less common. Small malignant potential.

Answer 171

History is the key- then physical examination to exclude SHD. Investigate from here if needed. Most treatment is reassurance- any treatment can cause more harm than good in terms of side effects

Answer 172

Repeated palpitations- may reflect underlying cardiomyopathy, atrial/pulmonary vein tachycardia or

Answer 173

Trigger for possible malignant arrhythmias. Treatment more hazardous and limited

Answer 174

Usually well-tolerated, benign and curable palpitation

Answer 175

Involves abnormalities in Na+/K+ channels causing susceptibility to polymorphic ventricular tachycardia. Common in drug-induced forms, genetic forms rare but being more recognized, and concealed forms may be common and can be the base of drug-induced Treated with drug therapy and potential ablation of pathways

Answer 176

Atrial fibrillation: Pacing and/or ablation Atrial flutter: Ablation of tricuspid valve-IVC isthmus Ventricular tachycardia: defibrillation or ablation Torsade de pointes: withdraw offending drugs and/or implant a defibrillator

Answer 177

Inadequate local blood supply to a tissue

Answer 178

A consequence of ischaemia- a deficiency of O2 causing cell injury by reducing aerobic respiration

Answer 179

Necrosis due to rapid or prolonged ischaemia

Answer 180

- External occlusion of a vessel- tumors, compression - Internal occlusion of a vessel- atherosclerosis, thrombosis, embolism - Vessel spasm (eg. frostbite) - Capillary blockage- sickle cell anaemia - Shock- circulatory failure with low arterial bp - Increased demand- increased tissue mass/workload - Venous obstruction

Answer 181

Those with higher energy requirements tend to be affected more severely Neurons are very sensitive, and irreversibly damaged by only 3 mins of anoxia Renal epithelium is sensitive- ion reabsorption is rapidly impaired Myocardium is sensitive- irreversible damage after 20 mins and functional impairment after 1min Skeletal muscle is less sensitive and capable of anoxic work Fibroblasts and macrophages are insensitive Neutrophils are enhanced by hypoxia, as the tissue they must clean up is often poorly perfused

Answer 182

Decrease in ATP availability, causing signal cascade activation for thrombosis Decreased pump activity, so increased Ca2+, Na+ and H2O, and decreased K+, causing swelling, death and bleb formation If the cells have enough ATP in hypoxic conditions they apoptose, and if not they die a necrotic death

Answer 183

The anatomy of the blood supply to the organ- ie collateral supply reduces susceptibility to hypoxia The size of the vessel- the larger, the more potential damage Speed of onset- collateral vessels may develop to compensate for slow stenosis Duration of occlusion- cells survive short periods, but may be killed by reperfusion injury Metabolic demands of tissue at time of ischaemia General adequacy of circulatory system- effects worse in heart failure, anaemia

Answer 184

No effect Functional defects due to less perfusion- eg. dysrhythmia due to poor conductance, renal insufficiency Reversible damage to isolated cells Apoptosis of isolated cells Infarction- necrosis due to overwhelming injury

Answer 185

``` Red infarcts: Occurs in tissue with a dual blood supply or in reperfused tissue- causes haemorrhage into damaged tissue White infarcts: Occurs in singularly supplied tissue, often wedge shaped with the point of wedge at occlusion, and base at organ surface Coagulative necrosis- loss of cell features and bright red color due to protein denaturing Liquifactive necrosis (brain) ```

Answer 186

In 24h, neutrophils are recruited. 1-3 days later is macrophages and some lymphocytes Fibroblasts and endothelial cells then recruited (organisation) and form granulation tissue which is remodeled into a fibrous scar. In some tissue, regeneration may occur

Answer 187

Usually caused by atherosclerotic narrowing of the coronary arteries, depriving the heart of blood. This causes 1. Angina pectoris- pain due to tissue death. Presents as transient constricting discomfort, and falls short of necrosis 2. Chronic ischaemic heart disease with heart failure 3. MI: may occur due to slowly growing plaque which suddenly enlarges- ie. rupture or thrombus formation. Causes full thickness of heart wall to infarc, or just the underlying endocardium This can cause mural thrombosis, dysrhythmias, heart failure, and reperfusion injury 4. Cerebrovascular injury- neurons are vulnerable, and as the brain needs 20% of normal blood supply it may be compromised

Answer 188

With thrombolitic agents Mechanical reexpansion of occluded vessel CABG

Answer 189

Non-severe/short-lived ischaemia causes a biology change to the cell, leading to adaptation. Prolonged causes death. Ranges from attempts at repair < atrophy < shut-down < apoptosis < necrosis

Answer 190

In short periods of ischaemia, reperfusion shows injury reversal. However, after long periods, damaging free radicals are produced in cells, which cause lipid peroxidation in membranes and damage enzymes and DNA In reperfusion, (ie after MI/transplant), this is severe. Vascular endothelial cells are particularly susceptible In skeletal muscle, reperfusion causes tissue swelling in the fascia, which can cause compartment syndrome, secondary ischaemia and necrosis.

Answer 191

Higher at nighttime Higher in elderly in wintertime Higher in older ages Lower in low salt, high exercise, low BMI people, non smokers

Answer 192

in 1950s it was only measured for renal and cardiac failure patients 1970s- GP screening introduced Now, BP is falling even though we are increasing in weight

Answer 193

Lifestyle Kidney disease Adrenal issues Coarctiation of aorta

Answer 194

``` Diagnosed over 3 visits, taking the average of the last 2 Easiest lowerers: 1. Drug therapy (triple test- ACE inhibitors, diuretics and Ca2+ blocker) 2. Exercise 3. Smoking cessation 4. Diet 5. Sodium intake 6. Alcohol intake 7. Weight loss ```

Answer 195

- Anything interfering with pump function (muscle and rhythm), which can cause hydrops (thickened skin around heart, effusions, ascites and hydrocardium/haemocardium) - Interference with stroke volume- valve regurgitation- or HR- arrhythmias.

Answer 196

Tricuspid regurgitation, causing heart hyperplasia and lung hypoplasia

Answer 197

- Critically ill fetuses become critically ill newborns - May have obstructed pulmonary veins or valve regurgitations, but don't often show RDS Heart murmurs can be present due to semilunar valve stenosis or AV regurgitations. May have cyanosis. Septal defects don't present yet

Answer 198

Ductal dependent lesions begin showing up at 24h-2 weeks- these begin to present when the ductus arteriosus begins closing, as children with ductal dependent lesions can function on a single chamber as the blood is still able to reach the other circuit with the duct open. Can be: Dependent for pulmonary blood flow, dependent for systemic blood flow, or dependent for mixing

Answer 199

- Mild cyanosis at birth - Gradual hypoxia at duct closure - Results in severe cyanosis, acidosis and lactaemia - Treated with prostaglandin E1 to reopen the duct, and eventual surgery

Answer 200

- Caused by aortic coarctation or LHS hypoplasia - Mild cyanosis at birth - acidosis and shock (grey skinned) - Tachypnoea, acidosis, lactaemia - Risk of organ damage- brain, guts, liver, renal - Treated with prostaglandin E1, inotropes, ventilation, organ repair and heart surgery

Answer 201

- Caused by the aorta coming off the RV and pulmonary arteries from LV- essentially separating the two circuits in the wrong way - Mild cyanosis at birth - Rapid cyanosis in the first few days - Acidosis and lactaemia if not treated - Treat with Prostaglandin E1, bullon septostomy to open the atrial septum, and surgery

Answer 202

Ventricular septal defects and patent ductus arteriosum. This is because pumonary resistance falls to the point that the blood going through the pulm. arteries is 2-5x higher than in the systemic circuit, as the pulmonary circuit becomes lower resistance than systemic. This results in congested, stiff lungs and increased heart work to supply the systemic circuit

Answer 203

- Breathlessness (>50/min) - Sweatiness due to increased metabolic rate - Tachycardia - Poor feeding and weight gain - Hepatomegaly - Larve VSDs Development of a pansystolic murmur in the tricuspid valve due to huge blood volume, and a middiastolic murmur due to mitral valve turbulence. - Small VSDs show a louder noise during systole

Answer 204

Present in 50s-60s Due to dilation of RA and V due to increased blood flow from the LA (higher P) to RA (lower P). The amount of flow is related to the diastolic compliance of the ventricles, and left ventricles become less compliant with age, especially in ischaemic heart disease and hypertension

Answer 205

Atrial arrhythmia and fibrillation- RHS failure and fibrillation after MI. Uncommon to have pulmonary hypertension Treat by closing valve- normal life if closed in childhood, risk persistent arrhythmias if closed in adulthood

Answer 206

``` Turns up in chest X rays Pulmonary blood flow murmur Split second heart sound Increased RV load so a greater RV ejection Equal RA/LA pressures Tricuspid valve murmur ```

Answer 207

It is where the clavicles meet in the midline

Answer 208

S: Thyroid, trachea, oesophagus A: Thymus (in children) M: Heart, trachea, oesophagus, great vessels P: Nerves

Answer 209

S: Goitre A: Thyroid, thymoma, lymphoma, teratoma M: Cardiac/vascular lesions, oesophageal abnormalities, lymphoma, bronchogenic cysts P: Neurogenic cysts

Answer 210

LHS presents with SOB and orthopnoea due to pulmonary involvement RHS presents with peripheral oedema and azygous vein involvement as the RHS is not draining Treat with diuretics to remove pulmonary fluid

Answer 211

Thyroid tumor: anterior and middle mediastinum involvement Lymphoma: LHS and RHS mediastinal involvement Seminoma: Mass in azygous recess Hiatus hernia: Air bubbles in chest

Answer 212

Put a catheter into the femoral artery and thread it back into the left ventricle

Answer 213

During diastolic filling, pressure increases slowly, then greatly, and volume increases greatly, then slowly. The end-systolic pressure-volume relationship is litear, while diastolic is exponential The pressure-volume loop fits between, as the two diastolic points (iso relax and end of vent. filling) are on the diastolic line, while end-systole is on the linear graph

Answer 214

It relates to the degree of stretch of the muscle just before contraction, due to the differing filament overlaps. At greater preloads, there is a greater stroke volume and a greater max. potential pressure (at aortic valve opening).

Answer 215

This is the pressure against which the ventricle contracts in order to open the aortic valve. It is determined mainly by systolic left ventricular and aortic pressures, which are increased by systemic hypertension. An increased afterload raises pressure, but decreases stroke volume

Answer 216

This is the intrinsic ability of the myocardium to contract at a given preload and afterload. Altering it adjusts the minimum pressure able to be developed, and shifts the linear end-systolic pressure-volume line. Stroke volume increases at increased inotropic states, and vice versa.

Answer 217

Digoxin- poisons the Na+/K+ pumps, increasing intracellular Na+, and meaning that the NCX pump brings in Ca2+ in exchange for Na+

Answer 218

Increasing heart rate increases CO as well as inotropic state. However, it decreases SV due to reduced filling time. However, this is only considerable at high HR

Answer 219

- Both hearts have to pump the same volume over time, so any changes must be balanced- additionally, increasing the afterload results in increased preload

Answer 220

- Increased left volume afterload - Decreased stroke volume - RV must do the same - Blood accumulates in the lungs - Left atrial filling increases - EDV increases - Increased stroke volume

Answer 221

- Blood volume - Venous tone - Posture - HR - Atrial contraction - Muscle pumps - Intrathoracic and intrapericardial pressures - Ventricular compliance

Answer 222

Hypertension Vasoconstriction Aortic stenosis Heart failure

Answer 223

``` ANS Catecholamines Force-frequency relationship AP changes Cardiomyopathy Positive inotropic and cardiac depressant drugs ```

Answer 224

ANS Reflexes Higher centres Catecholamines

Answer 225

It is SV/EDVx100. It is often measured using echocardiography, and sits around 55-60% normally, with 85% during exercise.

Answer 226

The maximum rate of ventricular pressure rise- this indicates cotnractility. In diastolic heart failure, ejection is conserved, but the heart has relaxation problems

Answer 227

They show preload vs. an index of ventricular performance. Stroke volume can be used, although stroke work is preferable as it is not affected by afterload

Answer 228

Stroke work is the pressure/volume work performed during each cardiac cycle Calculated by SW = MAP x SV As preload increases, SW increases - If MAP increases, SV decreases but SW stays the same Both move if you increase or decrease inotropy. SW represents everything but heart rate

Answer 229

Stenosis- impaired forward flow Regurgitation/incompetence- allowing reverse flow These can occur in isolation or together

Answer 230

Diastolic are mitral/tricuspid stenosis, or aortic/pulmonary incompetence Systolic are mitral/tricuspid incompetence, or aortic/pulmonary stenosis

Answer 231

``` Developmental defects of CT Calcification Infection Post-infection Hypercoaguability Carcinoid tumours ```

Answer 232

-Stenosis of the pulmonary or aortic valve Leaflet abnormailites (like bicuspid aortic valves) Myxomatous degeneration of the mitral valve- also known as mitral valve prolapse

Answer 233

Idiopathic, but commonly occurs in marfan syndrome and other inherited CT disorders Asymptomatic Can increase risk of endocarditis and mitral insufficiency

Answer 234

It occurs in local areas after extensive cell injury, when dead or dying cells accumulate calcium. This causes cumulative damage, most commonly in the form of annular calcification of the mitral valve, and stenosis of the aortic valve, which may render it unable to fully open or close

Answer 235

Infective endocarditis is the colonisation or invasion of heart valves by a microbe, often after seeding of blood with microbes. Small lesions called vegetations form, and the pathogens involved can be bacterial, fungal etc.

Answer 236

Acute: High virulence, often previously normal valve, destructive and high mortality rate. Caused by staph.a Subacute: Low virulence, often previously abnormal valve, insidious. Caused by strep. viridans

Answer 237

Rheumatic fever is a multi-system type II hypersensitivity reaction, which can cause scarrin, fibrosis, vegetations, aschoff bodies (oedematous CT with WBCs) and pericarditis Leads to valve deformities such as mitral stenosis Immune response against strep M proteins cross reacts to antigens in the heart

Answer 238

``` - Previous endocarditis Rheumatic heart disease Prosthetic valves Unrepaired congenital heart defects Congenital heart defects that were repaired less than 6mos ago ```

Answer 239

Involves deposition of fibrin and platelets on the heart valve without any pathogen responsibility. It's especially evident when the patient is in a hypercoagulable state due to an underlying cause such as cancer or sepsis, when Vichow's triad is turned on Prosthetic valves can also increase risk of thrombosis

Answer 240

A range of neoplasms arising from neuroendocrine cells Secrete a variety of bioactive products which cause plaque like thickenings on the RHS of the heart Composed largely of smooth muscle cells that affect the tricuspid and pulmonary valves.

Answer 241

P= CO x R, and when CO increases, R decreases and vice versa. An increase in resistance increases blood pressure upstream, whereas downstream flow is affected mainly by capillary flow (but with little effect on TPR).

Answer 242

The major pressure drop is in the small arteries (resistance vessels), which also show and inverse relationship between total X sectional area and flow rate. Max cross sectional area and minimum flow is seen in the capillaries.

Answer 243

The volume passing any point along a tube per unit time Q = mean velocity x cross sectional area, where velocity is proportional to 1/Area- the wider the cross sectional area, the slower the velocity. (This allows diffusion to occur in capillaries

Answer 244

``` Flow rate (Q) = change in P / R. Therefore, flow is directly proportional to pressure difference and inversely proportional to resistance. NB: Usually the delta P = Pa - Pv, although often Pv can be ignored as it's close to 0. Often, CO = MAP (100mmHg) /TPR (mainly controlleld by small arterioles) ```

Answer 245

The capillary beds are in parallel, rather than series, so that 1/resistance = 1/vessel1 + 1/vessel2 + 1/vessel3

Answer 246

The flow = change in P x (pi x r^4) / (8viscosityL) | As Q = p/R, R = the inverse of this

Answer 247

Vessel length Blood viscosity Radius of blood vessel

Answer 248

One of the most important factors due to the proportionality to the fourth power. This means flow will increase exponentially for minor changes in radius

Answer 249

It affects the amount of the friction between the vessel wall and fluid Relative viscosity of fluid = fluid viscosity / water viscosity

Answer 250

Temperature: Decreased temperature = increased viscosity Haematocrit: Increased Hct = Increased viscosity Shear rate: Low velocities, blood becomes non-newtonian. so that viscosity is no longer independent of shear rate, and viscosity increased as cells clump together Vessel diameter: In very small vessels, viscosity decreases as blood cells can only get through one at a time- most of the blood is plasma at this point

Answer 251

- Steady laminar flow (not profile) to get a parabolic velocity flow (max velocity in the centre, near zero close to vessel walls (newtonian flow) - Rigid vessels: OK assumption for the small arteries (most important), due to their thick muscular walls - Newtonean fluid- viscosity is independent of shear rate, and blood assumed to be homogeneous

Answer 252

As blood vessels' diameters can change, at increased pressures resistance decreases and flow rate increases, and vice versa There is also a critical closing pressure, beneath which the vessels will collapse

Answer 253

Force in the direction of flow along the inner surface of the blood vessel. Its magnitude depends on viscosity and rate of flow. It can damage and weaken the vessel walls. It influences the function of the endothelium, causing NO release and vasodilation when under great stress- therefore reducing flow velocity and reducing shear stress

Answer 254

Increased friction and flow resistance results, making flow proportional to the the square root of the pressure difference, rather than directly proportional

Answer 255

Velocity of blood flow and diameter of blood flow | Above reynold's number ( (density x velocity x diameter)/viscosity ) turbulence will occur.

Answer 256

Heart murmurs Atherosclerosis Post-stenotic dilation

Answer 257

The pressure inside the vessel minus the pressure outside the vessel

Answer 258

Given by laPlace's law: Wall tension is proportional to radius and pressure, and inversely pressure to wall thickness. As the diameter of the vessel increases, wall tension increases. This is important for capillaries- small diameter so low wall tension Aneurysm- larger vessel diameter, increased tension so more likely to rupure Heart failure- enlarged heart is inefficient as more wall tension is needed to develop the same pressures

Answer 259

Compliance relates the distension of a vessel to the distending force. It = change in volume / change in pressure Capacitance is a measure of the volume to pressure relationship over the entire V/P curve

Answer 260

``` Arterioles Metarterioles Precapillary sphincters True capillaries AV anastomoses Venules ```

Answer 261

Both have variable resistance, control the distribution of vascular pressure and flow, and have a thick layer of smooth muscle in their walls Metarterioles do not have continuous smoth muscle, and often branch off arterioles at right angles

Answer 262

They open and close in order to direct blood in and out of the capillaries. Opening is promoted by decreasing O2, or increased CO2, lactic acid, NO, adenosine, K+ or H_ in the ECF, inflammatory chemicals and increased temperature They are controleld by local mechanisms, not neural,

Answer 263

They are exchange vessels, and vary in concentration depending on the tissue. They have a high SA:V ratio and very thin walls, with a variety of holes and permeabilities. Blood flow through them is acheived through autoregulation, with myogenic control- increased stretch activates stretch that cause increased contraction

Answer 264

Diffusion: Driven by concentration gradient- mainly for exchange of solutes and water. Fick's law governs it: Diffusion = diffusion constant x (area/thickness) x concentration gradient. Transcapillary transport of small molecules is limited by the rate of delivery from the material to the vessel (flow limited). Transcapillary transport of large molecules is limited by pore size (diffusion limited)

Answer 265

A bulk flow of fluid across a membrane, driven by hydrostatic and osmotic pressure differences. A filtration coefficient is determined by the permeability of the capillaries to water, tissue type, and other influences. - Capillary hydrostatic pressure drops over the vessel, pushing fluid out - IF hydrostatic pressure is is normally around 0 - Blood colloid osmotic pressurenormally remains the same, drawing fluid into the vessel - IF colloid osmotic pressure draws fluid in and also remains the same

Answer 266

Fluid movement = filtration constant x (blood - IF hydrostatic pressure) - membrane reflection constant x (blood - IF colloid osmotic pressure) If Pa, Pv and rv increase, blood hydrostatic pressure increases, and outward fluid movement increases - If ra increases, blood hydrostatic pressure decreases, and outward filtration decreases

Answer 267

- normal: 50% each - Vasoconstriction: less filtration as Pa decreased, and absorption increases - Vasodilation- Pa increases, so filtration increases and absorption decreases - Increased Pv (heart failure)- Increased filtration, decreased absorption - Dehydration: Decreased filtration, increased absorption - Hypoproteinemia: Increased filtration, decreased absorption

Answer 268

``` Return blood components to the circulation Absorption from the gut (esp. fats) Removes RBCs to tissues Lymph noes Elephatiasis and lymphodema ```

Answer 269

Total energy of laminar flow without resistant is constant, and equals the sum of pressure energy (PxV), gravitational energy, and kinetic energy. Total energy= PV + pgh + 1/2pv^2

Answer 270

- velocity increases Kinetic energy increases Although: total energy remains the same Therefore, there must be a pressure drop

Answer 271

Due to the narrowing in heart valves during closure, the blood is sucked rapidly through the space, creating a sort of vacuum and sucking the leaflets closed. In delayed valve closure, the forward flow continues because of a kinetic energy difference, as ventricular blood has a higher total energy compared to the artery

Answer 272

Cardiac issues: MI, myocarditis, pericarditis, HF Aortic dissection Respiratory issues: Pulmonary embolism, infection, COPD, asthma, pneumothorax

Answer 273

ST elevation MI (STEMI) | Non-ST elevation MI (Non-STEMI)

Answer 274

MI is caused due to the rupture of an atherosclerotic plaque, causing platelets to aggregate and the thrombus to occlude the blood vessel.

Answer 275

Aspirin and similar, to overcome the activation of platelets Low molecular weight heparin (LMWH) as an anticoagulant Thrombolytics in less advanced centres, which break the clot down. Modern centres use a stent to open up the thrombus

Answer 276

STEMIs show elevation between the S and T wave, esp. on the V3 lead NSTEMIs show depression of the ST segment on V3

Answer 277

NSTEMIs and STEMIs: Morphine, nitrates for vasodilation, aspirin (+/- clopidogrel) beta blockers. NSTEMIs: LMWH STEMIs: LMWH, and either a thrombolytic or a stent

Answer 278

Given intravenously or via bolus It catalyses plasminogen to plasmin, to lyse the thrombus. Best given within 12 hours of chest pain onset. Streptokinase is non-human protein so may cause an allergic reaction, alteplase is human. Risks bleeding, and allergic reactions from non-human protein.

Answer 279

They are small chains, usually generated by depolymerisation of unfractioned heparin They inhibit factor Xa, which converts prothrombin to thrombin, and are injected subcutaneously. Side effects can be bruising and bleeding, or thrombocytopenia

Answer 280

It inhibits platelet cyclo-oxygenase, which prevents thromboxane production. (thromboxane causes vasoconstriction and platelet aggregation. It is used in acute MI, chronic angina, stroke and peripheral vascular disease. Side effects are dyspepsia and GI ulcers due to reduced PGE2 Also increased asthma exacerbation

Answer 281

It inhibits the purine platelet receptor, preventing ADP-induced thrombosis. This is done to cover another method of platelet activation than covered by aspirin. Side effects include upper GI symptoms and bleeding, as well as rash. Used with acute coronary syndromes, aspirin allergy, and vascular stenting

Answer 282

A new platelet inhibitor that is reversible. However, causes dyspnoea and bleeding

Answer 283

Used in acute MI and chronic angina. These can be absorbed rapidly through oral, IV, sublingual and transdermal methods. They increase the bioavailability of nitric oxide, allowing vasodilation. Their main side effect is headache. In sustained therapy, a tolerance can be built up, causing a loss of efficacy. This can be prevented by nitrate dosing and a nitrate free period

Answer 284

Beta blockers antagonise the B1 and B2 receptors, which cause an inhibition of sympathetic activity in the body. This allows the reduction of cardiac work by causing acute reduction in cardiac work and a negative chronotropy. There can be different selectivity (B1>B2 and vice versa) as well as differences in elimination location, solubility and half life. Side effects include asthma exacerbation, hypotension and bradycardia, fatigue, and withdrawal symptoms

Answer 285

Pain nature, duration, radiation and assoc. features Risk factors such as smoking, diabetes, lipids, blood pressure, family hx Past medical history

Answer 286

Vital signs, like bP Heart sounds and any bruits JVP and oedema

Answer 287

ECG | Blood troponin levels (released when contractile cells are damaged)

Answer 288

They contain radiofrequency coils that transmit to surface coils. H atoms align to the field and protons swing back into place once the transmission is over, and emit radiowaves. The computer reconstructs the image.

Answer 289

``` The structures are small Patients have to hold their breath Pictures have to be taken in time with the heartbeat Cardiac arrhythmias complicate things Need cooperation of patients ```

Answer 290

Can take a measure of LV size, a measure of LV lumen size, and subtract it.

Answer 291

Gadolinium contrast is taken up and removed from healthy tissue quickly, whereas it stays in tissues with a poor blood supply for longer. If the ventricle is only 50% or less black, healthy tissue, it is not viable

Answer 292

Involves feeding a tube from the femoral or radial artery into the coronary artery entrance, and injecting dye while taking photos. A multi-holed catheter can be used to see the chamber.

Answer 293

A way of reopening blocked coronary vessels. Pass a balloon into the vessel, inflate it into the stent, and then deflate and remove balloon- the stent stays open Stents are coated in drugs to prevent stenosis, and ensure patency. There is a slight risk of thrombosis if the stent doesn't fully inflate the vessel, or if the vessel wall tears during insertion- risk increased in multiple or long standing lesions, diabetes and restenosis procedures

Answer 294

Non-invasive, so it's cheap and with less risk Images both the vessel wall and the lumen Can see other thoracic issues Lower radiation and contrast Doesn't need a specialist facility

Answer 295

Poor images of tachycardics Requires patient cooperation Issues with calcified vessels More difficult to interpret.

Answer 296

Cardiac function Vascular function Blood volume

Answer 297

The body's Oxygen demands

Answer 298

Guyton built a model of the circulatory system with a pump for a heart. When the heart was pumping at 100ml/s, the Pa was 102 and Pv was 2. When the pump stopped, the pressures equalized to 7mmHg (a drop of 1mmHg in the veins for each 19mmHg in the arteries, due to the increased compliance of the veins). This is the mean systemic filling pressure

Answer 299

As the RAP falls, the return gradient increases, so venous return increases. However, below about 1mmHg, the curve plateaus. This is due to the fact that the large veins collapse at very low pressures, causing an increase in resistance and no further increase in VR At higher RAPs, venous return decreases to 0 at mean systemic filling pressure.

Answer 300

In transfusions, there is an increase in venous tone, so the venous return curve shifts up. This means there is more flow at a given RAP. In haemorrhage or decreased venous tone, the curve shifts down,

Answer 301

C = dV/dP. dP = C/dV If dV increases or venous tone (C) decreases, the there is higher systemic filling pressure- although the TPR (slope) is unchanged. Venous return always levels off at the same RAP.

Answer 302

Constriction causes decreased venous return, while dilation causes increased venous return.

Answer 303

Right atrial P Degree of filling in terms of the volume of blood Systemic vascular resistance

Answer 304

It's a curve of mean right atrial pressure vs. cardiac output. It's sigmoidal, similar to ventricular function curves. The output of the heart as a whole is dependent on the filling of the right heart. At increased input volume, CO increases Affected by Preload, afterload, inotropy and chronotropy

Answer 305

The point at which the two curves intersect. The two flows must be equal at all times

Answer 306

The cardiac function curve is unchanged, but the VR curve shifts up, finding a higher CO at a higher filling pressure. This is a similar response to that of venoconstriction

Answer 307

Cardiac function moves up and to the left. The VR curve moves up due to venous constriction, and tilts to be flatter- this is a small effect of increased arterial resistance. The new eq is a higher CO at a lower RAP.

Answer 308

Venous pooling increases capacity, causing a drop in ressure at the heart- VR curve shifts down. As a reflex, the SNS increases HR and inoropy, allowing the VR and CO curves to move upwards, putting the final eq slightly lower and to the left of the original

Answer 309

The CO curve shifts way up due to inotropy, HR, increased afterload and decreased mean arterial resistance due to skeletal muscle vessel dilation The VR curve shifts up massively due to increased venous tone, increased depth of inspiration pulling the blood into the chest, and activation of venous muscle pumps due to movement.

Answer 310

HF means the heart's ability to eject blood is impaired. CO falls, venous pressure rises, and the kidneys retain fluid, allowing the VR curve to shift up as in transfusion. In moderate HF this means that CO is maintained, but in more severe HF, CO falls at increased venous pressures.

Answer 311

Raised JVP Pulmonary Oedema Peripheral Oedema

Answer 312

Diuretics, to remove fluid, lower venous pressures and reduce ventricular size/wall stress Vasodilators reduce afterload and remodelling Beta blockers Positive inotropes Diet (reduction in salt)

Answer 313

Rheumatic heart disease begins as a sore throat called 'strep throat' due to the bacteria streptococcus

Answer 314

- Sore, swollen joints - Restless in school with poor handwriting - Shortness of breath

Answer 315

Maori and Pacific children, those in crowded circumstances or lower socioeconomic areas. This is because the bacteria spreads easily in children and in poor housing, or less sanitary environments you are more likely to contract it.

Answer 316

Improve housing quality and nutrition, reduce smoking, crowding. Increase awareness of sore throats and access to primary care Early identification of RF and RF register + penicillin

Answer 317

A cardiac condition characterized by SOB, exercise limitation and fatigue, as well as peripheral and pulmonary congestion secondary to cardiac abnormalities.

Answer 318

LHS is lung crackles, low SpO2, dyspnoea and GI symptoms | RHS is jugular venous distension, liver engorgement, ascites and peripheral edema.

Answer 319

Can do an ECG, take brain natriuretic peptide levels (elevated in HF), do a chest Xray and use chest ultrasounds

Answer 320

Heart failure with preserved ejection fraction is known as diastolic heart failure- an inability to fill the heart, with high left ventricular diastolic pressures. It's often due to remodelling secondary to increased afterload, as found in hypertension and aortic stenosis. Heart failure with reduced ejection fraction is known as systolic heart failure, showing an inability of the myocardium to contract, with increased EDV. It's due to dilated cardiomyopathy where myocytes have increased in length. Typically occurs after infarction.

Answer 321

Diastolic heart failure shows the muscle becoming thicker as sarcomeres are added deep and superficial to the existing muscle Systolic heart failure shows adding extra sarcomeres next to existing ones, causing lengthening and dilation of the chamber.

Answer 322

Systolic dysfunction: - When the heart begins to fail, less blood is ejected- stroke volume decreases. - The reduced cardiac output and increased stretch in the heart & pulm. vessels compensate for this by increasing venous return via aldosterone, allowing for an increase in EDV. However, the increased energy expenditure can worsen the existing problem

Answer 323

In diastolic heart failure, there is less space to take blood into, so EDV decreases and SV decreases. This increases the steepness of the venous pressure/volume curve - The reduced CO results in aldosterone release causing increased venous return, resulting in an increase in EDV, increasing stroke volume.

Answer 324

- LHS: Increased diastolic wall stress --> sarcomere addition --> myocyte elongation --> increased cavity volume- LaPlace's law states that this leads to increased wall stress -RHS: Increased systolic wall stress --> parallel sarcomere addition --> myocyte thickening --> increased wall thickness --> lessens wall stress

Answer 325

- Self-management is encouraged, especially weight monitoring, smoking cessation, exercise, and cutting salt. Drug treatment usually targets the RAA system and the sympathetic nervous system. The order of treatment severity goes diuretic --> beta blockers & ACE inhibitors -> aldosterone antagonist and angiotensin II blockers, digoxin and anticoagulants. +ve inotropic drugs are only for acute systolic failure and end stage failure Other treatments include heart transplants and assist devices.

Answer 326

Stress and negative emotions These cause increased HR and vasoconstriction, leading to lesions -Hormonal changes, reducing resilience - Changes in lipids - Stress hormones can inflame coronary arteries

Answer 327

Causes increased SNS and decreased PNS function Poor adherence to medication More stressful existence and poor health habits

Answer 328

Events can lead to cardiac invalidism, where there is a feeling of helplessness etc. Physcial components can be fatigue, hypervigilance, disability, aches and pains, and sleep problems Cognitive can be poor concentration and memory, and altered decision making and thinking patterns Emotional recations are roller coster emotions and loss of confidence Behaviour changes involve decreased motivation and social life, as well as relationship, adherence and work problems

Answer 329

It increases the risk of CVD in males, and also predicts survival following MI This is due to the behavioural and biological context associated with depression- lack of exercise, HPA axis issues, platelet dysfunction, inflammation etc.

Answer 330

Stress management, CBT and mindfulness Lifestyle changes Pharmacotherapy

Answer 331

A situation where the left ventricle balloons out after a sudden stress, usually occurring in post-menopausal women.

Answer 332

Chest pain and SOB secondary to severe stress EKG abnormalities No artery obstruction Ballooning and abnormal movement in LV

Answer 333

A fixed stenosis of a coronary vessel, rather than an acute rupture. In angina after exertion, there is a relative ischaemia due to the stenosis as the oxygen requirements go up.

Answer 334

Chest pain's nature, relieving/exacerbating factors and associations. Duration of pain Risk factors

Answer 335

BO, heart sounds, oedema and bruits

Answer 336

``` ECG CXR Exercise treadmill test Echocardiogram Angiography/angiogram ```

Answer 337

Pharmacological- reduces symptoms or CVS risk | Interventional- can do surgery if multiple vessels stenosed or stenting if 1-2 vessels stenosed

Answer 338

- Beta blockers - Nitrates - Calcium channel blockers

Answer 339

- Antiplatelets | - Lipid lowering drugs

Answer 340

The block L type Ca2+ channels within the resistance vessels, myocardium and conducting tissue. This causes vasodilation, causing decreased resistance and blood pressure. other varieties cause decreased contractility and SA rate in the heart

Answer 341

Dihydropiridines and benzothiazepines cause vascular relaxation Phenylalkylamine causes heart effects

Answer 342

It acts like a nitrate, as well as increasing K+atp channels, hyperpolarizing the myocytes and reducing contraction response

Answer 343

They inhibit an enzyme involved inc cholesterol formation, causing cells to increase their LDL receptors due to less cholesterol production (more sensitivity) and take up more cholesterol into themselves. It also blocks inflammatory pathways

Answer 344

- Prevents MI and CVA as well as mortality Side effects include myalgia, myositis, renal failure due to muscle brekdown and deranged liver function tests, as well as being a teratogen It has an interaction with cytochrome P450 and fibrates/