Cardio Flashcards

Question

types of angina?

Answer 1

``` Stable angina: • Induced by effort and relieved by rest Unstable (crescendo) angina: • Angina of recent onset (less than 24hrs) or deterioration in previously stable angina prinzemnatal angina - caused by coronary artery spasm ```

Answer 2

- more common in men | - can be due to; stenosis, valvular disease, atheroma, arrhythmia and anaemia

Answer 3

- smoking - sedentary lifestyle - T2DM - genetics - hypercholesterolaemia

Answer 4

Endothelial dysfunction and injury around sites of sheer and damage with subsequent lipid accumulation at sites of impaired endothelial barrier • Local cellular proliferation and incorporation of oxidise lipoproteins occurs • Mural thrombi on surface and subsequent healing and repeat of cycle

Answer 5

As plaque progresses to 50% of vascular lumen size the vessel can no longer compensate by re-modelling and becomes narrowed • This drives variable cell turnover within the plaque with new matrix surfaces and degradation of matrix • May progress to unstable plaque

Answer 6

The plaque continues to encroach upon the lumen and runs the risk of haemorrhage or exposure of tissue HLA-DR antigens which might stimulate T cell accumulation • This drives an inflammatory reaction against part of the plaque contents • Complications develop including ulceration, fissuring, calcification and aneurysm change

Answer 7

Fatty streak: - These show macrophages filled with abundant lipid (foam cells) - Also smooth muscle cells with fat Intimal cell mass: - These are collections of muscle cells and connective tissue without lipid - “cushions” The atheromatous plaque: - Characterised by distorted endothelial surface containing lymphocytes, macrophages, smooth muscle cells and a variably complete endothelial surface - There is local necrotic and fatty matter with scattered lipid rich macrophages - Evidence of local haemorrhage may be seen with iron deposition and calcification - Complicated plaques are those which show calcification and mural thrombus - making them vulnerable to rupture

Answer 8

- central chest tightness - worse on exertion - relieved by rest/GTN spray - pain radiate to arm, neck, jaw, teeth - sweating, SOB, nausea

Answer 9

1. Have, central, tight, radiation to arms, jaw & neck 2. Precipitated by exertion 3. Relieved by rest or spray GTN • 3/3 = Typical angina • 2/3 = Atypical pain • 1/3 = Non-anginal pain

Answer 10

- pericarditis - PE - chest infection - dissection of aorta - GORD

Answer 11

- may show ST depression | - flat or inverted t waves

Answer 12

- treadmill test/ ECG exercise - CT scan calcium scoring - SPECT/myoview -> radio-labelled tracer - cardiac catheterisation

Answer 13

- modifiable risk factors - aspirin (antiplatlet) - statin (HMG-CoA reductase inhibitor) - beta blockers - GTN spray (nitrate - vasodilator) - CCB (reduce after load) - revascularisation (PCI and CABG)

Answer 14

PCI -Dilating coronary atheromatous obstructions by inflating balloon within it - Insert balloon and stent, inflate balloon and remove it, stent persists and keeps artery patent - Expanding plaque = make artery bigger - PRO; less invasive - CON; risk of stent thrombosis CABG - Left Internal Mammary Artery (LIMA) used to bypass proximal stenosis (narrowing) in Left Anterior Descending (LAD) coronary artery - PRO; good prognosis - CON; invasive

Answer 15

umbrella term that includes STEMI, unstable angina, NSTEMI

Answer 16

ST-elevation myocardial infarction (STEMI): • Develop a complete occlusion of a MAJOR coronary artery previously affected by atherosclerosis • This causes full thickness damage of heart muscle • Can usually be diagnosed on ECG at presentation • Will produce a pathological Q wave some time after MI so also known as Q-wave infarction

Answer 17

Non-ST-elevation myocardial infarction (NSTEMI): • Occurs by developing a complete occlusion of a MINOR or a partial occlusion of a major coronary artery previously affected by atherosclerosis • Is a retrospective diagnosis made after troponin results and sometimes other investigation results are available • This causes partial thickness damage of heart muscle • Also known as a Non-Q wave infarction will see ST depression and/ or T wave inversion

Answer 18

- NSTEMI has rise in serum troponin or creatine kinase-MB

Answer 19

Type 1: - Spontaneous MI with ischaemia due to a primary coronary event e.g. plaque erosion/rupture, fissuring or dissection Type 2: - MI secondary to ischaemia due to increased O2 demand or decreased supply such as in coronary spasm, coronary embolism, anaemia, arrhythmias, hypertension or hypotension Type 3,4,5: - MI due to sudden cardiac death, related to PCI and related to CABG respectively

Answer 20

- family history of IHD - smoking - hypertension, T2DM - obesity

Answer 21

Rupture or erosion of the fibrous cap of a coronary artery plaque - Leading to platelet aggregation and adhesion, localised thrombosis, vasoconstriction and distal thrombus embolisation - The presence of a rich lipid pool within the plaque and a thin, fibrous cap is associated with an increased risk of rupture - Thrombus formation and the vasoconstriction produced by platelet release of serotonin and thromboxane A2 result in myocardial ischaemia due to reduction of coronary blood flow - Fatty streak → Fibrotic plaque → Atherosclerotic plaque → Plaque rupture/ fissure and thrombosis → MI or Ischaemic stroke or Critical leg ischaemia or Sudden CVS death - In unstable angina the plaque has a necrotic centre and ulcerated cap and the thrombus results in PARTIAL OCCLUSION - In myocardial infarction the plaque also has a necrotic centre but the thrombus results in TOTAL OCCLUSION

Answer 22

- Pallor - Increased pulse and reduced BP - Reduced 4th heart sound - chest pain - sweating

Answer 23

- angina - pericarditis - myocarditis - aortic dissection - PE - GORD

Answer 24

- can be normal - ST depression and T wave inversion - can get tall T waves

Answer 25

Troponin (T & I): - T & I are the most sensitive and specific markers of myocardial necrosis - Serum levels increase within 3-12 hours from the onset of chest pain and peak at 24-48 hours - They then fall back to normal over 5-14 days - Can act as prognostic indicator to determine mortality risk and define which patients may benefit from aggressive medical therapy and early coronary revascularisation CK-MB: - CK-MB can be used as a marker for myocyte death - but has low accuracy since it can be present in the serum of normal individuals and in patients with significant skeletal muscle damage - However it can be used to determine re-infarction as levels drop back to normal after 36-72 hours Myoglobin: - Becomes elevated very early in MI but the test has poor specificity since myoglobin is present in skeletal muscle

Answer 26

- pain relief; GTN spray, IV opiods - antiemetics - oxygen (94-98% sat, lower for those with COPD)

Answer 27

Atheromatous plaque rupture results in platelets being exposed to ADP/ Thromboxane A2/adrenaline/thrombin/collagen tissue factor • This results in platelet activation/aggregation via IIb/IIIa glycoproteins binding to fibrinogen (enables platelets to adhere to each other = aggregation) • Then thrombin (already present in surroundings) is able to enzymatically convert fibrinogen to fibrin (insoluble) resulting in the formation of a fibrin mesh over platelet plug and the formation of a thrombotic clot

Answer 28

blocks formation of thromboxane A2 thus | prevents platelet aggregation

Answer 29

Inhibit ADP-dependant activation of IIb/IIIa glycoproteins thereby preventing amplification response of platelet aggregation

Answer 30

Used in combination with aspirin and oral P2Y12 inhibitors in patients with ACS undergoing Percutaneous Coronary Intervention (PCI)

Answer 31

- male | - premature menopause

Answer 32

Rupture or erosion of vulnerable fibrous cap of coronary artery atheromatous plaque - This results in platelet aggregation, adhesion, local thrombosis, vasoconstriction and DISTAL THROMBUS EMBOLISATION resulting in PROLONGED COMPLETE ARTERIAL OCCLUSION resulting in myocardial necrosis within 15-30 minutes in a STEMI (since major artery occluded fully)

Answer 33

- chest pain that is severe >20 mins - SOB - pale, clammy

Answer 34

stable angina, unstable angina, NSTEMI, pneumonia, pneumothorax, GORD

Answer 35

- ST elevation - Tall t-waves - LBBB

Answer 36

- ST depression - T wave inversion - diagnosis retrospective after troponin result

Answer 37

- 300mg chewable aspirin ASAP - GTN - morphine - o2 if <95% - beta blocker - p2y12 inhibitor - PCI - CABG - risk factor modifications

Answer 38

- mitral incompetence - pericarditis - cardiac rupture; early and late

Answer 39

The inability of the heart to deliver blood and thus O2 at a rate that is commensurate with the requirement of metabolising tissue of the body

Answer 40

- 10% in elderly - African descent - men

Answer 41

- Ischaemic heart disease (IHD) - MAIN CAUSE • Cardiomyopathy (disease of heart muscles, where the walls have become thickened, stiff or stretched) • Valvular heart disease e.g. aortic stenosis, aortic and mitral regurgitation • Cor pulmonale • Hypertension • Alcohol excess • Any factor that increases myocardial work e.g. anaemia, arrhythmias, hyperthyroidism, pregnancy and obesity

Answer 42

When the heart begins to fail, there are many systems involved that initiate physiological COMPENSATORY CHANGES that try to maintain cardiac output and peripheral perfusion in order to negate the effects of the heart failure - However as heart failure progresses, these mechanisms are overwhelmed and become pathophysiological also known as DECOMPENSATION - mechanisms are preload, after load, sympathetic activation and RAAS.

Answer 43

Venous return (preload): - Myocardial failure leads to a reduction of the volume of blood ejected with each heart beat, and an increase in the volume of blood remaining after systole - This increased diastolic (or preload - the volume of blood in the ventricle before contraction) volume stretches the myocardial fibres and, as Starling’s law of the heart says, myocardial contraction is restored since the stretching of myocardial fibres will increase its force of contraction - However, in heart failure, the failing myocardium actually doesn't contract as much in response to increased preload meaning cardiac output cannot be maintained and may decrease

Answer 44

Outflow resistance (afterload) is the load or resistance against which the ventricle contracts - It is made up of: • Pulmonary and systemic resistance • Physical characteristics of the vessel walls • The volume of blood that is ejected - When there is an increase in afterload there is a increase in end- diastolic volume and a decrease in stroke volume and thus a DECREASE in cardiac output - This results in a increase of end-diastolic volume and dilatation of the ventricle itself (the more the ventricle is dilated the harder it must work i.e. the more resistance there is to contract against) which then further exacerbates the problem of afterload

Answer 45

When baroreceptors (located in the arterial wall of the aorta, carotid and in the heart walls and major veins) detect a drop in arterial pressure or an increase in venous pressure (due to back flow of blood) they stimulate sympathetic activation - This increases the force of contraction (positively inotropic) of the heart (which increases stroke volume) as well as heart rate - both resulting in an increase in cardiac output - However in heart failure there is chronic sympathetic activation which results in the receptors being acted on by the sympathetic system to down regulate resulting in their being less receptor to act on meaning the effect of sympathetic activation is diminished and cardiac output stops increasing in response to sympathetic activation

Answer 46

Reduced cardiac output leads to diminished renal perfusion, thereby activating the renin-angiotensin system whereby; angiotensinogen is converted to angiotensin I under the action of renin, angiotensin I is then converted to angiotensin II under the act of angiotensin converting enzyme (ACE), angiotensin II then stimulates the release of aldosterone from the adrenal cortex above the kidneys - This results in increased Na+ reabsorption and thus water reabsorption as well as the release of ADH which stimulates water retention - This results in the increased volume of the blood which in turn increases blood pressure and thus venous pressure which in turn increases pre-load thereby increasing the stretching of the heart and thus force of contraction and thus stroke volume and thus cardiac output - However, with increased force of contraction the cardiac myocytes require more energy and thus more blood however in heart failure (which is most commonly caused by ischaemic heart disease) there will be no increase in blood and thus the cardiac myocytes will die resulting in a decrease in force of contraction and thus a decrease in stroke volume and a decrease in cardiac output

Answer 47

Inability of the ventricle to contract normally resulting in a decrease in cardiac output • Caused by ischaemic heart disease, myocardial infarction and cardiomyopathy (disease of heart muscle thus impairing function)

Answer 48

Inability of the ventricles to relax and fill fully thereby decreasing stroke volume and decreasing cardiac output • Caused by hypertrophy (due to chronic hypertension which results in increased blood pressure thereby increasing afterload so heart pumps against more resistance and thus cardiac myocytes grow bigger to compensate for this) of ventricles resulting in there being less space for blood to fill in and thus decreased cardiac output • Also caused by aortic stenosis (the narrowing of the aortic valve) which also increases afterload and thus decreases cardiac output

Answer 49

Acute: • Often used exclusively to mean new onset or decompensation of chromic heart failure characterised by pulmonary and/or peripheral oedema with or without signs of peripheral hypotension Chronic - Develops slowly • Venous congestion is common but arterial pressure is well maintained until very late

Answer 50

- SOB - fatigue - ankle swelling - raised JVP - murmurs - ascites - hypotension - bi-basal crackles

Answer 51

blood tests; BNP (brain natuertic peptide) which is secreted by ventricles in response to increased myocardial wall stress - CXR; ACDE (alveolar oedema, cardiomegaly, dilated upper lobe vessels of lungs and effusions) - ECG - echocardiography

Answer 52

- lifestyle changes - diuretics; promote sodium and this water loss, reducing vernacular filling pressure (preload) - ACE inhibitors - Beta-blocker - digoxin - revascularisation - surgery - heart transplant - cardiac resynchronisation

Answer 53

Mitral valve is on the left side and is also known as the tricuspid valve, it separates the left atrium from the left ventricle

Answer 54

Obstruction of left ventricle inflow that prevents proper filling during diastole • Mitral valve has 2 cusps

Answer 55

more men than women history of rheumatic fever untreated strep. infections

Answer 56

Most common cause of mitral stenosis is rheumatic heart disease secondary to rheumatic fever due to infection with group A beta-haemolytic streptococcus e.g. Streptococcus Pyogenes - or IE - Or mitral annular calcification

Answer 57

Thickening and immobility of the valve leads to obstruction of blood flow from the left atrium to the left ventricle - In order for sufficient cardiac output to be maintained, the left atrial pressure increases and left atrial hypertrophy and dilatation occur - Consequently pulmonary venous, pulmonary arterial and right heart pressures also increase - The increase in pulmonary capillary pressure is followed by the development of pulmonary oedema - this is seen particularly when atrial fibrillation occurs, due to the elevation of left atrial pressure and dilatation, with tachycardia and loss of coordinated atrial contraction - This is partially countered by alveolar and capillary thickening and pulmonary arterial vasoconstriction (reactive pulmonary hypertension) - Pulmonary hypertension leads to right ventricular hypertrophy, dilatation and failure with subsequent tricuspid regurgitation

Answer 58

- usually no symptoms until stenosis <2cm - progressive SOB - haemoptysis - due to rupture of bronchial vessels due to elevated pulmonary pressure - signs of RHF - atrial fibrillation - malar flush - loud S1 snap

Answer 59

- gold standard -> echocardiogram - ECG - CXR

Answer 60

- stenosis is mechanical problem so meds don't prevent progression - treat symptoms with beta blockers and diuretics - percuataneous mitral balloon valvvotomy - mitral valve replacement

Answer 61

Backflow of blood from the left ventricle to the left atrium during systole • Mild physiological mitral regurgitation (MR) is seen in 80% of normal individuals

Answer 62

- females - lower BMI - advancing age - renal dysfunction - prior MI

Answer 63

``` Occurs due to abnormalities of the valve leaflets, chordae tendinae, papillary muscles or left ventricle - Most frequent cause is myxomatous degeneration (MVP) (weakening of the chordae tendinae) - resulting in a floppy mitral valve that prolapses (mitral valve prolapse) - Other causes include: • Ischaemic mitral valve • Rheumatic heart disease • Infective endocarditis • Papillary muscle dysfunction/rupture • Dilated cardiomyopathy ```

Answer 64

Regurgitation into the left atrium produces left atrial dilatation but little increase in left atrial pressure if the regurgitation is longstanding, since the regurgitant flow is accommodated by the large left atrium - Pure volume overload due to leakage of blood into left atrium during systole - Compensatory mechanisms: Left arterial enlargement, left ventricle hypertrophy (since left ventricle must put in same effort to pump less blood(due to regurgitation) so needs to pump harder to maintain cardiac output and thus hypertrophy to increase stroke volume) and increases contractility: • Progressive left atrial dilatation and right ventricular dysfunction due to pulmonary hypertension • Progressive left ventricular volume overload leads to dilatation and progressive heart failure

Answer 65

- auscultation - soft S1 and prominent third extra heart sound S3 - exertion dyspnoea - fatigue - palpitation - signs of right HF

Answer 66

- ECG - CXR - echocardiogram

Answer 67

- vasodilators, beta blockers, anticoagulants, diuretics - serial echocardiography to check for improvement - surgery; if symptoms is at rest or ejection fraction <60%

Answer 68

Narrowing of the aortic valve resulting in obstruction to the left ventricular stroke volume, leading to symptoms of chest pain, breathlessness, syncope and fatigue

Answer 69

Congenital bicuspid aortic valve (BAV) predisposes to stenosis and regurgitation - bicuspid valves are more likely to develop stenosis - Congenital BAV is predominant in males

Answer 70

- Calcific aortic valvular disease (CAVD) - essentially calcification of the aortic valve resulting in stenosis, most commonly seen in elderly • Calcification of a congenital bicuspid aortic valve (BAV) (valve has 2 leaflets instead of 3 due to genetic disease - this is the most common congenital heart disease) resulting in stenosis - Rheumatic heart disease - rare now due to eradication

Answer 71

• Supravalvular (above valve) e.g congenital fibrous diaphragm above the aortic valve • Subvalvular (below valve) e.g congenital condition in which a fibrous ridge or diaphragm is situated immediately below the aortic valve • Valvular - most common

Answer 72

Due to the narrowing there is obstructed left ventricular emptying and a pressure gradient develops between the left ventricle and the aorta resulting in an increased afterload - This results in increased left ventricular pressure and compensatory left ventricular hypertrophy - In turn, this results in relative ischaemia of the left ventricular myocardium (since hypertrophy results in increased blood demand), and consequent angina, arrhythmias and left ventricular failure - The obstruction to left ventricular emptying is relatively more severe on exercise - since exercise causes a many-fold increase in cardiac output, however due to the severe narrowing of the aortic valve, the cardiac output can hardly increase - thus, the blood pressure falls, coronary ischaemia worsens, the myocardium fails and cardiac arrhythmias develop - When this compensatory mechanism is exhausted left ventricular function decline rapidly

Answer 73

- syncope - usually exertional - angina - heart failure - dyspnoea - absence of second heart sound

Answer 74

aortic regurgitation and subacute bacterial endocarditis

Answer 75

- echocardiogram; left ventricular size&function and doppler derived gradient and valve area - ECG - CXR

Answer 76

- IE prophylaxis in dental procedures - surgery - TAVI - transcutaneous aortic valve implant

Answer 77

- IE prophylaxis in dental procedures - surgery - TAVI - transcutaneous aortic valve implant

Answer 78

``` Leakage of blood into the left ventricle from aorta during diastole due to ineffective coaptation (bringing together) of the aortic cusps, of which there are three ```

Answer 79

SLE, marfans and Ehlers Danlos syndrome, aortic dilation and IE

Answer 80

- Congenital bicuspid aortic valve (BAV) - chronic • Rheumatic fever - chronic • Infective endocarditis - acute

Answer 81

Aortic regurgitation is reflux of blood from the aorta through the aortic valve into the left ventricle during diastole - If net cardiac output is to be maintained, the total volume of blood pumped into the aorta must increase and, consequently, the left ventricular size must enlarge resulting in left ventricle dilation and hypertrophy - Progressive dilation leads to heart failure - Furthermore due to the fact that the remaining blood in the root of the aorta supplies the coronary arteries via the coronary sinus during diastole - regurgitation causes diastolic blood pressure to fall and thus coronary perfusion decreases - Also the large left ventricular size is mechanically less efficient, so that the demand for oxygen is greater and cardiac ischaemia develops

Answer 82

In chronic regurgitation, patients remain asymptomatic for many years before symptoms develop - Exertional dysponea - Palpitations - Angina - Syncope -Quincke’s sign - capillary pulsation in the nail beds - de Musset’s sign - head nodding with each heart beat - Pistol shot femoral - a sharp bang heard on auscultation

Answer 83

- HF - IE - mitral reguitation

Answer 84

- echocardiogram - CXR - ECG

Answer 85

- vasodilators | - surgery

Answer 86

An infection of the endocardium or vascular endothelium of the heart • Known as subacute bacterial endocarditis • Infection occurs on the following: - Valves with congenital or acquired defects (usually on the left side of the heart). Right sided endocarditis is more common in IV drug addicts - Normal valves with virulent organisms such as Streptococcus pneumoniae or Staphylococcus aureus - Prosthetic valves and pacemakers

Answer 87

- more common in developing countries - elderly with prosthetic valves - IV drug user - young with congenial heart disease

Answer 88

- Staphylococcus aureus (IVDU, diabetes and surgery) - most common cause • Pseudomonas aeruginosa - Streptococcus viridans (dental problems) - GRAM POSITIVE, alpha haemolytic and optochin resistant (Strep. mutans, strep, sanguis, strep. milleri & strep. oralis)

Answer 89

Usually the consequence of two factors; the presence of organisms in the bloodstream and abnormal cardiac endothelium that facilitates their adherence and growth - Bacteraemia may arise for patient-specific reasons: • Poor dental hygiene - bacteria in tooth plaque can cause gum disease which results in bleeding and inflammation of gums meaning when brushing/in dental procedure this bacteria can enter the bloodstream and reach the heart • IV drug use • Soft tissue infections - Damaged endocardium promotes platelet and fibrin deposition, which allows organisms to adhere and grow, leading to an infected vegetation - Aortic and mitral valves are most commonly involved - IV drug users are the exception since right-sided lesions are more common in them - Virulent organisms destroy the valve they are on resulting in regurgitation and worsening heart failure

Answer 90

- regurgitant murmur - embolic event - sepsis - renal infarction - fever - headache - finger clubbing - HF signs - splinter haemorrhages - embolic skin lesions - osler nodes - janeway lesion - roth spots - petechiae

Answer 91

- blood cultures - blood tests; CRP and ESR raised - urinalysis - CXR - ECG; long PR intervals - echocardiogram; transthoraic or thransoesphageal (better)

Answer 92

- if staph. -> vancomycin and rifampicin - if not staph. -> benzylpenicillin and getamyicin - surgery to remove valve and replace prosthetic - good oral health!

Answer 93

``` Group of diseases of the myocardium that affect the mechanical or electrical function of the heart ```

Answer 94

- All carry an arrhythmic risk - Can occur at younger ages - Restrictive cardiomyopathy is rare in childhood and has a poor outcome once symptoms develop - In general they are inherited genetic conditions although there are some acquired ones

Answer 95

- hypertrophic - dilated - restricted - arrythmogenic right ventricle

Answer 96

ventricular hypertrophy/thickening of the muscle

Answer 97

Quite common, second most common cardiomyopathy (behind dilated) • 1/500 people have it • Autosomal dominant - familial • May present at any age • Most common cause of sudden cardiac death in the young • HCM refers to otherwise unexplained primary cardiac hypertrophy

Answer 98

Caused by sarcomeric protein gene mutations e.g troponin T and B- myosin • All in the absence of hypertension and valvular disease • The hypertrophic, non-compliant ventricles impair diastolic filling resulting in reduced stroke volume and thus cardiac output • Another issue with thick powerful heart is that there is a disarray of cardiac myocytes so conduction is affected

Answer 99

- sudden death - chest pain - syncope - jerky carotid pulse

Answer 100

- ECG; show signs of LVH with T wave inversion and deep Q wave - echocardiogram - genetic analysis

Answer 101

- Amiodarone - anti-arrythmatic medication, if at high risk of arrhythmia then can place an implantable cardiac defibrillator • Calcium channel blocker e.g. Verampil • Beta-blocker e.g. Atenolol

Answer 102

Dilated left ventricle which contracts poorly/has thin muscle

Answer 103

Most common cardiomyopathy • Autosomal dominant - familial • Can be caused by; ischaemia, alcohol, thyroid disorder or familial/ genetic

Answer 104

Caused by cytoskeletal gene mutations • Left ventricle or right ventricle or all 4 chamber dilatation and thus dysfunction • Theory is that poorly generated contractile force leads to progressive dilatation of heart with some diffuse interstitial fibrosis

Answer 105

- SOB - HF - thromboembolism - sudden deatg - increased JVP

Answer 106

- CXR - ECG - ECHO

Answer 107

Causes are; amyloidosis, idiopathic, sarcoidosis, end-myocardial fibrosis

Answer 108

There is normal or decreased volume of both ventricles with bi-atrial enlargement, normal wall thickness, normal cardiac valves and impaired ventricular filing • Restrictive physiology • Poor dilation of the heart restricts its the ability of the heart to take on blood and pass it to the rest of the body • Rigid myocardium restricts diastolic ventricular filling

Answer 109

- SOB - increased JVP - hepatic enlargement

Answer 110

- CXR - ECHO - ECG - cardiac catheristisation

Answer 111

- no specific treatment | - poor prognosis, die within a year

Answer 112

Progressive genetic cardiomyopathy characterised by progressive fatty and fibrous replacement of ventricular myocardium • Cause is unknown • Familial form is usually autosomal dominant with incomplete penetrance but can be recessive

Answer 113

Desmosome (normally hold cardiac cells together) gene mutation • Right ventricle replaced by fat and fibrous tissue • Muscle dies and replaced by fat as part of inflammatory process

Answer 114

conductive issues - syncope - RHF; right heart failure

Answer 115

- genetic testing is gold standard - ECG; t wave inversion - ECHO

Answer 116

- beta blockers - amiodarone - cardiac transplant

Answer 117

- atrial septal defect | - persistence ductus arteriosis

Answer 118

- central cyanosis; due to right-left shunting of blood; seen in tetralogy of fallout and tricuspid atresia - pulmonary hypertension; due to left-right shunts; Eisenmenger’s complex - clubbing of fingers - growth retardation - syncope

Answer 119

Most common form of congenital heart disease, occurring in 1-2% of live births • More common in males than females

Answer 120

These can work well at birth and go undetected but can be severely stenotic in infancy or childhood • Degenerate quicker than normal valves • Become regurgitant earlier than normal valves • Are associated with coarctation and dilation of the ascending aorta • May eventually develop aortic stenosis (requiring valve replacement) with to without aortic regurgitation thereby predisposing to infective endocarditis

Answer 121

Often first diagnosed in adulthood and represents one third of congenital heart disease • More common in women than men

Answer 122

- abnormal connection between two atria - shunt left-right so acyanotic - increased flow into right heart and lungs - if not treated can develop right heart hypertrophy, pulmonary hypertension and risk of IE

Answer 123

- SOB - exercise intolerance - atria arrhythmia

Answer 124

- CXR - ECG; RBBB - echocardiogram

Answer 125

- surgical closure

Answer 126

VENTRICULAR SEPTAL DEFECTS (VSD): • Abnormal connection between the two ventricles • Many close spontaneously during childhood

Answer 127

Common - 20% of all congenital heart defects

Answer 128

Higher pressure in left ventricle than right ventricle • Thus left-to-right shunt • Thus does NOT go blue i.e. acyanotic • Increased blood flow through the lung

Answer 129

- tachycardia - SOB - increased respiratory rate - pulmonary hypertension - small defect; buzzing sensation and normal heart rate and size

Answer 130

- Medical initially since many will spontaneously close - Surgical closure - If small then no intervention is required - Prophylactic antibiotics - If moderately sized lesion; furosemide, ACE inhibitor e.g. ramipril and digoxin may suffice

Answer 131

ATRIO-VENTRICULAR SEPTAL DEFECTS (AVSD): • Associated with Downs syndrome • Basically a hole in the very centre of the heart • Involves; the ventricular septum, the atrial septum, the mitral and tricuspid valves • Can be complete or partial • Instead of two separate atrio-ventricular valves there is JUST ONE big malformed one which usually leaks

Answer 132

- breathlessness - poor weight gain and feeding - eisenmenger -> cyanosis over time - partial defect; it presents in late adulthood and symptoms are SOB, tachycardia

Answer 133

- Pulmonary artery banding if large defect in infancy - band reduces blood flow to lungs thereby reducing pulmonary hypertension and Eisenmenger’s syndrome - Surgical repair is challenging - A partial defect may be left alone if there is no right heart dilatation

Answer 134

Ductus arteriosus is a persistent communication between the proximal left pulmonary artery and the descending aorta

Answer 135

In foetal life pulmonary vascular resistance is high (since bronchioles are filled with fluid and vessels are vasoconstricted due to lack of O2) and the right heart pressure exceeds that of left - consequently flow is from right to left atrium through foramen ovale, and from pulmonary artery to aorta via ductus arteriosus • Normally, the ductus arteriosus closes within a few hours of birth in response to decreased pulmonary resistance; however in some cases e.g. in premature babies and in cases with maternal rubella, the ductus persists ``` • If it remains open then there is an abnormal left-to- right shunt (from aorta to pulmonary artery) and ``` eventually means that the lung circulation is overloaded with pulmonary hypertension (leading to Eisenmenger syndrome) and right side cardiac failure (due to right ventricular hypertrophy in response to increased afterload) subsequently • Also increases risk of infective endocarditis

Answer 136

- murmurs - bounding pulse - SOB - tachycardia - eisenmengers syndrome with clubbed blue toes and PINK fingers

Answer 137

- CXR - ECG - ECHO

Answer 138

- surgical closure | - indomethacin -? prostaglandin inhibitor

Answer 139

- more common in men than women | - associated with turners syndrome, berry aneurysms and patent ductus arterioles

Answer 140

A narrowing of the aorta at, or just distal to, the insertion of the ductus arteriosus (distal to the origin of the left subclavian artery) • The net result is a narrowing of the aorta just after the arch, with excessive blood flow being diverted through the carotid and subclavian vessels into systemic vascular shunts to supply the rest of the body, thus stronger perfusion to upper body compared to lower - decreased renal perfusion leads to systemic hypertension

Answer 141

- right arm hypertension | - headache and nose bleeds

Answer 142

- CXR - ECG - CT

Answer 143

- surgery | - balloon dilation and stenting

Answer 144

``` Most common form of cyanotic congenital heart disease • Consists of: - A large, maligned Ventricular Septal Defect (VSD) - An overriding aorta - Right ventricular outflow obstruction e.g. due to pulmonary stenosis - Right ventricular hypertrophy ```

Answer 145

- The stenosis of the right ventricle outflow leads to the right ventricle being at a higher pressure than the left • Thus blue blood passes from the right ventricle to the left ventricle • The patients are BLUE i.e CYANOTIC

Answer 146

Central cyanosis - Low birthweight and growth - Dysponea on exertion - Delayed puberty - Systolic ejection murmurs - CXR; boot shaped heart

Answer 147

Involves the aorta coming off the right ventricle and the pulmonary trunk coming off the left ventricle • Two closed circulations result • More common in men and associated with diabetes • Survival is only possible if there is communication between the two circuits and virtually all have some form of atrial septal defect with blood mixing

Answer 148

Acute inflammation of the pericardium; with or without effusion

Answer 149

Majority are idiopathic and most commonly seen in the young, previously healthy patient - Occurs in men more than women - Occurs in adults more than children

Answer 150

``` Infectious: - Viral (common): • Enteroviruses e.g. coxsackieviruses & echoviruses - Bacterial: • Mycobacterium tuberculosis (other bacteria are rare) - Fungal (very rare): • Histoplasma spp. - most likely to be seen in immunocompromised patient non infections - autoimmune; SLE - neoplastic - dresslers syndrome - traumatic ```

Answer 151

Pericardium becomes acutely inflamed, with pericardial vascularisation and infiltration with polymorphonuclear leukocytes - A fibrinous reaction frequently results in exudate and adhesions within the pericardial sac, and a serous or haemorrhagic effusion may develop

Answer 152

- severe, sharp and pleuritic chest pain - pericardial friction rub - fever - tachycardia

Answer 153

angina, mI, pulmonary infarction, pneumonia

Answer 154

- ECG; diagnostic; saddle shaped ST elevation and PR depression - CXR; cardiomegaly in cases of effusion - FBC; WBC count is high - ESR

Answer 155

- restrict physical activity - NSAID for 2 weeks - colchine for 3 weeks

Answer 156

pericardial effusion is a collection of fluid within the potential space of the serous pericardial sac

Answer 157

when a large volume collects in this space, ventricular filling is compromised, leading to the embarrassment of the circulation - this is a CARDIAC TAMPONADE

Answer 158

- soft and distant heart sounds - raised jVP - dyspnoea

Answer 159

- high pulse - low BP - high JVP - muffled 1st and 2nd heart sound - reduced CO

Answer 160

- CXR - ECG - Echo

Answer 161

- CXR - Becks triad; falling BP, raising JVP and muffled heart sounds - ECG - echo is diagnostic

Answer 162

- urgent drainage via pericardiocentesis

Answer 163

Certain causes of pericarditis such as tuberculosis, bacterial infection and rheumatic heart disease result in the pericardium becoming thick, fibrous and calcified - Cause is often unknown and can actually occur after any pericarditis

Answer 164

the pericardium becomes so inelastic as to interfere with the diastolic filling of the heart, CONSTRICTIVE PERICARDITIS is said to have developed As these changes are chronic, allowing the body time to compensate, this condition is not as immediately life-threatening as cardiac tamponade, in which the circulation is more acutely embarrassed

Answer 165

- kussamulas sign; rise in JVP - ascites - oedema - right heart failure signs

Answer 166

- CXR; small heart - ECG - echocardiogram

Answer 167

More than or equal to 140/90mmHg clinic BP - Daytime average Ambulatory blood pressure monitoring (ABPM - 24hr BP monitor) or Home blood pressure monitoring (HBPM); greater than or equal to 135/85mmHg

Answer 168

More than or equal to 160/100mmHg clinic BP - Daytime average ABPM or HBPM greater than or equal to 150/95mmHg

Answer 169

Clinic systolic BP greater than or equal to 180mmHg and/or | diastolic BP greater than or equal to 110mmHg

Answer 170

- primary cause unknown - accounts for majority of cases - multifactorial

Answer 171

- commonly caused by disease or pregnancy - endocrine causes eg, Cushing disease, conns syndrome, phaemochromocytoma - coarctation of aorta - medications

Answer 172

- vascular changes - heart - NS; intraceberal haemorrhage - kindly/renal disease - malignant hypertension; markedly raised diastolic blood pressure, usually over 120mmHg and progressive renal disease *very quick and sudden*

Answer 173

- look for end organ damage - urinalysis; protein, albumin, haemuturia - blood tests; serum creatine, glucose, eGFR - fundoscopy - ECH - echo

Answer 174

1- lifestyle change 2- ACD; ace inhibitor, CCB and diuretic (less than 55yrs old, diabetic and not black; ACE first)

Answer 175

Heart rate is slow (less than 60bpm during the day and less than 50bpm at night) • Usually asymptomatic unless the rate is very slow • Normal in athletes owing to increased vagal tone and thus parasympathetic activity

Answer 176

Heart rate is fast (more than 100bpm) • More symptomatic when the arrhythmia is fast and sustained • Subdivided into: - Supraventricular tachycardias - arise from the atrium or the AV junction - Ventricular tachycardias - arise from the ventricles

Answer 177

A chaotic irregular atrial rhythm at 300-600bpm; the AV node responds intermittently, hence an irregular ventricular rate

Answer 178

Around 5-15% of patients over age of 75 - Can either be paroxysmal (self terminating) or persistent (continues without intervention)

Answer 179

Acute: onset within the previous 48 hours • Paroxysmal: stops spontaneously within 7 days • Recurrent: two or more episodes • Persistent: continuos for more than 7 days and not self terminating • Permanent

Answer 180

- idiopathic - hypertension - HF - valvular heart disease - rheumatic heart disease

Answer 181

Atrial fibrillation (AF) is maintained by continuous, rapid (300-600/min) activation of the atria by multiple meandering re-entry wavelets - These are often driven by rapidly depolarising automatic foci, located predominantly within the pulmonary veins - The atria respond electrically at this rate but there is NO COORDINATED MECHANICAL ACTION and only a proportion of the impulses are conducted to the ventricles i.e. there is no unified atrial contraction instead there is atrial spasm - The ventricular response depends on the rate and regularity of atrial activity, particularly at the entry to the AV node, and the balance between sympathetic and parasympathetic tone - Cardiac output DROPS by 10-20% as the ventricles are not primed reliably by the atria

Answer 182

- paptitations - dyspnoea - fatigue

Answer 183

- atrial flutter | - supraventiuclar tachyarrhythmias

Answer 184

- ECG; absent P wave

Answer 185

Conversion to sinus rhythm achieved electrically by DC shock e.g. defibrillator - NOTE: give low molecular weight heparin e.g. Enoxaparin or Dalteparin to minimise the risk of thromboembolism associated with cardioversion - ventricular rate is controlled by drugs that block AV node; CCB, beta blocker, digoxin and amiodarone

Answer 186

1- rate control; AV nodal slowing agent and oral anti-coagulation 2- CHA2DS20VASC - calculate risk

Answer 187

usually an ORGANISED atrial rhythm with an atrial rate | typically between 250-350bpm

Answer 188

- less common than atrial fibrillation - more common in men - increase with age

Answer 189

- idiopathic 30% - CHD - obesity - COPD - pericarditis

Answer 190

palpations chest pain syncope fatigue

Answer 191

- ECG | - regular sawtooth like waves

Answer 192

- anticoagulant first -> LMWH - catheter ablation - amidorone and bisoprolol

Answer 193

- can occur at any level of conducting system - av block = block in AV node or bundle of his - Lower block = bundle branch block

Answer 194

This is simple prolongation of the PR interval to greater than 0.22 seconds - Every atrial depolarisation is followed by conduction to the ventricles but with delay - Causes: • Hypokalaemia • Myocarditis • Inferior MI • Atrioventricular node (AVN) blocking drugs e.g. beta blockers (Bisoprolol), calcium channel blockers (Verapamil) and Digoxin - ASYMPTOMATIC so no treatment!

Answer 195

Occurs when some P waves conduct and other do not - Acute MI may produce second degree heart block - mobitz I and mobitz II block

Answer 196

Also known as the Wenckebach block phenomenon • A progressive PR interval prolongation until beat is ‘dropped’ and P wave fails to conduct i.e. excitation completely fails to pass through the AVN/bundle of His • The PR interval before the blocked P wave is much longer than the PR interval after the blocked P wave • Causes: - Atrioventricular node (AVN) blocking drugs e.g. beta blockers (Bisoprolol), calcium channel blockers (Verapamil) and Digoxin - Inferior MI • Results in light headiness, dizziness and syncope • Does not require a pacemaker unless its poorly tolerated

Answer 197

PR interval is constant and QRS interval is dropped • Failure of conduction through the His-Purkinje system • Causes: - Anterior MI - Mitral valve surgery - SLE and Lyme disease - Rheumatic fever • Results in shortness of breath, postural hypotension and chest pain • High risk of developing sudden complete AV block and a pacemaker should be inserted

Answer 198

Complete heart block occurs when all atrial activity fails to conduct to the ventricles - Ventricular contractions are sustained by spontaneous escape rhythm which originates below the block - P waves are COMPLETELY INDEPENDENT of QRS complex - Causes: • Structural heart disease e.g. transposition of great vessels • Ischaemic heart disease e.g. acute MI • Hypertension • Endocarditis or Lyme disease

Answer 199

- pacemaker | - IV atropine

Answer 200

Usually asymptomatic | • The His bundle gives rise to the right and left bundle branches

Answer 201

This is associated with a wider QRS complex (larger than 0.12 seconds) - The shape of the QRS depends on whether the right or the left bundle is blocked

Answer 202

Causes; Pulmonary embolism, Ischaemic heart disease & Atrial/ Ventricular septal defect • Right bundle no longer conducts, meaning that the two ventricles do not get impulses at the same time, and instead spread from left to right • Produces the late activation of the right ventricle • MaRRoW; QRS looks like M in V1 and QRS looks like W in v5&6

Answer 203

Causes; Ischaemic heart disease and aortic valve disease • Produces the late activation of the left ventricle - on ECG; WiLLiam -> QRS looks like W in v1&v2 and QRS looks like M in v4-v6

Answer 204

- anaemia - anxiety - HF - PE

Answer 205

- atria or AV junction

Answer 206

- more common in women | - tea, coffee and alcohol can cause it

Answer 207

There are two pathways within the AV node in AVNRT: • One has a short effective refractory period (the window of time where cells cannot be excited again after they have already been excited) and SLOW conduction • One has a longer effective refractory period and FAST conduction - This sets up a RE-ENTRANT LOOP at the AV NODE hence why its AVNRT and the loop sends signals through the AV node at a MUCH FASTER RATE

Answer 208

- palpitations - chest pain - SOB - polyuria; (due to the realise of atrial natriuretic peptide in response to increased atrial pressures during the tachycardia)

Answer 209

- Large circuit involving the AV node, the His bundle, the ventricle and an abnormal connection of myocardial fibres from the ventricle back to the atrium - This ‘abnormal connection’ is called the accessory pathway or bypass tract and results from an incomplete separation of the atria and the ventricles during fetal development

Answer 210

WPW -> wolff Parkinson white syndrome | normal AV conduction but accessory pathway

Answer 211

- PALPATION - dizziness - SOB - syncope

Answer 212

- short PR interval | - wide QRS complex (delta wave)

Answer 213

- IV adenosine | - surgery; catheter ablation

Answer 214

Umbrella term encompassing: - Ventricular ectopics - Ventricular tachycardia - Sustained ventricular tachycardia - Ventricular fibrillation - cardiac channel-pathies; long QT syndrome

Answer 215

premature ventricular contraction

Answer 216

- post MIs

Answer 217

These premature beats have a broad (greater than 0.12 seconds) and bizarre QRS complex because they arise from an abnormal (ectopic) site in the ventricular myocardium - Following a premature beat, there is usually a complete compensatory pause because the AV node or ventricle is refractory (i.e. cannot accept new impulses) to the next sinus impulse - resulting in missed beat

Answer 218

- missed beat - uncomfortable - irregular pulse - faint, dizziness

Answer 219

wide QRS complex

Answer 220

beta blockers

Answer 221

- >100 bpm | - > 3 irregular heart beats in a row

Answer 222

Commonly found in patients with structurally normal hearts (known as idiopathic ventricular tachycardia), in these cases it is usually a benign condition with an excellent long-term prognosis • Occasionally it is pathological and known as Gallavardin’s tachycardia and if untreated may lead to cardiomyopathy

Answer 223

Essentially there is rapid ventricular beating so much so that they is inadequate blood filling of ventricles since they are filled in between beats and thus id beating faster there is less time to fill and thus less blood fills • Results in decreased cardiac output and thus a decrease in the amount of oxygenated blood that is circulated around the body

Answer 224

- SOB - chest pain - light headedness

Answer 225

Ventricular tachycardia for longer than 30 seconds

Answer 226

- broad and abnormal QRS complex

Answer 227

Involves very rapid and irregular ventricular activation with NO MECHANICAL EFFECT i.e NO CARDIAC OUTPUT • Patient is pulseless and becomes unconscious and respiration ceases (CARDIAC ARREST) Usually caused by a ventricular ectopic beat

Answer 228

congenital eg; Jervell-Lange-Nielsen syndrome (autosomal recessive) - mutation in cardiac potassium and sodium-channel genes • Romano-Ward syndrome (autosomal dominant) - acquired; hypocalcaemia, drugs, Bradycardia, acute MI

Answer 229

- syncope | - palpitations

Answer 230

IV isoprenaline

Answer 231

permanent dilatation of the artery to TWICE | the normal diameter

Answer 232

``` Abnormal dilatations that involve all layers of the arterial wall - Arteries most frequently involved are: • Abdominal aorta (most common) • Iliac, popliteal and femoral arteries • Thoracic aorta ```

Answer 233

Involves the collection of blood in the OUTER LAYER ONLY (ADVENTITIA) which communicates with the lumen e.g after trauma from a femoral artery puncture

Answer 234

- most common infra-renal - men > women - incidence increases with age

Answer 235

- severe atherosclerotic damage - family history - COPD - trauma - smoking

Answer 236

Degradation of the elastic lamellae resulting in leukocyte infiltrate causing enhanced proteolysis and smooth muscle cell loss - The dilatation affects ALL THREE LAYERS of the vascular tunic - If it doesn't then it is a pseudoaneurysm

Answer 237

unruptured; asymptomatic or pain in back, loin or groin | ruptured AAA; increased BP, female, abdominal pain, pulsatile abdominal swelling, collapse, tachycardia

Answer 238

- abdo ultrasound | - CT or MRI angiography

Answer 239

- lifestyle change - BP and lipid control - surgery

Answer 240

- ascending TAA; marfans syndrome and hypertension | - descending TAA; atherosclerosis and rare due to syphilis

Answer 241

- autosomal dominant trait - connective tissue disorders - weight lifting, cocaine and amphetamine use

Answer 242

Involves inflammation, proteolysis and reduced survival of the smooth muscle cells in the aortic wall - Once the aorta reaches a crucial diameter (around 6cm in the ascending and 7cm in the descending) it loses all distensibility so that a rise in BP to around 200mmHg can exceed the arterial wall strength and may trigger dissection or rupture

Answer 243

- most asymptomatic - pain in chest, neck, upper back - aortic regurgitation - cardiac tamponade

Answer 244

- CT or MRI - aortography - transesophageol echocardiogram - ultrasound

Answer 245

- surgery - BP control - smoking cessation

Answer 246

- men>females - >50+ - acute = <2 weeks, subacute 2-8 weeks and chronic >8 weeks

Answer 247

- inherited - atherosclerosis - inflammation - trauma

Answer 248

Aortic dissection begins with a tear in the intimal lining of the aorta - The tear allows a column of blood under pressure to enter the aortic wall, forming a haemotoma which separates the intima from the adventitia and creates a false lumen - The false lumen extends for a variable distance in either direction; anterograde (towards bifurcations) and retrograde (towards the aortic root) - The most common sites for the intimal tears are: • Within 2-3cm of the aortic valve • Distal to the left subclavian artery in the descending aorta

Answer 249

- sudden onset of chest pain that radiates to back and arms - hypertension - pain is maximal - neurological symptoms - aortic regurgitation and cardiac tamponde - peripheral pulse absent

Answer 250

- CXR - CT scan - transoesophageol echocardiography - MRI

Answer 251

- anti-hypertensive medication - analgesics - surgery - stents

Answer 252

- men>women | - smoking, diabetes, hypertension, obesity all risk factors

Answer 253

ALWAYS due to ATHEROSCLEROSIS of the arteries distal to the aortic arch - Atherosclerosis can result in many complications:

Answer 254

Stress-induced physiological malfunction - Exercise induced angina - Intermittent claudication: • This is a cramping pain that is induced by exercise and relieved by rest • Pain is distal to site of atheroma • Occurs when anaerobic metabolism comes into effect when O2 demand outstrips supply • Pain is the result of lactic acid production • Caused by inadequate blood supply to the affected muscles resulting in moderate ischaemia • Most commonly seen in the calf and leg muscles as a result of atheroma of the leg arteries • Leg pulses are often absent and the feet may be cold • Oxygen pressures in different activities with intermittent claudication:

Answer 255

Structural & functional breakdown - Ischaemic cardiac failure - Critical limb ischaemia: • Blood supply is BARELY ADEQUATE to allow basal metabolism • No reserve available for increased demand • Rest pain that is typically NOCTURNAL • Risk of gangrene and/or infection • CHRONIC CONDITION and the MOST SEVERE clinical manifestation of peripheral vascular disease

Answer 256

- infarction | - gangrene

Answer 257

- absent femoral, popliteal foot pulses?

Answer 258

- -colour duplex ultrasound - first line - ESR; exclude arthritis - FBC; excluse anemia - ABPI - ankle brachial pressure index <0.5 v. serious - MRI/CT angiography

Answer 259

Usually forms on a chronic atherosclerotic stenosis in a patient who has previously reported symptoms of claudication • Thrombus may also form in normal vessels in individuals who are hypercoagulable because of malignancy or thrombophilia defects • Popliteal aneurysms may thromboses or embolise distally

Answer 260

``` pain pallor perishing cold pulseless paralysis paraetheisa ```

Answer 261

- risk factor modification -> smoking cessation - hypertension, hyperlipidaemia and diabetes treatment - anti-platelet therapy - revascularisation

Answer 262

acute circulatory failure with inadequate or inappropriately distributed tissue perfusion (meaning there is inadequate substrate (glucose & oxygen) for aerobic cellular respiration), resulting in generalised hypoxia and/or an inability of the cells to utilise oxygen

Answer 263

Causes of shock: - Hypovolaemic shock - low blood volume (trauma, bleeding, dehydration) - Cardiogenic shock - heart isn't pumping (cardia tamponade, PE, MI) - Distributive shock: • Septic shock • Anaphylactic shock • Neurogenic shock - Anaemic shock - not enough oxygen carrying capacity - Cytotoxic shock - cells poisoned

Answer 264

* 15% blood loss * Pulse below 100 bpm * BP normal * Pulse pressure normal

Answer 265

15-30% blood loss • Pulse greater than 100 bpm (tachycardia - earliest sign) • BP normal due to autonomic response (increased sympathetic activity) • Pulse pressure decreased

Answer 266

30-40% blood loss • Pulse above 120 bpm • BP decreased • Pulse pressure decreased

Answer 267

``` Inadequate tissue perfusion: - Skin: cold, pale, clammy, slate-grey, - Brain: drowsiness and confusion • Increased sympathetic tone • Tachycardia - narrow pulse pressure and weak pulse • Sweating ```

Answer 268

Signs of myocardial failure • Raised jugular venous pressure (JVP) • Gallop rhythm • Basal crackles and pulmonary oedema

Answer 269

Pyrexia and rigors • Nausea and vomiting • Vasodilation with warm peripheries • Bounding pulse

Answer 270

Impaired oxygenation • Bilateral pulmonary fluid buildup • NO CARDIAC FAILURE • Normal pulmonary arterial pressure

Answer 271

``` Extrapulmonary: • Shock of any cause • Head injury • Drug reaction • Sepsis - Pulmonary: • Pneumonia • Chemical pneumonitis • Smoke inhalation • Near drowning ```

Answer 272

Alveolar capillary membrane injury results in leakage of fluid into the alveolar spaces - There is resulting neutrophil invasion which attracts more neutrophils = EXUDATIVE PHASE - Eventually fibroblasts come in and initiate healing = PROLIFERATIVE PHASE - And make scar tissue = FIBROTIC PHASE (scarring due to fibroblasts) - Results in severely stiff lungs and thus SEVERE DIFFICULTY IN VENTILATION and thus O2 BLOOD PERFUSION!