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CVS Flashcards

1
Q

Cardiac tamponade?

A

Fluid builds up in pericardium
Causes compression of heart, since outer fibrous layer is not elastic and can’t stretch
Restricts filling of the heart - limits EDV
–> affects both sides of the heart -> high central venous and low arterial blood pressure –> mechanical shock

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2
Q

Aortic valve stenosis?

A

Aortic valve narrowing - less blood pumped to aorta
- Increased LV pressure –> LV hypertrophy
- Left sided heart failure –> Syncope (fainting, crescendo and decrescendo murmur), angina (pain, early decrescendo murmur)
- Microangiopathic haemolytic anaemia (due to damage of RBCs being forced through small gap)
Due to: Degenerative (senile calcification), congenital (bicuspid form of valve instead of normal tricuspid), rheumatic fever

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3
Q

Aortic valve regurgitation?

A

Blood flows back into LV during diastole (early decrescendo diastolic murmur):
- Stroke volume increased
- Systolic pressure increased, diastolic decreased
- Bounding pulse (head bobbing, Quinke’s sign)
- LV hypertrophy
Due to: Aortic root dilation, valvular damage (endocarditis rheumatic fever)

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4
Q

Mitral valve stenosis?

A

Mitral valve narrowing - less blood flows to LV
Increase in LA pressure (snap as valve opens, diastolic murmur)
- Pulmonary oedema; hypertension, dyspnea –> RV hypertrophy
- LA dilation –> Atrial fibrillation –> thrombus formation
–> Oesophagus compression –> dysphagia
Due to: Rheumatic fever

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5
Q

Mitral valve regurgitation?

A

Some blood flows back from LV to LA, increases preload - more blood enters LV in subsequent cycles
Causes LV hypertrophy (holosystolic murmur)
Due to: Damage to papillary muscles, valve stretching due to left sided heart failure, rheumatic fever (fibrosis of valves)

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6
Q

Microangiopathic haemolytic anaemia?

A

Anaemia due to damage of RBC’s being forced through a narrow gap at high pressure
Eg sheer stress in aortic valve stenosis

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7
Q

Situs inversus?

A

Congenital condition -major visceral organs are positioned in the mirror image of the normal

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8
Q

Patent ductus arteriosus?

A

Persistent communication between descending aorta and pulmonary artery, mainly in infants
Due to failure of physiological closure of ductus arteriosus
Left to right shunt

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9
Q

Atrial septal defect?

A

Defect of ostium secondum (2nd septal hole)
Due to:
- septum primum (1st wall) resorbed or too short
- septum secondum (2nd wall) to smaller
Effects: Increased pulmonary flow, RV volume overload, rare pulmonary hypertension, eventually late onset right heart failure and arrhythmia
Asymptomatic until adulthood

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10
Q

Hypoplastic left heart syndrome?

A

Left ventricle/heart is underdeveloped (Congenital)
Ascending aorta very small
Leads to cyanosis
RV supports systemic circulation, R to L shunt required to stay open (ASD) and PDA req. for survival

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11
Q

Ventricular septal defect?

A

Membranous portion of ventricular septum affected (most commonly)
Effects: LV overload, pulmonary venous congestion –> pulmonary hypertension if not treated
Present in infancy with left heart failure

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12
Q

Transposition of the great arteries?

A

If aorta arises from RV and pulmonary trunk from LV, baby will have cyanosis
Due to incorrect formation of spiral conotruncal septum
2 non-communicating systems
Not viable unless there is mixing of blood between the two, eg like in the foetus (shunts - ASD, VSD, PDA)

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13
Q

Tetralogy of Fallot?

A 
Involves 4 heart defects: 
- Pulmonary stenosis
- Large ventricular septal defect
- RV hypertrophy
- Overriding aorta
Leads to cyanosis
Due to: Conotruncal septum formation defective, could be due to fault in neural crest cells 
Present in infancy (cyanoitic spells)
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14
Q

Coarctation?

A

Ductal tissue on aorta, causing obstruction

Both neonatal and adult variety (renal hypertension, left vent hypertrophy)

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15
Q

Tricuspid atresia?

A

Complete failure of formation of tricuspid valve
Leads to cyanosis
Effects: No RV inlet, so blood goes through foramen ovale, to LA and LV
LV pushes it through aorta and pulmonary artery (can do this because of either VSD or PDA)

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16
Q

Pulmonary atresia?

A

No RV outlet

Blood flows from RA to LA (ASD), and to lungs via shunt between aorta and pulmonary artery (PDA)

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17
Q

Hyperkalaemia?

A

Plasma K+ too high (>5.5mmol/L)
- Mild –> 5.5-5.9
- Moderate –> 6-6.4
- Severe –> >6.5
Membrane potential of myocytes depolarises - inactivates some voltage gated Na + channels
Slows down upstroke (there are less channels available)
Can cause: asystole, initial increased excitability
Treatment: Calcium gluconate, insulin+glucose
ECG could be: high T, prolonged PR, depressed ST, absent P (atrial standstill, AV block), ventricular fibrillation

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18
Q

Hypokalaemia?

A

Plasma K+ too low (<3.5mmol/L)
Lengthens AP, delays repolarisation
Effects: EAds formed, entricular fibrillation -> no cardiac output
ECG could be: low T, high U, low ST

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19
Q

Bradycardia?

A

Slow heart rate (<60bpm) Can be physiological - sleep, athletes etc
Due to:
-intrinsic SAN node issue/extrinsic problem -> sinus bradycardia
-conduction block (at AVN/Bundle of His)

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20
Q

Tachycardia?

A

Fast heart rate (>100bpm)
Can be physiological - exercise, anger etc
Due to: ectopic pacemaker activity, afterdepolarisations, atrial flutter/fibrillation, re-entry loops

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21
Q

Hypertension?

A

Sustained increase in BP
Stage 1: >140/90 mmHg
Stage 2: >160/100 mmHg
Severe: >180 sys, >110 dias
Leads to MI, heart failure, stroke, aneurysm, renal failure, retinopathy
Treatment: Exercise, diet, reduced Na intake, reduced alcohol intake, ACE inhibitors, Ang II inhibitors, L-type Ca channel blockers, diuretics

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22
Q

Primary hypertension?

A

No known cause: genetic, environmental

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23
Q

Secondary hypertension?

A

Known cause: renovascular disease (occlusion of renal artery->renin), renal parenchymal disease, hyperaldosteronism, renal disease, Cushing’s or Conn’s syndrome, adrenal tumour

24
Q

Haemodynamic shock?

A

Acute condition of inadequate blood flow throughout the body due to large fall in BP (fall in CO or TPR)
Fall in CO - cardiogenic, mechanical, hypovolemic
Fall in TPR (distributive) - toxic, septic

25
Cardiogenic shock?
Acute failure of heart to maintain cardiac output Due to: after MI, arrhythmias, heart failure Dramatic drop in BP, inadequate blood flow Tissues poorly perfused Could lead to renal failure - oliguria
26
Mechanical shock-cardiac tamponade?
Blood/fluid builds up in pericardial space, causing tamponade - limits EDV High central venous pressure Low BP, continued electrical activity Inadequate blood flow
27
Mechanical shock-pulmonary embolism?
Embolus occludes large pulmonary artery (PA) (due to DVT) PA pressure high RV can't empty - central venous pressure high, reduced return, LA pressure low, BP low - inadequate blood flow Causes chest pain, dyspnoea
28
Hypovolaemic shock?
Reduced blood volume (20-40%) Due to haemorrhage - venous pressure falls, CO falls, aBP falls --> detected by baroreceptors Compensatory response - high sympathetic, tachycardia, high contractility, peripheral vasoconstriction, venoconstriction Danger of decompensation To restore volume: RAAS, ADH Symptoms: tachycardia, weak pulse, pale skin, cold extremities
29
Distributive shock?
Decreased TPR - volume of circulation increases but blood volume constant - Toxic shock - Anaphylactic shock
30
Toxic/septic shock?
Due to sepsis Bacteria --> endotoxins Inflammation, vasodilation, fall in TPR, fall in aBP -impaired tissue perfusion, capillaries leaky - low blood volume Symptoms: hypotension, tachycardia due to baroreceptors), warm red extremities,
31
Anaphylactic shock?
Due to severe allergic reaction Mast cells - histamine --> vasodilation --> fall in TPR, fall in aBP Sympathetic response increased (high CO) to combat, but can't overcome vasodilation Impaired tissue perfusion Other mediators - bhronconstriction, laryngeal oedema Symptoms: hard to breathe, collapse, rapid heart rate, red warm extremities Treatment: adrenaline (epi pen)
32
Atrial fibrillation?
Impulses have chaotic random pathway in atria - no coordinated contraction Due to: re-entrant loops, mitral stenosis Atrial depolarisation chaotic Ventricles depolarise, contract regularly Decreased CO ECG- irregular baseline, no P waves, QRS normal (or narrow) but irregular Pulse- irregularly irregular
33
AV conduction block?
Delay/failure of conduction of impulses from atria to ventricles via AV node/bundle of His Due to: MI, degenerative changes 3 types: 1st degree, 2nd degree, 3rd degree (complete heart block)
34
1st degree heart block?
Slow conduction in AV node/His bundle: AV conduction lengthened - delay of conduction of impulses to ventricles ECG - P normal, PR prolonged, QRS normal
35
2nd degree heart block?
Mobitz type 1 (Wenkebach) - ECG: progressive lengthening of PR, till 1 P not conducted, then cycle begins again Mobitz type 2 - More dangerous than type 1 - Can progress to 3rd degree (CHB) - ECG: PR normal, sudden non-conduction of beat, dropped QRS
36
3rd degree heart block?
Complete heart block Atrial depolarisation normal but impulses not conducted to ventricles Ventricular pacemaker takes over (escape rhythm: 30-40bpm) HR too slow to maintain BP and perfusion ECG - wide QRS, R-R intervals constant but slow, no relationship b/w p and QRS) Treatment: pacemaker
37
Ventricular ectopic beats?
``` Ectopic focus in ventricle muscle - impulse not spread through His-purkinje system Slower depolarisation of ventricles No escape rhythm Due to: irritation eg ischaemia ECG - wide differently shaped QRS ```
38
Ventricular tachycardia?
``` Run of 3 or more ventricular ectopic beats Broad complex tachycardia Persistence is dangerous High risk of ventricular fibrillation Treatment: electrical shock ```
39
Ventricular fibrillation?
Abnormal chaotic fast ventricular depolarisation Impulses from many sites in ventricular muscle, no coordinated contraction No CO -> no pulse/HR -> heart failure Very rapid irregular heart rhythm
40
NSTEMI?
Non ST elevation MI Due to severe narrowing of arterial lumen ECG: normal -> T inversion or ST depression (acute) -> ST & T normal, no Q (weeks later)
41
STEMI?
ST elevation MI Due to complete occlusion of lumen by thrombus Muscle injury throughout endo and epicardium No perfusion -> necrosis ECG: normal -> ST elevation (normal) -> low R, Q begins-necrosis (hours) -> T inversion, Q deeper (1-2d) -> ST normal, T inverted (few days) -> ST, T normal, Q persists (weeks)
42
Bundle branch block?
Delayed conduction of impulse down one side of Bundle of His so it conducts across muscle instead - slower ECG - sinus rhythm with increased QRS
43
Pericarditis?
Inflammation of the pericardium Often secondary to viral illness M>F Symptoms: chest pain - restrosternal, sharp, localised (chest front), worse on inspiration & coughing & lying flat, eased by sitting up & leaning forward Pericardial rub heard - coarse heart sound ECG: ST elevated - saddle shaped
44
Stable angina?
Ischaemia occurs only when demands greater than what can be delivered Due to: stable atherosclerotic plaque, anaemia, hypovolemia, AV stenosis, hypertrophy, hypothyroidism Symptoms: dull retrosternal pain, triggered by excursion, relieved on rest, radiation to shoulders maybe, no sweat/unwell appearance, GTN relieves pain Tests: ECG (often normal), FBC etc, ischaemia tests (treadmill), angiogram Treatment: aspirin, beta blockers, statins, ACE inhibitors, GTN
45
Acute coronary syndrome?
Acute MI caused by atherosclerotic coronary artery disease - atherosclerotic plaque ruptures, thrombus forms, occludes artery Unstable angina -> NSTEMI -> STEMI (completely blocked artery - MI) Tests: ECG, blood tests (troponin I)
46
Unstable angina?
``` Heart pain which can lead MI Due to: coronary plaque rupture Symptoms: as per unstable angina except; Pain at rest, could be more intense, last longer, GTN doesn't work ECG: ST depression, T flat or inverted No troponin released (no muscle death) Treatment: reperfusion ```
47
Myocardial infarction?
Blood flow stopped to part of the heart causing damage to heart muscle Symptoms: dull severe retrosternal pain for >15mins, radiates to muscles/shoulders/arm, chest pain at rest, unwell appearance (sweaty, pale) -Type 1: spontaneous -Type 2: secondary to ischaemic imbalance Treatment: oxygen, pain relief, GTN sublingually, aspirin, reperfusion
48
Heart failure?
A state in which the heart fails to maintain an adequate circulation for the needs of the body despite an adequate filling pressure Due to: Ischaemic heart disease (primary), hypertension, LV systolic dysfunction, skeletal muscle changes, cardiomyopathy, valve/pericardial disease, arrhythmia -4 classes (increasing discomfort) -Effects: RAAS overactivated, natriuretic hormones, ADH, prostaglandins, NO released, oedema, renal effects, anaemia, pulmonary/venous congestion Treatment: ACE inhibitors, beta blockers, sacubitril, MRAs
49
Left ventricular systolic dysfunction?
Due to: Increased LV capacity, Reduced LV CO, Myocardial wall thinning by fibrosis, necrosis, proteinases, Mitral valve incompetence, Neurohormonal activation, arrhythmias Causes loss of muscle, uncoordinated contraction, cellular structure and function changes -> heart failure
50
Heart failure with preserved ejection fraction (HFpEF)?
Reduced LV compliance and relaxation due to thicker/shorter myocytes Impaired diastolic LV filling but ejection is same Triggers neuro-hormonal activation Common in elderly, female, obese hypertensive, diabetic patients
51
Left heart failure?
Symptoms : Fatigue, exertional dyspnoea, orthopnoea, paroxysmal nocturnal dyspnnoea Signs: tachycardia, cardiomegaly, 3rd/4th heart sound, mitral regurg. murmur, basal pulmonary crackles (lung fluid), peripheral oedema
52
Right heart failure?
Due to: LHF (most common), chronic lung disease, pulmonary embolism/hypertension Symptoms: fatigue, dyspnoea, anorexia, nausea Signs: high JVP, smooth hepatic enlargement, pitting oedema, ascites, plural effusion
53
Arrhythmia?
Abnormality of heart rate or rhythm - Tachycardia: ectopic pacemaker activity (due to infarction), afterdepolarisations (delayed, EAD), atrial flutter/fib, re-entry loop - Bradycardia: sinus bradycardia (intrinsic SAN dysfunction or extrinsic), conduction block (AVN or extrinsic)
54
Wolff-Parkinson-White syndrome?
Genetic defect which causes the heart to have an accessory pathway connection between atrium and ventricle Creates re entry loops - ventricle conducting at a different rate to AVN Causes supraventricular tachycardia (paroxysmal VF) Treatment: Amiodarone
55
Varicose veins?
Tortuous, twisted, lengthened veins Thin wall -> dilatation -> separation of valve cusps (become incompetent) Symptoms: heaviness, tension, aching along vein Could lead to: haemorrhage, thrombophlebitis (venous thrombosis with inflammation, pain), venous hypertension -> oedema , skin pigmentation, eczema, lipodermaotsclerosis (hard thick fat), ulceration
56
Acute limb ischaemia?
Normal to impaired blood supply in minutes (no time for collateral blood supply to form) Due to: mainly embolism Sudden onset Symptoms: 6 Ps -> pain, paralysis, paraesthesia, pallor, perishing cold, pulseless
57
Chronic peripheral arterial disease?
Intermittent claudication | Critical ischaemia - rest pain (foot pain when in bed - relieved by dangling foot off bed), ulceration/gangrene

Clinical Conditions (6 decks)

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