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Clinical Conditions > CVS > Flashcards

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
Q

Cardiogenic shock?

A

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
Q

Mechanical shock-cardiac tamponade?

A

Blood/fluid builds up in pericardial space, causing tamponade - limits EDV
High central venous pressure
Low BP, continued electrical activity
Inadequate blood flow

27
Q

Mechanical shock-pulmonary embolism?

A

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
Q

Hypovolaemic shock?

A

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
Q

Distributive shock?

A

Decreased TPR - volume of circulation increases but blood volume constant

  • Toxic shock
  • Anaphylactic shock
30
Q

Toxic/septic shock?

A

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
Q

Anaphylactic shock?

A

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
Q

Atrial fibrillation?

A

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
Q

AV conduction block?

A

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
Q

1st degree heart block?

A

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
Q

2nd degree heart block?

A

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
Q

3rd degree heart block?

A

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
Q

Ventricular ectopic beats?

A 
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
Q

Ventricular tachycardia?

A 
Run of 3 or more ventricular ectopic beats
Broad complex tachycardia
Persistence is dangerous 
High risk of ventricular fibrillation
Treatment: electrical shock
39
Q

Ventricular fibrillation?

A

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
Q

NSTEMI?

A

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
Q

STEMI?

A

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
Q

Bundle branch block?

A

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
Q

Pericarditis?

A

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
Q

Stable angina?

A

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
Q

Acute coronary syndrome?

A

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
Q

Unstable angina?

A 
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
Q

Myocardial infarction?

A

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
Q

Heart failure?

A

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
Q

Left ventricular systolic dysfunction?

A

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
Q

Heart failure with preserved ejection fraction (HFpEF)?

A

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
Q

Left heart failure?

A

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
Q

Right heart failure?

A

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
Q

Arrhythmia?

A

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
Q

Wolff-Parkinson-White syndrome?

A

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
Q

Varicose veins?

A

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
Q

Acute limb ischaemia?

A

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
Q

Chronic peripheral arterial disease?

A

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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