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Cardio > cardio patho > Flashcards

cardio patho Flashcards

1
Q

what HR is considered brady/tachycardia?

A

bradycardia: <60bpm
tachycardia: >100bpm

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2
Q

what are the possible causes of bradycardia? (2)

A
  1. disruption to impulse generation @SA node
  2. interrupted conduction from atrium to ventricle (AV node)
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3
Q

what are the manifestations of disruption to impulse generation @SA node? (3)

A
  1. asystole
  2. sinus bradycardia
  3. sinus arrhythmia
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4
Q

what is sinus bradycardia + its causes (5)

A
  • sinus rhythm with low HR
  • decreased rate of electrical discharge fr SA node

causes:
1. high vagal tone→ higher PNS activity (youths & athletes)
2. aging
3. drugs (B-blockers, Ca2+ channel blockers)
4. injury to SA node (ischaemia, infection)
5. hypothyroidism (decreased metabolism)

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5
Q

what is asystole?

A

no cardiac activity (flatline)

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6
Q

what is sinus arrythmia + causes?

A
  • PHYSIOLOGICAL irregular sinus rhythm
  • due to varying vagal tone on HR (inspiration: HR decrease, expiration: HR increase)
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7
Q

what are the causes of interrupted conduction from atrium to ventricles (AV node)? (3)

A
  1. first deg AV block
  2. second deg AV block
  3. third deg AV block
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8
Q

what is first deg AV block + causes? (3)

A
  • prolong duration of conduction from atrium to ventricle (gap betw P wave & QRS complex)
  • often asymptomatic
    1. high vagal tone
    2. drugs (B-blockers, Ca2+ channel blockers)
    3. aging
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9
Q

what is second deg AV block + causes? (3)

A
  • regular dropped AV conduction (every 2nd P wave is blocked→ not accompanied by QRS complex)
    1. aging
    2. injury to AV node (MI involving RCA, myocarditis)
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10
Q

what is third deg AV block + causes?

A
  • no relationship betw P and QRS (regular PP & RR intervals)
    1. aging
    2. injury to AV node or His bundle (MI involving RCA, myocarditis)
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11
Q

what are the symptoms of bradycardia? (5)

A
  1. lethargy
  2. giddiness
  3. syncope (periodic loss of consciousness)
  4. exertional dyspnoea
  5. asymptomatic
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12
Q

what are the causes of tachycardia?

A
  1. abnormal automaticity
  2. triggered activity
  3. re-entry
  4. disorganised activity
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13
Q

what is re-entry in atrium (atrial flutter) + causes?

A
  • atrial contracts repeatedly
  • no P waves, sawtooth baseline
  • regular/irregular RR intervals depending on deg of AV block
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14
Q

what is ventricular tachycardia? (re-entry)

A
  • HR>100
  • QRS broad & bizarre (ventricular depolarization doesn’t involve His bundle, occurs in diff direction)
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15
Q

what is atrial fibrillation? (disorganised activity)

A
  • no p waves
  • irregularly irregular RR intervals (AV nodes filters some signals irregularly)
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16
Q

what is ventricular fibrillation? (disorganised activity)

A
  • associated w cardiac arrest
  • no cardiac output
  • ecg is a mess of waves
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17
Q

what is atrial ectopic (AA/TA in atrium)?

A
  • ectopic beat (P wave w diff morphology) disrupting sinus rhythm
  • p wave occurs earlier than expected
  • QRS narrow (sinus)
  • due to atrium depolarising in opposite direction
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18
Q

what is atrial tachycardia (AA/TA in atrium)?

A
  • HR>100bpm
  • QRS narrow (sinus)
  • P preceding QRS but with diff P wave morphology
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19
Q

what is ventricular ectopics? (AA/TA in ventricles)

A

QRS broad & bizzare, interrupting normal sinus rhythm (depolarisation occurs in diff direction, takes longer, doesnt’ involve His bundle)

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20
Q

what is sinus tachycardia + causes (2)

A
  • high but regular HR w each P having a corresponding QRS wave
    1. physiological: exercise, stress/pain
    2. pathological: sepsis/pyrexia, hypovolemia, thyrotoxicosis (excess circulating thyroid hormones→ increased metabolism)
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21
Q

what are the symptoms of tachycardia? (5)

A
  1. palpitations
  2. giddiness
  3. syncope
  4. cardiac arrest
  5. asymptomatic
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22
Q

what is valvular stenosis?

A

narrowing of valve/failure to OPEN completely→ prevents forward flow

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23
Q

what are the possible causes of stenosis? (3)

A
  1. post inflammatory scarring/fibrosis
  2. calcifications (deposits)
  3. congenital
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24
Q

what is valvular regurgitation/incompetence?

A

failure of valves to CLOSE completely→ allows reverse flow

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25
Q

what are the causes of regurgitation/incompetence? (4)

A
  1. post inflammatory scarring
  2. genetic/developmental e.g. marfan syndrome
  3. degenerative
  4. infectious (destroys valves)
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26
Q

what is infectious endocarditis?

A

microbial infection of cardiac valves/endocardium→ vegetation→ tissue destruction
(affects MV/AV more aka left side)

27
Q

what is subacute vs acute infectious endocarditis?

A

acute:
- involves NORMAL valves
- highly virulent pathogenic organisms→ rapid destruction
- IVDA, open heart surgery, septicaemia
- staph aureus!! (IVDA)

subacute:
- insidious infection of ABNORMAL valves (eg. congenital, prosthetic)
- low pathogenic orgnisms fr normal flora
- staph epidermidis (no 1 cause of subacute endocarditis in prosthetic valves)
- strep viridans!! (normal oral flora, affects damaged heart valves)

28
Q

what is rheumatic fever?

A
  • abnormal response to grp A strep pharyngitis
  • leads to rheumatic heart disease!! (permanently damages heart valves)
29
Q

what is rheumatic heart disease?

A

acute phase:
- pancarditis (inflammation in all 3 layers of heart)
- inflammation comprises Aschoff bodies (T-cells, plasma cells, aschoff giant cells, activated macrophage/caterpillar nucleus)
- inflammation→ verrucae (small vegetations)

chronic phase:
- after cumulative damage
- inflammation, fibrosis & damage to valves (MV>AV>PV/TV)
- leads to stenosis/regurgitation

30
Q

what is pericardial effusion?

A
  • buildup of extra fluid in pericardium (eg hemopericardium, purulent pericarditis)
  • can lead to cardiac tamponade: compression of heart→ impedes filling of heart→ fall in CO)
31
Q

what is tetralogy of fallot?

A

CYANOTIC congenital heart disease
1. pulmonary stenosis
2. RV hypertrophy
3. VSD
4. overriding aorta

32
Q

what is transposition of great arteries?

A

CYANOTIC congenital heart diease
- aorta arise fr RV, PT from LV (swapped)
- deoxygenated blood fr body→ RA→ RV→ aorta→ rest of body

33
Q

what is coarctation of aorta?

A

ACYANOTIC congenital heart disease
- narrowing of aorta @ certain parts

34
Q

what is the definition of hypertension?

A

persistent high bp
systolic: >140mmHg
diastolic: >90mmHg

35
Q

what are some of the etiologies of primary hypertension?

A

(primary HT has no known cause)

increased resistance of arterioles & arterioles:
- sympathetic overdrive
- dysregulation of vascular smooth muscle tone (smoking, age)
- smooth muscle hypertrophy due to insulin resistance

kidneys:
- sympathetic overdrive (overactivation of RAAS)
- insensitivity of RAAS to salt (continues absorbing salt fr diet→ increase blood volume)

obesity:
- increased angiotensin release from adipocytes
- increased blood volume
- increased blood viscosity (increased resistance)

36
Q

what are the causes of secondary hypertension? (5)

A

Renal
Endocrine (hypercortisolism, pheochromocytoma)
Neurologic
Aortic (coarctation, atherosclerosis)
Labile (psychogenic, stress-related)

37
Q

what is the only cause of BOTH hypertension and tachycardia happening concurrently? (usually pt only has HT because heart compensates by decreasing HR)

A

pheocytochroma (tumour of adrenal gland) that causes activation of SNS→ tachycardia despite HT

38
Q

what are some of the consequences of hypertension?

A

HEART: congestive heart failure (LV pressure increases→ LV hypertrophies→ LV diastolic filling falls→ LA dilation→ LV failure)

BLOOD VESSELS: atherosclerosis, arteriolosclerosis, aneurysms, thrombosis→ damage organs the blood vessels supply
Brain: hypertensive encephalopathy
Heart: hypertensive cardiomyopathy
Kidney: hypertensive nephropathy
Eyes: hypertensive retinopathy
Aorta: aortic dissection

RENAL: kidney diseases

39
Q

what type of hypertension leads to what type of arteriolosclerosis? (2)

A

benign HT→ hyaline arteriolosclerosis
malignant HT→ hyperplastic arteriolosclerosis

40
Q

what are aneurysms?

A

localised abnormal dilation of blood vessels/heart (usually w superimposed atherosclerosis in vessel walls)

41
Q

what are the causes of aneurysms?

A
  • atherosclerosis
  • hypertension
  • fibrosis (e.g. trauma, infections, vasculitis)
  • congenital defects
42
Q

what are the clinical manifestations of aneurysms?

A
  • asymptomatic
  • rupture
  • embolism fr atheroma/thrombus formed
  • impingement on adjacent structures (pain, constipation)
43
Q

what is aortic dissection?

A

tear in intimal layer of aortic wall

44
Q

how does aortic dissection occur?

A

hypertension→ hypertrophy of vessels supplying aorta→ degenerative/ischaemic injury to arteriolar walls→ weakening/necrosis of aortic wall→ dissection

45
Q

what are the clinical presentations of aortic dissection?

A

obvious sharp shooting pain between scapulae (back)

46
Q

what is atherosclerosis?

A

thickening/blocking of arteries due to buildup of plaque

47
Q

what factors/modifiable risk factors predispose pts to atherosclerosis? (4)

A
  1. high cholesterol
  2. hypertension (cause damage to blood vessels→ fats in blood can collect there→ atheroma)
  3. smoking
  4. diabetes

(three highs + smoking)

48
Q

what is an atheroma?

A

plaque consisting of raised lesion w a soft, yellow core of lipid covered with a white fibrous cap

49
Q

what is the pathogenesis of atheroma formation?

A

(tend to develop in areas with turbulent blood flow)
endothelial injury→ response to injury (increased permeability, leukocyte adhesion, macrophage activation in intima)→ failure to engulf lipids→ “foam cells” aggregate→ fatty streak→ ECM deposition→ fibrous cap formed

50
Q

what are vulnerable/unstable plaques?

A
  • dangerous plaques with relatively larger lipid core & thin fibrous cap/collagen content (ruptures easily)
  • more likely to rupture, fissure, ulcerate & hemmorhage
51
Q

what are the clinical consequences of atherosclerosis? (3)

A
  1. vessel thickens→ narrows lumen→ poor tissue perfusion→ ISCHAEMIA & ANGINA
  2. loss of elasticity→ predisposition to ANEURYSM→ possibly rupture & hemorrhage
  3. endothelial changes→ ruptures→ release prothrombotic atheroma contentspre→ THROMBOSIS→ infarction
52
Q

what are the clinical manifestations of ischemic heart disease? (4)

A
  1. angina
  2. myocardial infarction
  3. chronic ischemic heart disease w heart failure
  4. sudden cardiac death
53
Q

what is angina?

A

mismatch between ability of coronary circulation to supply blood to HEART muscles, and its metabolic requirements

54
Q

name and describe the 3 forms of angina

A

stable angina
- myocardial demand>perfusion
- relieved by rest or vasodilation

prinzmetal angina
- episodic myocardial angina due to coronary artery spasm
- unrelated to physical activity/HR/BP
- relieved by vasodilation

unstable angina
- increasingly frequent pain, prolonged duration
- ppt during lower levels of activity or even during rest
- unresponsive to rest

55
Q

what are the characters of angina? (4)

A
  1. location: chest/epigastric area
  2. radiation: pain radiates fr chest to left arm
  3. nature: crushing pain, discomforting sensation
  4. precipitated by exertion, relieved by rest
56
Q

what are the causes of angina?

A

increased metabolic demand: physical activity

fall in blood supply of myocardium
- fall in diastolic pressure/rapid HR→ decrease blood suply LV→ stroke volume falls
- due to atherosclerosis blocking blood flows

57
Q

what is myocardial infarction?

A

death of cardiac muscle following impaired blood flow

58
Q

how is MI clinically diagnosed? (3)

A
  1. symptoms: severe, crushing central chest pain (radiates to arms)
  2. ECG changes
  3. elevated cardiac enzymes (released when myocyte cell membranes rupture)
59
Q

describe the change in heart morphology after MI overtime

A

0-12h: no visible change
12-24h:
- macroscopically: pale w bloody discolouration
- histology: infarcted muscle bright eosinophilic, no nucleus (ghost outlines), intercellular edema
24-72h:
- macro: soft & pale tissue, yellow
- histo: neutrophil infiltration
3-10days:
- macro: hyperaemic border w central yellowing
- histo: granulation tissue response (eg angiogenesis)
6-8 weeks: fibrous scar

60
Q

what part of the heart is affected when MI occurs in the left anterior descending artery? + ECG leads

A

antero-septal: leads V1, V2, V3, V4

61
Q

what part of the heart is affected when MI occurs in the left circumflex artery? + ECG leads

A

antero-lateral: leads 1, aVL, V5, V6

62
Q

what part of the heart is affected when MI occurs in the right coronary artery + ECG leads?

A

inferior: leads 2, 3, aVF
posterior: none

63
Q

what is chronic IHD w heart failure?

A

chronic atherosclerotic narrowing of coronary arteries→ slow/constant loss of myocardial fibres→ insidious cardiac failure→ death

Cardio (8 decks)

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