cardio patho Flashcards
what HR is considered brady/tachycardia?
bradycardia: <60bpm
tachycardia: >100bpm
what are the possible causes of bradycardia? (2)
- disruption to impulse generation @SA node
- interrupted conduction from atrium to ventricle (AV node)
what are the manifestations of disruption to impulse generation @SA node? (3)
- asystole
- sinus bradycardia
- sinus arrhythmia
what is sinus bradycardia + its causes (5)
- 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)
what is asystole?
no cardiac activity (flatline)
what is sinus arrythmia + causes?
- PHYSIOLOGICAL irregular sinus rhythm
- due to varying vagal tone on HR (inspiration: HR decrease, expiration: HR increase)
what are the causes of interrupted conduction from atrium to ventricles (AV node)? (3)
- first deg AV block
- second deg AV block
- third deg AV block
what is first deg AV block + causes? (3)
- 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
what is second deg AV block + causes? (3)
- 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)
what is third deg AV block + causes?
- no relationship betw P and QRS (regular PP & RR intervals)
1. aging
2. injury to AV node or His bundle (MI involving RCA, myocarditis)
what are the symptoms of bradycardia? (5)
- lethargy
- giddiness
- syncope (periodic loss of consciousness)
- exertional dyspnoea
- asymptomatic
what are the causes of tachycardia?
- abnormal automaticity
- triggered activity
- re-entry
- disorganised activity
what is re-entry in atrium (atrial flutter) + causes?
- atrial contracts repeatedly
- no P waves, sawtooth baseline
- regular/irregular RR intervals depending on deg of AV block
what is ventricular tachycardia? (re-entry)
- HR>100
- QRS broad & bizarre (ventricular depolarization doesn’t involve His bundle, occurs in diff direction)
what is atrial fibrillation? (disorganised activity)
- no p waves
- irregularly irregular RR intervals (AV nodes filters some signals irregularly)
what is ventricular fibrillation? (disorganised activity)
- associated w cardiac arrest
- no cardiac output
- ecg is a mess of waves
what is atrial ectopic (AA/TA in atrium)?
- 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
what is atrial tachycardia (AA/TA in atrium)?
- HR>100bpm
- QRS narrow (sinus)
- P preceding QRS but with diff P wave morphology
what is ventricular ectopics? (AA/TA in ventricles)
QRS broad & bizzare, interrupting normal sinus rhythm (depolarisation occurs in diff direction, takes longer, doesnt’ involve His bundle)
what is sinus tachycardia + causes (2)
- 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)
what are the symptoms of tachycardia? (5)
- palpitations
- giddiness
- syncope
- cardiac arrest
- asymptomatic
what is valvular stenosis?
narrowing of valve/failure to OPEN completely→ prevents forward flow
what are the possible causes of stenosis? (3)
- post inflammatory scarring/fibrosis
- calcifications (deposits)
- congenital
what is valvular regurgitation/incompetence?
failure of valves to CLOSE completely→ allows reverse flow
what are the causes of regurgitation/incompetence? (4)
- post inflammatory scarring
- genetic/developmental e.g. marfan syndrome
- degenerative
- infectious (destroys valves)
what is infectious endocarditis?
microbial infection of cardiac valves/endocardium→ vegetation→ tissue destruction
(affects MV/AV more aka left side)
what is subacute vs acute infectious endocarditis?
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)
what is rheumatic fever?
- abnormal response to grp A strep pharyngitis
- leads to rheumatic heart disease!! (permanently damages heart valves)
what is rheumatic heart disease?
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
what is pericardial effusion?
- 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)
what is tetralogy of fallot?
CYANOTIC congenital heart disease
1. pulmonary stenosis
2. RV hypertrophy
3. VSD
4. overriding aorta
what is transposition of great arteries?
CYANOTIC congenital heart diease
- aorta arise fr RV, PT from LV (swapped)
- deoxygenated blood fr body→ RA→ RV→ aorta→ rest of body
what is coarctation of aorta?
ACYANOTIC congenital heart disease
- narrowing of aorta @ certain parts
what is the definition of hypertension?
persistent high bp
systolic: >140mmHg
diastolic: >90mmHg
what are some of the etiologies of primary hypertension?
(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)
what are the causes of secondary hypertension? (5)
Renal
Endocrine (hypercortisolism, pheochromocytoma)
Neurologic
Aortic (coarctation, atherosclerosis)
Labile (psychogenic, stress-related)
what is the only cause of BOTH hypertension and tachycardia happening concurrently? (usually pt only has HT because heart compensates by decreasing HR)
pheocytochroma (tumour of adrenal gland) that causes activation of SNS→ tachycardia despite HT
what are some of the consequences of hypertension?
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
what type of hypertension leads to what type of arteriolosclerosis? (2)
benign HT→ hyaline arteriolosclerosis
malignant HT→ hyperplastic arteriolosclerosis
what are aneurysms?
localised abnormal dilation of blood vessels/heart (usually w superimposed atherosclerosis in vessel walls)
what are the causes of aneurysms?
- atherosclerosis
- hypertension
- fibrosis (e.g. trauma, infections, vasculitis)
- congenital defects
what are the clinical manifestations of aneurysms?
- asymptomatic
- rupture
- embolism fr atheroma/thrombus formed
- impingement on adjacent structures (pain, constipation)
what is aortic dissection?
tear in intimal layer of aortic wall
how does aortic dissection occur?
hypertension→ hypertrophy of vessels supplying aorta→ degenerative/ischaemic injury to arteriolar walls→ weakening/necrosis of aortic wall→ dissection
what are the clinical presentations of aortic dissection?
obvious sharp shooting pain between scapulae (back)
what is atherosclerosis?
thickening/blocking of arteries due to buildup of plaque
what factors/modifiable risk factors predispose pts to atherosclerosis? (4)
- high cholesterol
- hypertension (cause damage to blood vessels→ fats in blood can collect there→ atheroma)
- smoking
- diabetes
(three highs + smoking)
what is an atheroma?
plaque consisting of raised lesion w a soft, yellow core of lipid covered with a white fibrous cap
what is the pathogenesis of atheroma formation?
(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
what are vulnerable/unstable plaques?
- dangerous plaques with relatively larger lipid core & thin fibrous cap/collagen content (ruptures easily)
- more likely to rupture, fissure, ulcerate & hemmorhage
what are the clinical consequences of atherosclerosis? (3)
- vessel thickens→ narrows lumen→ poor tissue perfusion→ ISCHAEMIA & ANGINA
- loss of elasticity→ predisposition to ANEURYSM→ possibly rupture & hemorrhage
- endothelial changes→ ruptures→ release prothrombotic atheroma contentspre→ THROMBOSIS→ infarction
what are the clinical manifestations of ischemic heart disease? (4)
- angina
- myocardial infarction
- chronic ischemic heart disease w heart failure
- sudden cardiac death
what is angina?
mismatch between ability of coronary circulation to supply blood to HEART muscles, and its metabolic requirements
name and describe the 3 forms of angina
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
what are the characters of angina? (4)
- location: chest/epigastric area
- radiation: pain radiates fr chest to left arm
- nature: crushing pain, discomforting sensation
- precipitated by exertion, relieved by rest
what are the causes of angina?
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
what is myocardial infarction?
death of cardiac muscle following impaired blood flow
how is MI clinically diagnosed? (3)
- symptoms: severe, crushing central chest pain (radiates to arms)
- ECG changes
- elevated cardiac enzymes (released when myocyte cell membranes rupture)
describe the change in heart morphology after MI overtime
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
what part of the heart is affected when MI occurs in the left anterior descending artery? + ECG leads
antero-septal: leads V1, V2, V3, V4
what part of the heart is affected when MI occurs in the left circumflex artery? + ECG leads
antero-lateral: leads 1, aVL, V5, V6
what part of the heart is affected when MI occurs in the right coronary artery + ECG leads?
inferior: leads 2, 3, aVF
posterior: none
what is chronic IHD w heart failure?
chronic atherosclerotic narrowing of coronary arteries→ slow/constant loss of myocardial fibres→ insidious cardiac failure→ death
