week 3 Flashcards
how do semilunar valves operate (what is their key differentiation from AV valves)
They close and open according to pressure gradients
They lack papillary muscles and chordae tendinae
what are the three layers of valves
fibrosa (innermost)
spongiosum
Ventricularis/atrialis (superficial)
what is sound 1
av valves closing
what is sound 2
SL valves closing
what is sound 3
rapid ventricular filling
what is sound 4
atrial contraction and turbulent blood in filled ventricles
what are pathological causes for the splitting of second heard sound
bundle branch blocks
frank starling mech 7 steps
greater venous return
greater end diastolic volume
greater preload
greater muscle tension
greater force of contraction
greater ejection fraction
greater cardiac ouput
what regulates cardiac work
baroreceptor reflex
arterial pressure
physiological responses to exercise in terms of circulation 4
- vasodilation of skeletal muscle BVs
- vasoconstriction of GIT
- Increased muscle pumping
- sympathetic activation: noradrenaline and adrenaline release
arterial pressure
cardiac output is inversely proportional to peripheral resistance
parasympathetic response in cardiac control
vagal
acts on sa and av node, reduces rate of firing
fast action
sympathetic response
causes chronotropy and inotropy through noradrenaline release
also causes vasoconstriction
baroreceptor mech
baroreceptors in aortic arch and coronary sinues
signal to cardio centre in medulla
either parasympathetic or sympathetic result
key vasoconstricors 3
adrenaline
vasopressin/ADH
angiotensin 2
key vasodilators 2
tissue derived vasodilators (metabolically driven) ex. adenosine
endothelium derived vasodilators ex. nitric oxide
what is the autoregulatory method for blood flow to the brain
myogenic mechanism: increased intravascular pressure->cerebral arteries constrict to prevent excessive blood flow, decreased intravascular pressure-> dilate to increase blood flow
metabolite concentrations will also influence
three broad groups for HF causation and their subgroups
myocyte related: ischaemia, toxins, trauma, CAD, myocarditis
Conduction related: Arrhythmias
Loading related: Hypertension, PAD
Pathophysiology mech of HF 6 steps
index event
reduced cardiac output
compensatory mechanisms
secondary organ damage
LV remodelling
further decline
the 3 compensatory mechanisms in HF onset
RAAS activation
Sympathetic activation
Natiuretic peptide release
what are the physical changes in HF that occur
LV remodelling including dilatation, hypertrophy and fibrosis
history symptoms of HF 5
swelling
dyspnoea
orthopnoea
fatigue
exercise intolerance
clinical symptoms in HF 3 right sided
raised JVP
added S3 sound
pitting oedema
what does an echocardiogram assess in HF 3
LV ejection
dilatation
diastolic function
reason for dyspnoea in HF
reduced cardiac ouput
backflow
increased pulmonary pressure
pulmonary congestion and oedema
increased blood air barrier
impaired gas exchange
reason for peripheral oedema in HF
low cardiac output->backflow->increased venous pressure->fluid enters interstitium
acute management of HF
furosemide
Sublingual GTN
supportive care ex. oxygen
role of sublingual GTN in acute HF management
vasodilator to reduce preload and afterload
long term drug management Hf
ARNI
beta blocker
Mineralcorticoid receptor antagonist
SGLT2 inhibitors
what can worsen HF (think in terms of 3 broad categories CVD, health, external)
CVD: Arrhythmias, MI, CAD structural abnormalities
Health: Infection, hypertension
External: Drugs, chemo, diet
drugs which precipitate HF 4
some chemotherapy drugs
tricyclic antidepressants
NSAIDs
calcium channel blockers
r sided HF complications 5
L. HF
Peripheral oedema
hepatic congestion->cirrhosis
renal congestion->renal dysfunction
abdominal congestion->ascites
l. sided complications 5
pulmonary oedema
pulmonary congestion
pulmonary hypertension
fatigue
exercise intolerance
reasons for valvular regurgitation to occur (physiological) 3
abnormal leaflet closure
muscle dissection
congenital/structural abnormalities
reasons for valvular stenosis to occur (physiological)
calcification
stenosis pre/para valvular
pathological reasons for valvular disease 7
ageing
RHD
infective endocarditis
Medications
trauma
Connective tissue disorders
congenital abnormalities
characteristics of aortic stenosis 4
systolic, radiates to carotids, loudest on phonocardiogram, highest pressure
characteristics of aortic regurgitation 3
early diastolic murmur, second loudest on phonocardiogram, greatest volume
characteristics of mitral regurgitation 5
pan systolic murmur, low pressure, higher volume, radiates to axilla, third loudest
role of clinical geneticist
medical doctor
role of genetic counsellor
non directive advise about tests and diagnoses
people involved in the multidisciplinary genetics team 3
genetics counsellor
clinical geneticist
psychologist
