General aspects of CV diseases. Clinical aspects of Heart Failure Flashcards
What is the CV system comprised of?
Heart- pump and endocrine
Vessels- diameter and integrity
Blood- vol, viscosity, O2 carrying (PCV, Hgb, pH)
What id CV insufficiency and what are the 2 main causes
CO is not sufficient enough to deliver the required amount of O2 to the tissues
- Heart failure (can lead to central shock)
- Periph circ failure= periph shock
Periph circ failure: causes and compensatory mechanisms
Decreased BV and dilatoin of vessels!!
Acute compensatory reaction: symp alarm reaction- vasoC of non-vital organs, incr HR and contraction
Tre`tment: REPLACE blood vol
Heart failure:
primarily due to HD and secondary due to the cardiac changes (often induced by the HD)
- Phys and haemodynamic
- Neurohormonal
- Inflamm- cytokines and FR’s
Phys/ haemodynamic aspects of HF
Preload
Afterload
Contractility
HR
Distensibility
Synch of beats (rhythm)
Frank-Sterling law
Preload!!
Incr length of myocytes– incr sensitivity of myofibrils to Ca– incr amount of Ca released for SR
The greater the venous return- the greater the contraction required to pump it
PAtho: overdilation- because the venous return is too high– congestion in venous system– at this point the cobtractility does not increase anymore.
The P in the LV will transfer to the L atrium– puml veins– pulm edema
P in RV– ascites
Leplace Law
Afterload (the P the heart must overcome to open Aorta and pump blood)
Incr in wall thicknedd to overcome an incr in P
Incr ejection P is caused by a decreased volume
Tension should be high (using O2 and E) during dilation of the wall, even if arterial P is normal
Training hypertrophy- does not induce increased wall stress
Distensibility
Depends on the cardiac muscle itself e.g if there is hypertrophy OR if there is anything compressing the heart e.g fluid in the pericardium
Results: DECREASED left ventricular vol i.e diastolic filling i.e preload
Preload
Stretch of myocytes
It increases
Leads to congestion and an increased O2 demand (is this because the myocytes are stretching more therefore require more O2??)
Afterload
Increases at beginning, the decreases.
Hypertrophy which requires more O2.. always detrimental
Contractility
Increases!!
Higher O2 and E demand
HR
Increases and then decr.
Correlates with SV because if there is more blood to be pumped then will beat faster. But if v high (above 180)- could mean that there is not enough time for diastolic filling
Distensibility
Increases!! is always patho- there is an increased O2 and E demand
Rhythm
Decreases (sunch of heart beats)
Top priorities in compensation of HF
Sustain BP in vital organs (brain heart and kidneys)
Sustain BP in other organs
Keep preload low!!! i.e keep venous P low
Neurohormonal comp process (4)
Incr HR but decr diatolic filling and coronary flow
incr myocardial activity/contraction- leads to hypertrophy and incr O2 and E demands
Periph vasoC… but incr afterload
Incr blood vol- RAAS which incr preload, it is our third priority to keep this low– patho overcompensation (because the cells detect a decr in BP-salt and water reabs to incr circ vol, alsoc vasoC)
Neural compensation
baroreceptors Detects decr in BP– Incr symp tone!!!!- if chronic baroreceptor stim then down reg of beta1 especially
Later AT2 also incr symp
+ ino, lsuio and chrono tropic
VasoC
Arrhythmias
Incr renin
Decr parasymp
RAAS
Na and H2O reabs
K excretion
VasoC
Incr symp tone
Local: myocardial fibrosis, apoptosis and necrosis, hypertrophy
Cardiac remodelling (is this because of Aldosterone?)- ECM production
Arrhythmias
