LV dysfunction 2 Flashcards
What has evolution allowed us to do with regards to the blood pressure?
Development of renin-angiotensin system which has allowed us to conserve blood volume and pressure allowing correct perfusion of blood to all organs
What is the renin-angiotensin pathway?
Angiotensin released from the liver. Renin produced and released from the kidney. Renin converts angiotensin into Angiotensin I. ACE then converts Angiotensin I –> Angiotensin II which stimulates reabsorption of Na+, salt retention and release of aldesterone (which promotes Na+ conservation)
What are the impacts of the sympathetic NS on the heart?
Stimulates production of NA –> increased force of contraction, vasoconstriction, increased C.O, increased peripheral resistance
How are compensatory mechanisms advantageous in acute blood loss?
Tachycardia - increased cardiac output
Increased stroke volume
Vasoconstriction to increase the blood pressure
Retention of Na+/H20 to increase circulatory volume (and increase BP)
How are compensatory mechanisms bad in heart failure?
Increased HR and +ve inotrophic effects increase the work load of the heart and +ve inotrophic effects
Vasoconstriction = increased afterload
Chronic adrenergic stimulation = arrhythmias and toxicity of the myocardium
H20/Na+ retention - oedema and increased preload
What are angiotensin and Aldesterone?
Angiotensin – peptide hormone stimulates vasoconstriction and increased BP
Aldesterone – steroid produced in ther adrenal gland which promotes conservation of Na+ in various areas of the body
ACE INHIBITORS:
- clinical indicators
- mechanism
- impacts
ENALAPRIL
- prevent the ACE from producing Angiotensin II
- used to treat HF and hypertension
- Reduce left ventricular dysfunction, decreased mortality in patients that enter HF after MYOIN, decrease overall probability of death
ADVERSE EFFECTS ACE—–|s associated with downreg of mechanism of angiotensin II
Hyperkalaemia
Hypotension
Acute renal failure
Teratogenic effects during pregnancy
ADVERSE EFFECTS ACE—–|s associated with increased kinin levels
ACE also breaks down BRADYKININ (isnt inactivated therefore)
Cough, rash, allergic reactions —> inflammatory effects
B blockers
- clinical indicators
- mechanism
- impacts
PROPANOLOL / BISPROLOL
- prevent binding of NA to B1/B2 receptors –> treatment of angina, arrhytmia, HF and hypertension
- increased probability of survival / event-free survival
- have to use in very small doses and up titrate very slowly
B blocker selectivity –> some are more selective than others !!!
B blockers are cardioselective –> block mainly B1 receptors IN THE HEART
As you increase the dose, the less selective the drug becomes. Some drugs are more selective than others
ADVERSE EFFECTS OF B BLOCKERS
Headaches, depression, nightmares, fatigue, sleep disturbance
Vascular - hypotension, bradycardia, cold peripheries, erectile dysfunction
Can also worsen other illnesses – asthma, raynauds. heart failure !!!! (counteract the bodys mechanisms that work to solve heart failure – causes compensatory mechanisms of sympa NS to reverse)
IVABRADINE - how does it work? is it effective?
Slows the sinus node firing by inhibiting the funny current
Used to treat angina and heart failure
Significant benefit to hospitalisations
DIGOXIN - how does it work? is it effective?
- stimulates the contraction of the heart
- limited use in treatment of heart failure
- does improve hospitalisations
VALSARTAN - how does it work? is it effective?
AngiotensinII blocker
Decreases production of natriuretic peptides
Decreases CV deaths and hospitalisations
useful in combiation with ACE—|
