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L5: Heart Failure - Coggle Diagram
L5: Heart Failure
Symptoms
Shortness of breath
Less O2
Higher heart rate
Higher sympathetic tone (brain)
Stimulation of heart nerves to increase heart rate (for more O2 throughout body)
Larger heart size
Not sympathetic NS related
Blood remaining in heart --> expansion in volume
Peripheral Edema
Less renal perfusion (less Na+ excretion)
Renin release
angio I (inactive; converted to angiotensinogen)
angio II (POWERFUL VASOCONSTRICTOR)
aldosterone release
Na+ retention, H2O retention
Pulmonary edema
Left ventricle failure (pumps to body)
higher pulmonary vein pressure (less leave heart; more waiting to enter)
Fluid extrusion into interstitial lung spaces
Consequences
Less Ca2+ available for contraction
Need digitalis glycoside drug
More renal absorption of Na+ (less excreted)
Need diuretics
More renin/angiotensin activity upon conversion
Need ACE (converting enzyme) inhibitors
Less cAMP generation (weaker contractility)
Need phosphodiesterase inhibitor
Antioxidant impairment (Higher ox stress)
More MDA & less thiol group in plasma
Need antioxidant supplements
Therapeutic Management
Increase contractility :star:
Digitalis glycoside
E.g. Digoxin
More renal blood flow (to kidneys)
Increased Na+ excretion
Less blood volume, lessened heart workload
Selective inhibition on Na/K pump & ATPase
More intracellular Na+/Ca2+
Less K+ in cell
Cardiac arrythmia risk in elderly patients
Use with spironolactone (K+ sparing drug)
Stronger contractile heart force
Diuretics
More Na+/H2O excretion, less blood vol
Less heart workload (less pump)
Carbonic anhydrase inhibitors
Inhibition of carbonic anhydrase (for smaller heart size)
More Cl- excretion
NaHCO3 excretion
In proximal tubules
Loop diuretics
Less Na+ reabsorbed in loop of Henle (water impermeable) --> site of most reabsorption
Medulla becomes less hypertonic (less water; more conc)
SIgnificant increase in excretion
Thiazides (Outer cortical segment)
Less Na+ reabsorption (More excretion)
No interference with urine conc
K+ loss
Less peripheral resistance (vasodilation)
Long term antihypertensive drug (to lower BP)
Less effective than Loop diuretics
Act on distal convoluted tubule/cortical segment, not proximal tubule
Spironolactone
Competitive antagonist of aldosterone
No K+ loss (blocks aldosterone, which affects Na/K exchange)
Less effective than thiazides
ACE inhibitors
Reduce effects of renin-angiotensin activation
Suppress Na+ reabsorption, edema, renal vasoconstriction (to increase excretion)
E.g. Captopril
Effectiveness
: Loop diuretics > thiazides > spironolactone
Phosphodiesterase Inhibitors
Increase cAMP levels
Improve heart failure
Ivabradine
Slower heart rate
Less heart workload
Sacubitril
Inhibits neprilysin
Prevents breakdown of Na+ excretion causing peptides (promote excretion)
Less Na+, less blood volume
Less heart workload
Starling Relationship
increasing end-diastolic BP
stretching myocardial fibres
More contractility, higher cardiac output (more blood pumped)
BEYOND certain point
increasing end-diastolic BP
less cardiac output
Less venous return to the heart
