Heart failure and Cardiovascular Shock Flashcards
Preload
The volume of blood stretching the ventricles at the end of diastole, before the next contraction
Afterload
-The peripheral resistance against which the left ventricle must pump
- Afterload depends on the size of the ventricle, wall tension, and arterial BP
Contractility
- Ability of heart muscle to shorten or contract
- Contractility can be increased by Epinephrine and Norepinephrine released by the SNS
Ejection Fraction
- Percentage of end-diastolic blood volume that is ejected during systole
- Ejection fraction provides information about the function of the left ventricle during systole and is a calculation used to determine the severity of heart failure on the left side
Heart failure
A condition where the heart cannot pump blood effectively enough to meet the body’s needs
HF is caused by a loss of critical quantity of functional myocardial cells after injury to the heart from several different causes
equation
Stroke Volume (SV) x Heart Rate (HR) = Cardiac Output (CO)
Cardiovascular (Cardiogenic) Shock:
The heart is severely compromised that it cannot pump enough blood to supply vital organs
left sided heart failure
Blood can’t be pumped out, which results in it backing up into the L. atrium and pulmonary veins
*most common
left sided preload/ afterload
Increase in preload and an increase in afterload
right sided heart failure
Blood backs up into the r. atrium and systemic venous circulation
right side HF areas of blockage
Increases pressure in inferior vena cava and causes hepatic veins to become congested with blood and leads to hepatomegaly and systemic venous congestion
right sided hf preload/ afterload
Decrease in preload and an increase in afterload
systolic HF
Inability to pump blood forward, left ventricle is unable to eject blood properly
Increased preload and increased afterload
diastolic HF
Impaired ability of ventricle to relax and fill during diastole
less blood fills into ventricles
Decreased preload and increased afterload
structural change: thickening
decreased blood volume (holds less blood)-> heart is stiff and weak ->
prevention of proper filling (decreases amount of blood pumped out with each beat)
structural change: Stiff heart (due to collagen accumulation)
impairs hearts ability to contract and relax (decreased contractile force of ventricle)
–> decreased SV and decreased CO
structural change: thinning
dilation -> heart weak -> decreased contractility strength -> harder to pump blood out to the rest of the body (ineffective pumping) -> decreased CO -> decreased tissue perfusion -> increased fluid and sodium retention
structural change: Abnormal valve function
increased pressure -> insufficient blood flow and increased workload on chamber
cellular dysfunction: Sarcoplasmic reticulum disorganization
inefficient calcium handling -> impaired contractility (ultimately leading to decreased CO)
cellular: mitochondrial dysfunction
impaired contractility and decreased CO
cellular: cytoskeletal alterations
change in cell shape and stability -> impaired contractility
patho order
damage to heart-> weakening of heart-> Improper filling and relaxing, or improper pumping and ejecting of blood (can have both) ->
decreased CO
compensatory mechanisms: SNS
baroreceptors sense a decrease in arterial pressure, activating SNS, releasing NE, EP to stimulate beta- adrenergic receptors
result: Increase in HR and ventricular contractility
Increases CO (temporary fight or flight response)
neurohormonal response
Juxtaglomerular Apparatus senses decrease in renal perfusion
activate raas system
result:
Vasoconstriction and increased B/P
Increased CO
ventricular remodeling
initially increases contractility and CO
but Altered ventricle shape increases ventricular mass and wall tension due to myocyte hypertrophy
-Impaired contractility
-Ventricles become larger and less effective at pumping
dilation
Enlargement of chambers/thinning of ventricular wall
-heart muscle stretches
increases: CO/contraction
hypertrophy
Increased muscle mass/cardiac wall thickness (new development of tissue)
increases: CO/ contraction
counter-regulatory mechansims
nitric oxide
released and…
Relaxes arterial smooth muscle vasodilation and decreased afterload
counter-regulatory mechansims
Natriuetic peptides
ANP (arterial natriuretic peptide) and BNP (b-type natriuretic peptide)
Released in response to increased blood volume in heart
Natriuetic peptides result
Vasodilation -> decreased CO
Counteracts effects of SNS and RAAS
cardiovascular shock
1.) Damage to heart
2.) Weakens heart
3.) Decreased CO
4.) Decreased organ perfusion
