Heart Failure Flashcards
Def of heart failure
- inadequate cardiac output
- oxygen delivery reduced
New york heart association classification
limitation of physical activity
Class I- no limitation
II- slight limitation with ordinary physical activity
IV- inability to carry on any physical activity
pathophys of heart failure
impaired contractility, increased afterload, and impaired ventricular filling
heart failure, systolic dysfunction causes
problem with ability to generate force- diminished capacity to eject blood from affected ventricle due to impaired myocardial contractility or increased afterload–> decreased SV
-increased afterload (htn, pulmonic or aortic stenosis) or impaired contractility (MI, chronic volume overload, transient MI, dilated cardiomyopathy)
hf, diastolic dysfunction
impaired ventricular filling- increased stiffness of ventricular wall or reduced ventricular relaxation during diastole (impaired nrg production/cellular metabolism- impairs passive stretch)
-obstruction of ventricular filling (tricuspid or mitral stenosis, pericardial tamponade), or impaired ventricular relaxation-preload reduced–>
stroke volume reduced (ventricular hypertrophy, hypertrophy cardiomyopathy, restrictive cardiomyopathy, transient MI)
mean electrical axis
- look at lead 1 and lead avf
- magnitude and direction of ventricular depolarization determined by balance of currents in right and left ventricle
- since left ventricle normally is thicker, it will point towards left ventricle
normal mean electrical axis
lead 1 and avf is positive
net qrs in LAD
lead 1 positive, avf is negative
-hypertrophy due to aortic stenosis, pregnancy, aortic insufficiency
right axis deviation
lead 1 negative
avf is positive
-pulmonic stenosis, mitral stenosis, pulmonic insufficiency, infarct in left ventricle
hypertrophy causes
increased force of contraction- adequate SV
-however, cells will get bigger and this increases diffusion distance from interior of cell to capillaries- more likely to lead to hypoxia
hypertrophy caused by
pressure overload, volume overload, regional dysfunction with volume overload leading to inc cardiac work, inc wall stress, hypertrophy, inc heart size and mass, fibrosis, inadequate vasculature
-bc ventricles are bigger it can lead to arrythmias (fatal), heart failure (systolic/diastolic dysfunction)
progression of heart failure
-as cardiac output decreases, inc firing of sympathetic nerves–> neurohumoral activation–> further hypertrophy, ang II causes myocytes to enlarge, increased oxygen consumption–> apoptosis or necrosis–> systolic dysfunction
baroreflex compensatory responses to lower MAP will accelerate development of heart failure
50% mortality in 5 years
left and right heart are arranged in
series
-must pump same amt of blood per minute
CO=HRxSV
PBF=HRxSV
If left side fails, then return to right side will be lower and CO from right side will also decrease
SV=
SV=EDV - ESV
EF=
EF= SV/ EDV
Normal range is .5 to .7
EF is reduced in systolic, not diastolic dysfunction
systolic dysfunction ventricles will be
overfilled compared to normal
- congestive heart failure
- force of contraction is reduced- less blood is ejected- EDV is increased and ventricle is overfilled
- End diastolic pressure is increased- LA pressure and pulmonary venous pressure is increased; SV is decreased
- Reduced EF
- Po curve is shifted downwards compared to healthy person
in diastolic dysfunction EDV will
EDV will be reduced,
shift in passive filling curve upwards because compliance of ventricles are reduced
-results in decreased SV because not filling
-End diastolic pressure is elevated (LA and pulmonary venous pressure elevated)
-EDV and SV decreased- no change in EF
pulse in systemic artery in heart failure will feel
weaker than normal
-decrease in SV leads to decrease in pulse pressure
-
pulse pressure is
difference in arterial systolic and diastolic pressure
-decrease in SV leads to decrease in pulse pressure
Left sided symptoms
- pulmonary edema
- diaphoresis (sweating)
- dyspnea, orthopnea, paroxysmal nocturnal dyspnea
- fatigue
- tachycardia
Right sided
right upper quad discomfort (hepatic enlargement)
- peripheral edema, and JVD
- diaphoresis
- tachycardia
EDP is increased with
systolic (dec SV) and diastolic dysfunction (inc stiffness or impared relaxation of ventricle)
- pressures upstream will also be increased
- increased atrial and venous pressure
Force for driving fluid out and into interstitial space
hydrostatic pressure
-interstitial pressure low under normal conditions
interstitial pressure increased when
- capillary pressure increases when arterioles dilate or increased venous pressure (promotes filtration)
- oncotic pressure decreases (decreased plasma protein, decreased reabsorption)
- vascular permeability (mast cell degranulation, leukocyte adherence)
- lymphatic vessels obstructed (remove small amts of protein that leak out)
peripheral edema
- caused by right sided HF
- increase diffusion distance b/w capillaries and cells- impair O2 delivery to cells
- inc interstitial pressure will compress venules and veins- reducing organ blood flow
pulmonary edema
- impair diffusion from alveolar air to lung
- lower O2 levels resulting in tissue hypoxia
- pulmonary arterioles vasoconstrict in response to low O2 levels (systemic arterioles dilate in response to hypoxia) –> inc pulmonary vascular resistance–> pulmonary htn
common clinical signs in left hf
- dyspnea, orthopnea, paroxysmal nocturnal dyspnea
- due to pulmonary edema
why orthopnea in left hf?
when laying down, venous return to heart increases- increased filling of heart increases ventricular edp, atrial pressure, and venous pressure–> promotes pulmonary edema by increasing pulmonary capillary pressure, increasing filtration
baroreflex response to decreased MAP due to decreased CO
- dec firing of baroreceptors in carotid arteries and aorta will–>
- increased SYM firing will activate- beta1 receptors, increasing HR and SV; alpha1 receptors which cause arteriolar constriction (inc TPR) and venoconstriction (inc venous return)
- dec PARA firing increases HR
Renin-angiotensin system
Decrease in MAP increases renin release from kidney
- causes constriction of vasc smooth muscle (inc TPR)
- stimulate ventricular myocyte growth
- inc aldosterone release from adrenals (sodium and water retention)
- inc blood volume–> inc severity of edema
ADH
Dec MAP will inc release of ADH
- decrease water excretion and inc blood water
- inc venricular EDP and EVP, inc severity of edema
- ADH constricts systemic arterioles
Adrenergic nervous system
- Decrease in MAP results in inc SYM via baroreflex (dec PARA)
- Chronic sym of heart results in down regulation of beta 1 receptors
- decreases inotropic state of heart- lowering CO and decreases sensitivity of heart to catecholamines
- can also promote cell death
- can also cause oxidative stress via ROS within myocytes- -leakage of Ca from SR– inc Ca during diastole–> diastolic dysfunction
Using diuretic to prevent pulmonary edema
will reduce SV and CO– too much can result in shock
Inotropic state
down regulation of beta 1 receptors in some pts with HF
- not possible to inc CO by increasing inotropic state with catecholamines
- must inc SV by decreasing afterload
How to decrease afterload in pts with HF
- ACE inhibitors- will decrease afterload due to lower ang II levels (lower TPR) and this will inc SV
- Will decrease blood volume due to lower aldosterone levels- reducing EDV and dec likelihood of pulmonary edema
AE of ACE inhibitors in pts with HF
-ACE inhibits will decrease diastolic pressure
If diastolic pressure is too low, myocardial ischemia can occur because coronary blood flow to LV is greatest during diastole
ANP
Stretch of atria due to inc blood volume elicits ANP release
-ANP acts on kidney to induce sodium excretion into urine- reducing plasma volume
ANP is also a vasodilator
-Levels increased in CHF
