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IC > Heart Failure > Flashcards

Heart Failure Flashcards

1
Q

Def of heart failure

A
  • inadequate cardiac output

- oxygen delivery reduced

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2
Q

New york heart association classification

A

limitation of physical activity
Class I- no limitation
II- slight limitation with ordinary physical activity
IV- inability to carry on any physical activity

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3
Q

pathophys of heart failure

A

impaired contractility, increased afterload, and impaired ventricular filling

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4
Q

heart failure, systolic dysfunction causes

A

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)

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5
Q

hf, diastolic dysfunction

A

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)

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6
Q

mean electrical axis

A
  • 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
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7
Q

normal mean electrical axis

A

lead 1 and avf is positive

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8
Q

net qrs in LAD

A

lead 1 positive, avf is negative

-hypertrophy due to aortic stenosis, pregnancy, aortic insufficiency

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9
Q

right axis deviation

A

lead 1 negative
avf is positive

-pulmonic stenosis, mitral stenosis, pulmonic insufficiency, infarct in left ventricle

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10
Q

hypertrophy causes

A

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

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11
Q

hypertrophy caused by

A

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)

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12
Q

progression of heart failure

A

-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

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13
Q

left and right heart are arranged in

A

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

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14
Q

SV=

A

SV=EDV - ESV

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15
Q

EF=

A

EF= SV/ EDV

Normal range is .5 to .7
EF is reduced in systolic, not diastolic dysfunction

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16
Q

systolic dysfunction ventricles will be

A

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
17
Q

in diastolic dysfunction EDV will

A

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

18
Q

pulse in systemic artery in heart failure will feel

A

weaker than normal
-decrease in SV leads to decrease in pulse pressure
-

19
Q

pulse pressure is

A

difference in arterial systolic and diastolic pressure

-decrease in SV leads to decrease in pulse pressure

20
Q

Left sided symptoms

A
  • pulmonary edema
  • diaphoresis (sweating)
  • dyspnea, orthopnea, paroxysmal nocturnal dyspnea
  • fatigue
  • tachycardia
21
Q

Right sided

A

right upper quad discomfort (hepatic enlargement)

  • peripheral edema, and JVD
  • diaphoresis
  • tachycardia
22
Q

EDP is increased with

A

systolic (dec SV) and diastolic dysfunction (inc stiffness or impared relaxation of ventricle)

  • pressures upstream will also be increased
  • increased atrial and venous pressure
23
Q

Force for driving fluid out and into interstitial space

A

hydrostatic pressure

-interstitial pressure low under normal conditions

24
Q

interstitial pressure increased when

A
  • 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)
25
Q

peripheral edema

A
  • 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
26
Q

pulmonary edema

A
  • 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
27
Q

common clinical signs in left hf

A
  • dyspnea, orthopnea, paroxysmal nocturnal dyspnea

- due to pulmonary edema

28
Q

why orthopnea in left hf?

A

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

29
Q

baroreflex response to decreased MAP due to decreased CO

A
  • 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
30
Q

Renin-angiotensin system

A

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
31
Q

ADH

A

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
32
Q

Adrenergic nervous system

A
  • 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
33
Q

Using diuretic to prevent pulmonary edema

A

will reduce SV and CO– too much can result in shock

34
Q

Inotropic state

A

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
35
Q

How to decrease afterload in pts with HF

A
  • 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
36
Q

AE of ACE inhibitors in pts with HF

A

-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

37
Q

ANP

A

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

IC (31 decks)

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