PAT202 WINTER > Heart failure > Flashcards

Heart failure Flashcards

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1
Q

what is heart failure?

A

the inability of the ventricles to pump enough blood to meet the body’s metabolic demands.

  • inadequate circulatory volume & pressure
  • results in inadequate perfusion of tissues
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2
Q

what are some disorder that cause heart failure?

A
  • mitral stenosis
  • myocardial infraction (MI)
  • chronic hypertension
  • coronary artery disease (CAD)
  • diabetes mellitus
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3
Q

what are non pharmacological ways heart failure can be reduce?

A
  • controlling lipid levels
  • implementing a regular exercise program
  • maintaining optimum body weight
  • keeping blood pressure w/in recommended limits =reduces CAD and MI
  • HF is a PREVENTABLE condition
  • control salt intake
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4
Q

what is the right side of the heart responsible for?

A

-the right side of the heart receives blood from the venous system and pumps it to the lungs, where the blood receives oxygen and loses it carbon dioxide

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5
Q

what is the left side of the heart responsible for?

A

the right side return the blood to the left side of the heart, which pumps it to the rest of the body via the aorta
-the amount of blood received by the right side should exactly equal that sent out by the left side

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6
Q

what is cardiac output?

A

the amount of blood pumped by each ventricle PER min

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7
Q

what is preload?

A

the degree to which the myocardial fibres are stretched just prior to contraction

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8
Q

what is Frank-Starling law?

A

the greater the degree of stretch on the myocardial fibres, the greater will be the force by which they contract
-think of a rubber band- the more it is stretched, the more forcefully it will snap back
-BUT…as preload continues to rise it causes repeated stretching of myocardium
doesn’t snap back as forcefully
contractility & thus CO is decreased
=HF worsens

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9
Q

what is contractility?

A

the strength of contraction of the heart

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10
Q

what are drugs that increase contractility? (called positive inotropic agents)

A

-norepinephrine, epinephrine, and thyroid hormones

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11
Q

what are drugs that decrease contractility? (called negative inotropic agents)

A

drugs such as beta-adrenergic blockers

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12
Q

what is after load?

A

the pressure in the aorta that must be overcome for blood to be ejected form the left ventricle

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13
Q

what happens in left sided heart failure? (sometimes congestive HF)

A

excess blood accumulates in the left-ventricle

  • the wall of the left ventricle may become thicker (hypertrophies) in attempt to compensate for the extra blood retained in the chamber
  • since the left ventricle has limits to its ability to compensate for the increased preload, blood “backs up” into the lungs, resulting in S/S of SOB, crackles etc.
  • LHF is most common
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14
Q

what happens in RHF?

A

the blood backs up into the peripheral veins, resulting in peripheral edema and engorgement of organs such as the liver

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15
Q

what are the most common S/S of HF?

A
  • dyspnea
  • orthopnea
  • paroxysmal nocturnal
  • fatigue
  • weakness
  • exercise intolerance
  • dependent edema
  • cough
  • weight gain
  • abdominal distention
  • nocturia
  • cool extremities
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16
Q

what are some less common S/S of HF?

A
  • cognitive impairment
  • altered mentation or delirium
  • nausea
  • abdominal discomfort
  • oliguria
  • anorexia
  • cyanosis
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17
Q

what are natriuretic peptides?

A

are substances secreted in response to increased pressure in the heart

  • atrial NP is secreted by the atria
  • B-type NP- is secreted by the cardiac ventricles
  • C-type NP is secreted by the brain
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18
Q

what do ANP and BNP do?

A

they are secreted in response to the left ventricular volume overload and dysfunction
-they cause dieresis and reverse the negative effects of sympathetic nervous system and the renin-angiotensin aldosterone system activation on the heart

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19
Q

BNP is used

A

as a biomarker to diagnosis and establish the severity of HF

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20
Q

all pts w/ left ventricle that ejects less than 40% should

A

be treated w/ triple therapy either ACE or ARB, a beta blocker, and mineralocorticoids receptor antagonist (MRA)

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21
Q

what type of med would you give a pt w/ peripheral edema or pulmonary congestion?

A

diuretics

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22
Q

what are the primary pharmacotherapy goals of Hf?

A
  • reduction of preload
  • reduction of systemic vascular resistance (afterload reduction)
  • inhibition of both the renin-angiotensin aldosterone system (RASS) and the vasoconstrictor mechanisms of the SNS
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23
Q

when should ACE inhibitors be discontinued?

A

-if pt is experiencing angioedema (ex. facial swelling or difficultly breathing)

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24
Q

how do ACE inhibitors work?

A

act by preventing the conversion of angiotensin I to angiotensin II. angiotensin II is a potent vasoconstrictor and also contributes to aldosterone secretion

  • ace inhibitors decrease BP through systemic vasodilation
  • inhibits the aldosterone exception by enhancing excretion of sodium and water and decrease blood volume
  • reduces preload, after load, and blood volume= decrease workload of the heart
  • also dilates the veins
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25
common side effect of an ACE?
dry productive cough and orthostatic orthostatic hypotension (teach pt to get up slowly) - is reversed when pt is off med - switch to an ARB
26
what should be viewed prior to administration of an ACE inhibitor (Captopril)
the BUN and creatinine should be viewed bc renal insufficiency is another potential side effect of an ACE -hyperkalemia!!
27
what is the first line of drug for HF?
ACE/ARBS bc they reduce peripheral edema and increase cardiac output (replaced digoxin as the drug of choice)
27
what is the first line of drug for HF?
ACE/ARBS bc they reduce peripheral edema and increase cardiac output (replaced digoxin as the drug of choice)
28
what an angiotensin receptor nepriylsin inhibitors (ARNIs)?
a new class (ARNI'S) combo drug of neprilysin inhibitors and and ARB - neprilysin is an enzyme normally present in the body that breaks down natriuretic peptides and other substances that affect fluid balance - blocking neprilysin, the concentration of natriuretic peptides in the blood increase and cardiac efficiency improves
29
when are ACE/ARBS contraindicated?
-in pregnancy and lactation and in clients w/ HX of anigoedmea
30
why should we discontinue diuretics before administering ACE inhibitors?
-to prevent severe hypotension
31
beta-adrenergic blockers and HF?
- slows down the heart rate and decrease blood pressure | - can be used in combination w/ ACE inhibitors as first-line drug for HF
32
when are beta blockers contraindicated?
in clients w/ decompensated HF, chronic obstructive pulmonary disease, bradycardia, heart block, pregnant or lactating clients
33
what are some considerations with beta blockers?
- monitor BP and pulse- notify HCP if pulse is less than 50-60 BPM - report immediately S/S of worsening HF- SOB, edema, chest pain - do not stop taking abruptly - diabetic clients should monitor serum glucose carefully b/c these drugs can cause a change in blood sugar levels
34
what are the two beta blockers approved for treatment of HF?
carvedilol and metoprolol extended-release form
35
what should the nurse do before administering digoxin and why?
check the client's apical pulse before administering the drug bc digoxin slows the heart rate and heart failure may cause a pulse deficit
36
what are the earliest s/s of digoxin toxicity?
anorexia, nausea, and vomiting
37
digoxin and hypokalemia
-increase risk dysthymias (atrial fibrillation or bradycardia)
38
common s/s of digoxin toxicity
- abdo pain - anorexia - N&V - flickering flashes of light - coloured or halo vision - photophobia - blurring - diplopia - scotomata - seeing yellow spots - hypokalemia- tell pt to eat foods rich in potassium - dyshythmias
39
how does diuretic relieve S/S of HF?
reduces fluid volume and decreases blood pressure - great for reducing blood volume, edema, and pulmonary congestion - rarely used alone, usually prescribed w/ ACE and other HF drugs
40
when are diuretics contraindicated?
- pregnancy, lactation, renal dysfunction, fluid and electrolyte depletion and hepatic coma - to be used in caution with pt: hepatic cirrhosis, or nephritic syndrome and in infants and older adults
41
what does the nurse monitor when pt is on a furosemide (Lasix)
potassium- wasting diuretic - monitor serum potassium level - obtain order if potassium is low - check potassium before administering - loop diuretics can cause the excretion of potassium, sodium, and magnesium
42
what is the adverse effect of furosemide?
ototoxicity -the nurse should tell the client to immediately report S/S of hearing loss, dizziness, or tinnitus to prevent permanent ear damage
43
how are coronary artery disease (CAD), and MI r/t HF?
-affects supply of nutrients to cardiac muscle
44
how is chronic and sustained HTN r/t HF?
-heart must pump more powerfully to eject blood
45
how is diabetes mellitus r/t HF?
- insulin resistance, hyperinsulinemia, hyperglycemia have multiple effects on cardiovascular system including endothelial damage → atherosclerosis - also associated with dyslipidemia
46
what are the risk factors for HF?
- ischemic heart disease - obesity - cardiomyopathies - HTN - diabetes - myocarditis - age - renal failure - congenital heart disease - smoking - valvular heart disease - excessive alcohol use
47
how are inflammatory cytokines involved in HF?
- endothelial hormones - endothelin is a potent vasoconstrictor & is assoc. with a poor prognosis in individuals with HF -TNF-α TNF-α is elevated in HF & contributes to myocardial hypertrophy & remodeling it down-regulates synthesis of vasodilator nitric oxide (NO), induces myocyte apoptosis, and may contribute to weight loss and weakness in individuals with HF (cardiac cachexia) -IL-6 IL-6 is elevated in individuals with severe HF & cardiogenic shock & may contribute to further harmful immune activation
48
how is HF classified?
HF can be classified based on systolic failure vs diastolic failure -systolic – decreased contractility leading to decreased ejection fraction (EF) -diastolic – normal contraction (normal EF) but abnormal relaxation -can be left vs right HF -acute vs chronic (degree of physiologic response) acute-pronounced response in acute HF-rapid symptoms requires immediate care! chronic -more subtle response in chronic HF -many compensatory mechanisms operating
49
what is the normal ejection fraction?
65%
50
systolic HF
-HF with reduced ejection fraction (HFrEF) EF <40% (normal is ~65%) -heart cannot generate adequate CO to perfuse tissues & organs characterized by complex constellation of hemodynamic, neurohumoral, inflammatory, & metabolic processes interaction of these processes results in gradual decline in myocardial function Associated with right sided heart failure
51
diastolic HF
-HF with preserved ejection fraction (HFpEF) heart failure with preserved EF -decreased compliance of left ventricle & abnormal diastolic relaxation -ventricle cannot accept filling with blood without significant resistance Associated with left sided heart failure
52
what are the s/s of left HF?
- pulmonary congestion/edema (cyanosis, inspiratory crackles) - dyspnea, orthopena, cough with frothy sputum - fatigue - decrease urine output (oliguria) and edema
53
what are causes of left sided HF?
HTN, MI, & cardiomyopathy
54
what are causes of right HF?
- primary cause is left HF - conditions impeding blood flow into the lungs -pulmonary congestion, pulmonary HTN, COPD, severe pneumonia, PE - conditions compromising pumping effectiveness of right ventricle - right ventricular MI, cardiomyopathy
55
what are S/S of right HF?
jugular venous distention, peripheral edema, hepatosplenomegaly
56
pathophysiologic process of left HF?
-inability of the heart to generate adequate cardiac output to perfuse vital tissues
57
pathophysiologic process of right HF?
inability of the heart to provide adequate blood flow into the pulmonary circulation at a normal central venous pressure
58
how dose increase SNS activity (catecholamines released) make HF worse?
- triggered d/t decreased SV & decreased CO - increases HR & force of contraction, also increases peripheral vascular resistance - but combined, cardiac workload is increased & HF worsens
59
how does activation of RAAS system worsen HF?
- kidneys release renin d/t decreased CO _ decreased renal perfusion & decreased GFR - promotes vasoconstriction & volume retention _ raise BP - but aldosterone increase preload and angiotensin II increases afterload =HF worsens
60
how dose ADH (antidiuretic hormone vasopressin) make HF worse?
-causes peripheral vasoconstriction & renal fluid retention -but exacerbates hyponatremia & edema (preload) and afterload =HF worsens
61
how do NP's make HF worse?
secreted in response to increased volume overload & dysfunction ANP from atria BNP from ventricles biomarker to dx & establish severity of HF cause diuresis & reverse negative effects of -but chronic HF leads to depletion of NP'S =HF WORSENS
62
what is cardiomyopathies?
most are result of remodeling caused by effect of neurohumoral responses (increase SNS activity) to ischemic heart disease or HTN on heart muscle
63
what is dilated cardiomyopathy
Impaired systolic function, leading to increases in intracardiac volume, ventricular dilation, systolic dysfunction & HF
64
what are causes of dilated cardiomyopathy?
- ischemic heart disease - valvular disease - diabetes - alcohol - drug toxicity - renal failure - hyperthyroidism - deficiencies of niacin vitamin D, and selenium - infection
65
what is hypertensive hypertrophic cardiomyopathy?
``` -Occurs d/t increased resistance to ventricular ejection seen in HTN -Hypertrophy of myocytes attempts to compensate for increased myocardial workload -Myocyte dysfunction develops over time -first diastolic dysfunction -then systolic dysfunction -HF ```
66
what is premature ventricular contractions (PVCs)?
-not normally serious unless it occurs at high frequency- is is a common cause of irregular heart rhythms -effects= decreased cardiac output from loss of atrial contribution to ventricular preload for that beat treatment= -drugs to change thresholds & refractory periods reduce myocardial demand & increase supply
67
what is ventricular tachycardia?
-often >150 bpm up to 200 bpm -life threatening -high risk of sudden death -effect= decreased cardiac output from loss of atrial contribution to ventricular preload -increased myocardial demand d/t tachycardia
68
what is deep venous thrombosis? (DVT)
-Thrombosis/clot in large vein flow & pressure are lower in veins than in arteries -Detached thrombus thromboembolus can lead to PE -Venous stasis (associated with immobility, obesity, prolonged leg dependency, age, HF) test- d-dimer & droppler
69
what are the S/S of DVT?
- pain - unilateral leg swelling - dilation of superficial veins - calf tenderness - mottled or cyanotic skin - can be asymptotic so prevention is important!!
70
what is PE?
-PE is occlusion or partial occlusion of pulmonary artery or its branches by an embolus results from embolization of clot from DVT may also originate in right heart -Risk factors for PE conditions & disorders that promote blood clotting as result of venous stasis (immobilization, HF) -PE can cause infarction or occlusion if thrombus is large enough, infarction of lung tissue, dysrhythmias, decreased cardiac output, shock, & death are possible -Tests D-dimer & CT arteriography serum troponin I levels as risk increases with right ventricular dysfunction
71
what are the S/S of PE?
``` PE can present with sudden onset of pleuritic chest pain cough dyspnea tachypnea tachycardia unexplained anxiety occasionally syncope or hemoptysis with large emboli, pleural friction rub, pleural effusion, fever, and leukocytosis may be noted ```
PAT202 WINTER
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