Heart Failure Notes Flashcards

1
Q

What are the two ways that can cause heart failure within the heart?

A

Defect in ventricular systolic function/ LV contraction (HFrEF)
Defect in ventricular diastolic functioning/filling (HFpEF)

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2
Q

2 main RF for HF

A

HTN

CAD

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3
Q

Pathophysiology of Left Sided HF Systolic (HFrEF)

A

LV does not have enough pressure to push blood out of the aorta.
Heart dilates and enlarges to compensate but the heart cannot generate enough Stroke Volume (SV) and Cardiac Output (CO).
LV pressure increases.
LV fails and blood is backed up into the LA.
Lungs will have too much fluid and it will spread into the alveoli and interstitium.

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4
Q

Pathophysiology of Left Sided HF Systolic (HFrEF)

A

LV does not have enough pressure to push blood out of the aorta.
Heart dilates and enlarges to compensate but the heart cannot generate enough Stroke Volume (SV) and Cardiac Output (CO).
LV pressure increases.
LV fails and blood is backed up into the LA.
Lungs will have too much fluid and it will spread into the alveoli and interstitium.

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5
Q

LVEF in HFrEF (Systolic)

A

<40%

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6
Q

Pathophysiology of Left Sided HF Diastolic (HFpEF)

A

LV is stiff and noncompliant, creating high filling pressure.
Decreased ventricular filling leads to decrease SV and CO.
Too much fluid in the lungs because they can’t get into the heart and it will spread to alveoli and surrounding tissues.

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7
Q

LVEF in HFpEF (Diastolic)

A

41-49%

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8
Q

What are the 3 things that can determine if it is a HFrEF or HFpEF?

A

Based on
Signs and symptoms of HF
Normal LVEF
Evidence of LV diastolic dysfunction by echocardiography or cardiac catherization

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9
Q

Pathophysiology of Right Sided HF

A

RV does not pump effectively

Fluid backs up into the venous system aeb systemic symptoms (peripheral edema, abd ascites, etc.)

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10
Q

What is the most common cause of Right side HF?

A

Left sided HF

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11
Q

Pathophysiology of Biventricular HF

A

Both ventricles cannot pump ineffectively leading to fluid build up and systemic venous engorgement.

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12
Q

What are the compensatory mechanisms?

A

Renin Angiotensin Aldosterone System (RAAS)
Sympathetic Nervous System (SNS)
Ventricular Dilation
Ventricular Hypertrophy

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13
Q

RAAS purpose

A

Increase preload and ventricular contraction to maintain CO

Retains Sodium and Fluid, Excretes Potassium

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14
Q

Pathophysiology of RAAS

A

Decrease CO will let the kidneys activate Renin.
Renin will be converted to angiotensinogen to Angiotensin I.
Angiotensin I will be converted to Angiotensin II in the lungs.
Angiotensin II is a strong vasoconstrictor that stimulates water and sodium retention and allows aldosterone to be released from adrenal gland.
Aldosterone will also retain water and sodium, waste potassium and allow myocardial fibrosis (thickening of heart scar tissue).

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15
Q

Pathophysiology of SNS

A

Low arterial pressure will get the SNS to release Catecholamines (norepinephrine and epinephrine).
Catecholamines will stimulate B-adrenergic heart receptors into increasing HR and ventricular contractility.
This will increase O2 consumption of the heart.

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16
Q

What will happen with continuous neurohormonal responses (RAAS and SNS)?

A

High ADH (antidiuretic hormone) levels, endothelin and proinflammatory cytokines.

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17
Q

Endothelin and Proinflammatory purpose (Short and Long term use)

A

Reduce ventricular contraction.

Chronic use: Increase heart’s workload, progressive LV dysfunction, myocyte hypertrophy and ventricular remodeling.

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18
Q

Dilation

A

Enlargement of heart chambers that allows an increases in preload but no increase in CO.

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19
Q

Frank-Starling Law

A

Strength of heart’s contraction is directly proportional to its diastolic expansion.

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20
Q

Hypertrophy

A

Increase in muscle mass and heart wall thickness that develops slowly.
It leads to poor contractility, more O2 demand, poor coronary artery circulation and prone to dysrhythmias.

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21
Q

Remodeling

A

Change in heart structure due to pressure or volume overload, injury and compensatory mechanisms.
It increases ventricular mass, increased wall tension, increased O2 consumption, and impair contractility.

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22
Q

Renal effects of ANP and BNP

A

Increase GFR and diuresis

Sodium excretion

23
Q

Cardiovascular effects of ANP and BNP

A

Vasodilation and decrease BP

24
Q

Hormonal effects of ANP and BNP

A

Aldosterone Inhibition and Renin secretion

Interference with ADH release

25
Nitric Oxide (NO) and Prostaglandin
Relax arterial smooth muscle, vasodilation and decreased afterload.
26
Compensated HF
Compensatory mechanism can maintain adequate CO
27
Decompensated HF
Compensatory mechanisms can NOT maintain CO and inadequate tissue perfusion occurs.
28
Chronic HF C/M:
Fatigue - when doing daily activities and is an early symptom of Chronic HF Dyspnea - most common manifestation of chronic HF Orthopnea PND- paroxysmal nocturnal dyspnea Cough - chronic and nonproductive that’s worse in recumbent position Tachycardia - early sign of HF Palpitations - Atrial Fibrillation is the most common dysrhythmia associated with HF, Edema - most common sign of HF Decreased urine output Nocturia Mottling skin- blue or gray skin color Coolness or clammy to touch Dizziness, lightheadedness and Syncope Sleep apnea Insomnia Chest Pain or Angina Weight changes- due to fluid retention Cardiac cachexia with muscle wasting and fat loss.
29
Interprofessional Care: ADHF stable
``` High Fowler's position with dyspnes Assess v/s, pulse ox, q4hrs Record I&O, daily weights Treat underlying cause Supplemental O2 Drug therapy Circulatory Assist Device Daily weights Sodium and Fluid restricted diet ```
30
Interprofessional Care: ADHF unstable
Continual ECG and O2 saturation monitoring, v/s, urine output q1hr Hemodynamic monitoring- arterial BP, pulmonary artery pressure Continuous CO and Pulmonary Artery Wedge Pressure (PAWP) Supplemental O2 Ultrafiltration Mechanical Cardiac Assist Device Intraaortic Balloon Pump (IABP) Treat underlying cause
31
Ultrafiltration
Treatment for patients with volume overload and regular diuretics isn't working anymore.
32
Mechanical Cardiac Assist Device
Used temporarily for patients with worsening HF in ICU unit
33
Intraaortic Balloon Pump (IABP)
Increases coronary blood flow to heart muscles and decrease workload through counterpulsation.
34
Interprofessional Care: Chronic HF
``` Treat underlying cause Supplemental O2 with ongoing pulse ox Drug therapy Circulatory Assist Device Daily weights Sodium and Fluid restricted diet Severe HF- bed rest. Mild to Moderate - ambulatory with restricted activity Structured exercise program like cardiac rehabilitation Dietitician Consult PT and OT Consult Home Health Nursing Palliative or End-of-life Care ```
35
Digoxin
Weak positive inotrope Reduces SNS effects and suppress renin section Serum levels should be <0.9ng/mL Monitor renal function and serum potassium levels.
36
Lasix
Diuretics First line for volume overload Decrease sodium reabsorption to enhance sodium and water loss. Decrease fluid in preload to promote efficient LV pumping Reduces edema, pulmonary venous pressure, and preload Evaluate by increased urine output, decrease symptoms and fluid weight loss. Monitor serum potassium and serum levels A/e Hypokalemia, ototoxicity, allergic reaction to sulfa-type drugs Diuretic resistance can occur in chronic HF. Chronic HF pts should start with lowest dose.
37
Captopril
ACE inhibitor First line for chronic HF Block RAAS system, reduces afterload and SVR Monitor s/e Symptomatic hypotension, intractable cough, hyperkalemia, angioedema, and renal insufficiency. Monitor renal function and serum potassium levels Monitor for first-dose hypotension Skipping doses or discontinuing can result in rebound HTN.
38
Nesiritide
``` Vasodilator Used for short term treatment and after IV diuretic treatment fails Reduces PAWP and dyspnea A/e: Hypotension Monitor BP ```
39
Morphine
Opioid Dilates pulmonary and systemic blood vessels, reduces preload and afterload Given in small IV boluses for dyspnea Can cause respiratory depression
40
Dopamine
Positive inotrope Short term treatment for ADHF Dilates renal blood vessel and enhances urine output. Evaluate CO, BP, urine output and reduced filling pressures. Monitor IV site due to tissue necrosis and sloughing High doses produce ventricular dysrhythmia
41
Metoprolol
Beta-blocker Decreases negative effects of SNS and increase LVEF Caution with pts with volume overload Start with low dose and increase dose every 2 weeks as tolerated S/e: Worsening HF symptoms, hypotension, fatigue, and bradycardia
42
Nitroglycerine
Nitrate Vasodilator Dilate blood vessels and relaxes veins to reduce heart’s workload Treats chest pain and symptoms of HF Do NOT smoke because it decreases nitroglycerine effects.
43
Isosorbide & Hydralazine
Fixed combination of vasodilator Improve LVEF and exercise tolerance Effective in African Americans with systolic HF (HFrEF) after receiving optimal doses of other medications. Do NOT use phosphodiesterase inhibitors (sildenafil (Viagra)). S/e: Hypotension and headache
44
Nutritional Therapy
Do not add salt or seasonings containing sodium when preparing foods. Do not use salt at the table 1 tsp of salt equals 2.3 g sodium Avoid high sodium foods Canned soups, processed meats, cheese, frozen meals Limit milk products to 2 cups daily Degree of sodium restriction depends on severity of HF and effectiveness of Diuretic therapy Fluid restrictions for stage D HF pts with persistent fluid retention despite sodium restriction. Monitor fluid status, weigh the same time daily
45
2 gram sodium diet
All foods high in sodium (over 400 mg per serving) should be avoided.
46
Ambulatory Care
Include pt and caregiver in overall care plan. Effective home health care Teach pts signs of drug toxicity and self-care such as monitoring BP and HR Tailor exercise programs based on pt's interest and teach them to rest in between.
47
Heart Transplant Indications
End-stage HR Severe, decompensated, inoperable, valvular heart disease Recurrent, life-threatening dysrhythmias that are not responsive to interventions and defibrillator Heart abnormalities that limit normal function and greater or equal to 50% mortality risk within 2 years.
48
Heart Transplant Contraindications
Chronologic age over 70 years of physiologic age over 65 Illness that limits survival to less than 5 years Advance cerebral or peripheral vascular disease not amenable to correction Active infection Severe pulmonary disease that pt will be dependent on ventilator after transplant
49
Pt teaching: Diet
Monitor sodium and adhere to diet Weigh daily at the same time Eat small frequent meals Look at food and drug labels for sodium
50
Pt teaching: Exercise
Encourage cardiac rehab program Increase walking and other activities gradually Rest in between activities Avoid extreme heat and cold
51
Pt teaching: Drug therapy
Take each medication as prescribed Count HR and BP before taking certain medications Know signs and symptoms of orthostatic hypotension and internal bleeding Know INR and targeted warfarin range
52
Pt teaching: Ongoing monitor
``` Know signs and symptoms of worsening HF Notify HCP immediately when: Weight gain < or = to 3lbs Difficulty breathing, especially when lying flat Waking up breathless at night Frequent, dry, hacking cough Fatigue and weakness Swelling of ankles, feet, abd and face Dizziness or fainting Nausea with abd swelling, pain and tenderness ```
53
Pt teaching: Health Promotion
Obtain annual vaccines such as flu Reduce RF Implement regular rest periods in between activity