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Critical Care Med Surg > Heart Failure Notes > Flashcards

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
Q

Nitric Oxide (NO) and Prostaglandin

A

Relax arterial smooth muscle, vasodilation and decreased afterload.

26
Q

Compensated HF

A

Compensatory mechanism can maintain adequate CO

27
Q

Decompensated HF

A

Compensatory mechanisms can NOT maintain CO and inadequate tissue perfusion occurs.

28
Q

Chronic HF C/M:

A

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
Q

Interprofessional Care: ADHF stable

A 
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
Q

Interprofessional Care: ADHF unstable

A

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
Q

Ultrafiltration

A

Treatment for patients with volume overload and regular diuretics isn’t working anymore.

32
Q

Mechanical Cardiac Assist Device

A

Used temporarily for patients with worsening HF in ICU unit

33
Q

Intraaortic Balloon Pump (IABP)

A

Increases coronary blood flow to heart muscles and decrease workload through counterpulsation.

34
Q

Interprofessional Care: Chronic HF

A 
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
Q

Digoxin

A

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
Q

Lasix

A

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
Q

Captopril

A

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
Q

Nesiritide

A 
Vasodilator
Used for short term treatment and after IV diuretic treatment fails
Reduces PAWP and dyspnea
A/e: Hypotension
Monitor BP
39
Q

Morphine

A

Opioid
Dilates pulmonary and systemic blood vessels, reduces preload and afterload
Given in small IV boluses for dyspnea
Can cause respiratory depression

40
Q

Dopamine

A

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
Q

Metoprolol

A

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
Q

Nitroglycerine

A

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
Q

Isosorbide & Hydralazine

A

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
Q

Nutritional Therapy

A

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
Q

2 gram sodium diet

A

All foods high in sodium (over 400 mg per serving) should be avoided.

46
Q

Ambulatory Care

A

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
Q

Heart Transplant Indications

A

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
Q

Heart Transplant Contraindications

A

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
Q

Pt teaching: Diet

A

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
Q

Pt teaching: Exercise

A

Encourage cardiac rehab program
Increase walking and other activities gradually
Rest in between activities
Avoid extreme heat and cold

51
Q

Pt teaching: Drug therapy

A

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
Q

Pt teaching: Ongoing monitor

A 
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
Q

Pt teaching: Health Promotion

A

Obtain annual vaccines such as flu
Reduce RF
Implement regular rest periods in between activity

Critical Care Med Surg (17 decks)

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