323 Final Exam - Heart Failure

Front 1

Causes of heart failure

Back 1

• Eccentric ventricular hypertrophy (dilation of ventricles)

o Enlargement of the ventricles to compensate for increased BP -> muscle fibres stretch to adapt to maintain CO -> chronically leads to decreased CO as muscle fibres are overstretched and not able to contract properly

• Concentric ventricular hypertrophy (thiccckening of ventricles)

o Increase in muscle mass and cardiac wall thickness to compensate for extra work and strain from increased BP-> chronically leads to poor contractility and increased O2 needs -> decreased coronary artery circulation -> arrhythmia risk

• Valvular stenosis (aortic, mitral, tricuspid), hypertension, diabetes, MI (myocardial damage)

• Non ischemic cardiomyopathy

o Tachycardia, Alcoholic, Diabetic, Obesity, Viral, Non-compaction

o Chemotherapy & immunotherapy, Pacemaker induced

o Right Ventricular Arrhythmogenic Cardiomyopathy

o Infiltrative (e.g. amyloid or sarcoidosis)

o Filling disorders (Cardiac tamponade, restrictive pericarditis)

Front 2

Risk factors of HF

Back 2

Risk factors

o Hypertension

o Coronary artery disease

o Diabetes mellitus (d/t insulin resistance’s effect on ventricular remodelling)

o Anemia

Front 3

HF-causing neurohormonal response

Back 3

• SNS: Increased HR and contractility -> myocyte hypertrophy and necrosis -> vasoconstriction and vascular hypertrophy -> increases work of the heart

• RAAS: Increase BP from fluid retention -> increases work of the heart

• These responses in order to increase CO put additional pressure on the heart, however, only short-term benefits

o Long-term, heart and lungs become congested with too much fluid (leads to myocyte damage, ventricular remodelling, disease progression)

Front 4

HF counter-regulatory mechanisms

Back 4

• Natriuretic peptides (atrial natriuretic peptide/ANP & B-type natriuretic peptide/BNP)

• Hormones produced by the heart in response to increased blood volume

o Increased GFR and diuresis

o Excretion of sodium

o Vasodilation and decreased BP

o Inhibits aldosterone and renin secretion

o Interferes with ADH release

• Counters the effects of the SNS and RAAS on the heart in pt with HF

Front 5

HRrEF systolic dysfunction

Back 5

Most common cause

• Dysfunction of systole, LVEF <40% (normal is >55% of ventricular volume)

• Decrease ventricular filling time, decreased stroke volume from the LV

• Results from inability of the heart to pump due to impaired contractile function/weak ventricle (e.g., caused by myocardial infarction, hypertension)

• Venous engorgement in normal systolic function

Front 6

HRpEF diastolic dysfunction

Back 6

Preserved ejection fraction

• Comorbidities, aging, hypertension, DM, LV hypertrophy, coronary disease, cardiomyopathies

• Aka diastolic HF -> Left ventricle doesn’t relax, so it doesn’t fill fully, -> decreased LVEF

o Fluid backed up into left atrium, then pulmonary vasculature, then right ventricle and atrium (RV hypertrophy and hypokinesis, tricuspid regurgitation)

o Left ventricle cannot fully relax, so it become stiff and doesn’t respond well

o Elevated systolic pulmonary pressure (systemic overload -> edema)

• Many different phenotypes, therefore different treatments

Front 7

Newer classification of HF

Back 7

• HFmEF – HF with mid-range ejection fraction, HF 41%-49%

• Recovered Ejection Fraction – refers to those who previously had an EF < 40% that rises to above 40% following therapy

Front 8

Thinking of HF clinically: wet and dry

Back 8

• Hot & Dry – Compensated Heart Failure (HF)

• Hot & Wet – Acute Decompensated Heart Failure (AdHF)

• Cold & Wet – AdHF with low output state – hardest to manage

• Cold & Dry – low output state of HF, end stage

Front 9

Left-sided heart failure: path, S&S,

Back 9

• Most common form of HF d/t left ventricular dysfunction -> fluid backs up into left atrium -> backs up into the lungs -> pulmonary edema

• Symptoms

o Fatigue

o Dyspnea - Shallow respirations (up to 32/min)

o Orthopnea (patient must be elevated)

o Dry cough

o Pulmonary edema

o Nocturia (peeing at night)

o Paroxysmal nocturnal dyspnea (random onset, goes away with position change) -> Second space fluid shifts back into circulation when lying down/sleeping -> characterized by waking up suddenly and feeling suffocated

• Signs

o LV heaves

o Cheyne-Stokes respirations (fast/shallow, then slow/heavy)

o Increased heart rate

o PMI (point of maximal impulse) displaced inferiorly and posteriorly (LV hypertrophy)

o Decrease pO2, slight increase pCO2, (poor oxygen exchange)

o Crackles (pulmonary edema)

o S3 and S4 heart sounds

Front 10

Right-sided HF: path, S&S

Back 10

Most often caused by left-sided heart failure

• Backflow to right atrium -> back up into venous circulation -> edema in a lot of places

• Symptoms

o Fatigue, peripheral edema, upper right quadrant pain

o Anorexia and bloating, nausea

• Signs

o RV heaves, murmurs

o Peripheral edema, nocturia

o Weight gain

o Edema of dependent body parts

o Ascites

o Anasarca (massive, generalized body edema)

o Jugular venous distension

o Hepatomegaly

o Right-sided pleural effusion

Front 11

AdHF/Acute decompensated HF: manifestations, treatment

Back 11

• AdHF is the acute manifestation of the chronic condition

o the initial manifestation of heart failure

o may indicate exacerbation of chronic heart failure

o Exception: if HF has a reversible cause

• Develops rapidly (hours to days).

• Clinical manifestation is usually the acute rapid onset pulmonary edema, but it can also be RHF or biventricular

Front 12

AdHF/Acute decompensated HF: manifestations, treatment

Back 12

• AdHF is the acute manifestation of the chronic condition

o the initial manifestation of heart failure

o may indicate exacerbation of chronic heart failure

o Exception: if HF has a reversible cause

• Develops rapidly (hours to days).

• Clinical manifestation is usually the acute rapid onset pulmonary edema, but it can also be RHF or biventricular

Front 13

AdHF - PPT treatments

Back 13

• Oxygen (CPAP/BiPAP only if high respiratory rate and low saturation despite high flow 02), titrate to 02 sat >90%

• IV diuretic (lasix) in intermittent doses or as a drip

• IV vasodilator (Nitroglycerin) SBP>100mmHg

• Positive inotrope such as Milrinone or Dobutamine only if necessary (risk of arrhythmia)

o Raise BP first before administering diuretics

• Continuation of chronic b-blocker therapy unless hypotension/bradycardic, optimize GDMT if tolerated

• Treating reversible causes

o Hypertension - antihypertensives

o Valvular defects – surgery, minimally invasive procedures

o Ischemic heart disease – percutaneous interventions (PCI), cardiac surgery

o Arrhythmias - medical therapy, device therapy

o Obstructive Sleep Apnea – CPAP

o Toxic (e.g. ETOH, chemotherapy) – remove toxin

Front 14

Textbook interventions: HF impaired gas exchange

Back 14

(related to increased preload and alveolar–capillary membrane changes as evidenced by abnormal O2 saturation, hypoxemia, dyspnea, tachypnea, tachycardia, restlessness, and patient’s statement about being short of breath)

• GOAL: Maintains adequate O2/CO2 exchange at the alveolar–capillary membrane to meet O2 needs of the body

• Respiratory monitoring

o Monitor pulse oximetry, respiratory rate, rhythm, depth, and effort of respirations to detect changes in respiratory status.

o Auscultate breath sounds, noting areas of decreased or absent ventilation and presence of adventitious sounds to detect presence of pulmonary edema.

o Monitor for increased restlessness, anxiety, and work of breathing to detect increasing hypoxemia.

• Oxygen therapy

o Administer supplemental O2 or other non-invasive ventilator support (e.g., bilevel positive airway pressure) as needed to maintain adequate O2 levels.

o Monitor the O2 litre flow rate and placement of O2 delivery device to ensure O2 is adequately delivered.

o Change O2 delivery device from mask to nasal prongs during meals as tolerated to sustain O2 levels while patient is eating.

o Monitor the effectiveness of O2 therapy to identify hypoxemia and establish range of O2 saturation.

• Positioning

o Position patient to alleviate dyspnea (e.g., semi-Fowler’s position), as appropriate, to improve ventilation by decreasing venous return to the heart and increasing thoracic capacity.

Front 15

Textbook interventions: HF impaired gas exchange

Back 15

(related to increased preload and alveolar–capillary membrane changes as evidenced by abnormal O2 saturation, hypoxemia, dyspnea, tachypnea, tachycardia, restlessness, and patient’s statement about being short of breath)

• GOAL: Maintains adequate O2/CO2 exchange at the alveolar–capillary membrane to meet O2 needs of the body

• Respiratory monitoring

o Monitor pulse oximetry, respiratory rate, rhythm, depth, and effort of respirations to detect changes in respiratory status.

o Auscultate breath sounds, noting areas of decreased or absent ventilation and presence of adventitious sounds to detect presence of pulmonary edema.

o Monitor for increased restlessness, anxiety, and work of breathing to detect increasing hypoxemia.

• Oxygen therapy

o Administer supplemental O2 or other non-invasive ventilator support (e.g., bilevel positive airway pressure) as needed to maintain adequate O2 levels.

o Monitor the O2 litre flow rate and placement of O2 delivery device to ensure O2 is adequately delivered.

o Change O2 delivery device from mask to nasal prongs during meals as tolerated to sustain O2 levels while patient is eating.

o Monitor the effectiveness of O2 therapy to identify hypoxemia and establish range of O2 saturation.

• Positioning

o Position patient to alleviate dyspnea (e.g., semi-Fowler’s position), as appropriate, to improve ventilation by decreasing venous return to the heart and increasing thoracic capacity.

Front 16

Textbook interventions: HF decreased cardiac output

Back 16

(related to altered contractility, altered preload, altered stroke volume, or a combination of these as evidenced by decreased ejection fraction, increased CVP, decreased peripheral pulses, jugular venous distension, orthopnea, chest pain, S3 and S4, and oliguria).

• GOAL: Maintains adequate blood pumped by the heart to meet metabolic demands of the body

• Cardiac Care

o Perform a comprehensive assessment of peripheral circulation (e.g., check peripheral pulses, edema, capillary refill, colour, and temperature of extremity) to determine circulatory status.

o Note signs and symptoms of decreased cardiac output (e.g., chest pain, S3, S4, jugular venous distension) to detect changes in status.

o Monitor fluid balance (e.g., input/output, and daily weight) to evaluate patient’s fluid status.

o Monitor cardiac rhythm to detect dysrhythmias.

o Monitor respiratory status for symptoms of heart failure (e.g., dyspnea, fatigue, tachypnea, orthopnea) to identify involvement of respiratory system.

o Instruct patient and caregivers about activity restriction and progression to allay fears and anxiety.

o Establish a supportive relationship with patient and caregivers to promote adherence to the treatment plan.

o Inform patient of the purpose and benefits of the prescribed activity and exercise to enhance adherence.

Front 17

Textbook interventions: HF excess fluid volume

Back 17

(related to excessive fluid intake, excessive sodium intake [decreased renal perfusion secondary to heart failure] as evidenced by weight gain over short period of time, edema, adventitious breath sounds, oliguria)

• GOAL: Experiences reduction or absence of edema and stable baseline weight

• Hypervolemia Management

o Administer medications as per MD/NP to reduce preload (e.g., furosemide, spironolactone, morphine, and nitroglycerine) to treat hypervolemia.

o Monitor for therapeutic effects of medications (e.g., increased urine output, decreased CVP, decreased adventitious breath sounds) to assess response to treatment.

o Monitor potassium levels after diuretic medications to detect hypokalemia.

o Weigh patient daily and monitor trends to evaluate effect of treatment.

o Monitor intake and output to assess fluid status.

o Monitor respiratory pattern for symptoms anxiety, air hunger, orthopnea, dyspnea, tachypnea, cough, frothy sputum production, and shortness of breath to detect signs and symptoms of pulmonary edema.

o Monitor hemodynamic status, including HR, BP, MAP, PAP, PAWP, CO, and CI, if available, to evaluate effectiveness of therapy.

o Monitor adventitious breath sounds, adventitious heart sounds, JVD, and peripheral edema to assess response to treatment.

Front 18

HF dyspnea/SOB management

Back 18

Symptom management: dyspnea

• Diuretics for fluid overload (furosemide IV/PO/SC, spironolactone, metolazone)

• CRT-P;

• Thoracentesis or paracentesis (draining fluid)

• 02 therapy PRN;

• Low dose opiates

• Chronic cough – codeine linctus?;

• Constipation care;

• Changing the pace of life, frequent rests, but doing what is loved;

• Normalize sleeping in chair;

• Fans & airflow in the home.

• Correction of anemia

Front 19

CHF - path, S&S, manifestations

Back 19

Chronic heart failure (pt has HF, but controlled Sx)

• Chronic HF develops as the myocardium weakens over time -> ventricular remodelling

o “Is this my new baseline?”

• S&S of chronic HF

o Fatigue (decreased CO, impaired perfusion to vital organs, decreased oxygenation, anemia)

o Dyspnea (increased pulmonary pressures secondary to interstitial and alveolar edema)

o Tachycardia (compensation for decreased CO d/t SNS activation)

o Edema (mainly located in periphery, liver, abdo cavity, lungs)

o Nocturia (lying down moves interstitial fluid into blood, decreased cardiac workload -> increased renal blood flow and diuresis)

o Skin changes (decreased tissue oxygenation -> dusky skin, LEE shiny/swollen)

o Behavioural changes (restlessness, confusion, decreased attention & memory)

o Chest pain (angina from decreased coronary perfusion)

o Weight changes (fluid retention/renal failure, abdo fullness causes anorexia and nausea, cardiac cachexia results in muscle wasting/fat loss)

Front 20

What is ICD? Indications and contraindications? How does it work?

Back 20

implantable cardioverter defibrillator

• A pacemaker with a defibrillator wire

o Will defibrillate fast rhythms (over 180bpm), even if sinus (Ex. ventricular dysrhythmias like V-tach)

• Not recommended for NYHA IV as advanced HF is not expected to improve

• Indications for use

• Non-ischemic CMP (comprehensive metabolic panel), NYHA II-III, EF<35%,

o measured at least 3 months after optimization of GDMT (guideline-directed medical therapy).

o Ischemic CMP, NYHA II-III, EF<35%, measured at least 1-month post-MI, 3 months post revascularization procedure.

o Ischemic CMP, NYHA I, EF < 30%

• Viewed as “lifeboat”

o There should be some discussion about turning off shock function

o Deactivation often gives perception we are “giving up” on the patient

Front 21

What is ICD? Indications and contraindications? How does it work?

Back 21

implantable cardioverter defibrillator

• A pacemaker with a defibrillator wire

o Will defibrillate fast rhythms (over 180bpm), even if sinus (Ex. ventricular dysrhythmias like V-tach)

• Not recommended for NYHA IV as advanced HF is not expected to improve

• Indications for use

• Non-ischemic CMP (comprehensive metabolic panel), NYHA II-III, EF<35%,

o measured at least 3 months after optimization of GDMT (guideline-directed medical therapy).

o Ischemic CMP, NYHA II-III, EF<35%, measured at least 1-month post-MI, 3 months post revascularization procedure.

o Ischemic CMP, NYHA I, EF < 30%

• Viewed as “lifeboat”

o There should be some discussion about turning off shock function

o Deactivation often gives perception we are “giving up” on the patient

Front 22

What is CRT? Indications? How does it work?

Back 22

• Indications

o Use in patients with max medical therapy, who still have NYHA III symptoms, and have a wide QRS complex

o Symptomatic NYHA II to IV, QRS > 130ms, EF < 35% with a left bundle branch block on optimal medical therapy

• CRT will improve symptoms, especially for wide QRS

• Pacemaker with two ventricular leads, one attached to each ventricle

• Rationale is to promote synchrony in the beating of the ventricles to improve HF symptoms

Front 23

What is ICD? Indications and contraindications? How does it work?

Back 23

implantable cardioverter defibrillator

• A pacemaker with a defibrillator wire

o Will defibrillate fast rhythms (over 180bpm), even if sinus (Ex. ventricular dysrhythmias like V-tach)

• Not recommended for NYHA IV as advanced HF is not expected to improve

• Indications for use

• Non-ischemic CMP (comprehensive metabolic panel), NYHA II-III, EF<35%,

o measured at least 3 months after optimization of GDMT (guideline-directed medical therapy).

o Ischemic CMP, NYHA II-III, EF<35%, measured at least 1-month post-MI, 3 months post revascularization procedure.

o Ischemic CMP, NYHA I, EF < 30%

• Viewed as “lifeboat”

o There should be some discussion about turning off shock function

o Deactivation often gives perception we are “giving up” on the patient

Front 24

What is CRT? Indications? How does it work?

Back 24

• Indications

o Use in patients with max medical therapy, who still have NYHA III symptoms, and have a wide QRS complex

o Symptomatic NYHA II to IV, QRS > 130ms, EF < 35% with a left bundle branch block on optimal medical therapy

• CRT will improve symptoms, especially for wide QRS

• Pacemaker with two ventricular leads, one attached to each ventricle

• Rationale is to promote synchrony in the beating of the ventricles to improve HF symptoms

Front 25

AHA stages of HF

Back 25

AHA Stages of HF

• A (HF Risk Factors, no Heart disease, no symptoms)

• B (heart disease + no symptoms OR asymptomatic + LV dysfunction)

• C (prior or current HF symptoms)

• D (refractory, HF symptoms)

Front 26

NYHA classifications for HF

Back 26

NYHA (New York Heart Association) classification for pt with HF

• Class I

o No limitation of physical activity. Ordinary physical activity does not cause fatigue, dyspnea, palpitations, or anginal pain.

• Class II

o Slight limitation of physical activity. No symptoms at rest. Ordinary physical activity results in fatigue, dyspnea, palpitations, or anginal pain.

• Class III

o Marked limitation of physical activity. Usually comfortable at rest. Ordinary physical activity causes fatigue, dyspnea, palpitations, or anginal pain.

• Class IV

o Inability to carry on any physical activity without discomfort. Symptoms of cardiac insufficiency or of angina may be present even at rest. If any physical activity is undertaken, discomfort is increased.

Front 27

Patient teaching for

Back 27

• Nursing Care – Collaborative work with family

o assess the types of food eaten, food preparation

o identify foods low and high in sodium

o identify ways to enhance food flavors without salt

o develop strategies for monitoring salt intake

o instruct the patient on how to read labels for sodium

• Sodium restriction (2-3gm/day)

o PURPOSE: reduces preload (volume of blood in ventricle at end of diastole)

o Less than 150 mg/serving is okay

o More than 400 mg/serving is a lot

o Stop using the saltshaker

o Do not add salt to foods during preparation

o Read food labels carefully

o Stop eating processed or high-sodium foods

o Be aware of hidden sources of sodium (ex. 1 slice of bread contains 150 mg of sodium)

• Medication adherence

o (suggest checklist, pillbox, dosette

• Fluid restrictions (1.5-2L daily)

o Monitor for I&Os to track the patient’s progress

• Weight loss PRN

o A tool to monitor fluid retention

o instruct patient to weigh self-daily at around the same time (preferably before breakfast)

o instruct the patient to call their primary health care provider if there has been a sustained weight gain of 3 lbs or more over 2-5 days (sign of fluid retention)

• Supervised exercise/cardio rehab

o Nursing Care (Discuss exercise with patient. Provide patient with list of available resources for supervised exercise. Advise rest periods between exercise and ADL. Advise avoidance of extremes of heat and cold.)

o All patients with stable NYHA I – III heart failure should take part in a supervised, tailored, exercise program to improve quality of life and exercise tolerance (strong recommendation, moderate evidence).

o Recommend assessment by HF specialist physician before taking part in such a program (strong recommendation, low-quality evidence) (No change in NYHA in past 6 weeks, No hospitalizations, procedures, major events)

o Recommended weekly exercise is 30 to 40 minutes, 3-5 times /week including aerobic activity and resistance training.

• No smoking

o Be aware of smoking cessation programs in your hospital or community setting

• Reduction alcohol consumption

o 1-2 drinks/day for men, 1 drink for women

o Heavy drinking (6-8 drinks/day) associated with alcohol induced cardiomyopathy

o “Beer isn’t alcohol…

• Psychosocial & Spiritual

o Psychological needs (depression, anxiety, self-efficacy)

o Social needs (family, community, activities, work, travel)

o Changing homecare needs? Team approach

 SW need to be involved?

 Dietician ?

 Psychological support