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Heart failure
Heart failure
• Heart Failure is the inability of the heart to pump sufficient blood to meet the needs of the tissues for oxygen and nutrients.
• It is otherwise known as Congestive Cardiac Failure.
• Heart failure results in intravascular and interstitial volume overload and poor tissue perfusion.
causes
• Reduced ventricular contractility
• Ventricular outflow obstruction (pressure
overload )
• Ventricular inflow obstruction
• Ventricular volume overload
• Arrhythmia
• Diastolic dysfunction
Acute causes
• Acute myocardial infarction
• Dysrrhythmias
• Pulmonary emboli
• Thyrotoxicosis
• Hypertensive crisis
• Rupture of papillary muscle( eg: mitral valve)
• Ventricular septal defect
• Myocarditis
Chronic causes• Coronary artery disease
• Hypertension
• Rheumatic heart disease
• Congenital heart disease
• Cor pulmonale
• Cardiomyopathy
• Anemia
• Bacterial endocarditis
• Valvular disorders
•
RISK FACTORS
• Advancing age
• Hypertension
• Diabetes
• Obesity
• High serum cholesterol
• Cigarette smoking
PRECIPITATING CAUSES
• Anemia
• Infection
• Hypothyroidism
• Bacterial endocarditis
• Paget’s disease
• Nutritional deficiencies
• Hypervolemia
PATHO PHYSIOLOGY
Compensatory mechanism
• 1. Hemodynamic alterations
• 2. Neurohormonal responses
• 3. Ventricular dilation
• 4. Ventricular hypertrophy
Alterations in Beta-adrenergic Receptor pathway
• Increased NE concentration cause down regulation of
beta-1 adrenergic receptors in the ventricles.
• Beta- adrenergic receptor kinase(BARK) enzyme level
increases.
Role of Arginine Vasopressin (AVP)
• Circulating AVP is elevated. This leads to salt and water
retention and systemic vasoconstriction.
Role of cytokinine
• They have crucial roles in mediating the
changes in myocardial structure and function
in CHF.
Cellular and Molecular Mechanisms
• Role of calcium
• Calcium plays a central role in myocardial
contraction and relaxation. In CHF, there is
prolonged elevation of intracellular calcium
during relaxation
• Role of free radicals and apoptosis
• Altered mitochondrial oxygen metabolism
results in formation of free radicals.
• Free radicals produced by various mechanisms
have been shown to result in apoptosis of
cardiac myocytes in CHF.
DECOMPENSATED HEART FAILURE
• Ventricular remodeling
• Sustained neurohumoral activation
Counter regulatory mechanism
• ANP and BNP are hormones produced by the heart
muscle .
• ANP is released in response to stretch or increased
volume in the chambers.
• Levels of circulating ANP can be correlate with
functional class prognosis and hemodynamic state.
• Inhibit renin, aldosterone and ADH secretion and results
in excretion of sodium and water
• Promotes venous and arterial vasodilatation.
• BNP is released in response to an increase in wall stress
or triggered by pressure.
TYPES OF HEART FAILURE
• Left –sided heart failure or left ventricular
dysfunction
• Right sided heart failure or right
ventricular failure
• Biventricular heart failure
• Diastolic and systolic dysfunction
High output versus low output failure
High output failure occurs when the heart despite
normal output to high output levels is simply
not able to meet the accelerated needs of the
tissues
Low output failure occurs in most forms of heart
disease resulting in hypoperfusion of tissue
cells .
Backward versus forward failure
• Backward failure focuses on the ventricles inability to eject completely ,which increases ventricular filling pressures ,causing venous and pulmonary congestion .
• Forward failure is a problem of inadequate perfusion. It results when reduced contractility produces a decrease in stroke volume and cardiac output
• Acute versus chronic heart failure
CLINICAL MANIFESTATIONS
• Left Sided HeartFailure
• Acute LVF presents with a sudden onset of dyspnoea at rest.
• progresses to acute respiratory distress, orthopnoea and prostration.
• appears agitated ,pale and clammy
• Rapid pulse
• Cool periphery
• High BP
• Elevated JVP if associated with RVF.
• Auscultaition – crepitations,triple gallop rhythm.
• Displaced apex beat.
Respiratory system
• Tachypnea
• Capillary refill > 3 seconds
• Orthopnea
• Dyspnea on exertion
• Nocturnal dyspnea
• Cough with frothy sputum (indicative of
pulmonary edema)
• Basilar crackles or rhonchi
• Cyanosis
• Hypoxia (respiratory acidosis)
• Kussmaul’s sign
• Cheyne stokes respiration
Cardiovascular system
• Diaphoresis
• Audible S3 and S4 heart tones
• Murmur or mitral insufficiency
• Enlarged left ventricle on X-ray
• Enlarged left atrium on X-ray
• Narrowing pulse pressure
• Pulses alternans (alteration of weak and strong
beats)
• Basilar crackles or rhonchi
• Cyanosis
• Hypoxia (respiratory acidosis)
• Kussmaul’s sign
• Cheyne stokes respiration
• Elevated pulmonary artery pressures
• Elevate pulmonary artery occlusive pressures
Central nervous system
• Mental confusion
Generalized symptoms
• Weight gain.
• Fatigue/weakness/lethargy
Right sided heartfailure
Gastro intestinal system
• Hepatomegaly
• Splenomegaly
• Hepatojugular reflux
• Ascites
• Weight gain
• Weight loss and emaciation as a result of inadequate
intake of food and wasting of tissues. This picture is
termed as cardiac cachexia
Cardiovascular system
• Arrhythmias
• Elevated CVP
• Elevated right atrial pressure
• Elevated right ventricular pressure
• Narrowing pulse pressure
• Murmur or tricuspid insufficiency
• Audible S3 and S4 heart tones
• Enlarged right atrium on X-ray
• Enlarged right ventricle on X-ray
• Dependant pitting edema
• Venous distention
• Urinary system
• Oliguria
• Nocturia
Chronic heart failure
• Fatigue
• Dyspnea
• Orthopnea
• Paroxysmal nocturnal dyspnea
• Tachycardia
• Edema
• Nocturia
• Skin changes
Chronic swelling result in pigment changes
causing the skin to appear brown
• cool and damp to the touch
• Behavioral changes
• Chest pain
• Weight changes
COMPLICATIONS
• Pleural effusion
• Dysrhythmias
EF less than 35%have a high risk of fatal dysrhythmias and sudden cardiac death.
• Renal failure
• Impaired liver function & Cardiac cirrhosis
• Thromboembolism
Hypokalemia & Hyperkalemia
DIAGNOSTIC STUDIES
• History
• Physical Examination
• Electrocardiogram
• Laboratory data(cardiac enzymes, BNP,serum chemistries
,liver function studies ,thyroid function studies and
complete blood count). In severe CHF dilutional
hyponatremia occurs. BUN and creatinine are moderately
elevated.
• BNP levels are used to assess the HF.
• BNP<100pg/ml - heart failure very
improbable
• BNP100-500pg/ml -HF probable
• BNP>500pg/ml -HF very probabl
• Echocardiogram : EF less than 40% accepted as evidence
of systolic dysfunction.
• Asessment of myocardial viability
This can be done by using dobutamine or dipyridamole
stress echocardiography, nuclear imaging using thallium
or sestamibi and positron emission tomography
Identify patients who will benefit from long term therapy
with drugs such as ACE inhibitors
• Stress testing,(treadmill test, stress echocardiography and
nuclear perfusion studies)
• Cardiac catheterization and coronary angiography:
• Endomyocardial biopsy
This is indicated in patients with clinical indication of
myocarditis and systemic disease with possible cardiac
involvement such as hemochromatosis, amyloidosis,
sarcoidosis and those who have received adriamycin
chemotherapy.
MANAGEMENT OF ACUTE PULMONARY EDEMA
• Sit the patient up
• Give oxygen(high flow ,high concentration ).
non invasive positive pressure ventilation
(CPAP-5-10 mmhg)
• IV glceryl trinitrate 10-200 microgram
/minute until clinical improvement occurs or
systolic blood pressure falls to ˂110mmHg.
• loop diuretic such as frusemide 50-100mg IV
• continuous monitoring
• Ionotropic agents
• Intra aortic balloon pump
Management
• General measures
• Pharmacologic therapy
• Devices
• Surgery
• Newer evolving therapies
General measures
• Rest
• Correction of aggravating factors
• Salt restriction – sodium intake should be limited to ˂ 2g/day
• Fluid restriction- to 1-2l/day is advisable in patients with dilutional hyponatremia.
• Smoking cessation
• Avoid alcohol
• Management of co morbidities
Pharmacologic therapy
To Reduce workload
• Angiotensin converting enzyme inhibitors
• Angiotensin II receptor blockers
• Vasodilators
• Diuretics
• Beta blockers
ACE inhibitors
• Interrupts the vicious cycle of neurohumoral activation
• Prevents salt and water retension ,peripheral arterial and
venous vasoconstriction
• Also increase the concentrations of the vasodilator
bradykinin.
• Decreases SVR and improves myocardial performance.
• Enalapril: 2.5 mg 12 hrly
• Lisinopril 2.5 mg daily
• Ramipril :1.25 mg daily
• Captopril :50 mg tds
Adverse effects
• Persistant cough
• Hypotension
• Hyperkalemia
• \deteriorating renal function
• Loss of taste
Angiiotensin II receptor blockers
• Similar hemodynamic effects to ACE inhibitors
• Do not affect bradykinin metabolism
• Losartan, Valsartan, Irbesartan and Eprosartan
• Losartan :25 mg daily
• Candesartan:4 mg daily
• Valsartan : 40 mg daily
Vasodialators
• Venous dialation blood is trapped in the veins ,and venous return to the heart is decreased .This reduces preload
• eg: nitroglycerin and isosorbide dinitrate
• Dilation of arterioles: arteriolar vasodilators
decreases peripheral vascular resistance and
afterload
• Eg:ACE inhibitors
Combined action on veins and arterioles
• decrease both preload and afterload
• sodium nitroprusside relaxes the smooth muscle of both
veins and arterioles.it does not directly affect the heart
muscle or heart rate
Beta blockers
• Directly block the direct effects of the SNS
• Cardio selective agents block beta 1 adrenergic
receptors.non selective agents block beta 1 and beta 2
adrenergic receptors.
• Eg: atenolol,metoprolol , bisoprolol, bucindolol,
labetalol,carvedilol,esmolol (25-50 mg bd)
Diuretics
• To mobilize edematous fluid , reduce pulmonary venous
pressure ,and reduce preload
• Thiazide diuretics may be the first choice in chronic HF
• Eg;benzthiazide,chlorothiazide,chlorthalidone,metolazon
e
• Loop diuretics
• eg.Frusimide ,torsemide
• Spironolactone is an inexpensive ,potassium sparing
diuretic.
Human b-type natriuretic peptide
Nesiritide is a synthetic form of human BN
Beta adrenergic agonists
• short term treatment
• E.g.:-dopamine, dobutamine
Cardiac glycosides
• Eg ; Digoxin
• Slow the ventricular rate, improves cardiac function
• Optimum therapeutic level os digoxin in serum is 1-1.5
ng/ml
• Toxic level is above 2ng/ml
Calcium channel blockers
• Vasodilator
• Anti ischemic effects
• Eg: Verapamil, diltiazem, amlodipine
• Phosphodiesterase inhibitors:-
Eg: amrinone,milrinone
• Antidysrhythmic drugs
e.g.adenosine, digoxin, ibutilide, magnesium
Devices
• Implantable cardiac defibrillators and
resynchronization therapy
Ventricular assist devices
Extracorporeal membrane oxygenator
Surgery
• Heart transplantation
• Coronary revascularization
• Dynamic cardiomyoplasty
• Partial left ventriculectomy( Batista procedure)
• Aneurysmectomy
• Mitral annuloplasty and mitral valve repair
Newer evolving therapies
• Gene therapy
• To increase the myocardial contractility at molecular level
• Genes expressing SERCA2a are increased by using adenovirus transfection of myocytes
• NURSING ASSESSMENT
Nursing diagnosis
Decreased cardiac output r/t heart failure ,dysrhythmia or both
• Assess blood pressure for hypotension or hypertension
• Assess heart rate and rhythm
• Document rhythm strips q8h
• Auscultate heart rate q2h
• Monitor lung sounds
• Monitor intake and output
• Assess for change in mental status
• Administer prescribed medications
• Encourage physical and mental support
• Encourage client to eat small frequent feeds
• Excess fluid volume related to cardiac failure
as evidenced by edema ,dyspnea on exertion
,increased weight gain
• Monitor intake and output chart
• Assess for presence of peripheral edema
• Assess for jugular vein distention
• Follow low sodium or fluid restriction
• Auscultate breath sounds
• Administer diuretic therapy
Impaired gas exchange related to increased preload, mechanical failure or immobility as evidenced by increased respiratory rate, shortness of breath, and dyspnea on exertion
• Auscultate breath sounds q2h
• Assess respiratory rate
• Asses for cyanosis
• Monitor pulse oximetry
• Position the client to facilitate breathing
• Administer diuretic therapy
Ineffective tissue perfusion related to decreased
cardiac output
• Note colour and temperature of the skin q4h
• Monitor peripheral pulsesq4h
• Provide a warm environment
• Encourage active rang of motion
• Monitor urine output
• Activity intolerance related to fatigue secondary to cardiac insufficiency and pulmonary congestion as evidenced by dyspnea,shortness of breath ,weakness, increased in heart rate on exertion
• space nursing activities
• Schedule rest periods
• Monitor the clients response to activities
• Instruct the client to avoid activities that increase cardiac workload
• Anxiety r/t to dyspnea or perceived threat of death as
evidenced by restlessness, irritability
• Deficient knowledge related to disease process as
evidenced by questions about the disease and prognosis
References
• KV Krishnadas. Text book of Medicine. 5th
edition.Jaypee publications.New Delhi.2008
• Marscall S. Runge. Georege A.Netter’sCardiology .2nd ed. USA .2014
• Nicki R.Colledge,Brian R. Walker,StuartH.Ralston.Davidson’s Principles and Practice of Medicine 21st edition 2010 Churchil Living stoneElsevier page no 542-550
• Richard Hatchett, David R Thompson. Cardiac Nursing. Elsevier publications. USA.2007