Congestive Heart Failure (CHF)
Congestive Heart Failure
The heart is unable to provide adequate perfusion of peripheral organs to meet their metabolic requirements
What Is CHF ? ♥ The heart does not pump efficiently ♥ The heart is not able to move as much blood as it should with each beat ♥ Organs in the body do not get enough oxygen rich blood that they need to work well
The "heart failure" sound alarming, but they do not mean that your heart has suddenly stopped working. Instead, heart failure means your heart is not pumping as well as it should to deliver oxygen-rich blood to your body's cells. Congestive heart failure (CHF) happens when the heart's weak pumping action causes a buildup of fluid called congestion in your lungs and other body tissues.
Compensatory Mechanisms
• Neurohormonal system • Renin-angiotensin-aldosterone system • Ventricular hypertrophy
• Stimulated by decreased perfusion secretion of hormones • Epi— • Increases contractility • Increases rate and pressure • Vasoconstriction SVR
• Vasopressin— • Pituitary gland • Mild vasoconstriction, renal water retention
• Decreased renal blood flow secondary to low cardiac output triggers renin secretion by the kidneys • Aldosterone is released increase in Na+ retention water retention • Preload increases • Worsening failure
• Long term compensatory mechanism • Increases in size due to increase in work load ie skeletal muscle
Symptoms of CHF shortness of breath blood pooling in pulmonary veins fluid in lungs occurs during activity, rest, or sleeping
persistent coughing/wheezing produces white/blood mucus
edema (or excess fluid buildup in body tissues) venous pooling swelling in extremities necrosis
Symptoms of CHF
tiredness/fatigue
decreased O2 supply diversion of blood supply from limbs
lack of appetite/nausea decreased blood supply to digestive tract
confusion/impaired thinking increased heart rate baroreceptor reflex
Risk factors for CHF include Previous heart attacks Coronary artery disease High blood pressure (hypertension) Irregular heartbeat (arrhythmia) Heart valve disease (especially of the aortic and mitral valves) Cardiomyopathy (disease of the heart muscle) Congenital heart defects (defects you are born with) Alcohol and drug abuse
• Uncontrolled HTN doubles the chances of failure • With HTN, the chambers of the heart enlarge and weaken.
• Can result from disease, infection, or be congenital • Don’t open and/or close completely increased workload failure
• Tachycardias decreased diastolic filling time decreased SV. • Atrial dysrhythmias as much as 30% reduction in stroke volume
• The ischemic tissue is basically taken out of the equation, leaving a portion of the heart to do the work of the entire heart decreased SV CHF.
• Tend to be overweight • HTN • Hyperlipidemia
• Left Ventricular Failure with Pulmonary Edema • systolic heart failure
• Right Ventricular Failure • diastolic heart failure
Classification of heart failure New York Heart Association (NYHA) Class
Symptoms
Class I
No limitation of physical activity
Class II
Slight limitation of physical activity
Class III
Marked limitation of physical activity
Class IV
Unable to carry out physical activity without discomfort
Treatment Objectives Survival Morbidity Exercise capacity Quality of life Neurohormonal changes Progression of CHF Symptoms
Therapeutic Overview Problems
Reduced force of contraction Decreased cardiac output Increased TPR Inadequate organ perfusion Development of edema Decreased exercise tolerance Ischemic heart disease Sudden death
Goals alleviate symptoms improve quality of life arrest cardiac remodeling prevent sudden death
Order of Therapy 1. 2. 3. 4. 5. 6.
Loop diuretics ACE inhibitor (or ARB if not tolerated) Beta blockers Digoxin Hydralazine, Nitrate Potassium sparing diuretcs
Diuretics • Essential to control symptoms secondary to fluid retention • Prevent progression to HF • Spironolactone improves survival
Diuretics Cortex
Thiazides Inhibit active exchange of Cl-Na in the cortical diluting segment of the ascending loop of Henle
K-sparing
Inhibit reabsorption of Na in the distal convoluted and collecting tubul
Loop diuretics
Medulla Loop of Henle
Inhibit exchange of Cl-Na-K in the thick segment of the ascending loop of Henle
Collecting tubule
Diuretics • Loop diuretics • Furosemide, buteminide • For Fluid control, and to help relieve symptoms
• Potassium-sparing diuretics • Spironolactone, eplerenone • Help enhance diuresis • Maintain potassium • Shown to improve survival in CHF
Diuretics used in CHF to reduce extracellular fluid volume primarily used in patients with acute CHF with volume overload IV infusion causes immediate and predictable diuresis for immediate relief Goal: reduce preload/afterload overdosing can result in excessive reduction in preload, overreduction in stroke volume thiazide and loop diuretics (i.e. Furosemide)
Beta Blocker therapy • Certain Beta blockers (carvedilol, metoprolol, bisoprolol) can improve overall and event free survival in NYHA class II to III HF, probably in class IV. • Contraindicated: • • • • •
Heart rate <60 bpm Symptomatic bradycardia Signs of peripheral hypoperfusion COPD, asthma PR interval > 0.24 sec, 2nd or 3rd degree block
Hydralazine plus Nitrates • Dosing: • Hydralazine • Started at 25 mg po TID, titrated up to 100 mg po TID
• Isosorbide dinitrate • Started at 40 mg po TID/QID
• Decreased mortality, lower rates of hospitalization, and improvement in quality of life.
Digoxin â&#x20AC;˘ Given to patients with HF to control symptoms such as fatigue, dyspnea, exercise intolerance â&#x20AC;˘ Shown to significantly reduce hospitalization for heart failure, but no benefit in terms of overall mortality.
Management of Refractory Heart Failure • Inotropic drugs:
• Dobutamine, dopamine, milrinone, nitroprusside, nitroglycerin
• Mechanical circulatory support:
• Intraaortic balloon pump • Left ventricular assist device (LVAD)
• Cardiac Transplantation • • •
A history of multiple hospitalizations for HF Escalation in the intensity of medical therapy A reproducable peak oxygen consumption with maximal exercise (VO2max) of < 14 mL/kg per min. (normal is 20 mL/kg per min. or more) is relative indication, while a VO2max < 10 mL/kg per min is a stronger indication.
Acute Decompensated Heart Failure â&#x20AC;˘ Cardiogenic pulmonary edema is a common and sometimes fatal cause of acute respiratory distress. â&#x20AC;˘ Characterized by the transudation of excess fluid into the lungs secondary to an increase in left atrial and subsequently pulmonary venous and pulmonary capillary pressures.
ACE-i. Mechanism of Action VASOCONSTRICTION ALDOSTERONE VASOPRESSIN SYMPATHETIC Angiotensinogen RENIN Angiotensin I
A.C.E. ANGIOTENSIN II
Inhibitor
Digitalis. Mechanism of Action Blocks Na+ / K+ ATPase => Ca+ +
• Inotropic effect • Natriuresis • Neurohormonal control -
Plasma Noradrenaline Peripheral nervous system activity Vagal tone Normalizes arterial baroreceptors
What is digoxin?
Digoxin (Lanoxin) is a cardiac glycoside, obtained from the leaves of the foxglove, Digitalis lanata.
Digitoxin and Digoxin • Glycosides have similar action on the heart • Follow somewhat different paths through the body • Have different levels of toxicity in the body
Digitalis lanata • Although D. purpurea contains both digitoxin and digoxin, digitoxin levels are higher • Related species Digitalis lanata (wooly foxglove) is used for digoxin extraction • Both species are still used as sources of the glycosides
Digoxin vs Digitoxin • Also digoxin has shorter half-life in body • These factors led physician to believe digoxin was safe • Digoxin one of most widely prescribed drugs today much more so than digitoxin
Differences in pharmacokinetics â&#x20AC;˘ Digitoxin is more completely and predictably absorbed from the gastrointestinal tract â&#x20AC;˘ Serum concentration not altered significantly by other medications or changes in renal or hepatic function â&#x20AC;˘ Digitoxin also has a much longer elimination time (half life 5 to 7 days as opposed to digoxin which is 1 to 2 days)
Digitoxin • Highly lipophilic • Extensively bound to plasma proteins • Mainly eliminated in urine and feces • Does not accumulate during kidney dysfunction • Bioavailabilty not reduced
Digoxin • Less lipophilic • Show lower protein binding • Shorter half-life • Mainly elimimiated by kidney • Accumulated quite rapidly in cases of insufficient kidney function • In patients with toxic side effects, 70% had renal insufficiency
Function of Na+/K+ ATPase
Outside cell (blood)
Digitalis Na+/K+ ATPase K+ K+ K+ Na+ K+ K+
Na+/Ca2+ Exchange Na+
Myofilaments
Ca2+
Ca2+
K+ Na+ + + Na Na Na+ Inside cell Na+ â&#x2020;&#x2018;CONTRACTILITY
Outside cell (blood)
Digitalis Na+/K+ ATPase
What would happen if Ca2+ was given? What would happen if K+ was low?
Na+/Ca2+ Exchange
+ 2+ K+ K+ K+ Na+ K+ + Na Ca Na + + + Na+ K Na Na
K+ Na+
Ca2+ Myofilaments Ca2+ Ca2+
Inside cell
Ca2+ â&#x2020;&#x2018;CONTRACTILITY
Digoxin Properties of digoxin • • • •
Increases inotropy (contractility) of the heart Decreases chronotropy (heart rate) Natriuresis (sodium loss) minor effect Neurohormonal effects -
Plasma Norepinephrine Peripheral nervous system activity RAAS activity Vagal tone
Symptoms of poisoning Cardiac dysrhythmias
100%
Nausea Vomiting Weakness Fatigue Diarrhoea Dizziness Abdominal Pain Visual Symptoms Headache Sweating Confusion Fever and/or Chills Anxiety Abnormal Dreams
100% 100% 88% 86% 80% 67% 59% 36% 34% 20% 19% 5% 3% 3%
Vision Effects
yellow-tinted vision or yellow corona-like spots
الرؤيةه الملّ وةنةه أفصفره َأ وه قُيفصّفقُره قُبَقَعه شبَهه هالَة
chromatopsia Abnormal هcondition هin هwhich ه objects هappear هfalsely هcoloured. ه Depending هupon هthe هcolour هseen, ه the هchromatopsia هis هcalled ه xanthopsia (هyellow هvision), ه erythropsia (هred هvision), ه chloropsia (هgreen هvision) هor ه cyanopsia (هblue هvision). هThis ه condition هmay هappear هdue هto هsome ه damage هto هthe هareas هof هthe هvisual ه cortex هinvolved هin هthe هprocessing هof ه colour هperception, ه
Affects of cardiac glycasides to ECG (electrocardiography) A. Therapeutic dose: T-wave can become low, flat, isoelectric or inverted S-T segment falls below the isoelectric line P-R interval is lengthened, which is associated with slower or delayed A-V conduction Q-T interval is shortened, ERP and APD is shortened in Purkenje fibers B. Higher dose: arrhythmias
The affects on ECG T wave It is characterized by an descend ST segment on the ECG P-R Q-T P-P
Phosphodiesterase Inhibitors primarily used for management of acute heart failure positive inotropic effects increase rate of myocardial relaxation decrease total peripheral resistance and afterload
Direct acting sympathomimetics cause immediate increases in cardiac inotropy goal: to increase cardiac output but not effect total peripheral resistance used in treatment of acute life-threatening CHF
Dopamine
Dobutamine
Vasodilators Goal: reduce TPR without causing large decrease in BP reduce preload reduce afterload relieves symptoms increase exercise tolerance
Meds to AVOID in heart failure • NSAIDS • Can cause worsening of preexisting HF
• Thiazolidinediones • Include rosiglitazone (Avandia), and pioglitazone (Actos) • Cause fluid retention that can exacerbate HF
• Metformin • People with HF who take it are at increased risk of potentially lethic lactic acidosis
Implantable CardioverterDefibrillators for HF • Sustained ventricular tachycardia is associated with sudden cardiac death in HF. • About one-third of mortality in HF is due to sudden cardiac death. • Patients with ischemic or nonischemic cardiomyopathy, NYHA class II to III HF, and LVEF ≤ 35% have a significant survival benefit from an implantable cardioverter-defibrillator (ICD) for the primary prevention of SCD.