1. Congestive Heart Failure Dory Roedel Ferraro, DNP, ANP-BC, CBN

2. Heart Failure Complex syndrome resulting from any functional or structural disorder of the heart that results in or increases the risk of developing manifestations of low cardiac output and/or pulmonary or systemic congestion Can be prevented or progression slowed by early detection and intervention Conditions that reduce the pumping ability of the heart Coronary artery disease Hypertension Dilated cardiomyopathy Valvular heart disease

3. Heart Failure Systolic dysfunction  in cardiac myocardial contractility Impaired ability to eject blood from the left ventricle Diastolic dysfunction Abnormality in ventricular relaxation and filling

4. Cardiac Output = HR x SV Heart Rate sympathetic nervous system  Parasympathetic  Stroke Volume Preload Afterload Myocardial contractility

5. Systolic vs Diastolic Dysfunction Systolic DysfunctionDiastolic Dysfunction EF< 40%Normal (55-70%) Preload  Afterload  CO  Etiology  contractilityAbnormal ventricular relaxation and filling

6. Preload (Volume) Volume of the ventricle at the end of diastole Determined by venous return End diastolic volume Causes a lengthening of the muscle fibers

7. Afterload (Force) Force that the contracting heart muscle must generate to eject blood from the filled heart Components of afterload Systemic vascular resistance Ventricular wall tension

8. Myocardial Contractility (Inotropy) Contractile performance of the heart The ability of the actin and myosin filaments of the heart muscle to interact and shorten against a load Requires the use of energy supplied by the breakdown of ATP and the presence of Ca ++ ions

9. Manifestations of Right-sided and Left-sided Heart Failure

10. Right-sided CHF Impairs the ability to move deoxygenated blood from the systemic circulation to the pulmonary circulation Congestion of blood in the systemic venous system and the viscera  in RV end diastolic, RA and systemic venous pressure Peripheral edema, ascites and weight gain Caused by LVF, pulmonary HTN, valvular heart disease, RV infarct, cardiomyopathy

11. Left-sided CHF Impairs the movement of blood from the pulmonary circulation into the systemic circulation  in cardiac output to the systemic circulation  pulmonary venous pressure Shift of intravascular fluid into the interstitium of the lung and development of pulmonary edema Most common causes are HTN and acute MI

12. Pharmacological Management of CHF Diuretic To reduce pulmonary and systemic edema ACE inhibitor An inhibitor of the renin-angiotensin-aldosterone system (RAAS) to lower aldosterone and normalize Na+ and K+ levels β-blocker To reduce heart rate Digoxin Increase myocardial contractility

13. Compensatory Mechanisms Frank-Starling mechanism Activation of neurohumoral influences RAAS mechanism Cardiac natriuretic hormones Locally produced vasoactive substances Myocardial hypertrophy and remodeling

14. Frank-Starling Mechanism Serves to match the outputs of the two ventricles Operates through an increase in preload Increased stretching of the myocardial fibers with a resultant increase in the force of the next contraction  ventricular wall tension  myocardial oxygen consumption  ischemia

15. Frank-Starling Curve

16. Sympathetic Nervous System Activity Cardiac sympathetic tone and catecholamine levels (epinephrine and norepinephrine) are elevated in late stages of CHF Helps to maintain perfusion of various body organs Augments BP and cardiac output  sympathetic activity by stimulation of β-adrenergic receptors leads to tachycardia, vasoconstriction and cardiac arrhythmias

17. RAAS  CO  reduction in renal blood flow and GFR  sodium and water retention  reduction in renal blood flow  Renin,  angiotensin II  aldosterone production  reabsorption of water and sodium  edema

18. Natriuretic Peptides (NPs) Peptide hormones produced and secreted by the cardiac muscle (four known NPs) Potent diuretic, natriuretic, and vascular smooth muscle effects Atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) are most commonly associated with heart failure In response to increased chamber stretch and pressure they promote rapid and transient natriuresis and diuresis through an increase in GFR and inhibition of tubular sodium and water reabsorption Inhibit the SNS, RAAS, endothelin inflammatory cytokines, vasopressin Used clinically in the diagnosis of heart failure

19. Myocardial Hypertrophy and Remodeling Principle mechanism by which the heart compensates for an increase in workload Series of complex events at both the molecular and cellular level Three types Symmetric hypertrophy (proportionate  in length and width) “athletes” Concentric hypertrophy (  in wall thickness) Eccentric hypertrophy (disproportionate  in muscle length) “cardiomyopathy”

20. Clinical Manifestations of Heart Failure Respiratory manifestations Fatigue, weakness and confusion Fluid retention and edema Cachexia and malnutrition Cyanosis Arrhythmias and sudden cardiac death

21. Treatment of Heart Failure Non-pharmacologic Oxygen therapy Resynchronization and AICDs Mechanical support and heart transplant Pharmacologic Diuretics ACE inhibitors β-Adrenergic receptor blockers Digitalis Vasodilators (  preload)

22. Circulatory Failure (Shock) Acute failure of the circulatory system to supply the peripheral tissues and organs of the body with adequate blood supply An imbalance between oxygen supply and demand Hypotension and hypoperfusion usually present Syndrome that occurs in the course of many life-threatening traumatic conditions or disease states

23. Pathophysiology of Shock Cellular responses Cell metabolism becomes anaerobic because of decreased availability of oxygen Excess amounts of lactic acid accumulate Limited amounts of ATP are produced Intracellular accumulation of sodium and loss of potassium Cellular edema Increased cell permeability Cell death with release of intracellular contents into the extracellular space

24. Pathophysiology of Shock Compensatory mechanisms which maintain CO and BP Sympathetic nervous system Stimulation of α receptors causes constriction of blood vessels Stimulation of β 1 receptors increases heart rate and force of myocardial contraction Stimulation of β 2 receptors causes vasodilation of the skeletal muscle beds and relaxation of the bronchioles Renin-angiotensin mechanism Augments vasoconstriction and leads to aldosterone mediated increase in sodium and water retention by the kidneys

25. Hypovolemic Shock Occurs when there is an acute loss of 15% or more of the circulating blood volume (loss of whole blood, plasma, extracellular fluid or excessive dehydration) 10% of the total blood volume can be lost without changing CO or arterial pressure (blood donation) Compensatory mechanisms are triggered with >15% loss

26. Manifestations of Hypovolemic Shock Depend on its severity Thirst, tachycardia, cool and clammy skin, decreased BP and urine output, changes in mentation Tachypnea, weak and thready pulse Restlessness, agitation and apprehension

27. Treatment of Hypovolemic Shock Directed toward correcting or controlling the underlying cause and improving tissue perfusion Ongoing loss of blood must be corrected Replacing volume is the first priority Intravenous administration of fluids, blood and blood products Vasopressor and inotropic medications

28. Cardiogenic Shock When the heart fails to pump blood sufficiently to meet the body’s demands Decreased cardiac output, hypotension, hypoperfusion and indications of tissue hypoxia despite an adequate intravascular volume Causes Acute MI Myocardial contusion Acute mitral valve regurgitation due to papillary muscle rupture Sustained arrhythmias Severe dilated cardiomyopathy Cardiac surgery

29. Manifestations of Cardiogenic Shock Cyanotic lips, nailbeds and skin Decreased mean arterial and systolic BP Decreased urine output Alterations in cognition and poor cerebral perfusion

30. Treatment of Cardiogenic Shock Improving CO and reducing the workload and oxygen needs of the heart Regulation of fluid volume to optimize the filling pressure and stroke volume and decrease oxygen demands of the heart Increase coronary artery perfusion and BP Decrease ventricular wall tension Pharmacotherapy: inotropic and vasopressor agents Mechanical support: intraaortic balloon pump

31. Other Types of Shock Obstructive shock: dissecting aortic aneurysm, cardiac tamponade, pneumothorax, ruptured hemidiaphragm, pulmonary embolism Distributive shock (normovolemic shock) Neurogenic shock: decreased sympathetic control of blood vessel tone (spinal cord injury) Anaphylactic shock: immunologically mediated systemic allergic reaction Septic shock: systemic immune response to severe infection

32. Complications of Shock Acute lung injury/ARDS Acute kidney injury GI Disseminated intravascular coagulation (DIC) Multiple organ dysfunction syndrome