Chapter 20: Heart Failure of Shock Flashcards
Define the terms preload, afterload, and cardiac contractility.
Preload**
“End -diastolic volume”
Determined by venous return to the heart
Afterload
Amount of force needed to eject filled heart
Determined by by SVR and ventricular wall tension
Contractility
Performance of cardiac muscle
Positive iontrop increases positive contractility
Discuss the risk factors for developing heart failure
common causes of heart failure are coronary artery disease, hypertension, dilated cardiomyopathy, and valvular heart disease.
Primary the elderly Vessel stiffness -ASHD Hypercholesterolemia Hyperlipedemia Decreased estrogen production for women
Differentiate between systolic versus diastolic heart failure, right-sided versus left-sided heart failure, and high-output versus low-output heart failure.
Systolic Heart Failure
-Impaired ejection of blood
-EF(ejection fraction, the amount of blood ejected from Ventricle) less than 40%
Causes: Muscle issues (CAD, myocarditis, cardiomyopathy, conduction issues)
Volume overload (valvular insufficiency, kidney failure)
Pressure overload (HTN, Valvular stenosis, pulmonary disease)
Diastolic Heart Failure
- Impaired filling during diastole
- Presence of signs and symptoms of HF in the absence of systolic dysfunction (LVEF > 40%)
- Myocardium is “stiff” (and often hypertrophied) and does not relax normally after contraction
Causes:
Impaired ventricular stretch (pericardial effusion, pericarditis, amyloidosis)
Increased wall thickness (hypertrophy, myopathy)
Delayed diastolic relaxation (aging, CAD)
Aggravated by tachycardia
At Risk: women, obesity, HTN, DM
Left-Sided Heart Failure
- decreased CO
- pulmonary congestion
Right-Sided Heart Failure
- systemic
- hepatomegly
- cor pulmonale
- liver congestion
High-Output Failure
Caused by excessive need for CO
Severe anemia
Thyrotoxicosis/thyroid storm
Low-Output Failure
Caused by conditions decreasing pumping ability
Explain how the Frank-Starling mechanism, sympathetic activity, renin-angiotensin-aldosterone mechanism, natriuretic peptides, endothelins, and myocardial hypertrophy and remodeling contribute to the initial adaptation to heart failure and then to its progression.
Frank-Starling Mechanism
- increase in end-diastolic volume (preload) will increase stroke volume
- stretch increases wall tension, increasing oxygen requirement = may lead to ischemia
Sympathetic Activity
- Increase in circulating catecholamines increase, increase HR, contractility, PVR, SV,CO
- Increased workload
- quickly becomes maladaptives = quickly becomes tachycardia, vasoconstriction, cardiac arrhythmias
Renin-angiotensin-aldosterone Mechanism
- Increased concentration of renin, angiotensin II, & aldosterone d/t decreased renal perfusion
- Increased preload, increased workload
- angiotensin 2 and aldosterone are also involved with inflammatory process and the reparative process that follows tissue injury in which Fibroblast and collagen deposition results in ventricular hypertrophy and myocardial wall fibrosis, which decreases compliance (increases stiffness), ultimately causing inappropriate remodeling of the heart and progression of both systolic and diastolic ventricular dysfunction.
Natriuretic Peptide (ANP & BNP)
- Released in response to stretch, pressure, fluid overload (promote diuresis)
- Decreases preload, decreases CO
- The NPs also inhibits the sympathetic nervous system, the renin-angiotensin-aldosterone system, and vasopressin.
- the NPs directly affect the central nervous system and the brain, inhibiting the secretion of the antidiuretic hormone (ADH) and the function of the salt appetite and thirst center.
Endothelins
- Responds to pressure changes (vasoconstrict, myocyte hypertrophy, ANP & catecholamine release)
- Increased workload
- progressively induces vascular smooth muscle proliferation and cardiac myocyte hypertrophy
- increase the release of ANP, aldosterone, and catecholamines; and exert antinatriuretic effects on the kidneys. They also have been shown to have a negative inotropic action in patients with heart failure
Myocardial hypertrophy
-Symmetric hypertrophy
Proportionate increase in muscle length & width (athlete)
- Pressure overload (hypertension)
Concentric hypertrophy d/t replication of myofibrils, thickening of myocytes
Increase in wall thickness (hypertension) - Volume overload (dilated cardiomyopathy)
Eccentric hypertrophy d/t replication of myofibrils, disproportionate elongation of muscle cells (decreased wall thickness)
Describe the pathophysiologic impact of compensatory mechanisms that ultimately contribute to heart failure.
Last question
Discuss the pathophysiology and manifestations associated with atrial fibrillation
Why does it happen:
MI/HF
Valvular damage
Patho: disorganized current flow within the atria (atrial fibrillation) or ventricle (ventricular fibrillation). Fibrillation interrupts the normal contraction of the atria or ventricles Quivering muscle Poor emptying of atria Poor filling of ventricle = decreased CO
How will your patient present?
Irregularly irregular HR
Pulses will be irregular with varying strength
Low BP
Possibility of angina
Possibility of thrombin (because of increased turbulence of the heart and valves)
Relate the effect of left ventricular failure to the development of and manifestations of pulmonary edema
-left ventricular failure causes fluid overload in which increases pulmonary pressure in the lungs due to fluid backed up into the left atria and into the lungs
- Accumulation of capillary fluid in alveoli
- Impairs gas exchange & limits lung expansion
Manifestations -Sob, dypsnea, tachypnea -Tachycardia, moist/cool skin -Fine to course crackles -Frothy, blood-tinged sputum -Cyanotic lips, nailbeds CNS: confusion, stupor
Describe the methods used in diagnosis and assessment of cardiac function in persons with heart failure.
History, physical assessment -Signs and symptoms ECG CXR Echocardiography -Ejection fraction -Wall motion, thickness -Chamber size -Structural defects (valves, tumors)
Blood tests: BNP, CBC
Central venous pressure/jugular vein distension
Pulmonary artery catheter pressures/volumes
Describe the various treatments available to individuals with heart failure.
Non-pharmacological
Exercise program, fluid/Na restriction, weight control, dietary counseling
Non-surgical and surgical medical management
-heart transplant
-pacemaker
Pharmacological
Diuretics, ACE inhibitors, cardiac glycoside (digoxin), ARBs, B-blockers
Oxygen Therapy
Explain the difference between anaerobic and aerobic energy production as it pertains to shock.
Anaerobic energy production
Cytoplasm uses glucose to create ATP and pyruvate
Less efficient
Aerobic energy production
Oxygen and pyruvate create ATP in mitochondria
If no oxygen, pyruvate converts to lactic acid
Compare the pathophysiological processes, manifestations, and typical treatments for cardiogenic shock and hypovolemic shock.
Cardiogenic Shock
Heart failure, uncompensated, failure to eject blood, hypotension and inadequate cardiac output
Causes: Myocardial infarction Myocardial contusion Acute mitral valve regurgitation – d/t papillary muscle rupture Arrhythmias Severe dilated cardiomyopathy Cardiac surgery
Manifestation Similar to extreme heart failure CVS: decreased stroke volume, mean arterial pressure, systole blood pressure Narrow pulse pressure Normal diastolic blood pressure Cyanosis dysrhythmias
Renal: oliguria, anuria
CNS: altered mentation (GCS 15-0)
Treatment
Balance!
Fluid volume management
Treat cause & symptoms
Improve CO, avoid increasing workload of heart
Inotropes (dopamine, dobutamine)
Hypovolemic Shock Any condition which decreases blood volume >15% External Loss Hemorrhage, burns, severe dehydration/vomiting/diarrhea Internal Loss 3rd spacing, hemorrhage Immediate compensation SNS, RAAS, Hypothalamus, fluid shift
Manifestation: CVS -Tachycardia, weak/thready pulses -Skin cool/clammy/mottled -Hypotension -Decreased central venous pressure CNS -ADH release, thirst -Altered mentation (CGS 15-0) Respiratory: tachypnea, deep resps Renal: oligura, anuria
Treatment:
Treat cause
Increase oxygen delivery by maintaining adequate vascular volume
IV crystalloids (increases volume)
IV colloids (rbc’s, plasma volume expanders)
Vasoactive pharmacology (not usually recommended)
State the causes of obstructive shock.
Mechanical obstruction of blood to or through great veins, heart, lungs
Pulmonary embolus Dissecting AA Tamponade Pneumothorax Atrial myxoma –benign tumor in the atrium Abdominal evisceration
The primary physiologic result of obstructive shock is elevated right heart pressure due to impaired right ventricular function. Pressures are increased despite impaired venous return to the heart.
Signs of right heart failure occur, including elevation of CVP and jugular venous distention.
Treatment modalities focus on correcting the cause of the disorder, frequently with surgical interventions such as pulmonary embolectomy, pericardiocentesis (i.e., removal of fluid from the pericardial sac) for cardiac tamponade, or the insertion of a chest tube for correction of a tension pneumothorax or hemothorax. In severe or massive pulmonary embolus, fibrinolytic drugs may be used to break down the clots causing the obstruction.
Compare the pathophysiology of neurogenic shock, anaphylactic shock, and septic shock as they relate to the pathophysiology of distributive shock.
Distributive Shock - Loss of vascular tone usually d/t loss of sympathetic control
Neurogenic Shock: Rare, often transitory depending on the cause Decreased SNS control of vessel tone Brain stem defect Spinal cord injury Drugs General anaesthesia Hypoxia Insulin reaction
Anaphylactic Shock: Immunological mediated reaction of histamine release causing v/d of arterioles and venuoles Increased capillary permeability -The vascular response in anaphylaxis is often accompanied by life-threatening laryngeal edema and bronchospasm, circulatory collapse, contraction of gastrointestinal and uterine smooth muscle, and urticaria (hives) or angioedema. Causes: Medication Foods Insect venom latex
Manifestations dependent on: Level of sensitivity Rate/quantity of antigen exposure Pruritus, urticaria Angioedema Laryngeal edema/bronchospasm Rapid hypotension; circulatory collapse
Treatment:
Remove cause
Epinephrine, oxygen, antihistamines, corticosteroids
Septic Shock:
Systemic inflammatory response to a severe infection
-Neutrophils increase capillary permeability & damage to endothelial cells result
-Cytokines, nitric oxide, & coagulation products are released, damaging cells/tissues and causing massive vasodilation
Manifestations:
CVS: vasodilation (decreased SVR), hypovolemia, hypotension, tachycardia, skin flushed, edema
CNS: pyrexia, abrupt change in mentation
Renal: oligura, anuria
Hemat:leukocytosis, metabolic acidosis,
Treatment: Treat cause Support circulation Oxygen Aggressive fluids Aggressive management of fluids Inotropes Recombinant human activated protein C (rhAPC), a naturally occurring factor that Inactivates clotting factors Inhibits cytokine production
Describe the following complications of shock: acute respiratory distress syndrome, acute renal failure, disseminated intravascular coagulation, multi-organ dysfunctional syndrome, and gastrointestinal complications.
Acute Respiratory Distress Syndrome:
Rapid onset of hypoxemia unrelieved by supplemental oxygen
Ventilation-perfusion mismatch
Atelactasis, impaired gas exchange, fluid limits inflation
Tx: mechanical ventilation, oxygen
Acute Renal Failure:
Ischemia/injury of renal tubules >20 minutes
Disseminated Intravascular Coagulation:
Widespread activation of coagulation cascade (not the primary disease)
Tx: anticoagulation, platelets, plasma
Multi-organ dysfunctional Syndrome:
Failure of multiple organs such that homeostasis cannot be achieved
Disease of mass destruction
Gastrointestinal Complication:
GI bleeding
Tx: proton pump inhibits, histamine-2 receptor antagonists
