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44 Cards in this Set
- Front
- Back
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Define heart failure.
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The inability of the pumping fn of the heart (CO) to meed the metabolic demands of tissues and venous return
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What condition results from heart failure?
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Congestion
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What are the features of passive congestion? (3)
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1. Dilation of chamber
2. Excess blood in chamber 3. Decreased flow out of chamber |
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What % of HF cases have antecedent HTN?
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75%
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What is the ability to increase CO during increased activity called, and how much can it be increased?
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Cardiac Reserve; can increase CO 5-6 times resting values
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The loading condition of the heart at the end of diastole:
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Preload
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The force tt the contracting heart must generate to eject blood:
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Afterload
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Mechanical performance of the heart; the ability of contractile elements to interact & shorten to eject blood from the heart:
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Cardiac contractility
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Two main categories of factors tt cause HF:
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Factors tt affect the contracting ability of the heart
Factors tt affect the workload placed on the heart (2ndary) |
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What are the factors tt affect the contracting ability of the heart? (2)
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Primary myocardial diseases
Restrictions of ventricular filling |
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What are the primary myocardial diseases tt cause HF? Which is the most common?
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AMI - most common
Coronary heart disease Toxic myocarditis Cardiomyopathies EtOH Dysrythmias Inflammation etc. |
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What are the restrictions of ventricular filling that cause HF?
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Diseases of the endocardium (valvular stenosis/regurgitation)
Diseases of the pericardium (cardiac tamponade, constrictive pericarditis, pericardial effusion) |
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What are the factors tt affect the workload of the heart? (3) What are some examples of these factors?
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Increases in peripheral resistance or pressure overload (due to HTN, coarctation of the aorta, aortic stenosis)
Conditions tt increase volume of blood tt heart receives (renal failure, arteriovenous shunt, aortic regurgitation) Excessive work demands (hyperthyroidism, septicemia, severe anemia) |
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What are two types of heart failure (hint: one is forward failure, the other is backward failure)
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Systolic dysfn (forward failure)
Diastolic dysfn (backward failure) |
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What is systolic dysfn?
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The impaired ejection of blood from the heart during systole
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What % of HF cases are from systolic dysfn?
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60-70%
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What is the normal heart ejection fraction?
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SV/DSV = 60-65%
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What happens when ejection fraction decreases? (4)
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Increase in diastolic volume
Increase in ventricular dilation Increase in ventricular wall tension Increase in ventricular end-diastolic pressure |
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What is diastolic dysfn?
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The impaired filling of blood into the heart during diastole
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What % of HF cases are from diastolic dysfn?
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40%
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What are the characteristics of diastolic dysfn? (4)
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Congestive symptoms
Smaller ventricular chamber Ventricular hypertrophy Decreased ventricular compliance |
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What conditions can cause diastolic dysfn?
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Mitral stenosis
Ischemic heart disease Aging - delay in relaxation Increase in ventricular wall tension Rise in ventricular end-diastolic pressure |
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Heart failure tt is accompanied by congestion of body tissue:
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Congestive Heart Failure (CHF)
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What are the clinical manifestations of CHF?
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Systemic venous or pulmonary congestion
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What are some adaptive or compensation mechanisms for heart failure? (5)
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Frank-Starling mechanism
Sympathetic activation RAAS Endothelin Hypertrophy/cardiac remodeling |
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How does sympathetic activation compensate for HF?
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Cardiac sympathetic tone & catecholamine levels increase in HF (stimulated via the baroreceptors when CO is first reduced). This helps maintain perfusion by increasing both rate & force of contraction of heart. Selective vasoconstriction (to increase venous return) stimulates RAS.
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What are the negative aspects of sympathetic activation in HF? (4)
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An increase in afterload puts more strain on the heart;
Prolonged stimulation will eventually produce downregulation of beta-adrenergic receptors; Increase in O2 demand; May contribute to arrhythmias |
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How does HF lead to activation of the RAAS, and how does RAAS compensate for HF?
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Decreased CO leads to decreased renal flow, leading to renin release.
Ang II stimulates aldosterone & ADH synthesis. Aldosterone & ADH both increase volume |
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How does endothelin compensate for HF?
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It is a potent vasoconstrictor and can induce VSM proliferation. It can induce myocyte hypertrophy & may be a partial reason for the development of pulmonary HTN in HF pts
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How does HF lead to cardiac remodeling, and how is hypertrophy an adaptive mechanism?
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Increase in volume leads to dilation of the heart chambers, eventually leading to hypertrophy. Some myocyte hypertrophy is beneficial because can increase cardiac contractility, but non-myocytes (fibroblasts) increase production of collagen synthesis, leading to fibrosis and increased wall thickness
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What other elements also lead to hypertrophy in HF, and how? (3)
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Endothelin, ANP, and Ang II: produce trophic factors tt cause hypertrophy (growth promoters, a non-hemodynamic process)
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What are the 3 types of cardiac hypertrophy? Describe them.
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Symmetric: proportional increase in length & width, seen in athletes;
Concentric: increase in wall thickness, seen in HTN, induced by pressure overload, eventually leads to ischemia; Eccentric: disproportional increase in length over width, occurs in dilated cardiomyopathy, induced by volume overload, can lead to decrease in ventricular wall thickness & increase in diastolic volume & wall tension |
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Signs & symptoms of the manifestations of HF compensation: (7)
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1. Fluid retention & edema
2. SOB 3. Fatigue & ltd exercise tolerance 4. Cyanosis 5. Wt. loss & malnutrition 6. Distention of the jugular veins in R-sided heart failure 7. Diaphoresis (sweating) & tachycardia |
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What is another term for weight loss associated with a chronic disease (such as HF)?
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Cachexia
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Possible causes of L-sided HF: (4)
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Aortic stenosis or mitral regurgitation
L ventricular infarction Cardiomyopathy HTN |
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Mechanisms of L-sided HF (7):
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Dilation of L ventricle
CO falls, blood remains in chamber Increase L ventricular volume increases workload on heart Increase workload of L atria causes dilation & hypertrophy of L atria Capillary pressure exceeds oncotic pressure & fluid leaks into lungs Oxygen exchange is compromised Compensatory mechanisms aggravate congestion |
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Manifestations (signs/symptoms) of L sided HF from congestion: (5)
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Dyspnea on exertion
Fatigue, weakness, dizziness, disorientation Orthopnea Paroxysmal nocturnal dyspnea Pulmonary edema |
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The inability to breathe while lying down:
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Orthopnea
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Labored breathing:
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Dyspnea
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Manifestations of L-sided HF from decreased CO:
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Activation of the sympathetic compensatory mechanisms, leading to:
Increase in HR Oliguria Cyanosis Fatigue Forgetfulness |
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Possible causes of R-sided HF (6):
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Conditions tt restrict blood flow into the lungs
Stenosis or regurgitation of the tricuspid or pulmonic valves R ventricular infarction Cardiomyopathy Persistent L-sided failure Acute or chronic pulmonary disease |
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Manifestations of R-sided HF (4):
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Systemic edema (usually first in lower limbs)
Liver & spleen enlargement Ascites Peripheral vein distention (usu. in neck & hands) |
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Free fluid in the abdominal area is called:
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Ascites
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Classes of heart disease pts
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Class I: have cardiac disease but no limitations in physical activity
Class II: with slight limitations in physical activity Class III: with marked limitation of physical activity Class IV: inability to have physical activity without discomfort |
