Cardiac Function
• A.O. was an 89-year-old woman with a long history of congestive heart failure secondary to a large left ventricular infarct. She had poor activity tolerance and required assistance with activities of daily living. Even minimal activity was associated with moderately severe dyspnea and exertionalchest pain, which was relieved by rest. A.O. also exhibited marked pedal edema bilaterally. She took digitalis, furosemide(Lasix), KCl, and sublingual nitroglycerin.
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1. Which type of heart failure (left or right sided) is usually associated with dyspnea? What other clinical findings are likely to be present with this type of heart failure?
œ Left-sided heart failure is usually associated with both exertionaldyspnea and paroxysmal nocturnal dyspnea.
œ Signs of pulmonary congestion such as basilar crackles, orthopnea, and cough.
œ Chest x-ray shows cardiomegaly.
2 œ Echocardiogram indicates ejection fraction less than 50.
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œ Increased heart rate and S3 heart sound upon auscultation. œ Forward effects include anxiety, confusion, restlessness, oliguria, and fatigue
2. What compensatory mechanisms are likely to be operative in A.O. to enhance cardiac output?
œ Baroreceptorsdetect low BP and CO and excite the sympathetic system resulting in increased heart rate. Eventually the ß receptors will down-regulate and this mechanism will be less effective.
œ Prolonged stretch on the myocardium results in myocardial hypertrophy.
œ Renin-angiotensin system activation causes decreased glomerular filtration rate and fluid retention, which results in increased preload.
4 Cardiac Function 3. What is the most likely cause of A.O.'spedal edema?
œ Prolonged left-sided failure causes back pressure on the right ventricle and eventual biventricular involvement.
œ Right-sided failure causes pedal edema.
5 Cardiac Function 4. What is the cause of A.O.'sexertionalchest pain? What laboratory tests would be useful to confirm this diagnosis?
œ Exertionalchest pain is likely due to angina.
• Normal CK with normal isoenzymes.
• Normal troponins.
• Normal myoglobin.
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• Resting ECG shows no ST elevation.
œ Diagnostic MI ECG
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5. What is the rationale for the use of each of A.O.'smedications in managing her heart disease?
œ Furosemideis a loop diuretic that activates prostaglandins in the kidney to dilate vessels and results in:
• Decreased preload and central venous pressure, thus reducing ventricular filling pressure
• Decreased blood pressure, thus reducing peripheral vascular resistance; decreased systolic vascular resistance; reduced central venous pressure; and decreased left ventricular end-diastolic pressure.
9 Thick Lumen - ascending Interstitium - urine limb blood
sodium/potassium chloride symporter Na+ Na+ ATP K+ - 2Cl K+
K+ (+) K+ potential Cl-
Mg2+, Ca2+
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œ Potassium is given to replace that lost as a result of the effects of furosemide.
œ Digitalis is a cardiac glycoside that functions as:
• Positive inotropic: increase force and velocity of myocardial contractions to increase stroke volume.
• Negative chronotropic: decrease heart rate
• Negative dromotropic: decrease automaticityat SA node, AV node, and bundle of His, and prolong atrialand ventricular refractory periods.
• Promote diuresisdue to improved kidney perfusion.
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œ Nitroglycerin is a nitrate that acts to:
• Dilate blood vessels by relaxing the smooth muscles that surround the vessel, especially veins and coronary arteries. Venous dilation decreases preload and decreases cardiac workload
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• K.R. is a 46-year-old man admitted to the emergency department with unremitting chest discomfort. The pain started while he was shoveling snow from his walkway. He had experienced chest discomfort with activity previously, but the pain had subsided with rest and he sought no medical help. This time the pain did not subside and became increasingly severe, radiating to his left arm and lower jaw. In the emergency department, an ECG and cardiac enzymes were obtained. The cardiac monitor showed sinus tachycardia with occasional premature ventricular complexes. K.R. was treated with 2 L nasal oxygen, tissue plasminogen activator, sublingual nitroglycerin, and IV morphine sulfate. When he was pain free, he was transferred to the cardiac unit for monitoring.
13 Cardiac Function • Angina Pectoris œ chest pain associated with intermittent myocardial ischemia
œ Stable Angina (Classic or Typical Angina)
• Most common
• Stenotic atherosclerotic coronary blood vessels
• When work load of heart increases can‘t supply myocardium with adequate amounts of oxygen
• Cause of pain predictable and is relieved by rest and nitroglycerine
• Candidate for future MI, preventative measures taken, frequent evaluation
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15 Cardiac Function œ PrinzmetalVariant Angina
• Unpredictable, unrelated to physical or emotional stress
• Believed to be the result of vasospasms of unknown cause
• Responds well to Ca2+ channel blockers
œ Unstable Angina
• Very similar to MI œ grouped with MI as Acute Coronary Syndrome (ACS)
• Plaque ruptures and results in formation of a thrombus
œ May resolve
œ May progress to an MI
16 Cardiac Function 1. What electrocardiographic changes would indicate that K.R. has acute coronary syndrome (ACS) or myocardial infarction (MI)?
œ Convex ST -segment elevation with upright or inverted T waves is diagnostic of ACS.
œ ST depression and T-wave changes may also indicate the development of a nonœQ-wave MI.
• TransmuralInfarct
• Non-Q-wave Infarct
œ An old MI is evidenced by larger-than-normal Q waves.
17 Cardiac Function 2. What changes in —cardiac enzymes“ would be consistent with a diagnosis of MI?
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œ Troponins(I and T specific to cardiac muscle cells)
• Markers of choice.
• Elevated between 4 and 6 hours after the onset of an acute MI and remains elevated for 8 to 12 days.
œ Myoglobin
• Levels rise within 1 to 4 hours after the onset of chest pain.
• Myoglobin is highly sensitive but not very specific.
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œ Creatinekinasecomprises three isoenzymes
• Creatinekinasewith muscle subunits (CK-MM), which is found mainly in skeletal muscle
• Creatinekinasewith brain subunits (CK-BB), predominantly found in the brain
• Myocardial muscle creatinekinase (CK-MB), which is found mainly in the heart.
œ CK-MB levels increase within 3 to 12 hours of onset of chest pain
œ Reach peak within 24 hours, and return to baseline after 48 to 72 hours.
œ Levels peak earlier if reperfusion occurs.
œ Sensitivity is approximately 95%, with very high specificity.
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3. What is the most common precipitating event for MI?
œ In most cases of MI plaque rupture followed by thrombus formation at the site is the precipitating event.
4. What is the rationale for using tissue plasminogen activator in the management of ACS?
œ Tissue plasminogen activator is fibrin specific.
œ It binds to the fibrin of fresh clots, and the resulting compound converts adjacent plasminogen into plasmin creating localized thrombolysis.
21 Cardiac Function 5. Why are morphine and nitroglycerin used to manage ischemic chest pain?
œ Pain relief is a high priority to reduce myocardial stimulation by the sympathetic nervous system.
œ Morphine sulfate reduces anxiety and catecholamine secretion and is a preload reducer.
œ Nitroglycerin causes relaxation of vascular smooth muscle, which decreases preload and reduces MVO2 (myocardial oxygen consumption).
22 Cardiac Function • C.J. is a 16-year-old high school student who is in the clinic for a sports physical prior to beginning basketball practice. He has no known significant medical history, takes no medications, and has no allergies. A review of systems reveals only that C.J. gets —winded“ earlier than most boys on the team. He attributes this to needing to get in better shape. The physical exam is unremarkable except for a grade III systolic murmur heard over the entire precordium. An echocardiogram and cardiac cathreveals a ventricular septaldefect (VSD) with moderate pulmonary hypertension.
23 Cardiac Function 1. A VSD is usually an acyanotic defect. Why is this?
œ The blood being shunted is oxygenated blood from the left ventricle shunted to the right because pressures on the left are higher.
24 Cardiac Function 1. What is the mechanism and significance of pulmonary hypertension?
œ The mechanism of pulmonary hypertension is due to increased blood volume within the pulmonary circuit from the VSD. Pressure is the product of CO and vascular resistance. In this case pressure is high secondary to increased CO. In the case of primary pulmonary hypertension, the cause is increased pulmonary vascular resistance.
œ Pulmonary hypertension can lead to cor pulmonale (right ventricular hypertrophy) and right-sided heart failure.
25 Cardiac Function 2. What other disorders besides VSD can produce a systolic murmur? How can character of the murmur and pattern of radiation be used to differentiate among these etiologic factors?
œ Systolic murmurs can be produced by mitralvalve prolapse, aortic or pulmonary stenosis, mitralor tricuspid regurgitation.
œ Heart sounds are produced in different areas of the heart and have different characteristics.
• Aortic stenosis
œ Right second intercostalspace
œ Midsystolic
œ Crescendo-decrescendo and radiates to the neck.
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• Mitralregurgitation
œ Apex and is radiates to the left axilla.
œ Loud, pansystolic, high pitched
œ Mitralregurgitation - difficult to distinguish from VSD murmur
œ
28 Cardiac Function 3. Is it necessary to close a VSD? What are the common complications of untreated VSD?
œ No, it's not always imperative to close VSDsdepending on patient's age, size of defect, and degree of shunt. Some VSDsclose spontaneously at a young age, whereas others generally require surgical correction.
œ Common complications include
• Pulmonary hypertension
œ If pulmonary hypertension develops, the shunt may reverse to a right-to-left pattern and cause hypoxemia.
• Cardiomegaly
• Atrialdysrhythmia
• Right-sided heart failure.
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