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Cardiovascular Case Study

Cardiovascular Case Study. Case Study.

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Cardiovascular Case Study

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  1. Cardiovascular Case Study

  2. Case Study Mr. Alex Borg is a 70 year old retired black male, who presented to the emergency department at 1000 on Saturday September 23rd via ambulance. He was accompanied by his wife. His primary complaints were of chest pain and shortness of breath. This was the Mr. Borg’s third visit to the emergency department in the last 2 weeks, with the same symptoms. On arrival, his chest pain was rated 9/10, and did not subside with rest.

  3. Vitals Upon Arrival • T – 35.9 oC • P – 118 bpm • R – 30 rpm • BP – 168/88 mm/Hg • SpO2 – 88% on RA

  4. Oxygen was applied by nasal prongs at 4L/min which brought his oxygen saturation levels up to 92%. Further clinical assessments were performed in order to confirm suspected diagnosis and treatment. The patient’s lungs were auscultated for decreased air entry and exit, but were clear throughout. Heart sounds were auscultated and a third sound, S3, was heard. Blood was drawn and sent to the lab for cardiac workup and routine chemistry. Peripheral edema was noted with +1 pitting around the ankles. Telemetry monitoring and a 12 lead ECG was performed. ECG results were obtained and showed the following rhythm.

  5. Medications administered: All other systems had no significant findings. An IV was started in the R forearm, N/S TKVO. • Nitrospray spray q 5 minutes x3 doses under the tongue beginning at 1005 • Aspirin 650mg PO given at 1005

  6. Shortly after medications were administered, Mr. Borg’s chest pain decreased to 5/10. • Mr. Borg was admitted to 4W Medical floor for observation. At that point a patient history was obtained with the following significant factors: • His mother died from a heart attack at age 53. • His father had hypertension. • He smokes 1 pack of cigarettes a day • He consumes 4 or more alcoholic drinks a day • He is obese • Wt. 109kg and ht. 5’9” • He has Type II Diabetes Mellitus

  7. Vitals q4h Keep SpO2 >92% with 3L oxygen Cardiac diet AAT IV TKVO NS 30mL/h Daily in & outs Telemetry CXR Repeat cardiac profile in 12 hours. Daily CBC, BUN, Cr, Lytes EC ASA 325mg po daily Metoprolol 100mg po daily Norvasc 2.5mg po daily Nitrospray spray prn Doctors Orders Upon Admission

  8. Diagnosis? Coronary Artery Disease with Anginal Episode

  9. What are coronary arteries?

  10. Coronary Arteries Cont’

  11. Cholesterol • High density lipoprotein (HDL) • A protein bound lipid that transports cholesterol to the liver for excretion in the bile. • Composed of a higher proportion of lipids than the LDLss. • Exerts a beneficial effect on the arterial wall. • Low density lipoprotein (LDL) • Protein bound lipids that transport cholesterol to tissues in the body. • Composed of a lower proportion of protein than the HDLs. • It exerts a harmful effect of the arterial wall.

  12. Coronary Artery Disease (CAD) • LDLs travel through the blood stream and adhere to the walls of the coronary arteries. • Over time, a fibrous layer composed of platelets and other clotting factors envelope the fatty deposits and form a plaque.

  13. Coronary Artery Disease (CAD) • Eventually the plaque buildup becomes so large that the coronary arteries become occluded and blood is unable to pass through. The lack of blood decreases the amount of oxygen that is being delivered to the myocardial cells and myocardial tissue become ischemic. • An occlusion can happen 2 ways: • The vessel becomes totally occluded and blood is unable to pass through at all. • A piece of the plaque breaks off the vessel wall, called a thrombus, and occludes a smaller coronary artery.

  14. How CAD Causes Ischemia

  15. Modifiable Dyslipidemia Hypertension Smoking Diabetes Type II Obesity Sedentary Lifestyle Alcoholism Non-Modifiable Advanced age Males under 60 Race Genetics Diabetes Type I Coronary Artery DiseaseRisk Factors

  16. Diabetes • Diabetic dyslipoproteinemia includes: • increased LDL • increased triglycerides • deceased HDL • Glycation of LDL protein decreases uptake by the liver, increases hepatic synthesis of LDL, and increases LDL oxidation. • Smoking and diabetes also increase LDL oxidation. • Oxidized LDL is toxic to endothelial cells and causes smooth muscle proliferation and abnormal vasoconstriction.

  17. Hypertension • Mr. Borg is currently in a hypertensive state. He has never been diagnosed with hypertension but may have unknowingly had it for years. Hypertension causes hypertrophy of the myocardial cells which increases the myocardial need for coronary flow.

  18. Smoking • Mr. Borg has been a smoker for 40 years. He smokes approximately 1 pack a day. Nicotine in the cigarettes stimulates the release of catecholamines which increases heart rate and vascular constriction. This causes blood pressure to rise and the cardiac workload and need for oxygen to increase.

  19. Obesity • Mr. Borg is an obese man (112 kg). He has lived with obesity for many years. HDL (good cholesterol) levels decrease with obesity. Obesity also causes the heart to increase in size, and therefore increases the workload of the heart. This makes it more difficult to pump blood to the body.

  20. Alcohol • Mr. Borg has been ingesting 4 or more alcoholic drinks each day for the past 35 years. • Alcohol ingestion increases body weight, LDL levels, and blood pressure which are all other leading causes of CAD.

  21. Clinical Manifestations • Chest pain from myocardial ischemia (angina) • Feels like heaviness or pressure • May radiate to the neck, jaw, left arm, shoulder, back, or right arm • Pallor • Diaphoresis • Dyspnea

  22. Angina • When a blood vessel becomes occluded for a long period of time, blood flow is limited and myocardial tissue becomes ischemic. • Length of occlusion time is approx. 10-20 minutes. • The thrombus then breaks apart or vasodilation occurs and myocardial perfusion returns before significant tissue necrosis occurs.

  23. Improving respiratory function Monitor vital signs Bedrest or sitting until pain subsides Oxygen if SpO2 levels are low. Reducing anxiety Develop a trusting relationship Provide privacy Reassure patient Improving cardiac flow Elevate head of the bed Monitor fluid volume status Monitor peripheral pulses Nursing Interventions

  24. Treatment and Evaluation • 3rd heart sound, S3 was heard on auscultation • This indicates left ventricle failure • ECG and telemetry • Laboratory tests

  25. Telemetry • The process of continuous electrocardiographic monitoring by the transmission of radiowaves from a battery-operated transmitter worn by the patient. • Anagram: • L: Smoke (black) over fire (red) • M: White on the right • R: Bear (Brown, on bottom) in the bush (green, on top)

  26. Act on the blood vessels in venous circulation and the coronary arteries Cause generalized vascular and coronary vasodilation which causes: Increased blood flow through the coronary arteries into the myocardial cells. Decreased cardiac preload and afterload Decreased myocardial oxygen demand Side Effects: Headaches from vasodilation Hypotension Dizziness and weakness Faintness *Be careful when using with other vasodilators, Viagra and alcohol because together they can enhance the effects of hypotension. Nitrates - Nitrospray

  27. Act on the B1 receptor sites and decrease the effects of the SNS by blocking the release of catecholamines (epi & norepi) causing: Decreased heart rate Decreased blood pressure Decreased myocardial oxygen demand Decreased anginal pain Side Effects Decreased pulse Decreased blood pressure Bronchospasm Behavioural repsonses Beta-Adrenergic Blockers – Metoprolol

  28. Calcium activates the myocardial cells to contract, increasing cardiac workload and oxygen demand. When these channels are blocked the heart rate slows and the demand for oxygen is decreased. Side Effects Headache Hypotension Dizziness Flushing of the skin Reflex tachycardia Liver and kidney changes Calcium Channel Blocker - Norvasc

  29. Aspirin prevents platelet activation and is used to inhibit clot formation. Aspirin reduces the incidence of MI and death in patients with CAD. Aspirin does not dissolve clots that are already present, but it works prophylactically to prevent clots from forming or enlarging. Aspirin will also help to reduce the pain a patient is experiencing because it is also a non-opioid analgesic. Side Effects GI bleeding Increased bleeding time Anemia from bleeding Anaphylaxis Heartburn, N & V, abdominal pain Hepatotoxicity Anti-Coagulants - Aspirin

  30. While on the floor for the past 2 days, Mr. Borg has been stable with no complaints of chest pain or shortness of breath. Lab reports and CXR came back with no significant findings. Mr. Borg is ready to be discharged tomorrow if no complications occur.

  31. At 1235, Monday September 25th, Mr. Borg’s wife approaches the nursing station in a frantic state. • She states “My husband doesn’t feel very well. He says he feels like he is dying.”

  32. Signs and Symptoms What do we see? • Mr. Borg is sitting at the side of his bed, clutching his chest. • He is diaphoretic and cyanotic around his lips and nail beds. • He has obvious dyspnea because he is gasping for his breath • He seems quite anxious and restless • Upon palpation, his skin is cool and clammy.

  33. Vitals • T – 37.9 • P – 180 bpm • R – 30 rpm • BP – 120/70 • SpO2 – 90% on 3L/min

  34. Assessments and Interventions • Oxygen is increased to 5L/min • Heart auscultated – a third and fourth heart sound are heard, S3 and S4 • Lung ausculation – decreased air entry and exit, chest is clear. • Elevate the head of the bed to 45 degrees, semi-fowlers position

  35. Medications • Nitrospray spray sl q5min x3 • After nitrospray has been administered, Mr. Borg’s chest pain is not relieved • His ECG shows the following:

  36. ECG

  37. ST elevation Altered Q waves Inverted T waves

  38. Altered Q waves • When a thrombus becomes permanently lodged in the coronary artery the infarct (tissue necrosis) spreads from the endocardium through to the epicardium. This results in altered Q waves. • ST Elevation • Myocardial injury also causes ST segment changes. The injured myocardial cells depolarized normally, but repolarize more rapidly then normal cells, causing the ST segment to rise at least 1mm above the isoelectric line. • Inverted T Waves • Myocardial injury causes the T wave to become enlarged and symmetric. As the area of injury becomes ischemic, myocardial repolarization is altered and delayed, causing the T wave to invert.

  39. Diagnosis? Acute Myocardial Infarction

  40. Myocardial Infarction • Plaque progression, disruption, and subsequent clot formation is the same for myocardial infarction as it is for other acute coronary syndromes, such as angina and coronary artery disease. • The same process occurs, but happens along a different point of the continuum. • In an acute MI, the thrombus is lodged for a prolonged period of time, depriving the cells of oxygen and causing cellular injury. The longer the deprivation of oxygen, there is more tissue necrosis that occurs.

  41. Cardiac Tissue Surrounding the Infarct • Myocardial stunning • Temporary loss of contractile functioning • Hibernating myocardium • Tissue that is persistently ischemic and undergoes metabolic adaptation • Myocardial remodeling • Causes myocyte hypertrophy and loss of contractile function

  42. Functional Changes Post MI • Decreased cardiac contractility with abnormal wall motion • Altered left ventricular compliance • Decreased stroke volume • Decreased ejection fraction • Increased left ventricular end diastolic pressure • SA node malfunction • Dysrhythmias and heart failure often follow MI

  43. “Time is Muscle!” • Within 8 seconds oxygen reserves of the myocardial cells are used up, glycogen stores are decreased, and anaerobic metabolism begins. This can put the patient into a state metabolic acidosis. • After 8 – 10 seconds of decreased blood flow the affected myocardium becomes cyanotic and cooler. • After 30 – 60 seconds of hypoxia, ECG changes are visible. • Even if cells are metabolically altered and dysfunctional, they can be saved if blood flow returns within 20 minutes. • Within an hour, tissue necrosis results in the release of certain intracellular enzymes through the damaged cell membranes. These enzymes are evident on the laboratory results.

  44. Creatinine Kinase (CK-MB) This is a cardiac specific enzyme found mainly in cardiac cells and, therefore, rises only when there is damage to these cells. It is the most specific index for the diagnosis of an MI Levels start to increase within a few hours and peak within 24 hours of an acute MI Normal values: 5 – 100 IU/L Patient value 152 IU/L This level is elevated, clearly indicating Mr. Borg has had an MI Laboratory Findings

  45. Myoglobin (Myo) Heme protein that is found in cardiac and skeletal muscle that helps to transport oxygen. Levels begin to increase within 1 – 3 hours, and peak within 12 hours from the onset of symptoms. If these values are negative it is a good indicator that the patient has not had an acute MI If the first test is negative, repeat the test in 3 hours. If the second test is negative it is confirmed that the patient did not have an MI Normal Values <100 ng/mL Patient Value 154 ng/mL Laboratory Findings

  46. Troponins Cardiac and skeletal muscle is controlled by intracellular calcium concentrations. When calcium levels rise, the muscles contract, and when the levels fall the muscles relax. Long filament that calcium binds to. There are 3 types of trops: Trop T Trop I Trop C Trop levels are normally quite low so even slight elevations are indicative of heart damage. Levels of TropT will begin to elevate within 4 hours of myocardial damage and are normally elevated for 1 – 2 weeks post-damage. Normal Values <0.1 ng/mL Patient Values 0.15 ng/mL Laboratory Findings

  47. Serum Glucose Arterial occlusion causes the myocardial cells to release catecholamines. Catecholamines mediate the release glycogen, glucose, and stored fat from body cells. These levels are increased on lab values. Normal values 3.9 – 6.1 Patient Values 7.8 Electrolytes Oxygen deprivation is accompanied by electrolyte disturbances Loss of K Loss of Ca Loss of Mg These electrolytes are released into the blood stream and are evident on lab results. Normal Values Na: 125 - 145 K: 3.5 – 5.0 Mg: 0.74 – 1.23 Patient Values Na: 152 K: 5.3 Mg: 1.36 Laboratory Findings

  48. White Blood Cells WBC levels increase with tissue necrosis and inflammation of the heart. Specifically the neutrophils will have the greatest increase. Normal Findings (Neutrophils) 0.54 – 0.75 Patient Value 0.97 Laboratory Findings

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