Question

Ms. X, age 55 years, has been complaining of severe fatigue and...


Ms. X, age 55 years, has been complaining of severe fatigue and "indigestion" on and off, but it seems to be getting worse over the past several hours. Her son is quite concerned and decides to take her to the emergency department. On arrival, she appears very anxious, and her facial skin is cool and clammy; her blood pressure is 90/60, and the pulse is around 90, weak and irregular. She is given oxygen, an intravenous line is opened, and leads for ECG are attached. Blood is taken for determination of serum enzymes and electrolytes. Tentative diagnosis is myocardial infarction involving the left ventricle. Her son provides information that indicates Ms. X is a long-time smoker, has a stressful job as a high school teacher, is recently separated after 20 years of marriage, and is fearful of losing the family home. She has also seemed to be more fatigued, and stopped going to the gym about 18 months ago. She has begun to rely on "fast foods" like pizza and fried chicken and cooks infrequently. Her father died of a heart attack at age 50. She has also noticed more fatigue and intermittent leg pain when walking or climbing stairs at work. Generalized atherosclerosis is suspected.




    What do you suspect Ms. X was experiencing when she reported "indigestion"? Was this true indigestion or related to her cardiac condition? Explain the pathophysiology behind this pain


   Think about the normal or typical presenting signs of myocardial Infarction. What is atypical in Ms. X's symptoms? How does this affect treatment and prognosis?


   What serum enzyme and electrolyte levels do you anticipate being checked in the ED. How are these levels related to the changes happening in Ms. X's cardiovascular system?

Answer & Explanation
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What do you suspect Ms. X was experiencing when she reported "indigestion"? 

  • I think that she was experiencing heartburn.  Heartburn or indigestion/feeling of fullness is a symptom of myocardial infarction. As presented in the history, she frequently rely on  fastfood as her meal and had a lot of stress lately which are a risk factor for myocardial infarction

Was this true indigestion or related to her cardiac condition? Explain the pathophysiology behind this pain.

  • Heartburn, or acid indigestion, happens when your stomach acid flows back into your esophagus. It causes an uncomfortable burning feeling or pain in your chest that can move up to your neck and throat. It is the main symptom of myocardial infarction. It can be differentiated from a simple indigestion (gastric pathology) to myocardial infarction by the presence of other associated symptoms which includes shortness of breath (patient is given oxygen) and sweating (cold clammy skin). 
  • attached in the explanation is the pathophysiology with symptoms associated to myocardial infarction

   Think about the normal or typical presenting signs of myocardial Infarction. What is atypical in Ms. X's symptoms? How does this affect treatment and prognosis?

  • typical presenting signs of myocardial infarction:
    • Angina: Chest pain or discomfort in the center of the chest; also described as a heaviness, tightness, pressure, aching, burning, numbness, fullness or squeezing feeling that lasts for more than a few minutes or goes away and comes back. It is sometimes mistakenly thought to be indigestion or heartburn.
    • Pain or discomfort in other areas of the upper body including the arms, left shoulder, back, neck, jaw, or stomach.
    • Trouble breathing or feeling shortness of breath.
    • Sweating or "cold sweat."
    • Fullness, indigestion, or choking feeling (may feel like "heartburn").
    • Nausea or vomiting.
    • Light-headedness, dizziness, extreme weakness or anxiety.
    • Rapid or irregular heart beats.
  • atypical presentation: intermittent leg pain when walking or climbing stairs (atherosclerosis)
    • Atherosclerosis is the predisposing factor of having myocardial infarction. Atherosclerosis is a slow, progressive disease. Although the exact cause is unknown, atherosclerosis may start with damage or injury to the inner layer of an artery. The damage may be caused by High blood pressure, High cholesterol, High triglycerides, Smoking and other sources of tobacco, Insulin resistance, obesity or diabetes, and inflammation from diseases, such as arthritis, lupus or infections, or inflammation of unknown cause. Once the inner wall of an artery is damaged, blood cells and other substances often clump at the injury site and build up in the inner lining of the artery. Over time, fatty deposits (plaque) made of cholesterol and other cellular products also build up at the injury site and harden, narrowing your arteries. The organs and tissues connected to the blocked arteries then don't receive enough blood to function properly. Eventually, pieces of the fatty deposits may break off and enter your bloodstream. In addition, the smooth lining of the plaque may rupture, spilling cholesterol and other substances into your bloodstream. This may cause a blood clot, which can block the blood flow to a specific part of your body, such as occurs when blocked blood flow to your heart causes a heart attack. A blood clot can also travel to other parts of your body, blocking flow to another organ.  (see explanation for the diagram)

 What serum enzyme and electrolyte levels do you anticipate being checked in the ED. How are these levels related to the changes happening in Ms. X's cardiovascular system? (see 3rd photo in the explanation)

  • C-reactive protein
    • increase due to tissue necrosis leading to local myocardial inflammation
  • Serum Troponin levels
    • increase, most sensitive and specific marker for myocardial necrosis
  • Serum CK-MB levels
    • less sensitive and specific than troponins but has faster clearance to the circulation


 

Step-by-step explanation
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Image transcriptions
Myocardial Infarction: Myocardial infarction Findings on Physical Exam (tissue necrosis) Systolic function Diastolic compliance Necrosis of (necrotic myocardium (necrotic myocardium does not relax papillary cannot contract as well) as well to accommodate blood) muscles: J Force of ventricular J Stroke volume (SV), Blood "backs up" Atrial Papillary muscle contractions cardiac output (CO) into L atrium -> contraction dysfunction or into pulmonary forces blood rupture circulation > into non- Diffuse Reflexive T in Left ventricle pulmonary blood compliant LV (fainter), sympathetic pressure at end diastole Valve leaflets activity (to try to T HR (LV) becomes Dyskinetic overfilled with not properly maintain CO) supported (uncoordinated) residual blood Pulmonary apex beat congestion/edema: (4th heart exudative fluid fills sound) T Sweating Generalized Turbulent early Mitral valve some alveoli, (diaphoresis) vasoconstriction diastolic flow regurgitation collapsing them from L atrium Vasoconstriction into "full" LV Clammy of skin arterioles On inspiration, air Pansystolic murmur skin enters + opens (best heard at apex) Cool skin S3 alveoli, > makes (3rd heart crackling sound sound) Note: BP is determined by cardiac output (CO) & Inspiratory Crackles systemic vascular resistance (SVR). MI may J.CO & (aka. rales) on auscultation thus may JBP. But generalized vasoconstriction Tes SVR in attempt to maintain BP. Hence, BP may be normal in MI, and low BP is NOT a specific sign of MI. Legend: Pathophysiology Mechanism Sign/Symptom/Lab Finding Complications
Atherosclerosis: Development of an "atheroma" (lipid-filled inflammatory plaque) in the artery wall Complications (atherosclerosis) If the plaque's fibrous cap remains Rupture of the fibrous cap overlying stable (does not rupture): the atheromatous plaque: Plaque expansion intrudes into The rough surfaces of the fibrous cap and the contents lumen of the blood vessel, of the lipid core are exposed to the lumen of the artery severely occluding bloodflow with local activation of coagulation pathway Embolism of Effects vary depending on location: Persistent 02 supply-demand Thombosis at mismatch, especially on exertion site of rupture thrombus Heart Acute Coronary Syndromes (ACS) (in the lumen of Coronary artery Stable stenosis on epicardial coronary angina If no myocyte death If myocytes have died arteries) angiography Unstable Angina Myocardial Infarction (MI) Brain Embolization of thrombotic material on plaque TOTAL occlusion of artery lumen (in the lumen of carotid or cerebral arteries) Transient Ischemic Attack (TIA) Cerebrovascular Accident (CVA) - (aka. Stroke) Vessel occlusion & calcification /weakening of Aortic Aneurysms Aorta Peripheral the aortic wall > parts of the wall bulge out (can rupture and hemorrhage) Arteries Peripheral vascular disease Legs Occlusion of iliac, popliteal, or other leg arteries (can lead to claudication, gangrene & amputation) Bowel Occlusion of the celiac or mesenteric arteries -Bowel Infarction Legend: Pathophysiology Mechanism Sign/Symptom/Lab Finding Complications
Myocardial Infarction: Findings on Investigations Myocardial infarction Tissue necrosis > Dead, damaged cardiac Tissue ischemia disrupts normal Local myocardial myocytes release inner cardiac electrical conduction inflammation contents into the blood (detected on serial ECG) Inflammatory 2-4 hours after MI: 3-8 hours after MI: Ischemia of sub- Acute, trans-mural cytokines can spread troponin proteins Creatinine-kinase endocardial myocardial systemically released into blood MB-isozymes myocardium ischemia released into blood C-Reactive Stimulation of T serum Cardiac ST-segment ST-segment Protein (CRP) neutrophil and Troponins: cTnT, cTnl 1 serum CK-MB depression elevation monocyte migration (Sensitive and most (less sensitive and (non-localizing) (localizes to site towards area of specific serum marker specific for myocardial of ischemia) inflammation for myocardial necrosis) necrosis than Troponins) If ischemia progresses to T WBC count Relatively slower Relatively faster tissue infarction (on CBC) clearance from clearance from circulation circulation Pathologic Q-waves (localizes to site of ischemia) Serum Troponin Serum CK-MB levels normalize levels normalize within 14 days within 3 days Note: Both types of ST-segment changes are non-specific: they can indicate Myocardial Infarctions , but can also be false positives Note: Measuring both CK-MB and Troponins gives a timeline (i.e. caused by left ventricular hypertrophy, to the MI. For instance, if CK-MB is normal but Troponins are bundle branch blocks, and other non- high, it means the MI happened >3 days but <14 days ago. myocardial ischemic causes)