Approach to Common Cardiac Symptoms PDF

CM 109: INTEGRATED BASIC SCIENCES II (PHYSICAL DIAGNOSIS) APPROACH TO COMMON CARDIAC SYMPTOMS: CHEST PAIN/PALPITATIONS/EDEMA DR. JERELYN ADVIENTO| 21 AUGUST 2024...

CM 109: INTEGRATED BASIC SCIENCES II (PHYSICAL DIAGNOSIS) APPROACH TO COMMON CARDIAC SYMPTOMS: CHEST PAIN/PALPITATIONS/EDEMA DR. JERELYN ADVIENTO| 21 AUGUST 2024 → Dyslipidemia TABLE OF CONTENTS → Hyperglycemia → High Blood Pressure → Obesity I. ASSESSMENT OF SUSPECTED CARDIAC SYMPTOM 1 → (older age, race/ethnicity, and sex differences) A. NEW YORK HEART ASSOCIATION CLASSIFICATION 1 → Smoking B. ASSESS FOR RISK FACTORS 1 → Kidney dysfunction II. CHEST PAIN 1 → Genetics/ familial hypercholesterolemia A. CASE VIGNETTE 1 B. CHEST PAIN 1 C. APPROACH TO CHEST PAIN 1 D. CHEST PAIN HISTORY 1 E. CONSIDERATIONS IN ASSESSMENT OF PATIENT WITH CHEST DISCOMFORT 2 F. CHEST PAIN CHARACTERISTICS 2 G. CHEST PAIN CHARACTERISTICS AND PROBABILITIES 2 H. PE IN PATIENTS WITH CHEST PAIN 2 III. PALPITATIONS 5 A. APPROACH TO PALPITATIONS 5 B. CAUSES OF PALPITATIONS 6 IV. EDEMA 6 Figure 1. The Cardiovascular Continuum Retrieved from PPT of Dr. Jerilyn Adviento A. EDEMA 7 II. CHEST PAIN B. APPROACH TO PATIENTS WITH EDEMA 7 C. IS EDEMA LOCALIZED? 7 A. CASE VIGNETTE Which patient is more likely to have acute coronary syndrome? D. IS EDEMA GENERALIZED? 7 → 35 y.o. Male, Luis health buff with good functional capacity. E. MEDS THAT CAUSE EDEMA 7 Sudden onset of sharp substernal chest pain, 6/10 aggravated by F. APPROACH TO PATIENT WITH EDEMA: PHYSICAL bending over, relieved by lying supine EXAMINATION 8 → 55 y.o. Female, May is a CEO, while during a business meeting had sudden onset of sharp substernal chest pain 6/10 radiating to G. DIAGNOSTIC APPROACH TO UNILATERAL LOWER the left arm, not relieved by lying supine, and worsens during EXTREMITY EDEMA 8 walking H. APPROACH TO UNILATERAL SWELLING AND IN SUSPECT FOR DEEP VEIN THROMBOSIS 8 PRECEPTOR NOTES I. DIAGNOSTIC APPROACH TO BILATERAL LOWER For cases like these, the clue lies in the description of chest pain EXTREMITY EDEMA 9 First case → Probable esophageal pain / costochondritic / positional V. SUMMARY: APPROACH TO CARDIAC SYMPTOMS 9 Second case is more probable VI. REFERENCES 9 → Ischemic description of chest pain → Highly likely to have acute coronary syndrome I. ASSESSMENT OF SUSPECTED CARDIAC SYMPTOM B. CHEST PAIN Be systematic as you think through the range of possible etiologies: One of the most serious of all patient complaints, and accounts for → Cardiac, Pulmonary, and Extrathoracic 1% of primary care outpatient visits When assessing cardiac symptoms it is important to quantify the The most common symptom of coronary heart disease (CHD) patient’s baseline level of activity CHD is the leading killer of both men and women → In the patient’s chest pain, does the pain occur with climbing C. APPROACH TO CHEST PAIN stairs? How many flights? How many steps? How about when 1. Identify life-threatening causes thorough Hy PE - carrying groceries, How does this compare with these activities in 2. Determine clinical stability the past? 3. Assess need for hospitalization versus safety of outpatient evaluation Know the onset and timing of symptoms and management → If the patient is short of breath, does this occur at rest, during exercise, or after climbing stairs? PRECEPTOR NOTES → This would dictate the phasing of how would you go with the PE In identifying life-threatening causes, you’ll get this from a thorough Quantifying the baseline level of activity will establish both the history and PE severity of the patient’s symptoms and their significance as you consider the next steps for management D. CHEST PAIN HISTORY Focused history OLD CARTS Chest pair- PQRST A. NEW YORK HEART ASSOCIATION CLASSIFICATION Begin with open-ended question S I Location , Aggravation intensity (o) , radiating , Table 1. New York Heart Association Classification → “Please tell me about any symptoms you might be having in your NYHA Class Symptoms chest.” associated sympters → Elicit more specific details I No limitations in normal physical activity → Ask the patient to point the pain and describe all seven features II Mild symptoms only in normal activity of the symptom → Clarify “Is the pain related to exertion?” and “What kinds of III Marked symptoms during daily activities, activities bring on the pain?” asymptomatic only at rest → “How intense is the pain, on a scale of 1 to 10?” → “Does it spread into the neck, shoulder, back, or down your arm?” IV Severe limitations, symptoms even at rest → “Are there any associated symptoms like shortness of breath, sweating, palpitations, or nausea?”...”Does it ever wake you up at PRECEPTOR NOTES night?”...”What do you do to make it better?” This is how you’ll quantify the patient’s functional capacity using NYHA Classification PRECEPTOR NOTES In NYHA Class IV, symptoms are present like Chest pain and For chest pain: Shortness of breath → Focused history and begin with open-ended questions ▪ OLD CARTS B. ASSESS FOR RISK FACTORS ▪ PQRST for the chest pain Top 10 CVD Risk Factors → Unhealthful nutrition → Physical inactivity/ sedentary life Trans 2 B6: Lareza, Marchan, Martinez, Moral, Napoles, Pecson, Rico, Salvo, Sernias, Tadiosa, Villar, Yaneza TH: Saysay 1 of 12  E. CONSIDERATIONS IN ASSESSMENT OF PATIENT WITH → Severe pain, 10/10, for 3 days, that is highly unlikely to present MI CHEST DISCOMFORT and needs to check the veracity of the patient’s account/statement Provoking and Alleviating Factors → Patients with myocardial ischemic pain are relieved by rest. → Changes in intensity of pain with position or movement are less likely with myocardial ischemia suggest a musculoskeletal etiology. → Positional such as pain worse on supine and relieved by sitting upright and leaning forward is more likely pericarditis → Gastroesophageal reflux may be exacerbated by alcohol, some foods, or a reclined position. → Exacerbation by eating suggests a gastrointestinal etiology such as peptic ulcer disease, cholecystitis, or pancreatitis. Peptic ulcer disease tends to become symptomatic 60-90 min after meals → Pain relieved by use of nitroglycerin ▪ Within mins is suggestive but not sensitive for diagnosis of ischemia ▪ With a delay of 10 or more mins may or may not indicate ischemia or severe ischemia such as acute MI PRECEPTOR NOTES Pain that is related to food intake before, after, and the middle of morning, or lie down on the right side = gastroesophageal reflux Associated Symptoms → Symptoms that may be associated with myocardial ischemia may include: ▪ Diaphoresis, dyspnea, nausea, fatigue, faintness, and eructations/burping → Dyspnea + chest pain suggests a cardiopulmonary etiology → Sudden onset of significant respiratory distress should lead to Figure 2. Considerations in assessment of Pt. with Chest Discomfort consideration of pulmonary embolism and spontaneous Retrieved from PPT of Dr. Jerilyn Adviento. pneumothorax → Hemoptysis may occur with pulmonary embolism or as F. CHEST PAIN CHARACTERISTICS blood-tinged frothy sputum in severe heart failure but usually Location / Radiation points toward a pulmonary parenchymal etiology of chest → Substernal location with radiation to the neck, jaw, shoulder, or symptoms arms is typical of myocardial ischemic discomfort → Presentation with syncope or presyncope should prompt → Radiation to both arms has a particularly high association with MI consideration of hemodynamically significant pulmonary → Pain that is highly localized – e.g. that which can be demarcated embolism or aortic dissection as well as ischemic arrhythmias by the top of one finger – is highly unusual for angina → Retrosternal location should prompt consideration of esophageal G. CHEST PAIN CHARACTERISTICS AND PROBABILITIES pain → Pain radiating to abdomen and epigastrium - gastrointestinal conditions → Severe pain radiating to the back, particularly between the shoulder blades, should prompt consideration of an acute aortic syndrome Figure 4. Index of Suspicion Than Chest “Pain” is Ischemic in Origin on the Basis of Commonly Used Descriptors Retrieved from PPT of Dr. Jerilyn Adviento. PRECEPTOR NOTES If the chest pain is NOT described as acute, it is likely a STABLE ANGINA Figure 3. Chest Pain Locations and Radiations Retrieved from PPT of Dr. Jerilyn Adviento. Pattern → Myocardial ischemic discomfort starts with a low level of pain and the pain intensity increases wherein it is exacerbated with activity Figure 5. Chest Pain Characteristics and Responsibilities and mitigated by rest Retrieved from PPT of Dr. Jerilyn Adviento. → Pain that reaches its peak intensity immediately means a 10/10, reaping, and lancinating is highly suggestive of aortic dissection, radiating to the back → High intensity with difficulty breathing could be a pulmonary embolism → Fleeting pain lasts a few seconds to less than 2 minutes is rarely ischemic in origin CM 109 B6: Lareza, Marchan, Martinez, Moral, Napoles, Pecson, Rico, Salvo, Saysay, Sernias, Tadiosa, Villar, Yaneza 2 of 12  H. PE IN PATIENTS WITH CHEST PAIN DIAGNOSTICS: 12 LEAD ECG Table 2. PE in Patients with Chest Pain. In all patients who present with acute chest pain regardless of the Clinical Syndrome Findings setting, an ECG should be acquired and reviewed for STEMI within 10 minutes of arrival Emergency ACS Diaphoresis, tachypnea, tachycardia, hypotension, crackles, S3, MR murmur; examination may be normal in uncomplicated cases PE Tachycardia + dyspnea → 90% of patients; pain with inspiration Aortic Dissection Connective tissue disorders (eg, Figure 6. 12 Lead ECG Marfan syndrome), extremity Retrieved from PPt of Dr. Jerilyn Adviento. pulse differential (30% of patients, type PRECEPTOR NOTES A>B) Check ECG if there is STEMI or ST Elevated Myocardial Infarction Severe pain, abrupt onset + Sinus Rhythm pulse → Upright P, R and T is normal differential + widened mediastinum on CXR > 80% probability of dissection Frequency of syncope > 10%, AR 40%-75% (type A) Esophageal Rupture Emesis, subcutaneous emphysema, pneumothorax (20% patients), unilateral decreased or absent Figure 7. 12 Lead ECG breath Retrieved from PPt of Dr. Jerilyn Adviento. sounds Normal sinus rhythm with lateral, septal, and anterolateral myocardial infarction with inferior ischaemia Reading: Sinus rhythm with anteroseptal and lateral wall MI Other Left main heart disease → this patient is a possible bypass Noncoronary cardiac : AS : Characteristic systolic AS, AR, HCM murmur, tardus or parvus carotid pulse AR : Diastolic murmur at right of sternum, rapid carotid upstroke HCM : Increased or displaced left ventricular impulse, prominent α wave in jugular venous pressure, systolic murmur Figure 8. 12 Lead ECG Pericarditis Fever, pleuritic chest pain, Retrieved from PPt of Dr. Jerilyn Adviento. increased in supine position, friction rub Myocarditis Fever, chest pain, heart failure, S3 Esophagitis, peptic ulcer Epigastric tenderness disease, gallbladder disease Right upper quadrant tenderness, Murphy sign Pneumonia Fever, localized chest pain, may be pleuritic, friction rub may be present, regional dullness to percussion, egophony Pneumothorax Dyspnea and pain on inspiration, Figure 9. Arteries of the Heart unilateral absence of breath Retrieved from PPt of Dr. Jerilyn Adviento. sounds PRECEPTOR NOTES Costochondritis, Tietze Tenderness of costochondral 12 Lead ECG Localization: syndrome joints → In ECG, you have 6 leads I, II, III, aVR, aVL, AVF, v1, v2, v3, v4, v5, v6 Herpes zoster Pain in dermatomal distribution, ECG can tell which area/wall of the heart is compromised triggered by touch; characteristic If there’s a problem in the localization, then they are compromised rash (unilateral and dermatomal which pertains to their electrical activity such as: distribution) → OLDLead I and aVL - the lateral wall of the heart ▪ pertains to the electrical activity in lateral wall of the heart → Lead II, III, aVF - inferior wall of the heart → Lead V1 and V2 - septal wall of the heart → Lead V3 and V4 - anterior wall of the heart → Lead V5 and V6 - lateral wall of the heart ▪ Ex. ST elevation → MI while ST depression/inversion → ischemia − Lead I and aVL has ST elevation = lateral wall MI CM 109 B6: Lareza, Marchan, Martinez, Moral, Napoles, Pecson, Rico, Salvo, Saysay, Sernias, Tadiosa, Villar, Yaneza 3 of 12  − Lead II, aVF, III has ST inversion = inferior wall ischemia − Lead V1 and V2 has ST elevation = septal wall MI − Lead V3 and V4 has ST elevation = anterior wall MI − Lead V5 and V6 has ST elevation = lateral wall MI Diagnosis or Reading is Sinus Rhythm with Lateral, Septal, Antero-lateral walls Myocardial Infarction, and Inferior wall Ischemia In Myocardial Infarction, it is important to know which artery is involved and know how many arteries is expected to have an occlusion: → Aorta → Right Coronary Artery (RCA) → Lead II, III, aVF - inferior wall of the heart → Left Coronary Artery → Left Circumflex Artery (LCX) → Lead I, aVL, V5 and V6 - the lateral wall of the heart → Left Anterior Descending Artery (LAD) → Lead V1 and V2 - septal wall of the heart and Lead V3 and V4 - anterior wall of Figure 11. Normal Chest X-ray the heart Retrieved from PPt of Dr. Jerilyn Adviento ▪ This means the Left Main Artery (left Coronary Artery) could probably be affected because both the LCX and LAD are PRECEPTOR NOTES affected The Chest X-ray is in AP view since clavicles are in front ▪ The affectation is LCX + LAD or LMA → 2 vessels disease or There are 4 borders of the heart: a left main heart disease meaning this patient is possible for → Right border - right atrium and right hilum a bypass → Left side heart - left ventricle and left atrium Anatomy of coronary artery → Superior border - great vessels (aorta & pulmonary) → Aorta supplies right coronary → Inferior border - right ventricle → Circumflex supplies lateral wall Note for the the ST elevations in the ECG ST elevation in lateral wall pertains to left circumflex affected → Inferior wall - ARC affected → Septal wall - left anterior descending affected I. ECG DIRECTED MANAGEMENT ALGORITHM OF CHEST PAIN Figure 12. Abnormalities in Chest X-ray Retrieved from PPt of Dr. Jerilyn Adviento Cardiomegaly → Enlarged heart → The normal CT ratio is the widest diameter of the heart divided by the thoracic ratio or the widest diameter of the thorax; should not be more that 0.52-0.54 PRECEPTOR NOTES Know which part of the heart is enlarged RA is enlarged = right side RV is enlarged= _____ LV is enlarged = left border is enlarged Congestive Heart Failure (CHF) Figure 10. ECG and Chest Pain Decision Tool → The angle is not visible Retrieved from PPt of Dr. Jerilyn Adviento. → Basal congestion right → Full fuzzy hilum PRECEPTOR NOTES Tetralogy of Fallot First thing to do when patient complains of chest pain: Do a → Boot-shaped heart or like a shoe thorough and focused physical exam and history taking → Enlarged RV (RV hypertrophy) Follow with ECG within 10 minutes. The ECG results will dictate → LV hypertrophy which guidelines you should follow ST-elevation seen in ECG → Follow STEMI guidelines Diffuse ST-elevation consistent with pericarditis → Pericarditis: Positional chest pain, relieved upon leaning forward → Follow the non ST-elevation guidelines If ECG is nondiagnostic (no ischemia/elevation) or patient has normal ECG → Follow up with repeat ECG if symptoms persist → Check for cardiac markers New arrhythmia seen on ECG → Follow arrhythmia specific guidelines DIAGNOSTICS: CHEST X-RAY Figure 13. Abnormalities in Chest X-ray In patients presenting with acute chest pain, a chest radiograph is Retrieved from PPt of Dr. Jerilyn Adviento useful to evaluate for other potential cardiac, pulmonary, and Lung mass thoracic causes of symptoms. → There’s a haziness at the left upper lung field which is equal to a Normal chest x-ray mass **Non-ST-Elevation Acute Coronary Syndrome (NSTE-ACS)** refers to a spectrum of conditions ranging from unstable angina (UA) to non-ST-elevation myocardial infarction (NSTEMI). Management of NSTE-ACS is guided by Pneumonia various clinical guidelines, which are regularly updated by organizations like the American College of Cardiology (ACC) and the American Heart Association (AHA). → Also presents with consolidation or infiltrates (ex. shown in picture ### Key Points from Current NSTE-ACS Guidelines: #### 1. **Initial Assessment and Risk Stratification:** is the left and right infiltrates) - **History and Physical Examination**: Evaluate symptoms (e.g., chest pain), risk factors, and clinical signs. - **Electrocardiogram (ECG)**: Perform immediately to assess for ischemic changes (e.g., ST-segment depression, T-wave inversion). Thoracic-aorta/thoraco-aortic aneurysm (TAA) - **Cardiac Biomarkers**: Measure troponin levels to detect myocardial injury. Troponin is typically elevated in NSTEMI but not in unstable angina. - **Risk Scores**: Use tools like the **TIMI** (Thrombolysis in Myocardial Infarction) or **GRACE** (Global Registry of Acute Coronary Events) scores to stratify risk and guide management decisions. → Normal: The aorta should be at the superior border of the heart #### 2. **Medical Management:** and has a small shadow that forms the mediastinum of the heart → Widened mediastinum = widened aorta - **Antiplatelet Therapy**: - **Aspirin**: Administer immediately and continue indefinitely unless contraindicated. - **P2Y12 Inhibitors**: Clopidogrel, ticagrelor, or prasugrel may be added, particularly in patients undergoing percutaneous coronary intervention (PCI). - **Anticoagulation**: - **Heparin**: Use unfractionated heparin (UFH) or low-molecular-weight heparin (LMWH) to prevent clot propagation. → Prominent ascending and descending arc - **Direct Oral Anticoagulants (DOACs)**: May be considered in specific cases, though more commonly used in atrial fibrillation. - **Beta-Blockers**: Administer to reduce myocardial oxygen demand unless contraindicated (e.g., in acute heart failure or bradycardia). → Prominent means it’s aneurysmal - **Nitrates**: Provide relief of chest pain. Avoid in hypotension or right ventricular infarction. - **Statins**: High-intensity statin therapy should be initiated or continued to lower LDL cholesterol and stabilize plaque. #### 3. **Invasive Strategies:** - **Early Invasive Approach**: Recommended for high-risk patients (e.g., those with elevated troponin, significant ECG changes, or high TIMI/GRACE scores). This involves coronary angiography within 24-72 hours of presentation. - **Ischemia-Guided Strategy**: May be appropriate for lower-risk patients or those with significant comorbidities. This involves a more conservative approach with medical therapy and non-invasive testing (e.g., stress testing) to guide further intervention. CM 109 #### 4. **Revascularization:** B6: Lareza, Marchan, Martinez, Moral, Napoles, Pecson, Rico, Salvo, Saysay, Sernias, Tadiosa, Villar, Yaneza 4 of 12 - **Percutaneous Coronary Intervention (PCI)**: The preferred method for revascularization, especially in patients with suitable anatomy and those at high risk.  DIAGNOSTICS: BIOMARKERS → Trans-telephonic event monitors In patients presenting with acute chest pain, serial cTn I or T levels → Diary or an electronic marker to indicate the timing of are useful to identify abnormal values and a rising or falling pattern palpitations senses by the patient is essential for appropriate indicative of acute myocardial injury interpretation Their most important application in clinical practice is for the rapid identification or exclusion of myocardial injury Creatine kinase myocardial (CK-MB), isoenzyme and myoglobin are not useful for diagnosis of acute myocardial injury PRECEPTOR NOTES Troponin increase at 6 hours after onset of MI Troponin I can last to 14 days Therefore, troponin can be used as a rapid identification of myocardial injury. SUMMARY In patients presenting with acute chest pain, a chest radiograph is useful to evaluate for other potential car Figure 15. Sinus Rhythm (NORMAL) Retrieved from PPt of Dr. Jerilyn Adviento PRECEPTOR NOTES Sinus rhythm → PQRST waves consisting of: → 3 upward waves = P R T → 2 downward waves = Q and S ▪ Downward Q which is not usually present in some. Other tests → Stress test - running on a treadmill connected to ECG → Holter monitor- carry ECG (hand carry) for 24 hrs recording for 24 hours, high yield → ILR- implanted under skin → Diary- write down time and date of palpitation for accuracy APPROACH TO PALPATION: ECG Figure 16. Sinus Rhythm and Sinus Tachycardia Retrieved from PPt of Dr. Jerilyn Adviento Figure 14. Summary of Chest Pain Retrieved from PPT of Dr. Jerilyn Adviento III. PALPITATIONS Defined as a "thumping." "pounding," or "fluttering" sensation in the chest. Can be intermittent or sustained and either regular or irregular. As an unusual awareness of the heartbeat and become especially concerned when they sense that they have had "skipped" or "missing" heartbeats. Palpitations are often noted when the patient is quietly resting, during which time other stimuli are minimal. Positional generally reflect a structural process within (e.g., atrial myxoma) or adjacent to (e.g., mediastinal mass) the heart Figure 17. Sinus Rhythm, Skipped Beats, and 3rd Degree Block Retrieved from PPt of Dr. Jerilyn Adviento PRECEPTOR NOTES Positional - meaning it has an anatomical quality to it. There is a structural process, a mass in the heart and moves together with movement, it triggers the arrhythmia. A. APPROACH TO PALPITATIONS Principal Goal → To determine whether the symptom is caused by a life-threatening arrhythmia (irregular rhythm) Check risk factors → CAD, trauma, CVD, hypertension, congenital heart disease, thyroid disease, obstructive sleep apnea, electrolyte imbalances, drug use, alcohol use Figure 18. Sinus Rhythm, Skipped Beats with Sinus arrest,, and Sinus Check for associated symptoms and signs Pause → Check for hemodynamic compromise: syncope or Retrieved from PPt of Dr. Jerilyn Adviento lightheadedness, blurring of vision, chest pain, dyspnea Check physical examination → Check for hemodynamic compromise: syncope or lightheadedness, blurring of vision, chest pain, dyspnea Check physical examination → Vital signs (heart rate and blood pressure) → Cardiac physical examination: regular or irregular rhythm Check 12 lead ECG → To document the arrhythmia Other diagnostics → Stress test- if palpitations are associated with exertion → Holter monitoring- If palpitations are infrequent, indicate if the Figure 19. Sinus Rhythm, Premature Atrial Contractions, and Premature etiology of palpitations cannot be determined from the patient’s Ventricular Contractions history, physical examination, and resting ECG Retrieved from PPt of Dr. Jerilyn Adviento → Implantable loop recorder- If infrequent recurrent unexplained palpitations, when palpitations occur unpredictably or do not occur daily CM 109 B6: Lareza, Marchan, Martinez, Moral, Napoles, Pecson, Rico, Salvo, Saysay, Sernias, Tadiosa, Villar, Yaneza 5 of 12  Figure 22. Causes of Heart Palpitations Retrieved from PPt of Dr. Jerilyn Adviento B. CAUSES OF PALPITATIONS Cardiac (43%) Figure 20. Atrial Fibrillation and Atrial Flutter Psychiatric (31%) Retrieved from PPt of Dr. Jerilyn Adviento Miscellaneous (10%) Unknown (16%) Figure 21. Ventricular Fibrillation and Ventricular Tachycardia Retrieved from PPt of Dr. Jerilyn Adviento PRECEPTOR NOTES Sinus Tachycardia → Every big box has 5 small boxes → Count from R to R, divide 1500 by 24 → 1500 divided by the number of squares from R to R → NSR 60-100 bpm Figure 23. Causes of Heart Palpitations → > sinus tachycardia Retrieved from PPt of Dr. Jerilyn Adviento → < sinus bradycardia Skipped Beat ALGORITHM FOR PALPITATIONS → There are areas that are irregular P wave and QRs → Repetitive (similar appearances) 3rd AV Block → One of the worst → P wave are followed by other p waves → R is far apart → Not in an orderly manner → Abnormal impulse conduction Sinus Arrest → Skipped Beat : pause is present between P wave - QRS (signified by the bold horizontal double headed arrows) Sinus Pause → Sinus pause: If sinus arrest lasts more than 3 seconds ▪ Sinus arrest - sinus node has stopped beating / dysfunctional ▪ Necessitates a pacemaker if seen on a patient Premature Atrial Contractions → There is a normal PQRST → However, in the 3rd complex, there is a premature beat, but there is an identified P wave. Premature Ventricular Contractions → Bizarre looking (read it from left to right) Figure 24. Algorithm for Palpitations → The 1st two complexes are normal. Retrieved from PPt of Dr. Jerilyn Adviento → The 3rd complex/beat has no P wave and a widened QRS with more than 3 small boxes wide (4 small boxes wide in the PRECEPTOR NOTES example). Which means that this is a premature ventricular How to manage and approach palpitation if your patient presents contraction. with a complaint for palpitation? → The trigeminal abnormal pattern (happens every 3rd beat) → The first thing to do is to take the history, Physical Exam (PE) Atrial Fibrillation and then request for ECG. → No more P wave → An example of structural disease is congenital heart disease &, → Quite small tumor → Irregular rhythm with no identifiable P wave → R-R is irregular IV. EDEMA Atrial Flutter Accumulation of excessive fluid in the extravascular interstitial → Numerous P waves space. → Saw-tooth like pattern Interstitial tissue can absorb up to 5L of fluid, accommodating up to → P wave-P wave-QRS a 10% weight gain, before pitting edema appears. Atrial fibrillation & flutter carries higher risk for stroke and A detailed history can help narrow the differential diagnosis of embolization edema Ventricular fibrillation Questions: → The most dangerous of all → “Have you had any swelling anywhere? Where? Anywhere else? → The patient is already dead hence no pulse and needs CPR → When does it occur? Does it worsen in the morning or at night? → There is no isoelectric line, no baseline, and no identifiable P → Do your shoes get tight? Are the rings tight on your fingers? and QRS waves → Are your eyelids puffy or swollen in the morning? Have you had to → only chaotic fluctuations let out your belt? Also, have your clothes gotten tight around the → Ventricular fibrillation comes from the ventricle middle? → they follow no pattern\ Ventricular tachycardia → 2nd to Ventricular fibrillation as the most dangerous. → May have regular small notches that can be P-waves → Identifiable qrs complex but no identifiable P-wave → Just QRS that are more than 3mm wide, regular, and repetitive Figure 25. Different Manifestations of Edema Retrieved from PPT of Dr. Jerilyn Adviento. APPROACH TO PALPITATION: FREQUENCY CM 109 B6: Lareza, Marchan, Martinez, Moral, Napoles, Pecson, Rico, Salvo, Saysay, Sernias, Tadiosa, Villar, Yaneza 6 of 12 PRECEPTOR NOTES WATER IN VASCULAR BED In bilateral edema think of diseases that affect the vessels like the lymph and veins. It can also be a systemic problem such as CHF. TOTAL BODY WATER DISTRIBUTION Figure 29. Water in Vascular Bed Retrieved from PPT of Dr. Jerilyn Adviento A. EDEMA Edema is the accumulation of fluid in the interstitial compartment It occurs because of an imbalance of capillary hemodynamics → Increased oncotic pressure of the interstitial space → Increased intravascular hydrostatic pressure → Increased permeability of the endothelial barrier Figure 26. Total Body Water Distribution → Decreased oncotic pressure within the capillary Retrieved from PPT of Dr. Jerilyn Adviento → Poor lymphatic drainage How does decreased CO and SVR cause Edema? Figure 27. Total Water Balance Retrieved from PPT of Dr. Jerilyn Adviento WATER CYCLE Figure 30. Clinical conditions in which a decrease in cardiac output (A) and systemic vascular resistance (B) Retrieved from PPT of Dr. Jerilyn Adviento PRECEPTOR NOTES Increased oncotic pressure of the interstitial space → Increased solutes in the interstitial space make the fluid move inward to the interstitial space Figure 28. Water Cycle Increased intravascular hydrostatic pressure Retrieved from PPT of Dr. Jerilyn Adviento → Fluid moves outward from the blood capillary to the interstitial space Water goes through various part of the body Increased permeability of the endothelial barrier → The pressure that balances and controls the intravascular PRECEPTOR NOTES compartment is already ruined Water inputs → Can be from the water we produce from metabolism (350 mL) B. APPROACH TO PATIENTS WITH EDEMA → Water in ingested food (0.5-1 L) 1. Is it generalized or localized? → Water in ingested fluids (2-3 L) 2. Is it unilateral or bilateral? Water Outputs 3. Is it acute or chronic? → Variable in sweat a. Acute < 3 weeks → 150 mL in feces b. Chronic >3 weeks → 1-2 L in urine 4. What do the chemistry panel say? Is there hypoalbuminemia? → 0.45 -1.9 L insensible loss a. Check for i i. Renal Blood Chem ii. Cardiac Blood Test i CM 109 B6: Lareza, Marchan, Martinez, Moral, Napoles, Pecson, Rico, Salvo, Saysay, Sernias, Tadiosa, Villar, Yaneza 7 of 12  iii. Liver Test i iv. Other Metabolic Tests 5. Check medication history 6. Thorough Physical examination, check for systemic disease C. IS EDEMA LOCALIZED? See Table 1 appendix D. IS EDEMA GENERALIZED? See Table 2 appendix E. MEDS THAT CAUSE EDEMA Figure 33. Grading of Edema Retrieved from PPT of Dr. Jerilyn Adviento Figure 34. Edematous feet Retrieved from PPT of Dr. Jerilyn Adviento Figure 31. Drugs Associated with Edema Formation PRECEPTOR NOTES Retrieved from PPt of Dr. Jerilyn Adviento. (Leftmost image) check for the quality of the skin → Lots of varicosities Table 3. Common Medications That Cause Edema. → Ulcer on the medial malleolus (non healing wound) MEDICATION CLASS EXAMPLES → This leg probably has chronic venous insufficiency (Center image) Antihypertensives Amlodipine (Norvasc). Beta → Very thick verrucous swelling, which can be a sign of blockers, Clonidine, Diltiazem, lymphedema Hydralazine, Minoxidil, Nifedipine (Rightmost image) → Erythema: can be a sign of DVT Anti-inflammatory Corticosteroids, nonsteroidal anti-inflammatory drugs (NSAIDs) Chemotherapy Cyclophosphamide, Cyclosporine (Sandimmune), Docetaxel (Taxotere), Gemcitabine, targeted immunotherapy Gabapentinoids Gabapentin (Neurontin), pregabalin (Lyrica) Hormones Estrogen (Estratest), progesterone, testosterone Thiazolinediones Pioglitazone (Actos) Other Acyclovir, antipsychotics, monoamine oxidase inhibitors Figure 35. Elephantiasis (Left) and Lymphedema (Right) Retrieved from PPt of Dr. Jerilyn Adviento F. APPROACH TO PATIENT WITH EDEMA: PHYSICAL EXAMINATION PRECEPTOR NOTES Pitting Edema Left image shows an elephant leg which can be a sign of → An indentation that remains in the edematous area after pressure elephantiasis. is applied. Right image is an example of a patient with Lymphedema. → Lower extremity examination should focus on the medial (+) Kaposi - Stemmer sign is the failure to tent the skin overlying malleolus, the bony portion of the tibia, and the dorsum of the foot the dorsum of the second toe using a pincer grasp. Tenderness on Palpation Check for systemic causes Changes in skin temperature, color, and texture provide clues to the → Heart failure (jugular venous distension, crackles) cause of edema. → Renal disease (oliguria, anuria, swelling in hands, legs and feet) ▪ Non-dependent edema → Hepatic disease (jaundice, ascites, asterixis) → Thyroid disease (exophthalmos, tremor, weight loss) Figure 32. Bilateral Pitting Edema Retrieved from PPT of Dr. Jerilyn Adviento CM 109 B6: Lareza, Marchan, Martinez, Moral, Napoles, Pecson, Rico, Salvo, Saysay, Sernias, Tadiosa, Villar, Yaneza 8 of 12  G. DIAGNOSTIC APPROACH TO UNILATERAL LOWER I. DIAGNOSTIC APPROACH TO BILATERAL LOWER EXTREMITY EDEMA EXTREMITY EDEMA Figure 38. Bilateral Lower Extremity Edema Approach Retrieved from PPt of Dr. Jerilyn Adviento V. SUMMARY: APPROACH TO CARDIAC SYMPTOMS Comprehensive History and Physical Exam are crucial Utilize appropriate diagnostic tools early Prioritize and stratify risk for immediate intervention VI. REFERENCES Adviento, J. (2024). Lecture Slides Figure 36. Unilateral Lower Extremity Edema Approach Retrieved from PPt of Dr. Jerilyn Adviento H. APPROACH TO UNILATERAL SWELLING AND IN SUSPECT FOR DEEP VEIN THROMBOSIS Figure 37. Well’s Scoring for DVT Retrieved from PPt of Dr. Jerilyn Adviento PRECEPTOR NOTES Unilateral lower extremity edema → Find out if chronic or acute ▪ Acute (72 hrs) − Look for the history of cancer, pelvic surgery or trauma o Yes (pelvic magnetic resonance venography) → check for the tumor or thrombus → yes then confirmed if not test for lymphedema CM 109 B6: Lareza, Marchan, Martinez, Moral, Napoles, Pecson, Rico, Salvo, Saysay, Sernias, Tadiosa, Villar, Yaneza 9 of 12  APPENDIX Table 4. Diagnosis and Management of Common Causes of Localized Edema Etiology Onset and Location Examination findings Evaluation methods Treatment Unilateral Predominance Chronic venous Onset: chronic; begins in Soft pitting edema with Duplex Compression stockings insufficiency middle to older age reddish-hued skin ultrasonography predilection; predilection Pneumatic compression Location: lower for medial ankle calf Ankle brachial index to device if stockings are extremities; evaluate for arterial Contraindicated bilateral distribution in later Associated findings insufficiency venous ulceration over Horse chestnut seed medial malleolus extract weeping erosions Skin care such as emollients topical steroids Complex regional pain Onset: chronic; following Soft tissue edema distal History and Systemic steroids syndrome type 1 trauma or other inciting to affected limb Examination (reflex sympathetic event Topical dimethylsulfoxide dystrophy) Associated findings: Radiography solution Location: upper or lower Early warm tender skin extremities; contralateral with the operas is late in Three-phase bone Physical therapy limbs at risk regardless of chinese skin with scintigraphy trauma atrophic changes Tricyclic antidepressant Magnetic resonance imaging Calcium channel blockers DVT Onset: acute Pitting edema with D-dimer assay Anticoagulation therapy tenderness with or Location: upper or lower without erythema; Duplex Compression stockings to extremities positive Homans sign ultrasonography prevent post-thrombotic syndrome Magnetic resonance venography to rule out Thrombolysis in select pelvic or thigh DVT (if patient clinical suspicion is high) or extrinsic venus compression (May-Thurner syndrome in patients with unexplained left-sided dvt) Consider hypercoagulability workup Lymphedema Onset: chronic insidious Early: dough-like skin Clinical diagnosis Complex decongestive often following lymphatic Pitting lymphoscintigraphy Physiotherapy obstruction from trauma or T1 weighted magnetic surgery Late: Thickened resonance Compression stockings verrucous fibrotic lymphangiography with Location : upper or lower hyperkeratotic skin Adjuvant extremities bilateral in 30% of patients Associated findings : pneumatic compression Inability to tent skin over devices second digit swelling of dorsum of foot with Skin care surgery in limited squared off digits painless kisses heaviness in extremity Cases Bilateral predominance Lipedema Onset: chronic begins Non pitting edema Clinical Diagnosis No effective treatment around or after puberty increase distribution of soft adipose tissue Weight loss does not Location: predominantly improve edema lower extremities; involves Associated findings: thighs, legs, buttocks, Medial thigh and tibial spares feet, ankles and tenderness; fat pad upper torso anterior to lateral malleolus Medication-induced Onset: weeks after Soft-pitting edema Clinical history Cessation of medication edema initiation of medication; suggesting recent resolve within days of initiation of offending stopping offending medication medications Location: lower extremities Obstructive sleep Onset: chronic Mild, pitting edema Suggestive clinical Positive pressure apnea history ventilation CM 109 B6: Lareza, Marchan, Martinez, Moral, Napoles, Pecson, Rico, Salvo, Saysay, Sernias, Tadiosa, Villar, Yaneza 10 of 12  Location: lower extremities Associated findings: daytime fatigue snoring Polysomnography Treatment of pulmonary obesity hypertension if suggested Echocardiography on echocardiography Table 5. Principal Causes of Generalized Edema: History, Physical Examination, and Laboratory Findings Organ System History Physical Examination Laboratory Findings Cardiac Dyspnea with exertion prominent - often Elevated jugular venous pressure, Elevated urea associated with orthopnea - or ventricular (S3) gallop; occasionally nitrogen-to-creatinine ratio paroxysmal nocturnal dyspnea with displaced or dyskinetic apical common; serum sodium often pulse; peripheral cyanosis, cool diminished; elevated natriuretic extremities, small pulse pressure peptides when severe Hepatic Dyspnea uncommon, except if Frequently associated with ascites; If severe, reductions in serum associated with significant degree of jugular venous pressure normal or albumin, cholesterol, other hepatic ascites; most often a history of low; blood pressure ↓ JVP proteins (transferrin, fibrinogen); ethanol abuse lower than in renal or cardiac disease; liver enzymes elevated, depending one or more additional signs of chronic on the cause and liver disease (jaundice, palmar acuity of liver injury; tendency erythema, toward hypokalemia, respiratory Dupuytren’s contracture, spider alkalosis; macrocytosis from folate angiomata, male gynecomastia; deficiency asterixis and other signs of encephalopathy) may be present Renal (CRF) Usually chronic: may be associated with Elevated blood pressure; hypertensive Elevation of serum creatinine and uremic signs and symptoms, including retinopathy; nitrogenous fetor; cystatin C; albuminuria; decreased appetite, altered (metallic or pericardial friction rub in advanced hyperkalemia, metabolic acidosis, fishy) taste, altered sleep pattern, cases with uremia hyperphosphatemia, difficulty concentrating, restless legs, or hypocalcemia, anemia (usually myoclonus; dyspnea can be present, but normocytic) generally less prominent than in heart failure Renal (INS) Childhood diabetes mellitus; plasma cell Periorbital edema; hypertension Proteinuria (≥3.5 g/d); dyscrasias hypoalbuminemia; hypercholesterolemia; microscopic hematuria Figure 36. Unilateral Lower Extremity Edema Approach Retrieved from PPt of Dr. Jerilyn Adviento CM 109 B6: Lareza, Marchan, Martinez, Moral, Napoles, Pecson, Rico, Salvo, Saysay, Sernias, Tadiosa, Villar, Yaneza 11 of 12  Figure 38. Bilateral Lower Extremity Edema Approach Retrieved from PPt of Dr. Jerilyn Adviento CM 109 B6: Lareza, Marchan, Martinez, Moral, Napoles, Pecson, Rico, Salvo, Saysay, Sernias, Tadiosa, Villar, Yaneza 12 of 12