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Hemodynamic Monitoring and Heart Failure: A Comprehensive Guide for Nursing Students, Lecture notes of Nursing

A comprehensive overview of hemodynamic monitoring, including its principles, techniques, and clinical applications. It delves into the assessment and management of heart failure, covering its causes, risk factors, compensatory mechanisms, and nursing interventions. The document also explores various cardiac dysrhythmias, their ecg characteristics, and treatment strategies. It includes numerous questions and answers to reinforce learning and promote critical thinking.

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CHAPTER 34: DIC (738-741)
Disseminated Intravascular Coagulation
DIC Definition: A serious bleeding and clotting disorder caused by abnormally initiated and accelerated
clotting, leading to depletion of clotting factors and platelets, which can result in uncontrollable bleeding.
Cause: DIC is not a primary disease but occurs secondary to another condition (e.g., cancer, infection,
trauma). The underlying cause must be treated to resolve DIC.
Pathophysiology:
Clotting Cascade: DIC is triggered by an underlying condition causing overactivation of the clotting
cascade.
Thrombosis & Bleeding: Excessive clot formation occurs due to intravascular thrombin, leading to
thrombosis and depletion of clotting factors, followed by profuse bleeding.
Fibrinolysis: The fibrinolytic system is activated, breaking down clots and creating fibrin split products
(FSPs), which inhibit further clotting.
Risk Factors:
Shock
oCardiogenic
oAnaphylaxis
oHemorrhagic
Vascular Disorders
oAortic Aneurism
Clinical Manifestations:
1. Bleeding Manifestations:
a. Skin: Petechiae, purpura, oozing blood, hematomas.
b. Respiratory: Tachypnea, hemoptysis.
c. Cardiovascular: Tachycardia, hypotension.
d. GI: Bloody stools, abdominal distention.
e. GU: Hematuria.
f. Neuro: Vision changes, dizziness, mental status changes.
2. Thrombotic Manifestations:
a. Skin: Cyanosis, necrosis.
b. Respiratory: Pulmonary embolism, dyspnea.
c. Cardiovascular: ECG changes, venous distention.
d. GI: Abdominal pain, paralytic ileus.
e. Renal: Oliguria, kidney failure.
f. Neuro: Delirium, coma.
Diagnostics:
Labs:
oDecreased platelets and fibrinogen.
oProlonged PT and aPTT.
oIncreased D-dimer (fibrin degradation products).
oFragmented RBCs (schistocytes) on blood smear.
Treatment:
1. Address Underlying Cause: Treat the condition causing DIC (e.g., infection, cancer).
2. Supportive Care:
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CHAPTER 34: DIC (738-741)

Disseminated Intravascular CoagulationDIC Definition : A serious bleeding and clotting disorder caused by abnormally initiated and accelerated clotting, leading to depletion of clotting factors and platelets, which can result in uncontrollable bleeding.  Cause : DIC is not a primary disease but occurs secondary to another condition (e.g., cancer, infection, trauma). The underlying cause must be treated to resolve DIC. Pathophysiology:Clotting Cascade : DIC is triggered by an underlying condition causing overactivation of the clotting cascade.  Thrombosis & Bleeding : Excessive clot formation occurs due to intravascular thrombin, leading to thrombosis and depletion of clotting factors, followed by profuse bleeding.  Fibrinolysis : The fibrinolytic system is activated, breaking down clots and creating fibrin split products (FSPs), which inhibit further clotting. Risk Factors:  Shock o Cardiogenic o Anaphylaxis o Hemorrhagic  Vascular Disorders o Aortic Aneurism Clinical Manifestations:

  1. Bleeding Manifestations : a. Skin: Petechiae, purpura, oozing blood, hematomas. b. Respiratory: Tachypnea, hemoptysis. c. Cardiovascular: Tachycardia, hypotension. d. GI: Bloody stools, abdominal distention. e. GU: Hematuria. f. Neuro: Vision changes, dizziness, mental status changes.
  2. Thrombotic Manifestations : a. Skin: Cyanosis, necrosis. b. Respiratory: Pulmonary embolism, dyspnea. c. Cardiovascular: ECG changes, venous distention. d. GI: Abdominal pain, paralytic ileus. e. Renal: Oliguria, kidney failure. f. Neuro: Delirium, coma. Diagnostics:Labs : o Decreased platelets and fibrinogen. o Prolonged PT and aPTT. o Increased D-dimer (fibrin degradation products). o Fragmented RBCs (schistocytes) on blood smear. Treatment:
  3. Address Underlying Cause : Treat the condition causing DIC (e.g., infection, cancer).
  4. Supportive Care :

a. Blood Products : Platelets, cryoprecipitate, and fresh frozen plasma (FFP) for patients with significant bleeding. b. Cryoprecipitate : Replaces fibrinogen and factor VIII. c. FFP : Replaces clotting factors except platelets.

  1. Anticoagulation Therapy : a. Heparin may be used for thrombosis if the benefits outweigh bleeding risks. b. AT III replacement for severe cases, but it increases bleeding risk. Nursing Management:
  2. Early Detection : Monitor for signs of bleeding (e.g., petechiae, IV site bleeding) and clotting (e.g., cyanosis, decreased urine output).
  3. Monitor Vital Signs : Watch for tachycardia, hypotension, and changes in mental status.
  4. Administer Blood Products : Ensure correct administration of platelets, cryoprecipitate, and FFP based on deficiency.
  5. Minimize Bleeding Risk : Avoid trauma or procedures that could cause bleeding; use gentle care techniques.
  6. Monitor Labs : Regularly assess coagulation panels and organ function test QUESTIONS (GPT) Question 1: A nurse is caring for a patient diagnosed with Disseminated Intravascular Coagulation (DIC) secondary to sepsis. Which of the following interventions is the priority in managing this patient's condition? A. Administer intravenous fluids to maintain blood pressure. B. Monitor for signs of bleeding at intravenous (IV) sites. C. Administer fresh frozen plasma (FFP) to correct clotting factor deficiency. D. Identify and treat the underlying infection. Correct Answer: D. Identify and treat the underlying infection. Rationale: DIC is a secondary condition, meaning it occurs as a result of another underlying cause, such as infection, trauma, or cancer. The priority in managing DIC is to treat the underlying cause (in this case, sepsis) to stop the abnormal clotting and bleeding cascade. While administering blood products (like FFP) and monitoring for bleeding are important, they do not address the root cause of the condition. Therefore, identifying and treating the infection is crucial for controlling the progression of DIC.  A. Administer intravenous fluids : While maintaining blood pressure is important, it does not address the primary cause of DIC.  B. Monitor for signs of bleeding : This is important for early detection of complications but is not the primary intervention.  C. Administer fresh frozen plasma (FFP) : FFP may help replenish clotting factors, but treating the underlying cause takes priority. Question 2: The nurse is assessing a patient with suspected Disseminated Intravascular Coagulation (DIC). Which of the following clinical manifestations would the nurse expect to find in this patient? (Select all that apply) A. Petechiae and oozing blood B. Hypotension and tachycardia C. Cyanosis of extremities D. Oliguria and hematuria E. Increased platelet count Correct Answers: A, B, C, D Rationale: Disseminated Intravascular Coagulation (DIC) involves both clotting and bleeding, leading to a variety of clinical manifestations:  A. Petechiae and oozing blood : These are signs of bleeding, which occurs due to the depletion of clotting factors in DIC.  B. Hypotension and tachycardia : These signs indicate cardiovascular involvement, possibly due to bleeding or organ ischemia from microthrombi.  C. Cyanosis of extremities : Thrombotic events in DIC can lead to decreased blood flow, resulting in cyanosis.  D. Oliguria and hematuria : Thrombosis can lead to kidney injury, resulting in decreased urine output (oliguria), while hematuria is a sign of bleeding in the urinary system.  E. Increased platelet count : Incorrect. In DIC, platelets are consumed, leading to decreased platelet levels, not increased.

Measurements : Systolic, diastolic, and mean arterial pressure (MAP). The system must be zeroed at the phlebostatic axis for accurate measurements.  Dynamic Response Testing : Ensures the monitoring system is optimally damped and responsive.  Complications : Hemorrhage, infection, thrombus formation, neurovascular impairment, and potential loss of limb. Risks of dislodgment and catheter infection can be minimized by using proper connections and sterile technique.

2. Arterial Pressure-Based Cardiac Output (APCO)Function : Measures continuous cardiac output (CO) by analyzing the arterial pulse pressure.  Indications : Monitoring a patient’s ability to increase stroke volume (SV) in response to fluid administration, especially in critically ill patients.  Measurements : Continuous CO and SV, using demographic data (gender, age, height, weight), arterial pulse pressure, and heart rate (HR).  Technology : A sensor attached to an arterial line provides continuous updates of CO and stroke volume variation (SVV), which helps predict fluid responsiveness. 3. Pulmonary Artery (PA) Pressure MonitoringIndications : PA pressure monitoring is useful for managing heart and lung conditions such as heart failure, shock, and pulmonary hypertension.  Catheter : A PA catheter (e.g., Swan-Ganz) measures PA pressure and PA wedge pressure (PAWP), reflecting left atrial pressure and left ventricular end-diastolic pressure.  Procedure : A multi-lumen catheter is inserted, and the pressure waveforms are observed to guide placement. The catheter tip is positioned in the PA, and a balloon is inflated to obtain PAWP.  Measurements : Right atrial pressure (central venous pressure), right ventricular pressure, and mixed venous oxygen saturation (SvO2). Thermodilution can be used to measure CO.  Complications : Dysrhythmias, infection, and potential catheter misplacement. PA pressure monitoring use has decreased due to the invasive nature and associated risks, with less invasive methods becoming more prevalent. 4. Complications of Invasive Pressure MonitoringHemorrhage : Often occurs if the catheter becomes dislodged. To prevent this, ensure secure connections, activate alarms, and monitor the arterial waveform.  Infection : Proper site care, routine inspection, and timely replacement of equipment are essential to minimize infection risks.  Thrombus Formation : Continuous slow flushing (1–3 mL/hr) with a pressure bag inflated to 300 mm Hg helps prevent clots.  Neurovascular Impairment : Regular assessment of the insertion site and extremities (e.g., temperature, color, capillary refill) can detect early signs of compromised blood flow.  High- and Low-Pressure Alarms :  Ensure alarms are set based on the patient's specific status, as conditions such as heart failure (HF) or volume depletion can alter pressure readings. In HF, the systolic upstroke may be slower, while in volume depletion, systolic pressure drops during inspiration.  For patient safety, Luer-Lok connections should be used, and continuous monitoring of arterial waveforms is essential.  Infection Control :  Inspect the insertion site for signs of infection or inflammation.  Replace pressure tubing, flush bags, and transducers every 96 hours (or per institutional policy). Notify healthcare providers (HCP) if infection is suspected and replace equipment as necessary.  Complications of Catheter Insertion :  Thrombus formation, emboli, or arterial spasm can lead to circulatory impairment. Assess the neurovascular status of the distal limb hourly.  Perform the Allen test before radial artery catheterization to confirm adequate ulnar circulation.

Flush System Management :  Maintain line patency and prevent thrombus formation by ensuring the flush system delivers a slow continuous flush (1-3 mL/hr). Keep the pressure bag inflated to 300 mm Hg. APCO Monitoring :  This minimally invasive technique measures continuous cardiac output (CCO) and stroke volume (SV), integrating arterial waveform data with patient demographics (age, gender, height, weight). APCO also helps evaluate preload responsiveness through stroke volume variation (SVV). Pulmonary Artery Catheters (Swan-Ganz):  These are used to assess fluid status and cardiac function by monitoring pulmonary artery pressures, including pulmonary artery diastolic pressure (PADP) and pulmonary artery wedge pressure (PAWP).  PA pressures can guide fluid therapy, helping avoid over- or under-resuscitation.  PA catheter insertion carries risks (e.g., dysrhythmias, infection), so monitoring the ECG during insertion is critical to detect abnormal heart rhythms. Central Venous Pressure (CVP) Monitoring:  CVP reflects right ventricular preload and overall fluid status, measured via a central venous catheter or the proximal port of a pulmonary artery catheter.  High CVP indicates fluid overload or right ventricular failure, while low CVP suggests hypovolemia.  Nursing Assessment :  Evaluate the patient’s general appearance, skin temperature, peripheral pulses, urine output, and mental status to assess hemodynamic status.  Continuous observation and correlation of clinical data with hemodynamic values (e.g., ECG, arterial and PA pressures, central venous oxygenation levels) are crucial.

1. Blood Studies & Cardiac Biomarkers:Troponin (cTnT, cTnI) : Specific markers for myocardial infarction (MI). Detected within 4-6 hours of injury, peak at 10-24 hours, and remain detectable for 10-14 days. High-sensitivity assays (hs-cTnT, hs-cTnI) detect events within 1-3 hours.  Creatine Kinase-MB (CK-MB) : Rises in 3-6 hours post-MI, peaks in 12-24 hours, and returns to normal within 12-48 hours. Less commonly used now for MI diagnosis.  C-Reactive Protein (CRP) : Indicates inflammation and is associated with atherosclerosis. Can predict future cardiac events.  Homocysteine (Hcy) : Elevated levels are linked to cardiovascular disease (CVD) and stroke risk.  B-Type Natriuretic Peptide (BNP) : Marker for heart failure (HF). Helps distinguish between cardiac and respiratory causes of dyspnea. 2. Serum Lipid Panel:Triglycerides : Elevated levels are linked to coronary artery disease (CAD).  Cholesterol : Total cholesterol levels alone do not provide sufficient information about CAD risk. LDLs (bad cholesterol) and HDLs (good cholesterol) are more relevant indicators. High LDL is linked to CAD; high HDL has a protective effect.  Lipoprotein (a) [Lp(a)] and Lipoprotein-associated phospholipase A2 (Lp-PLA2) : Indicators of atherosclerosis and increased CAD risk. 3. Electrocardiography (ECG):12-Lead ECG : Basic heart rhythm assessment for detecting abnormalities like MI.  Holter Monitoring : Continuous ECG monitoring for 24-48 hours to assess intermittent arrhythmias.  Event Monitor : For patients with less frequent symptoms; records ECG during specific events.  Exercise Stress Testing : Evaluates the heart’s response to physical stress to assess CVD.

A. Assess for signs of infection at the insertion site. B. Monitor the patient’s urine output. C. Perform a neurovascular assessment of the limb distal to the catheter insertion site. D. Check for signs of fluid overload. Correct Answer: C. Perform a neurovascular assessment of the limb distal to the catheter insertion site Rationale: One of the major complications of arterial catheterization is neurovascular impairment. Assessing the distal limb for color, temperature, and capillary refill ensures the circulation is intact and prevents ischemic complications.A. Signs of infection are important but neurovascular impairment is more urgent in the acute phase.B. Urine output may reflect overall fluid status but is not directly related to catheter complications.D. Fluid overload is relevant but less immediately critical in this situation. Question 3: The nurse is interpreting a patient's pulmonary artery wedge pressure (PAWP). The patient's PAWP is elevated. Which condition is the nurse most likely to suspect? A. Hypovolemia B. Left ventricular failure C. Pulmonary embolism D. Right-sided heart failure Correct Answer: B. Left ventricular failure Rationale: Pulmonary artery wedge pressure (PAWP) reflects left atrial pressure and left ventricular end-diastolic pressure. An elevated PAWP is a sign of left-sided heart failure or fluid overload.A. Hypovolemia would cause a decreased PAWP.C. Pulmonary embolism does not directly increase PAWP but may increase pulmonary artery pressure.D. Right-sided heart failure affects central venous pressure (CVP), not PAWP. Question 4: A nurse is caring for a patient with an arterial catheter placed for arterial blood pressure (ABP) monitoring. To ensure accurate pressure readings, the nurse should position the transducer at which anatomical location? A. Fifth intercostal space, midclavicular line B. Second intercostal space, midaxillary line C. Fourth intercostal space, midaxillary line D. Xiphoid process Correct Answer: C. Fourth intercostal space, midaxillary line Rationale: The phlebostatic axis is located at the 4th intercostal space, midaxillary line. This is the correct reference point to zero the transducer for accurate pressure readings.A. Fifth intercostal space, midclavicular line is the location for heart auscultation, not hemodynamic monitoring.B. Second intercostal space is incorrect.D. Xiphoid process is irrelevant for this purpose. Question 5: A nurse is caring for a patient with a pulmonary artery catheter in place for hemodynamic monitoring. Which of the following findings is most concerning and requires immediate intervention?

A. Systolic blood pressure of 140 mmHg B. PAWP of 22 mmHg C. Heart rate of 85 bpm D. Central venous pressure (CVP) of 5 mmHg Correct Answer: B. PAWP of 22 mmHg Rationale: A normal PAWP is 6-12 mmHg. A PAWP of 22 mmHg indicates severe fluid overload or left ventricular failure, which requires immediate intervention.A. Systolic blood pressure of 140 mmHg may be elevated but is not immediately concerning.C. Heart rate of 85 bpm is within normal range.D. CVP of 5 mmHg is within the normal range (2-8 mmHg). Question 6: The nurse is assessing a patient with a central venous catheter. Which of the following would indicate a potential infection at the catheter insertion site? A. Localized warmth and erythema around the insertion site B. A MAP of 70 mmHg C. Blood pressure readings higher than baseline D. Increased urine output Correct Answer: A. Localized warmth and erythema around the insertion site Rationale: Signs of infection at the catheter site include localized warmth, erythema, swelling, and purulent drainage. This requires immediate attention to prevent systemic infection.B. A MAP of 70 mmHg is within normal range and doesn’t indicate infection.C. Blood pressure readings may change due to many reasons unrelated to infection.D. Increased urine output is not a sign of infection. Question 7: A critically ill patient is being monitored using arterial pressure-based cardiac output (APCO) monitoring. Which of the following assessments is the nurse likely to use to evaluate fluid responsiveness? A. Central venous pressure (CVP) B. Pulmonary artery pressure (PAP) C. Stroke volume variation (SVV) D. Pulmonary artery wedge pressure (PAWP) Correct Answer: C. Stroke volume variation (SVV) Rationale: Stroke volume variation (SVV) is used in arterial pressure-based cardiac output (APCO) monitoring to evaluate fluid responsiveness, especially in critically ill patients.A. CVP measures right ventricular preload but is less accurate for fluid responsiveness.B. Pulmonary artery pressure (PAP) assesses pulmonary function but does not directly indicate fluid responsiveness.D. PAWP assesses left ventricular preload but SVV is more commonly used in APCO monitoring. Question 8: A nurse is caring for a patient receiving hemodynamic monitoring. The patient’s systemic vascular resistance (SVR) is elevated. Which of the following medications is the nurse most likely to administer to reduce SVR?

CHAPTER 36: HYPERTENSION (814-816)

Definition:Hypertensive Crisis : SBP > 180 mm Hg and/or DBP > 120 mm Hg. o Hypertensive Emergency : Evidence of target organ damage (e.g., brain, heart, kidneys). Requires immediate treatment and hospitalization. o Hypertensive Urgency : No organ damage. Outpatient management possible. Causes:Primary causes : o Exacerbation of chronic hypertension o Medication non-adherence or withdrawal (e.g., clonidine, beta-blockers) o Drug use (cocaine, amphetamines) o Pheochromocytoma o Head injury, preeclampsia, aortic dissection o MAOIs with tyramine-containing foods Clinical Manifestations:Hypertensive Emergency : Often presents hypertensive encephalopathy. o Symptoms : Severe headache, nausea, vomiting, seizures, confusion, coma, blurry vision, chest pain, dyspnea, nosebleeds, seizures. o End-organ damage signs :  Brain : Cerebral edema, seizures, coma  Heart : Unstable angina, MI, pulmonary edema  Kidneys : Renal insufficiency to renal failure  Aortic dissection : Sudden chest/back pain, reduced peripheral pulses o Retinal signs : Exudates, hemorrhages, papilledema Assessment and Monitoring:Vital Signs : Continuous BP, O2 saturation, ECG monitoring.  Heart/Lung sounds : Auscultation for abnormalities.  Neurologic Checks : Level of consciousness, pupillary reactions, movement of extremities.  Renal Function : Measure urine output hourly.  Ongoing monitoring : Cardiac, lung, and renal system decompensation. Interventions:Initial Management : o IV Antihypertensive Therapy : For hypertensive emergencies (e.g., sodium nitroprusside, labetalol, nicardipine). o MAP Control : Initial goal: Decrease MAP by no more than 20%-25% or reduce MAP to 110-115 mm Hg. o Caution : Avoid rapid BP reduction to prevent ischemic events (e.g., stroke, MI, renal failure). o Special Cases :  Aortic Dissection : SBP < 100-120 mm Hg ASAP.  Stroke : May maintain higher BP initially for perfusion. o Titrate Drugs : Based on MAP or SBP. Check BP every 2-3 minutes during initial treatment. o Continuous Monitoring : ECG, urine output, BP.  Oxygen Therapy : Administer as per protocol.  IV Access : For drug administration and monitoring.  Bed Rest : Limit movement to prevent cerebral ischemia and fainting.

Medications:IV Agents (used for emergencies): o Vasodilators : Sodium nitroprusside, nicardipine o Adrenergic Inhibitors : Labetalol, esmolol o CCBs : Clevidipine o Frequent BP Monitoring : 2–3-minute intervals with titration based on response.  Oral Medications (used for urgency): o Captopril o Labetalol o Clonidine o Amlodipine Patient Education:  Importance of medication adherence.  Management of risk factors and ongoing monitoring.  Follow-up care to prevent future crises. Complications if Untreated:Hypertensive Emergency mortality rate >79% within a year.  Complications : Stroke, MI, renal failure, aortic dissection, pulmonary edema, encephalopathy. QUESTIONS (GPT) Question 1: A patient is admitted with a hypertensive emergency. The nurse notes the patient has blurred vision, a severe headache, and confusion. Which of the following interventions is most important to initiate immediately? A. Administer oral clonidine. B. Begin IV antihypertensive therapy. C. Encourage the patient to rest and remain calm. D. Place the patient in a semi-Fowler’s position. Correct Answer: B. Begin IV antihypertensive therapy. Rationale: In a hypertensive emergency, the priority is to lower the blood pressure to prevent further end-organ damage, and this is done through IV antihypertensive therapy. Oral medications, such as clonidine (choice A), are too slow-acting for a hypertensive emergency, which requires rapid blood pressure control. Encouraging rest (choice C) and positioning (choice D) may be helpful but are not the priority interventions in this situation. Question 2: A patient is admitted with an aortic dissection and a systolic blood pressure (SBP) of 185 mmHg. Which of the following is the priority goal for this patient’s blood pressure management? A. Decrease the SBP to < 150 mmHg within the first hour. B. Maintain the SBP at 140-160 mmHg. C. Decrease the SBP to < 100-120 mmHg as quickly as possible. D. Reduce the mean arterial pressure (MAP) by no more than 25% within the first hour. Correct Answer: C. Decrease the SBP to < 100-120 mmHg as quickly as possible. Rationale: In patients with aortic dissection , rapid reduction of systolic blood pressure is critical to reduce the risk of rupture. The goal is to decrease the SBP to less than 100-120 mmHg as quickly as possible. The other options are incorrect because they suggest less aggressive management, which is not appropriate for aortic dissection, a life-threatening condition. Question 3: The nurse is caring for a patient with a hypertensive urgency. Which of the following is an appropriate intervention for this patient? A. Administer IV nitroprusside. B. Start the patient on oral labetalol. C. Initiate continuous BP monitoring. D. Begin oxygen therapy immediately. Correct Answer: B. Start the patient on oral labetalol. Rationale: In hypertensive urgency , there is no evidence of target organ damage, so the treatment can be managed with oral medications such

CHAPTER 37: CORONARY SYNDROME (832-855)

Unstable AnginaDefinition : Caused by the rupture of unstable plaque, exposing thrombogenic surface.  Characteristics : o New-onset angina. o Chronic stable angina that increases in frequency, duration, or severity. o Occurs at rest or with minimal exertion. o Pain lasts longer than 10 minutes. Interprofessional and Nursing Care for Chronic Stable AnginaProgression Risk : Chronic stable angina can progress to Acute Coronary Syndrome (ACS) or Myocardial Infarction (MI). Any change in angina pattern should be evaluated.  Goals of Treatment : o Pain relief. o Immediate and appropriate treatment. o Preservation of heart muscle if MI is suspected. o Effective coping with anxiety. o Participation in rehabilitation. o Reduction of risk factors. Acute Care Protocol for Chest Pain

  1. Position patient upright and apply supplemental oxygen.
  2. Assess vital signs.
  3. Continuous ECG monitoring.
  4. Obtain a 12-lead ECG.
  5. Provide prompt pain relief (Sublingual or IV Nitroglycerin followed by IV opioid if needed).
  6. Obtain cardiac biomarkers.
  7. Assess heart and breath sounds.
  8. Obtain chest x-ray. Assessment of Patient with Angina  Describe and rate pain (0 to 10).  Look for restlessness, ECG changes, and nonverbal cues.  Monitor skin for pallor and temperature.  Use a calm approach to reduce anxiety. Treatment Elements for Angina (Mnemonic: ABCDE)A : Antiplatelet/anticoagulant therapy, Antianginal therapy, ACE inhibitors/ARBs.  B : Beta-blockers, BP control.  C : Cigarette smoking cessation, Cholesterol management, Calcium channel blockers, Cardiac rehabilitation.  D : Diet (weight management), Diabetes management, Depression screening.  E : Education, Exercise. Patient Teaching for Chronic Stable AnginaRisk Factor Modification : Identify and reduce risk factors for coronary artery disease (CAD).  Diet : Low in salt and saturated fats; maintain ideal body weight.  Physical Activity : Regular program (e.g., brisk walking).  Avoid Triggers : Identify and avoid precipitating factors (e.g., heavy meals, extreme weather).  Medication Knowledge : Educate on medications, their use, and side effects.

Drug Therapy OverviewNitrates : First-line for acute angina; monitor for orthostatic hypotension.  ACE Inhibitors/ARBs : For patients with EF ≤40%, diabetes, hypertension, or chronic kidney disease.  Beta-Blockers : Indicated for relieving angina; monitor for bradycardia and hypotension.  Calcium Channel Blockers : For those intolerant to beta-blockers; monitor for peripheral edema and constipation.  Lipid-Lowering Agents : Essential for managing cholesterol levels.  Sodium Current Inhibitor (Ranolazine) : Used if other treatments are ineffective; does not affect BP/HR. Important Drug AlertsNitrates : o Store in dark, airtight container. o Sit before taking SL NTG; it should cause a tingling sensation. o Do not combine with erectile dysfunction medications. o Monitor for headaches and orthostatic hypotension. Diagnostic and Intervention Studies for Chest Pain and CAD Initial AssessmentPatient History : Detailed health history and physical assessment for new-onset chest pain or changes in chronic stable angina.  12-Lead ECG : Compare with previous ECG to identify changes indicating acute coronary syndrome (ACS).  Laboratory Tests : o Cardiac Biomarkers : Determine presence of ACS. o Lipid Profile & CRP : Identify CAD risk factors.  Chest X-ray : Assess for heart enlargement, aortic calcifications, and pulmonary congestion.  Echocardiogram : Detects resting left ventricular (LV) wall motion abnormalities suggestive of CAD. Stress Testing  If ECG and biomarkers are negative: o Exercise Stress Test : May include imaging (echocardiography or nuclear imaging). o Pharmacologic Stress Test : For patients unable to walk (e.g., adenosine or dobutamine). o Imaging : Abnormal if blockages >50% in left main artery or >70% in other vessels. o EBCT or CCTA : Considered if ACS is ruled out and the patient is pain-free. Cardiac CatheterizationGold Standard Test : For increasing angina symptoms.  Indications : Positive ECG changes or biomarkers; abnormal stress test.  Revascularization Options : o Percutaneous Coronary Intervention (PCI) : Includes balloon angioplasty and stent placement.  Stents : Bare metal (BMS) vs. drug-eluting (DES) to prevent restenosis.  DAPT : Dual antiplatelet therapy (e.g., aspirin + clopidogrel) post-PCI. Potential Complications of PCI

  1. Abrupt closure
  2. Vascular injury
  3. Acute MI
  4. Stent embolization
  5. Failure to cross blockage
  6. Coronary spasm
  7. Dye allergy

Ischemic ProcessTimeline : o Heart muscle cells become hypoxic within 10 seconds of total occlusion. o Viability lasts about 20 minutes without collateral circulation. o Complete necrosis can take 4-6 hours for full thickness of the heart muscle, up to 12 hours if not completely occluded.  Metabolic Changes : o Initial anaerobic metabolism leads to lactic acid accumulation. o Restoration of blood flow allows aerobic metabolism to resume. Unstable Angina (UA)Characteristics : o New onset, occurs at rest, or increases in frequency/duration with less effort. o Lasts 10 minutes or more. o ECG may show ischemic changes (ST depression/T wave inversion). Myocardial Infarction (MI)Classification : o STEMI : Caused by an occlusive thrombus. Requires emergency intervention (PCI or thrombolytic therapy) within 90 minutes. o NSTEMI : Caused by a nonocclusive thrombus. No ST elevation; managed with catheterization within 12-72 hours. Thrombolytics are not used.  Risk Factors : o Most MIs occur in individuals with preexisting coronary artery disease (CAD).  Location of Infarction : o Right Coronary Artery : Supplies inferior/posterior walls. o Left Anterior Descending (LAD) Artery : Supplies anterior wall. o Left Circumflex Artery : Supplies lateral wall.  Collateral Circulation : o The degree of collateral circulation influences the severity of the MI. Older patients may have developed collateral circulation, providing better outcomes compared to younger individuals with similar blockages. Diagnostic ConsiderationsCardiac Biomarkers : Serum levels increase with myocardial damage; crucial for distinguishing NSTEMI from UA.  Echocardiogram : May show hypokinesis or akinesis in the affected area, indicating contractility issues. Nursing ImplicationsImmediate Assessment : Compare current ECG with previous ECG if available.  Monitoring : Regular assessment of vital signs, ECG changes, and cardiac biomarkers.  Patient Education : Importance of seeking immediate medical attention for chest pain. Summary Points for NCLEX  Recognize signs and symptoms of ACS and different types of MI.  Understand the urgency of STEMI treatment.  Differentiate between UA, NSTEMI, and STEMI based on clinical presentation and ECG changes.  Be aware of the importance of collateral circulation in MI outcomes.

Diagnostic Studies for Acute Coronary Syndrome (ACS)

  1. Primary Diagnostic Tools : a. 12-Lead Electrocardiogram (ECG) b. Serum Cardiac Biomarkers Electrocardiogram (ECG) FindingsPurpose : Essential for diagnosing UA, NSTEMI, and STEMI. Compare new ECG with any previous ECGs.  ECG Changes : o ST-Elevation : Indicates STEMI; significant if ≥1 mm in at least 2 contiguous leads ( ≥2 mm in leads V2 and V3). o T Wave Changes : Inversion may occur with ischemia and is a later sign if reperfusion is delayed. o Pathologic Q Waves : Develop if treatment is delayed and remain permanently on ECG.  Types of ACS on ECG : o STEMI : Complete occlusion, ST elevation in leads facing the infarcted area. o NSTEMI/UA : Transient thrombosis/incomplete occlusion; may show ST depression and/or T wave inversion but no pathologic Q waves.  Dynamic Process : o Serial ECGs are important to observe changes over time in ischemia, injury, and infarction. Serum Cardiac BiomarkersImportance : Distinguish between UA (negative biomarkers) and NSTEMI (positive biomarkers).  Key Biomarkers : o Troponins :  cTnT and cTnI : Rise within 4-6 hours , peak at 10-24 hours , and return to baseline in 10- days. Serial measurements recommended every 6 hours for 24 hours.  High-Sensitivity Cardiac Troponin (hs-cTn) : Rises within 1 hour of injury; levels remain high for 7-14 days. o Creatine Kinase (CK) :  CK-MB : Rises about 6 hours post-MI, peaks at 18 hours , and normalizes in 24-36 hours. Specific for heart muscle injury but less sensitive than troponins. Cardiac CatheterizationIndications : o STEMI : Must undergo catheterization within 90 minutes of ED presentation or receive thrombolytics within 30 minutes if no PCI capability. o NSTEMI/UA : Usually scheduled within 12-72 hours for evaluation and treatment (e.g., PCI or CABG). Acute Coronary Syndrome (ACS) OverviewDefinition : A spectrum of conditions associated with sudden, reduced blood flow to the heart.  Importance of Quick Treatment : Early diagnosis and intervention are crucial to preserve heart muscle. Emergency Management of ACS Initial Assessment and Interventions
  2. Vital Signs : Monitor and record baseline vital signs, including oxygen saturation.
  3. ECG : Obtain a 12-lead ECG and start continuous monitoring.
  4. Patient Positioning : Position upright unless contraindicated.
  5. Oxygen Therapy : Administer O2 via nasal cannula to maintain saturation above 93%.

Post-Acute Care:  Focus on effective coping with anxiety, participation in rehabilitation, and risk reduction. Nutrition Therapy  Start NPO (nothing by mouth) until stable; advance to a heart-healthy diet. Implementation of Care in Acute Coronary Syndrome Monitoring and AssessmentVital Signs : Monitor vital signs and pulse oximetry frequently (every hour initially) and continuously in ICU/telemetry settings.  ECG Monitoring : Start continuous ECG monitoring and obtain serial 12-lead ECGs. Monitor for dysrhythmias, especially sustained VT and VF.  Cardiac Biomarkers : Draw serial cardiac biomarkers to assess heart function.  Physical Assessment : Regularly assess for signs of heart failure (HF) such as dyspnea, tachycardia, and peripheral edema. Check input/output and for nasal cannula irritation. Pain ManagementMedications : Administer nitroglycerin (NTG), morphine, and supplemental oxygen as needed for chest pain.  Documentation : Continuously evaluate and document pain relief and the effectiveness of interventions.  Patient Education : Educate patients about the importance of ongoing treatment even after pain relief. Treatment ProtocolsUnstable Angina (UA) and NSTEMI : Use heparin (unfractionated or low molecular weight) to prevent microemboli. Dual antiplatelet therapy (DAPT) with aspirin and ticagrelor is recommended.  STEMI Treatment : Initiate reperfusion therapy (emergent PCI preferred) as soon as possible. Use thrombolytics if PCI is unavailable. Rest and ComfortGradual Activity : Encourage gradual increase in activity; patients may sit in a chair post-event if stable.  Comfort Measures : Create a quiet environment and employ relaxation techniques to promote comfort. Phases of Cardiac Rehabilitation

  1. Phase I (Hospital) : Focus on early mobility and management of symptoms and complications.
  2. Phase II (Early Recovery) : Outpatient rehabilitation; gradually increase activity under supervision.
  3. Phase III (Late Recovery) : Long-term individualized activity programs; lifestyle changes should be sustained. Anxiety and Emotional SupportAnxiety Management : Identify sources of anxiety and provide reassurance. Encourage family presence.  Patient Teaching : Begin teaching based on the patient's understanding and readiness; answer questions simply and repetitively. Emotional and Behavioral Reactions  Recognize patterns of emotional responses (anger, denial, anxiety, dependency, depression, acceptance).  Support coping strategies and assess the patient’s support system. Patient Education TopicsSigns and Symptoms : Teach recognition of angina and myocardial infarction (MI) symptoms and how to respond.  Heart Anatomy : Provide education on heart function, coronary artery disease (CAD), and its implications.

Lifestyle Changes : Discuss risk factors and management strategies, importance of cardiac rehabilitation, and gradual activity resumption.  Expectations for Recovery : Offer anticipatory guidance on recovery, work, and lifestyle changes. Physical Activity and Cardiac Rehabilitation

  1. Importance of Physical Activity : a. Essential for physiologic and psychologic well-being. b. Benefits include: i. Increased maximal O2 uptake ii. Improved cardiac output (CO) iii. Decreased blood lipids and blood pressure (BP) iv. Enhanced blood flow to coronary arteries v. Increased muscle mass and flexibility vi. Weight loss and control c. Even after years of inactivity, physical activity is beneficial.
  2. Metabolic Equivalent (MET) Units : a. 1 MET = 3.5 mL of O2/kg/min (or 1.4 cal/kg/min). b. Energy expenditure categorized: i. Low-Energy (<3 METs) : Eating, resting supine. ii. Moderate-Energy (3–6 METs) : Showering, walking at 3–4 mph. iii. High-Energy (6–8 METs) : Mowing lawn, walking at 5 mph. iv. Very-High-Energy (>9 METs) : Cross-country skiing, running at >6 mph.
  3. Activity Guidelines for Patients : a. AHA recommends 30 minutes of moderate aerobic activity (e.g., brisk walking) 5 days a week. b. Gradually increase activity, especially for those recovering from acute coronary syndrome (ACS). c. Patients should listen to their bodies to avoid overexertion. d. Teach patients to check their heart rate (HR) during activity.
  4. Types of Physical Activity : a. Isometric (static) : Minimal joint movement, e.g., lifting heavy objects. Limit isometric exercises due to rapid HR/BP changes. b. Isotonic (dynamic) : Involves joint movement, e.g., walking, swimming. Safer for cardiovascular health.
  5. Factors Affecting Adherence to Exercise : a. Women and patients with depression may have poor adherence to exercise post-MI. b. Regularly screen for depression and refer for treatment as needed. Cardiac Rehabilitation
  6. Definition : Restoration of optimal function across multiple areas (physiologic, psychologic, mental, spiritual, economic, vocational).
  7. Recommendation : All patients with UA, MI, PCI, or CABG should be referred for cardiac rehabilitation.
  8. Barriers : Participation is often low due to cost and logistical issues; home-based programs are a viable alternative.
  9. Long-term Management : Emphasize that coronary artery disease (CAD) is chronic; lifestyle changes are essential for recovery. Resuming Sexual Activity
  10. Counseling : Address sexual activity post-ACS; often more stressful than the act itself.
  11. Guidelines : a. Resume sex when able to exercise ≥3-5 METs without symptoms. b. Encourage daily physical activity during recovery. c. Avoid heavy meals and alcohol before sex; foreplay is beneficial.