Cardiac Output, Oxygen Delivery and Myocardial Infarction

Cardiac Output

• Cardiac output (CO) refers to the volume of blood pumped by the heart each minute.
• Stroke volume is the volume of blood pumped by the left ventricle with each heartbeat.
• Preload is the end diastolic pressure or volume that stretches the right or left ventricle, reflecting the patient's fluid volume status.
• Afterload is the force or resistance ventricles must overcome to eject blood into the pulmonary circuit or aorta.
• Contractility is an inherent ability of the heart muscle to contract independent of preload and afterload.

Oxygen Delivery

• Oxygen delivery is the amount of oxygen delivered to the tissues.
• Oxygen utilization and consumption show the relationship between oxygen delivery and oxygen extraction at the tissue level, which is normally 60-75%.

Myocardial Infarction (MI) Epidemiology

• There are approximately 659,000 deaths per year due to MI.
• One in four deaths is due to heart disease.
• More than one in three adults live with one or more types of cardiovascular disease.
• There are around 805,000 MIs per year.
• Approximately 25% of MIs are recurrent
• 1 in 5 MIs are silent, showing no symptoms.

Myocardial Infarction Risk Factors

• Risk factors include smoking, high LDL, Type 2 diabetes, elevated adrenaline, obesity, inactivity, and hypertension.

Myocardial Infarction Pathophysiology

• Destruction of heart muscle occurs from a lack of oxygenated blood supply.
• Atherosclerosis is the most common cause.
• The process involves plaque in the artery rupturing, leading to thrombus formation and obstruction of blood flow.

Acute Coronary Syndrome (ACS)

• ACS is an umbrella term used when there is concern for myocardial ischemia.
• ACS encompasses unstable angina, Non-ST Elevation Myocardial Infarction (NSTEMI), and ST Elevation Myocardial Infarction (STEMI).
• Stable angina involves episodes of intermittent chest pain when an artery is narrowed due to CAD, and is associated with activity and relieved by rest and serves as a warning sign for potential heart muscle damage.
• Unstable angina is pain not associated with exercise and not relieved by rest, and it involves, ECG changes but no elevation in cardiac markers, and requires immediate treatment.
• Unstable angina may present with nonspecific or transient ST segment depressions or elevations.
• NSTEMI involves ST depressions (0.5 mm at least) or T wave inversions (1.0 mm at least) without Q waves in 2 contiguous leads with prominent R wave or R/S ratio >1, accompanied by elevated cardiac markers.
• STEMI shows ST elevations and elevated cardiac markers.

Myocardial Infarction Clinical Manifestations

• Obstructed blood flow to the heart muscle is a cause.
• Chest pain (stable/unstable angina) and referred pain to the shoulder/arm (left side) or jaw and tooth may occur.
• Other manifestations include shoulder blade pain, upper back pain, shortness of breath (SOB), nausea/vomiting (N/V), diaphoresis, and generalized fatigue.
• Left coronary artery MI or left ventricle infarction has a worse prognosis with the highest risk of sudden death and congestive heart failure (CHF).
  • Signs include dyspnea, tachycardia, and hypertension due to loss of CO and stimulation of sympathetic compensatory mechanisms, potentially leading to hypotension.
• Right coronary artery MI or right ventricle infarction - JVD, hypotension.

Myocardial Infarction Medical Management—Diagnosis

• Laboratory tests include troponin, creatine kinase (CK), and creatine kinase myocardial band (CK-MB).
  • Troponin is a specific marker of cardiac muscle damage, elevating within 4 hours of injury and staying elevated for up to 10 days.
  • CK is a general marker of cellular injury, released from brain, skeletal muscle, and cardiac tissue when there is muscle damage.
  • CK-MB is a isoenzyme marker specific to cardiac tissue, released from myocardial damage cells rising at 3 hrs & remain up for 36 hrs.
• Diagnostic testing: An EKG is the gold standard for diagnosing STEMI because it's inexpensive and easy to perform.

Myocardial Infarction Medical Management—Treatment

• Maximize oxygenation, control pain, dilate coronary arteries, prevent clots, decrease myocardial workload, and increase blood flow to cardiac tissue via reperfusion therapy.
• Administer nitroglycerin SL, aspirin, then a pain medication like morphine sulfate if pain persists despite nitroglycerin.
• Oxygen: Administer only for patients with suspected MI who display respiratory distress and when arterial saturation is < 90% or at high risk of hypoxia.

Myocardial Infarction Medical Management—Medications

• Oxygen: All patients receive this.
• Nitroglycerin SL dilates coronary arteries, increases cerebral blood flow, controls pain.
  • Administer one tablet every 5 minutes, up to a maximum of 3 doses.
• Aspirin acts as an antiplatelet to prevent clot growth.
• Pain medication: Administer morphine for pain, which may mask changes in condition.

Myocardial Infarction Reperfusion Therapy

• Percutaneous coronary intervention involves interventional caths opening blocked blood vessels from MI.
  • A catheter with a small balloon is inserted into the artery to the left side of the heart & coronary arteries.
  • The balloon is inflated and deflated to open the lumen of the blocked artery.
  • The goal is a door-to-balloon time of 90 minutes.
  • Once the lumen is open, a stent is inserted to maintain adequate blood flow.
  • The radial artery is preferred; if the femoral artery is used, the patient must lie flat without bending the leg for 2-6 hours to allow healing and risk of bleeding.
  • After removing the catheter from the radial artery, a compression device is placed around the wrist to apply pressure.
• Fibrinolytics are used if PCI is not available and should be administered within 6 hours.

Myocardial Infarction Surgical Management

• Coronary artery bypass graft (CABG) is a revascularization intervention that bypasses blockages in coronary arteries causing myocardial muscle damage.
  • A healthy artery or vein (internal thoracic artery or saphenous vein) is grafted to the blocked coronary artery.
  • One end the artery or vein is attached to the aorta, and the other end is attached to the blocked coronary distal to the occlusion. - This bypasses the blocked portion of the artery to allow blood flow to the cardiac tissue.
  • Complications: bleeding, dysrhythmias, MI, stroke, nonunion of sternum, sternal infection, renal failure, and heart failure.
  • Complications of bypass: systemic inflammatory response resulting in vasodilatory shock, heparin-induced thrombocytopenia & activation.

Myocardial Infarction Complications

• Heart failure: An MI can cause a large amount of heart muscle to die, decreasing left ventricular function. - It causes an inability to produce adequate CO to maintain the body's metabolic demands and decreasing heart function due to myocardial tissue death.
• Arrhythmias: Includes asystole, symptomatic bradycardia, and heart block. - These are associated with SA node dysfunction, common after inferior wall MI because the right coronary artery supplies the SA node and may need temporary pacemakers. - Ventricular arrhythmias may also occur.

Myocardial Infarction Nursing Management—Assessment and Analysis

• Assess for signs and symptoms related to lack of oxygen delivery:
  • Chest pain, shoulder/arm pain (left arm), jaw & neck pain, upper back pain, SOB, N/V, diaphoresis, pallor, generalized fatigue.
• Female patients often present with neck, shoulder blade, jaw pain, abdominal pain, and fatigue.
• Older adults present with dyspnea, syncope, weakness, or confusion.

Myocardial Infarction Nursing Management—Nursing Diagnoses

• Decreased CO r/t poor cardiac contractility secondary to MI.
• Decreased cardiac tissue perfusion r/t coronary artery occlusion secondary to MI.
• Pain r/t inadequate blood supply by the heart.

Myocardial Infarction Nursing Interventions—Assessments

• Vital Signs & Pulse Oximetry: Tachycardia with borderline low BP and decreased O2 sat is a sign of inadequate cardiac output & O2 delivery.
• Characteristics of pain: Chest pain is an indication of MI, and continued or changing in pain characteristics indicate worsening.
• ECG: ST depression shows ischemia, ST elevation is injury, Q Wave indicates MI.
• Restlessness: It is early stages to severe anxiety & sense of doom.
• Skin Color & Temperature, Peripheral Pulses, Diaphoresis: Decreased pulses & cold, clammy, pale skin. - Inadequate tissue perfusion & inadequate cardiac output (CO). - Activation of the sympathetic system with low CO will stimulate diaphoresis.
• Urine Output: Decreased or absent urine output means decreased renal perfusion related to decreased CO.
• Labs: Troponin is protein released from damaged cardiac muscle. - It elevates within 4 hours & stay elevated for 10 days.

Post-CABG Nursing Interventions—Assessments

• HR & BP: Continuously with arterial catheter q 15 mins initially, then q 4 hrs until stable. - Tachycardia, bradycardia, hypotension, and hypertension may be signs of decreased cardiac output or compensatory mechanisms.
• Hemodynamic monitoring: Decreased preload indicates decreased cardiac output, leading to poor tissue perfusion.
• Continuous cardiac monitoring: Dysrhythmias are common after CABG.
• Heart Tones: Muffled heart tones indicate tamponade.
  • S3 and S4 crackles indicate heart failure.
• Breath sounds & continuous oxygen saturation: Decreasing sat indicates pulmonary complications.
  • Diminished or unilaterally absent sounds indicate atelectasis, pleural effusions, or pneumothorax.
• Core Temperature: Hypothermia during surgery reduces metabolic rate & risk of organ ischemia.
  • Rewarming can produce hypotension from vasodilation.
• LOC, Pupils, Responsiveness: Assessing effectiveness of sedation & neurological function.
• Hourly I&O: Notify MD if output is < 30 ml/hr for 2 hours.
  • Decreased urine output sign of renal damage or decreased cardiac output.
• Skin color, temperature, pulses, edema, capillary refill:
  • Pale, cool skin, delayed cap refill, and weak pulses indicate decreased cardiac output.
  • Edema is expected after CABG due to fluid resuscitation during surgery.
• Chest tube output, color, volume hourly:
  • A sudden increase in output > 100 to 200 ml associated with position changes or if increased bright-red drainage indicates hemorrhage & need to return to the operating room.
• Labs: Assess hgb/hct, electrolytes, creatinine, BUN, glucose.
  • Changes indicate bleeding, fluid shifts, or renal dysfunction.
  • Tight glucose control is associated with improved outcomes.
• Incisions: Assess incisions for drainage, warmth, redness, swelling.
  • Redness, warmth, swelling, or purulent drainage indicates infection.

Myocardial Infarction Nursing Interventions—Actions:

• Administer oxygen if < 93%: Oxygen consumption & demand increases.
• Insert two large-bore IVs: IV access for medication delivery & fluid resuscitation
• Administer medications as ordered:
  • Aspirin & heparin prevent new clot formation.
  • Nitroglycerin SL dilates coronary arteries, increases blood flow & decreases pain.
  • Morphine provides pain relief if nitroglycerin is not effective.
  • Beta-blockers decreases sympathetic response to MI, decreases cardiac workload & oxygen consumption.
• Continuous ECG Monitoring: Electrocardiogram monitoring to evaluate MI, effectiveness of treatment monitor for dysrhythmias.
• Bed Rest: To decreases oxygen and cardiac demands
• BP is monitored because hypotension may result in graft collapse, and hypertension may result in bleeding.
• Administer fluids & medications as ordered:
  • Give vasodilators, vasoconstrictors, inotropes, diuretics as needed.
  • Maintains hemodynamic stability.
• Rewarm patients slowly:
  • Warm fluids, blankets, air flow devices.
  • Rapid rewarming causes dysrhythmias and/or hypotension due to vasodilation and shivering increase oxygen needs.
• Administer pain medication & continuous sedation medications:
  • Used to decrease anxiety & pain, potentially increasing cardiac workload.
• Wound care: Initial dressing to be removed or changed by a surgeon.
• Pulmonary hygiene is administered while intubated
  • Reposition frequently, suction prn, and provide oral care every 4 hours.
• Pulmonary hygiene is provided after extubation:
  • Incentive spirometry, cough & deep breathe q 1 - 2 hrs while awake, and encourage chest splinting when coughing.
  • This can help with weaning toward extubation, and oral care prevent ventilator-associated PNA.
• Early mobility or ambulation reduces complications r/t immobility, DVT, PNA, constipation, and skin breakdown.

Myocardial Infarction Nursing Interventions—Teaching

• Report s/s of MI: Chest pain or chest discomfort or increased SOB.
  • Understanding s/s MI allows patients to have earlier intervention, decreasing complications & severity of present or future MIs.
• Medication education: Purpose, dose, and side effects of medications.
  • To treat effects of MI & prevent future MIs.
• American Heart Association "Life's simple 7" are as follows,
  1. No smoking of cigarettes or tobacco products: e-cigarettes or vaping.
  2. Maintain normal body weight.
  3. Exercise for at least 150 mins w/ moderate-intensity activity, or 75 mins of vigorous-intensity activity, or combination of each per week.
  4. Eat healthy diet: whole foods, fruits, vegetables, lean protein, nuts, seeds, cooking in healthy oils.
  5. Maintain the total cholesterol level <200mg/dL.
  6. Keep BP < 120/80 mmHg.
  7. Keep fasting blood glucose < 100 mg/dl.
• In the instance the patient had CABG:
  • Signs of infection: Wound infection requires prompt intervention to promote healing.
  • Sternal precautions: Do not lift weight over 10 lbs, raise arms overhead, bend at waist, participate in vigorous activity until cleared.
  • This will help interfere with sternal wound healing.
  • Cardiac rehabilitation: Exercise training & physical activity counseling, coronary risk factor reduction/secondary prevention, nutritional counseling, and weight management.
    • It also includes psychosocial support, education regarding diet, wt management, purpose of meds, drug side effect assess tolerance, and reinforcement for med adherence.

Myocardial Infarction Nursing Management - Evaluating Care Outcomes

• Resume normal activity
• Pain free
• Anxiety free

Cardiogenic Shock Pathophysiology

• Heart muscle cannot contract, which leads to a decrease in cardiac output, decreased ejection fraction, and decreased contractility with increased ventricular filling pressures.
• A precipitating event such as myocardial damage or stunning leads to decreased contractility with decreased CO, also decreased O2 to tissues = anaerobic metabolism = increased lactate.
• Decreased CO leads to sympathetic stimulation (tachycardia, renal retention, vasoconstriction), increasing myocardial workload, and causing myocardial.

Cardiogenic Shock Clinical Manifestations

• Decreased cardiac output - Hypotension, Tachycardia, systemic vasoconstriction, venous congestion, decreased urine output, lactic acidosis, end-organ dysfunction and crackles
• Also decreased peripheral pulses, cool pale skin, decreased bowel sounds, restlessness.
• Chest pain, Nausea, Vomiting, Diaphoresis are also noted

Cardiogenic Shock Medical Management—Diagnosis

• Diagnosis is based on patient presentation, exclusion of other causes and laboratory testing. Specific tests include ABG, which reveals hypoxia, lactic acidosis, and liver and renal function.

Cardiogenic Shock Medical Management—Medications

• Medications are used to increase BP and cardiac output.
• Vasoactives, Vasodilators.
• Positive Inotropes

Medications to Treat Cardiogenic Shock

• Various medications are used for cardiogenic shock, including multiple vasopressors and inotropes.
  • Epinephrine increases contractility and chronotropy by activating beta-1- and beta-2-adrenergic receptors, increasing CO, MAP, and HR. - There is also a risk of dysrhythmias and increased SVO2. - It stimulates glycolysis, which can increase lactate and causes hyperglycemia.
  • Norepinephrine (Levophed) provides vasopressor and inotropic support through alpha- and beta-adrenergic receptors and is a strong vasoconstrictor associated with improved outcomes in cardiogenic shock.
  • Dopamine increases chronotropy, with low doses increasing renal perfusion and higher doses working as a vasopressor. - It increases SVO2 and is not a first-line choice due to an increase in cardiac workload.
  • Vasopressin is a hormone analogue, providing pure vasoconstriction. - It is useful for treating vasoplegic states, with no effect on heart rate. Usually, an adjunct drip
  • Angiotensin II (Giapreza) is a hormone analogue that mimics angiotensin II and causes vasoconstriction and increased aldosterone release. - It can increase lactate and cause hyperglycemia, increase in HR, and increase the risk of clotting
  • Phenylephrine (Neo-Synephrine) causes vasoconstriction through alpha adrenoceptors, avoiding inotropy and can cause intrapulmonary shunting.
  • Nitroglycerin causes vasodilation in both arterial and venous systems and promotes coronary circulation, potentially causing hypotension and headaches. - It Can also cause profound hypotension in RCA occlusions
  • Nitroprusside (Nipride) causes vasodilation through nitric oxide relaxation of vascular smooth muscle, reducing preload and afterload, and dilating coronary arteries and is effective but short-acting. - It can cause coronary steal phenomenon with partially vascularized patients. - Thiocyanate can accumulate leading to cyanide toxicity, in renal failure patients.
  • Nicardipine is a calcium channel blocker with direct arterial vasodilating effects on the system and coronary arteries.
    • Used to prevent vasospasm and lower blood pressure.
  • Milrinoneis a phosphodiesterase inhibitor that increases CO by improving contractility and reducing SVR and PVR. - It increases CO, lowers HR, and decreases filling pressures and requires monitoring for hypotension, dysrhythmias, and thrombocytopenia. - There is reduced clearance with renal insufficiency.
  • Dobutamine is considered with activation of beta-1 adrenoceptors to increase heart rate and myocardial contractility, as well as beta-2 adrenoceptors, which provide vasodilation.. - Typically used in right-sided ventricular dysfunction but requires monitoring for increased HR and pro-arrhythmic effects.

Cardiogenic Shock Surgical Management

• Intra-aortic balloon pump (IABP): provides mechanical circulatory support (MCS).
• Includes mechanical pumps used to assist ventricles & decrease the workload of the heart
• Ventricular assist device - LVAD works by pulling blood from the left ventricle into a pump, then ejects the blood into the aorta.
• RVAD works by pulling blood from the right ventricle, then ejecting the blood into the pulmonary artery.
• Extracorporeal membrane oxygenation (ECMO): Deoxygenated blood.
• Blood is diverted from the vascular system via a central vein and returned to circulation after being oxygenated and warmed outside the body to enhance cardiac output.
• Heart transplant when all other medical & surgical therapies have been exhausted.

Cardiogenic Shock Nursing Management—Assessment and Analysis

• Signs and symptoms resulting from decreased cardiac output include:
  • Hypotension, tachycardia with weak pulses, tachypnea, and severely decreased level of consciousness.
  • Other indicators are cold, cyanotic, and mottled skin; decreased or absent urine output; severely decreased or absent bowel sounds.
• Without successful intervention, multiple organ systems begin to fail, leading to severe hypotension, bradycardia, hypoxia, hypoglycemia, DIC, and severe coagulopathy.

Cardiogenic Shock Nursing Management—Nursing Diagnoses

• Altered tissue perfusion r/t inadequate CO

Cardiogenic Shock Nursing Interventions—Assessments

• Vital Signs: Hypotension, decreased CO, and increased left ventricular filling volumes are present because of ineffective contractile ability of the heart.
  • Increased SVR & tachycardia occur as a compensatory mechanism to increase BP and CO. RR increases to improve oxygenation.
• Breath sounds & Oxygen saturation: Decreasing 02 and/or auscultation of crackles indicate the presence of left heart weakening & pulmonary edema.
• Neurologic status: Decreased level of consciousness occurs as a result of decreased CO.
• Skin Color and Temperature: Cold and clammy skin may be a sign of progressing shock.
• Labs as follows:
  • ABGs reflect a metabolic acidosis due to anaerobic metabolism.
  • Hgb/Hct is essential to support oxygenation.
    • Metabolic Profile to track organ function through liver function and renal function tests.
  • Lactate: Increasing lactate levels is an indicator of anaerobic metabolism.
    • SvO2 (mixed venous oxygen saturation) decreases, and that indicates increased oxygen utilization at the tissue level decreases due to low CO.

Cardiogenic Shock Nursing Interventions—Actions

• Apply 100% non-rebreather oxygen mask.
• Anticipate Intubation & mechanical ventilation:
  • Intubation with mechanical ventilation decreases myocardial workload & will improve oxygenation.
• Prepare for invasive hemodynamic monitoring arterial, central, and PA catheters:
  • Invasive monitoring allows more precise evaluation & adjustment of medications.
• Administer inotropic & vasoactive meds as prescribed:
  • Inotropic meds increase contractility and vasoactive meds increase BP to improve stroke volume & systemic tissue perfusion.
• Administer fluid replacement
  • Fluid is administered to improve CO and preload only if filling pressures are low
• Administer diuretics as prescribed
• Restrict activity and allow rest periods to decrease cardiac workload & oxygen consumption.
• Morphine decreases preload with its action as a venous dilator.
• Maintain IABP anticipate potential placement and will help to increase coronary circulation & decrease SVR.
  • Assure IABP catheter is secured, head of bed is elevated <30 degrees, & affected leg is kept straight at all times to avoid catheter migration.
    • Also, assess catheter tubing for brown flecks, blood, which will indicate balloon rupture.

Cardiogenic Shock Nursing Interventions—Teaching

• Rest periods: Increased activity or stress levels cause increased myocardial oxygen consumption & can worsen a shock state.
• Allow family visitation: To help decrease a patient's anxiety & stress levels.
• Maintain fluid & Na+ restrictions to decrease the risk of heart failure. - Symptoms of heart failure, notify MD right away that early treatment of heart failure prevents progression to shock.

Cardiogenic Shock Nursing Management—Evaluating Care Outcomes

• Return to activities of daily living.
• The patient should have comfortable sleep and articulate feelings of control.