CJ

Exam2: Cardiovascular

I. Cardiac Disorders & Management

Heart Failure

Left-sided Heart Failure (LHF)
: Occurs when the left ventricle fails to pump blood efficiently to the body, leading to blood backing up into the lungs.

Symptoms
: Dyspnea (shortness of breath), orthopnea (difficulty breathing when lying flat), paroxysmal nocturnal dyspnea (PND, sudden awakenings due to dyspnea), crackles (rales) in the lungs, pulmonary edema (can lead to pink frothy sputum in severe cases), fatigue, weakness, activity intolerance, hacking cough (worse at night).

Causes
: Hypertension, coronary artery disease (CAD), myocardial infarction (MI), valvular diseases (e.g., aortic stenosis).

Right-sided Heart Failure (RHF)
: Occurs when the right ventricle fails to pump blood to the lungs, causing blood to back up into the systemic circulation.

Symptoms
: Jugular vein distension (JVD), peripheral edema (swelling in extremities), ascites (fluid accumulation in the abdomen), hepatomegaly (enlarged liver), splenomegaly, weight gain, nausea, anorexia.

Causes
: Most commonly caused by LHF, but can also result from pulmonary hypertension (e.g., due to chronic lung disease).

Diagnostics

  • B-type Natriuretic Peptide (BNP)
    : A hormone released from the ventricles in response to fluid overload; levels > 100\,pg/mL usually indicate heart failure. Higher levels correlate with severity.

  • Echocardiogram (Echo)
    : Assesses cardiac structure and function, including ejection fraction (EF), chamber enlargement, and valvular function. EF < 40\% is indicative of systolic heart failure.

  • Chest X-ray (CXR)
    : May show cardiomegaly, pulmonary congestion, or pleural effusions.

  • ECG
    : Can show arrhythmias, ventricular hypertrophy, or signs of ischemia.

Treatment
: Goals include improving cardiac output, reducing symptoms, and preventing disease progression.

  • Diuretics (e.g., Furosemide, Hydrochlorothiazide)
    : Reduce fluid volume and preload, alleviating pulmonary and peripheral edema.

  • ACE Inhibitors (ACEI) / Angiotensin Receptor Blockers (ARBs)
    : Reduce afterload and preload, improve cardiac remodeling, and decrease mortality (e.g., Lisinopril, Valsartan).

  • Beta Blockers (e.g., Metoprolol, Carvedilol)
    : Reduce heart rate, improve ventricular filling, and decrease myocardial oxygen demand, initiated once stable (contraindicated in acute decompensated HF).

  • Angiotensin Receptor-Neprilysin Inhibitors (ARNI) (e.g., Sacubitril/Valsartan)
    : Newer class for chronic HF with reduced EF.

  • Oxygen Therapy
    : Administered to improve oxygenation, especially if hypoxic.

  • Fluid Restriction
    : To manage fluid overload in severe cases.

  • Sodium Restriction
    : Dietary sodium intake should be limited to 2-3\,grams/day to prevent fluid retention.

  • Daily Weights
    : Monitor for sudden weight gain (e.g., > 2-3\,lbs in a day or > 5\,lbs in a week) which indicates fluid retention.

Valvular Heart Disease

Aortic Stenosis (AS)
: Narrowing of the aortic valve opening, obstructing blood flow from the left ventricle to the aorta.

Symptoms
: Classic triad of syncope, angina, and dyspnea on exertion (SAD), crescendo-decrescendo systolic murmur best heard at the right upper sternal border, often radiating to the carotid arteries; Left Ventricular (LV) hypertrophy due to increased pressure workload.

Causes
: Calcification in elderly, congenital bicuspid aortic valve.

Treatment
: Valve replacement (surgical or transcatheter aortic valve replacement - TAVR) is definitive.

Mitral Regurgitation (MR)
: Incomplete closure of the mitral valve, leading to backflow of blood from the left ventricle into the left atrium during systole.

Symptoms
: Holosystolic (pansystolic) murmur best heard at the apex and radiating to the axilla, pulmonary edema (due to increased left atrial pressure), atrial fibrillation (AFib) risk, fatigue, dyspnea.

Causes
: Mitral valve prolapse, ischemic heart disease, rheumatic fever.

Treatment
: Diuretics, vasodilators, surgical repair or replacement.

Mitral Stenosis (MS)
: Narrowing of the mitral valve opening, impeding blood flow from the left atrium to the left ventricle.

Symptoms
: Rumbling diastolic murmur heard at the apex, open snapping sound, pulmonary hypertension, dyspnea, hemoptysis, atrial fibrillation.

Causes
: Almost always rheumatic fever.

Treatment
: Diuretics, beta blockers, anticoagulation (for AFib), balloon valvuloplasty, or valve replacement.

Aortic Regurgitation (AR) / Aortic Insufficiency
: Incomplete closure of the aortic valve, causing backflow of blood from the aorta into the left ventricle during diastole.

Symptoms
: Bounding pulses (Corrigan's pulse), widened pulse pressure (systolic-diastolic), diastolic murmur (high-pitched, decrescendo) heard at the left sternal border, angina, dyspnea, head bobbing (Musset's sign).

Causes
: Rheumatic fever, Marfan syndrome, endocarditis.

Treatment
: Vasodilators, diuretics, aortic valve replacement.

Coronary Artery Disease (CAD) & Acute Coronary Syndromes (ACS)

Pathophysiology

  • Endothelial injury
    : Damage to the inner lining of arteries (e.g., due to hypertension, hyperlipidemia, smoking, diabetes).

  • Fatty streak formation
    : Lipids accumulate in the damaged endothelium.

  • Fibrous plaque formation
    : Smooth muscle cells proliferate, collagen is deposited, forming a fibrous cap over the lipid core. This narrows the arterial lumen.

  • Plaque rupture
    : The fibrous cap can rupture, exposing the thrombogenic lipid core.

  • Thrombosis
    : Platelets aggregate at the site of rupture, leading to thrombus formation, which can acutely occlude the artery.

Stable Angina
: Chest pain (angina) that is predictable, occurs with exertion or stress, and is relieved by rest or nitroglycerin. It's due to fixed atherosclerotic plaque limiting blood flow.

Unstable Angina (UA)
: Chest pain that is new in onset, occurs at rest, is worsening, or is not relieved by rest/nitroglycerin. It indicates partial occlusion of a coronary artery and is a precursor to MI.

Acute Coronary Syndromes (ACS)
: A spectrum ranging from UA to MI, characterized by acute myocardial ischemia.

  • Non-ST Elevation Myocardial Infarction (NSTEMI)
    : Partial occlusion of a coronary artery, resulting in myocardial cell death. ECG shows ST depression or T-wave inversion (no ST elevation). Cardiac biomarkers (troponins, CK-MB) are elevated.

  • ST-Elevation Myocardial Infarction (STEMI)
    : Complete occlusion of a coronary artery, leading to significant myocardial necrosis. ECG shows ST-segment elevation in two or more contiguous leads. Cardiac biomarkers are significantly elevated.

Treatment (Acute Management)
:

  • AONM Protocol (Acute MI)
    :

    • Aspirin: Antiplatelet, prevents further clot formation.

    • Oxygen: If SpO_{2} < 90\% or respiratory distress.

    • Nitroglycerin: Vasodilator, reduces preload and coronary spasms, improves blood flow.

    • Morphine: For pain relief, reduces myocardial oxygen demand, causes vasodilation.

  • Antiplatelets
    : Dual antiplatelet therapy (aspirin + P2Y_{12} inhibitor like Clopidogrel) for at least 12 months post-ACS.

  • Anticoagulants
    : Heparin drip, LMWH to prevent further thrombus growth.

  • Beta-blockers
    : Reduce myocardial oxygen demand, risk of arrhythmias.

  • ACE Inhibitors/ARBs
    : Started within 24 hours to prevent ventricular remodeling.

  • Statins
    : Lower cholesterol, stabilize plaque.

  • Reperfusion Therapy (for STEMI)
    :

    • Percutaneous Coronary Intervention (PCI)
      : Balloon angioplasty and stent placement to open the occluded artery. Primary PCI is preferred within 90\, minutes of first medical contact.

    • Post-PCI Care
      : Monitor for bleeding at access site (femoral or radial), re-occlusion (chest pain), sheath removal complications, vasovagal reactions, arrhythmias, renal function (contrast-induced nephropathy).

    • Fibrinolytic (Thrombolytic) Therapy
      : Administered if PCI is not available within 120\, minutes (e.g., Alteplase). Dissolves the clot.

  • Coronary Artery Bypass Graft (CABG)
    : Surgical procedure to create new pathways for blood flow around blocked coronary arteries using grafts (e.g., internal mammary artery or saphenous vein).

    • Indications
      : Multi-vessel disease, left main coronary artery disease, failed PCI, or poor ventricular function.

    • Post-CABG Care
      : Intensive Care Unit (ICU) monitoring, management of chest tubes (monitor drainage, air leaks), sternal precautions (avoid heavy lifting, pushing/pulling, arm abduction to protect sternum), pain management, early ambulation, monitoring for arrhythmias (AFib common), neuro status, renal function.

Infective & Inflammatory Disorders

Infective Endocarditis (IE)
: Infection of the endocardium, typically involving heart valves.

Symptoms
: Fever (most common), new or changed heart murmur, systemic emboli (e.g., Janeway lesions, Osler's nodes, Roth's spots), splinter hemorrhages, fatigue, chills.

Causes
: Bacterial (e.g., Staphylococcus aureus, Streptococcus viridans) or fungal infection, often associated with IV drug use, prosthetic valves, or dental procedures.

Diagnostics
: Positive blood cultures, echocardiogram (showing vegetations).

Treatment
: Long-term (4-6 weeks) IV antibiotics, sometimes valve replacement surgery.

Pericarditis
: Inflammation of the pericardium (the sac surrounding the heart).

Symptoms
: Sharp, pleuritic chest pain (worse with inspiration, coughing, lying flat), often relieved by leaning forward; pericardial friction rub (scratchy sound heard on auscultation), fever.

Causes
: Viral infection (most common), MI, autoimmune diseases, renal failure.

Diagnostics
: ECG (diffuse ST elevation with PR depression), echocardiogram (pericardial effusion), elevated inflammatory markers (CRP, ESR).

Treatment
: NSAIDs (e.g., Ibuprofen) or colchicine for pain and inflammation. Corticosteroids if severe.

Myocarditis
: Inflammation of the heart muscle (myocardium).

Symptoms
: Can vary widely from asymptomatic to severe chest pain, dyspnea, palpitations, signs of heart failure or arrhythmias.

Causes
: Viral infections (e.g., Coxsackievirus, adenovirus) are the most common cause. Can lead to dilated cardiomyopathy, heart failure, or arrhythmias.

Diagnostics
: ECG abnormalities, elevated cardiac enzymes, elevated inflammatory markers, cardiac MRI, endomyocardial biopsy is definitive.

Treatment
: Supportive care, managing heart failure symptoms (diuretics, ACEI/ARBs), antiarrhythmics if needed. Abstinence from strenuous activity.

Cardiogenic Shock & Cardiac Tamponade

Cardiogenic Shock
: The heart's inability to pump enough blood to meet the body's needs, leading to inadequate tissue perfusion.

Clinical picture
: Hypotension (systolic BP < 90\,mmHg), weak thready pulses, cool clammy skin, decreased urine output (< 0.5\,mL/kg/hr), altered mental status, pulmonary congestion.

Causes
: Most commonly severe MI (loss of >40\% of LV myocardium), severe heart failure, arrhythmias, valvular rupture.

Treatment

  • Inotropes (e.g., Dobutamine, Milrinone)
    : Improve myocardial contractility.

  • Vasopressors (e.g., Norepinephrine)
    : Maintain blood pressure.

  • Intra-Aortic Balloon Pump (IABP)
    : Mechanical circulatory support, inflates during diastole (increases coronary perfusion) and deflates during systole (reduces afterload, increases cardiac output).

  • Diuretics
    : If pulmonary edema is present, cautiously administered.

  • Treat underlying cause (e.g., revascularization for MI).

Cardiac Tamponade
: Compression of the heart caused by fluid accumulation in the pericardial sac, preventing adequate ventricular filling.

Symptoms
: Manifests as Beck's Triad (Muffled heart sounds, Hypotension, Jugular Vein Distension); pulsus paradoxus (an exaggerated drop in systolic BP > 10\,mmHg during inspiration); dyspnea, narrow pulse pressure.

Causes
: Trauma, pericarditis, post-cardiac surgery, malignancy, aortic dissection.

Diagnostics
: Echocardiogram (confirms pericardial effusion and cardiac compression).

Treatment
: Emergency pericardiocentesis (percutaneous needle aspiration of fluid from the pericardial sac) to relieve pressure. Sometimes a surgical pericardial window is created.

Disorders of the Aorta

Abdominal Aortic Aneurysm (AAA)
: Localized dilation or bulging of the abdominal aorta.

Symptoms
: Often asymptomatic until rupture. May present with back pain, flank pain, or a pulsatile mass in the abdomen. Rupture is a surgical emergency, leading to severe pain, hypotension, and signs of shock.

Risk Factors
: Age, smoking, hypertension, male gender, hyperlipidemia, family history.

Diagnostics
: Ultrasound screening, CT scan with contrast confirms diagnosis and size.

Treatment

  • Small aneurysms (< 5.5\,cm): Monitor with regular ultrasounds, blood pressure control.

  • Large/symptomatic aneurysms: Surgical repair (open repair or endovascular aneurysm repair - EVAR).

  • Ruptured AAA
    : Emergency surgery with high mortality.

Aortic Dissection
: A tear in the inner layer (intima) of the aorta, allowing blood to surge between the layers and create a false lumen.

Symptoms
: Sudden, severe, tearing or ripping chest and/or back pain (often described as migrating pain as the dissection extends), differential blood pressure between arms (> 20\,mmHg), pulse deficits, neurological deficits (if cerebral arteries involved), surgical emergency.

Causes
: Hypertension (most common), Marfan syndrome, Ehlers-Danlos syndrome, trauma.

Classification
: Stanford Type A (involving ascending aorta, surgical emergency) or Type B (involving descending aorta, often medically managed initially).

Treatment
: Aggressive blood pressure control (e.g., beta-blockers, nitroprusside), surgical repair for Type A, and sometimes for complicated Type B.

II. Hemodynamics & Critical Care

Hemodynamic Monitoring

Cardiac Output (CO)
: The amount of blood pumped by the heart per minute. CO = Heart Rate (HR) \times Stroke Volume (SV). Normal range 4-8\,L/min.

Mean Arterial Pressure (MAP)
: Average arterial pressure during a single cardiac cycle. Represents the perfusion pressure seen by organs. Target MAP ≥ 65\,mmHg for adequate organ perfusion.

Central Venous Pressure (CVP)
: Measures right ventricular preload (pressure in the right atrium). Normal range 2-8\,mmHg. Elevated CVP indicates fluid overload or right ventricular dysfunction. Decreased CVP indicates hypovolemia.

Pulmonary Artery Wedge Pressure (PAWP) / Pulmonary Capillary Wedge Pressure (PCWP)
: Measures left ventricular preload (end-diastolic pressure in the left ventricle). Normal range 6-12\,mmHg. Elevated PAWP indicates left ventricular failure or fluid overload. Decreased PAWP indicates hypovolemia.

Systemic Vascular Resistance (SVR)
: Resistance to blood flow offered by the systemic vasculature. Reflects afterload. Elevated SVR indicates vasoconstriction, reduced SVR indicates vasodilation.

Devices

Arterial Line (A-line)
: Invasive catheter inserted into an artery (radial, femoral) to continuously monitor blood pressure and allow for arterial blood gas (ABG) sampling.

  • Zero at phlebostatic axis
    : For accurate readings, the transducer must be leveled at the phlebostatic axis (fourth intercostal space, midaxillary line), which approximates the level of the right atrium.

  • Complications
    : Hemorrhage, infection, thrombus formation, nerve damage.

Intra-Aortic Balloon Pump (IABP)
: A temporary mechanical circulatory support device placed in the descending aorta via a femoral artery. Synchronized with the ECG.

  • Inflates during diastole
    : Increases diastolic pressure, augmenting coronary artery perfusion.

  • Deflates during systole
    : Decreases afterload (reduces resistance the LV pumps against), increasing cardiac output.

  • Indications
    : Cardiogenic shock, acute MI, unstable angina, bridge to transplant or other definitive therapy.

  • Complications
    : Limb ischemia, bleeding, aortic dissection, infection, balloon rupture.

Central Venous Catheters (CVCs)
: Multi-lumen catheters inserted into large veins (subclavian, jugular, femoral) for medication administration, fluid resuscitation, and CVP monitoring.

  • Monitor for infection
    : Site care, sterile dressing changes, assess for redness, swelling, drainage.

  • Monitor for air embolism
    : During insertion or removal if not properly clamped or sealed. Place patient in Trendelenburg and on left side if suspected.

  • Complications
    : Pneumothorax (during insertion), arterial puncture, arrhythmias.

Shock States

General Principles of Shock Management
: Optimize oxygen delivery, administer IV fluids, identify and treat the underlying cause.

  • Hypovolemic Shock
    : Due to inadequate circulating blood volume (e.g., hemorrhage, severe dehydration). Markers include decreased CVP/PAWP, increased SVR, decreased CO. Treatment: Rapid administration of IV fluids (crystalloids like NS or LR) or blood products.

  • Cardiogenic Shock
    : Due to primary cardiac pump failure. Markers include increased CVP/PAWP, increased SVR, decreased CO. Treatment: Inotropes (dobutamine, milrinone), vasopressors (norepinephrine), IABP. Avoid aggressive fluid administration unless hypovolemic.

  • Septic Shock
    : A type of distributive shock caused by severe infection leading to widespread vasodilation and organ dysfunction. Markers include decreased SVR, variable CVP/PAWP, decreased CO (early) or increased CO (late). Treatment: Early and aggressive fluid resuscitation (crystalloids), broad-spectrum antibiotics, vasopressors (norepinephrine) for persistent hypotension, source control.

  • Anaphylactic Shock
    : A severe, life-threatening allergic reaction causing widespread vasodilation and increased capillary permeability. Markers include decreased SVR, decreased CVP/PAWP. Treatment: Epinephrine (priority), IV fluids, H{1} and H{2} blockers, corticosteroids, airway management.

  • Neurogenic Shock
    : A type of distributive shock resulting from loss of sympathetic tone due to spinal cord injury, leading to widespread vasodilation, bradycardia, and hypotension. Markers include decreased SVR, decreased CVP/PAWP. Treatment: IV fluids, vasopressors (phenylephrine, norepinephrine), atropine for bradycardia.

Post-PCI & CABG

Post-PCI Care
: Focuses on monitoring for complications related to the procedure and access site.

  • Monitoring for bleeding
    : Especially at the vascular access site (femoral or radial artery). Assess for hematoma, ecchymosis, active bleeding. Maintain pressure post-sheath removal. Closely monitor Hgb/Hct.

  • Monitoring for re-occlusion
    : New or recurrent chest pain, ECG changes, dysrhythmias. Indicates potential restenosis or stent thrombosis.

  • Monitoring for pain
    : Angina vs. access site pain.

  • Monitoring for complications
    : Retroperitoneal bleed (especially with femoral access, back/flank pain, hypotension), pseudoaneurysm formation, arterial dissection, contrast-induced nephropathy (monitor creatinine).

  • Patient Education
    : Activity restrictions, medication adherence (dual antiplatelets).

Post-CABG Care
: Intensive management in the ICU for several days, followed by step-down care.

  • ICU monitoring
    : Continuous ECG, hemodynamic monitoring (arterial line, CVP, PA catheter), chest tube output, urine output, neurological status, core body temperature.

  • Chest tubes
    : Monitor drainage volume (excessive > 100-200\,mL/hr may indicate hemorrhage), color. Assess for proper function (tidaling, air leaks).

  • Sternal precautions
    : Avoid lifting, pushing, or pulling more than 5\,lbs; do not raise elbows higher than shoulders; hug a pillow when coughing or sneezing to prevent sternal dehiscence.

  • Pain management
    : Both incisional and sternal pain. IV opioids initially, transitioning to oral.

  • Fluid and electrolyte balance
    : Often have fluid shifts, monitor for hypovolemia or hypervolemia, administer replacements (potassium, magnesium) per protocol.

  • Arrhythmias
    : Atrial fibrillation is common post-CABG (peak incidence on post-op days 2-4); require rate and/or rhythm control.

  • Neurological status
    : Monitor for stroke, transient ischemic attack (TIA).

  • Risk for infection
    : Surgical site (sternal wound), pneumonia.

  • Early ambulation
    : Prevents complications such as DVT/PE and pneumonia.

III. Cardiac Rhythms

Sinus Rhythms

Normal Sinus Rhythm (NSR)
: Electrical impulse originates in the SA node, rate 60-100\,bpm. Regular rhythm, P wave precedes every QRS, PR interval 0.12-0.20\,s, QRS duration 0.04-0.12\,s.

Sinus Bradycardia
: SA node fires at < 60\,bpm.

  • Symptoms
    : If symptomatic (hypotension, dizziness, altered mental status, chest pain, syncope), due to decreased cardiac output.

  • Treatment
    : If symptomatic, Atropine (first-line drug to increase HR) or transcutaneous/transvenous pacing.

Sinus Tachycardia
: SA node fires at > 100\,bpm.

  • Symptoms
    : Palpitations, dizziness, dyspnea. Increased myocardial oxygen demand may lead to angina in patients with CAD.

  • Treatment
    : Primarily treat the underlying cause (e.g., fever, pain, anxiety, hypovolemia, anemia, hyperthyroidism, stimulants).

Atrial Dysrhythmias

Atrial Fibrillation (AFib)
: Disorganized atrial electrical activity, leading to rapid, irregular ventricular response. No discernible P waves; instead, fibrillatory waves are seen. Irregularly irregular pulse.

  • Risk
    : High risk of thrombus formation in the atria due to blood stasis, leading to stroke.

  • Treatment
    : Anticoagulation (e.g., Warfarin, DOACs) to prevent stroke, plus rate control (e.g., beta-blockers, calcium channel blockers like Diltiazem) to keep ventricular rate < 100\,bpm. Rhythm control (electrical or pharmacological cardioversion) may be used.

Atrial Flutter
: Rapid, regular atrial activity from a re-entrant circuit, typically in the right atrium. Produces characteristic "sawtooth" flutter waves (F waves) on ECG. Atrial rate 250-350\,bpm. Ventricular response may be regular or irregular (e.g., 2:1, 3:1 block).

  • Treatment
    : Rate control (beta-blockers, calcium channel blockers), anticoagulation (similar to AFib). May need cardioversion (electrical or pharmacological) or catheter ablation to restore sinus rhythm.

Ventricular Dysrhythmias

Premature Ventricular Contractions (PVCs)
: Early wide QRS complexes of ventricular origin. P wave is usually absent. Can be isolated, bigeminy (every other beat), trigeminy (every third beat), or coupled (two in a row).

  • Significance
    : Usually benign in healthy hearts. May indicate ischemia, electrolyte imbalances (hypokalemia, hypomagnesemia), or medication toxicity.

  • Treatment
    : Assess frequency, monitor for underlying cause, check K/Mg levels. Antiarrhythmics (e.g., beta-blockers) if frequent and symptomatic.

Ventricular Tachycardia (VTach)
: A run of three or more PVCs. Rapid, regular or irregular wide QRS rhythm. Ventricular rate 100-250\,bpm. Can be monomorphic (QRS complexes look similar) or polymorphic.

  • Pulse = amiodarone/cardiovert
    : If the patient has a pulse and is stable: IV Amiodarone or other antiarrhythmics. If unstable with a pulse (e.g., hypotensive): Synchronized cardioversion.

  • Pulseless = CPR + defib
    : If the patient is pulseless VTach: Treat as ventricular fibrillation (CPR + immediate defibrillation).

Ventricular Fibrillation (VFib)
: Disorganized, chaotic electrical activity in the ventricles, leading to no effective cardiac output. ECG shows irregular, wavy baseline with no discernible QRS complexes. Patient is pulseless and unconscious.

  • Treatment
    : Medical emergency. Immediate high-quality CPR + defibrillation. Followed by epinephrine, then amiodarone if recurrent.

Torsades de Pointes
: A form of polymorphic VTach characterized by a twisting of the QRS complexes around the isoelectric line. Associated with prolonged QT interval.

  • Treatment
    : IV Magnesium Sulfate (MgSO_{4}). Defibrillation if pulseless. Overdrive pacing if refractory.

AV Blocks & Asystole

First-Degree AV Block (1° Block)
: Prolongation of the PR interval (> 0.20\,s) consistently, but all P waves are followed by a QRS complex. All impulses are conducted, just slowly.

  • Treatment
    : Usually no treatment required, monitor for progression.

Second-Degree AV Block, Type I (Mobitz I or Wenckebach)
: Progressive lengthening of the PR interval until a QRS complex is dropped. The pattern then repeats.

  • Treatment
    : If symptomatic, Atropine or pacing.

Second-Degree AV Block, Type II (Mobitz II)
: Consistent PR interval for conducted beats, but some P waves are not followed by a QRS complex, indicating an intermittently blocked impulse. Often progresses to third-degree block.

  • Treatment
    : High risk for progression to complete heart block and asystole. Often requires pacemaker insertion (transvenous or permanent) even if asymptomatic due to high risk.

Third-Degree AV Block (3° Block / Complete Heart Block)
: No electrical impulses are conducted from the atria to the ventricles. The atria and ventricles beat independently (AV dissociation). Regular P waves with a faster atrial rate, slower regular ventricular rhythm (escape rhythm from junctional or ventricular pacemaker).

  • Treatment
    : Requires urgent pacemaker insertion (temporary followed by permanent) due to severe bradycardia and associated symptoms (hypotension, syncope).

Asystole
: Complete absence of electrical and mechanical cardiac activity. Appears as a flat line on the ECG (confirm in two leads).

  • Treatment
    : Immediate high-quality CPR + Epinephrine. It is not shockable (no electrical activity to defibrillate). Identify and treat reversible causes (H's and T's).

Pacemakers & ICDs

Pacemakers
: Electronic devices used to generate electrical impulses to initiate heartbeats when the heart's natural pacemaker fails or conduction is blocked.

  • Temporary Pacemakers
    : Transcutaneous (pads on chest), transvenous (electrode inserted into vein), epicardial (wires sutured to myocardium during open-heart surgery).

  • Permanent Pacemakers
    : Implanted subcutaneously with leads placed in the right atrium and/or right ventricle. Used for chronic bradycardia, AV blocks, sick sinus syndrome.

  • Monitoring
    : Assess for capture (pacer spike followed by a P wave or QRS), sensing (pacemaker's ability to recognize intrinsic heart activity), battery function, lead migration, infection.

Implantable Cardioverter-Defibrillators (ICDs)
: Devices that monitor heart rhythm and deliver electrical shocks (defibrillation or cardioversion) to terminate life-threatening ventricular tachyarrhythmias (VT/VF).

  • Shock for VF/VT
    : Automatically detects and treats ventricular fibrillation and ventricular tachycardia. Also includes pacemaker functions for bradycardia.

  • Teaching = avoid magnets
    : Patients should avoid strong magnetic fields (e.g., MRI unless MRI-conditional ICD, industrial magnets, large speakers) that can interfere with ICD function or reprogram it. Should carry an ICD identification card.

  • Patient Education
    : How to respond to a shock, when to call physician, avoiding physical activities that could damage the device or leads, warning signs of infection.

IV. Medication Calculations

Medications

Vasopressors
: Medications that cause vasoconstriction to increase blood pressure and systemic vascular resistance (SVR). Primarily act on alpha-adrenergic receptors.

  • Norepinephrine (Levophed)
    : Potent vasoconstrictor, moderate inotropic effect. Often first-line for septic shock.

  • Dopamine
    : Dose-dependent effects: renal vasodilation (low dose), inotropic (medium dose), vasoconstrictor (high dose). Less commonly used for shock now due to side effects compared to norepinephrine.

  • Vasopressin
    : ADH analog, causes vasoconstriction independent of adrenergic receptors. Used in refractory shock.

  • Phenylephrine
    : Pure alpha-agonist, causes vasoconstriction. Can cause reflex bradycardia.

  • Calculation
    : Often calculated in mcg/kg/min or mcg/min. Requires careful titration based on patient's blood pressure response.

Inotropes
: Medications that increase myocardial contractility, thereby increasing cardiac output.

  • Dobutamine
    : Primarily beta-1 agonist, increases contractility with minimal effect on HR/BP at lower doses. Used in heart failure with low cardiac output and adequate BP.

  • Milrinone
    : Phosphodiesterase inhibitor, increases contractility and causes vasodilation (decreases SVR). Can cause hypotension. Used in severe heart failure.

Vasodilators
: Medications that decrease vascular resistance, reducing preload and/or afterload.

  • Nitroglycerin
    : Venous and arterial dilator (primarily venous), reduces preload, improves coronary blood flow. Used for angina, acute MI, hypertensive emergencies.

  • Nitroprusside
    : Potent arterial and venous dilator, rapid onset and short duration. Used for acute severe hypertension, decompensated heart failure. Requires arterial line and close monitoring due to risk of cyanide toxicity.

Anticoagulants
: Medications that prevent clot formation or extension.

  • Heparin
    : Inhibits clotting factors (especially Factor Xa and Thrombin). Requires close monitoring of aPTT. Often administered as a weight-based continuous IV infusion.

  • Warfarin
    : Vitamin K antagonist. Oral anticoagulant, monitored by INR. Used for long-term anticoagulation (e.g., AFib, prosthetic valves).

  • Direct Oral Anticoagulants (DOACs)
    : E.g., Rivaroxaban, Apixaban, Dabigatran. Do not require routine monitoring, but have specific indications and contraindications.

Practice: IV drip rates, safe dose ranges
: Critical for safe medication administration. Nurses must be proficient in calculating drug doses, IV infusion rates, and checking safe dose ranges based on patient weight and clinical condition.

  • Formulas include
    : Dose = (Desired\,Dose \times Volume) / Have\,Dose; Rate\,(mL/hr) = (Dose\,(mg/kg/min \,or\,mcg/kg/min) \times Weight\,(kg) \times 60\,min) / Concentration\,(mg/mL\,or\,mcg/mL); Drip\,Rate = (Volume\,(mL) \times gtt/mL) / Time\,(min).

  • Emphasis
    : Double-checking calculations, using drug references for safe ranges, and understanding the physiological effects of each medication.