CCRN (Adult)

The heart is a four-chambered muscular organ responsible for pumping blood throughout the body. The right side receives deoxygenated blood from the systemic circulation and pumps it to the lungs. The left side receives oxygenated blood from the pulmonary circulation and pumps it to the body. The cardiac cycle consists of systole (contraction) and diastole (relaxation).

Coronary arteries supply the myocardium with oxygenated blood. The left main coronary artery branches into the left anterior descending artery and the circumflex artery. The right coronary artery supplies the right ventricle and inferior wall of the left ventricle in most individuals. Coronary artery dominance refers to which artery supplies the posterior descending artery.

The cardiac conduction system initiates and coordinates electrical impulses. The sinoatrial node is the primary pacemaker with an intrinsic rate of 60 to 100 beats per minute. The atrioventricular node delays impulse transmission to allow atrial contraction before ventricular contraction. The bundle of His, bundle branches, and Purkinje fibers rapidly conduct impulses throughout the ventricles.

Cardiac output equals heart rate multiplied by stroke volume. Stroke volume is determined by preload, afterload, and contractility. Preload is the volume of blood in the ventricle at end-diastole. Afterload is the resistance the ventricle must overcome to eject blood. Contractility is the inherent strength of myocardial contraction independent of preload and afterload.

Arterial blood pressure monitoring provides continuous waveform analysis. The arterial waveform displays systolic upstroke, dicrotic notch, and diastolic runoff. Mean arterial pressure represents average perfusion pressure during the cardiac cycle. Normal MAP ranges from 70 to 105 mmHg.

Central venous pressure reflects right ventricular preload. Normal CVP ranges from 2 to 8 mmHg. Elevated CVP may indicate fluid overload, right ventricular failure, tricuspid regurgitation, or cardiac tamponade. Low CVP suggests hypovolemia or vasodilation.

Pulmonary artery catheterization provides comprehensive hemodynamic data. Pulmonary artery systolic pressure normally ranges from 15 to 30 mmHg. Pulmonary artery diastolic pressure normally ranges from 4 to 12 mmHg. Pulmonary artery wedge pressure reflects left ventricular preload with normal values of 4 to 12 mmHg.

Cardiac output can be measured using thermodilution or continuous monitoring methods. Cardiac index adjusts cardiac output for body surface area with normal values of 2.5 to 4.0 L/min/m². Systemic vascular resistance indicates afterload with normal values of 800 to 1200 dynes·sec/cm⁵. Pulmonary vascular resistance normally ranges from 100 to 250 dynes·sec/cm⁵.

Acute coronary syndromes encompass unstable angina, non-ST-elevation myocardial infarction, and ST-elevation myocardial infarction. The underlying pathophysiology involves atherosclerotic plaque rupture with subsequent thrombus formation. Complete occlusion typically produces STEMI while partial occlusion causes UA or NSTEMI.

Clinical presentation includes chest pain or pressure, diaphoresis, dyspnea, nausea, and anxiety. Atypical presentations are more common in women, elderly patients, and diabetics. Silent ischemia occurs without chest pain but with other symptoms or ECG changes.

Electrocardiographic changes help differentiate ACS types. ST-segment elevation indicates transmural ischemia requiring emergent reperfusion. ST-segment depression and T-wave inversion suggest subendocardial ischemia. Reciprocal changes in opposite leads support the diagnosis.

Cardiac biomarkers confirm myocardial necrosis. Troponin I and T are highly specific for myocardial injury. Troponin elevation occurs within 2 to 4 hours of infarction and remains elevated for 7 to 14 days. High-sensitivity troponin assays allow earlier detection.

Management of STEMI focuses on rapid reperfusion. Primary percutaneous coronary intervention is preferred when available within 90 minutes. Fibrinolytic therapy is indicated when PCI cannot be performed within 120 minutes. Door-to-balloon time should not exceed 90 minutes for primary PCI.

Antiplatelet therapy includes aspirin and a P2Y12 inhibitor. Aspirin should be given immediately upon presentation. Clopidogrel, prasugrel, or ticagrelor are added based on treatment strategy. Glycoprotein IIb/IIIa inhibitors may be used during PCI.

Anticoagulation prevents thrombus propagation. Unfractionated heparin, low-molecular-weight heparin, fondaparinux, or bivalirudin may be used. Choice depends on treatment strategy and bleeding risk. Duration varies based on intervention performed.

Beta-blockers reduce myocardial oxygen demand. They should be initiated within 24 hours in stable patients. Contraindications include hypotension, bradycardia, heart failure, and cardiogenic shock. Metoprolol, carvedilol, and bisoprolol are commonly used.

ACE inhibitors provide mortality benefit and ventricular remodeling prevention. They should be started within 24 hours in patients with anterior MI, heart failure, or ejection fraction below 40%. Angiotensin receptor blockers are alternatives for ACE inhibitor-intolerant patients.

Heart failure occurs when the heart cannot meet metabolic demands of tissues. It may be classified as systolic (reduced ejection fraction) or diastolic (preserved ejection fraction). Left-sided failure causes pulmonary congestion while right-sided failure causes systemic congestion.

New York Heart Association classification grades functional limitation. Class I indicates no limitation of physical activity. Class II involves slight limitation with ordinary activity. Class III involves marked limitation with less than ordinary activity. Class IV indicates symptoms at rest.

Clinical manifestations of left-sided failure include dyspnea, orthopnea, paroxysmal nocturnal dyspnea, fatigue, and pulmonary crackles. Right-sided failure produces jugular venous distention, peripheral edema, hepatomegaly, and ascites. Biventricular failure combines features of both.

B-type natriuretic peptide elevation supports the diagnosis. BNP levels above 400 pg/mL strongly suggest heart failure. NT-proBNP above 900 pg/mL in patients under 50 years indicates heart failure. Levels correlate with severity and prognosis.

Acute decompensated heart failure requires aggressive management. Diuretics relieve congestion through sodium and water excretion. Loop diuretics such as furosemide are first-line agents. Continuous infusion may be more effective than intermittent boluses in severe cases.

Vasodilators reduce preload and afterload. Nitroglycerin is useful for patients with elevated blood pressure and pulmonary congestion. Sodium nitroprusside provides balanced arterial and venous dilation. Vasodilators are avoided when the patient is hypotensive.

Inotropic support may be necessary in cardiogenic shock. Dobutamine is a beta-agonist that increases contractility. Milrinone is a phosphodiesterase inhibitor with inotropic and vasodilatory effects. These agents increase mortality and should be used cautiously.

Chronic heart failure management includes neurohormonal blockade. ACE inhibitors or ARBs reduce mortality and improve symptoms. Beta-blockers with evidence include carvedilol, metoprolol succinate, and bisoprolol. Aldosterone antagonists provide additional mortality benefit in severe heart failure.

Guideline-directed medical therapy includes newer agents. Sacubitril-valsartan (ARNI) is preferred over ACE inhibitors in HFrEF. Sodium-glucose cotransporter 2 inhibitors reduce hospitalizations and mortality. Ivabradine reduces heart rate in patients already on maximized beta-blocker therapy.

Device therapy benefits selected patients. Implantable cardioverter-defibrillators prevent sudden cardiac death in patients with EF below 35%. Cardiac resynchronization therapy improves symptoms in patients with wide QRS and reduced EF. Left ventricular assist devices provide mechanical circulatory support as bridge to transplant or destination therapy.

Cardiogenic shock is circulatory failure due to severe cardiac dysfunction. Mortality rates remain high at 40 to 50% despite advances in treatment. The most common cause is acute myocardial infarction with left ventricular dysfunction.

Hemodynamic criteria include systolic blood pressure below 90 mmHg, cardiac index below 2.2 L/min/m², and pulmonary capillary wedge pressure above 15 mmHg. Clinical signs include altered mental status, cool extremities, oliguria, and pulmonary congestion.

Management priorities include rapid identification and treatment of underlying cause. Emergent revascularization is indicated for MI-related cardiogenic shock. At the first procedure, only the culprit lesion is treated; routine immediate multivessel intervention is not recommended.

Vasopressor support maintains perfusion pressure. Norepinephrine is the preferred first-line vasopressor. Dopamine increases mortality compared to norepinephrine. Vasopressin may be added for refractory hypotension.

Sinus bradycardia is a heart rate below 60 beats per minute with normal sinus rhythm. Causes include medications, hypothyroidism, increased vagal tone, and inferior MI. Treatment is required only for symptomatic bradycardia. Atropine is the first-line medication followed by transcutaneous pacing if needed.

Atrial fibrillation is characterized by irregularly irregular rhythm without discrete P waves. It increases stroke risk fivefold. Rate control with beta-blockers, calcium channel blockers, or digoxin is initial therapy. Rhythm control with cardioversion or antiarrhythmics may be appropriate in some patients.

Anticoagulation is required based on CHA₂DS₂-VASc score. Direct oral anticoagulants are preferred over warfarin in most patients. Scores of 2 or higher in men and 3 or higher in women indicate anticoagulation. Left atrial appendage closure is an alternative for patients who cannot tolerate anticoagulation.

Atrial flutter presents with regular atrial rate of 250 to 350 beats per minute. Characteristic sawtooth flutter waves are visible in inferior leads. Management is similar to atrial fibrillation. Ablation is highly effective for typical atrial flutter.

Supraventricular tachycardia includes AVNRT, AVRT, and atrial tachycardia. Vagal maneuvers such as Valsalva or carotid massage may terminate the rhythm. Adenosine 6 mg followed by 12 mg is first-line pharmacological treatment. Synchronized cardioversion is indicated for hemodynamically unstable patients.

Ventricular tachycardia is three or more consecutive ventricular beats at a rate above 100 per minute. Sustained VT lasts longer than 30 seconds or causes hemodynamic instability. Monomorphic VT has uniform QRS morphology while polymorphic VT shows varying morphology.

Pulseless VT requires immediate defibrillation with CPR. Stable monomorphic VT may be treated with amiodarone, procainamide, or sotalol. Synchronized cardioversion is indicated for unstable VT with a pulse. ICD placement prevents sudden cardiac death in high-risk patients.

Ventricular fibrillation is chaotic ventricular electrical activity without effective contraction. It is the most common initial rhythm in sudden cardiac arrest. Immediate defibrillation is the definitive treatment. Each minute without defibrillation decreases survival by 7 to 10%.

Heart blocks involve impaired conduction through the AV node or His-Purkinje system. First-degree block shows prolonged PR interval without dropped beats. Second-degree Mobitz I (Wenckebach) shows progressive PR prolongation before a dropped beat. Second-degree Mobitz II shows constant PR interval with intermittent dropped beats.

Third-degree (complete) heart block shows AV dissociation with independent atrial and ventricular rhythms. Ventricular escape rhythm may be junctional (40 to 60 bpm) or ventricular (20 to 40 bpm). Permanent pacemaker implantation is indicated for symptomatic bradycardia or Mobitz II and complete heart block.

Aortic stenosis causes left ventricular pressure overload. Classic symptoms include angina, syncope, and heart failure. Physical examination reveals harsh crescendo-decrescendo systolic murmur. Severe AS has valve area below 1.0 cm² and mean gradient above 40 mmHg. Transcatheter or surgical aortic valve replacement is indicated for symptomatic severe AS.

Aortic regurgitation causes left ventricular volume overload. Acute AR from endocarditis or dissection presents with pulmonary edema and shock. Chronic AR allows compensatory LV dilation. Physical findings include widened pulse pressure and diastolic murmur. Surgery is indicated for symptomatic AR or asymptomatic severe AR with LV dysfunction.

Mitral stenosis typically results from rheumatic heart disease. Symptoms include dyspnea, orthopnea, and atrial fibrillation. Opening snap and diastolic rumble are characteristic findings. Percutaneous balloon commissurotomy is preferred for favorable valve anatomy. Surgical commissurotomy or replacement is alternative.

Mitral regurgitation may be primary (valve disease) or secondary (ventricular dysfunction). Acute MR from papillary muscle rupture or chordal rupture causes pulmonary edema. Chronic MR leads to progressive LV dilation. Surgical repair is preferred over replacement when feasible.

Hypertrophic cardiomyopathy involves asymmetric septal hypertrophy. Left ventricular outflow tract obstruction may be present. Sudden cardiac death risk stratification guides ICD placement. Beta-blockers and avoiding dehydration and vasodilators are management principles.

Cardiac tamponade occurs when pericardial fluid compresses the heart. Beck's triad includes hypotension, jugular venous distention, and muffled heart sounds. Pulsus paradoxus shows greater than 10 mmHg inspiratory decrease in systolic pressure. Echocardiography confirms diagnosis showing right atrial and ventricular diastolic collapse. Emergent pericardiocentesis is life-saving.

Acute aortic dissection involves a tear in the aortic intima with blood tracking into the media. Stanford type A involves the ascending aorta and requires emergent surgery. Stanford type B involves only the descending aorta and may be managed medically. Severe tearing chest pain radiating to the back is the classic presentation.

Blood pressure control is essential to prevent propagation. Target systolic blood pressure is 100 to 120 mmHg. Esmolol provides rapid titratable beta-blockade. Nicardipine or nitroprusside may be added for additional pressure control after adequate beta-blockade.

Acute limb ischemia presents with the six Ps: pain, pallor, pulselessness, paresthesias, paralysis, and poikilothermia. Causes include arterial embolism, thrombosis, and trauma. Urgent revascularization within 6 hours prevents irreversible tissue loss. Anticoagulation with heparin should be initiated immediately.

Pulmonary embolism occurs when venous thrombus embolizes to the pulmonary arteries. Risk factors include immobility, malignancy, surgery, and hypercoagulable states. Symptoms include dyspnea, pleuritic chest pain, and hemoptysis. Tachycardia and hypoxemia are common findings.

Risk stratification guides treatment intensity. Massive PE with hemodynamic instability requires thrombolysis or embolectomy. Submassive PE with RV dysfunction may benefit from escalated therapy. Low-risk PE is treated with anticoagulation alone.

Anticoagulation is the cornerstone of PE treatment. Direct oral anticoagulants are preferred for most patients. Low-molecular-weight heparin is preferred in malignancy-associated PE. Duration is typically 3 months for provoked PE and indefinite for unprovoked or recurrent PE.

Infection and inflammation can involve the valves, the myocardium, or the pericardium. Each may present with chest pain, fever, or new heart failure, and each can deteriorate quickly.