Comprehensive Nursing Care for Cardiovascular and Vascular Diseases

Cardiovascular and Vascular Pathologies: Nursing Care

Shock

Definition and Etiology: Shock is a critical condition characterized by cellular hypoxia and energy failure due to an imbalance between oxygen supply and demand. It can appear acutely or insidiously. The body attempts to survive through homeostatic mechanisms to restore tissue perfusion. Etiologies include hypovolemia, cardiogenic pump failure, and maldistribution (neurogenic, spinal, and septic). Alterations in cellular oxygen uptake also occur, particularly in septic shock.

Stages of Shock

• 1. Level 1 (Mild/Compensated): Cellular changes detected clinically as normal blood pressure (BP) within normal limits, normal heart rate (HR), respiratory rate (RR), skin tone, and preserved consciousness.
• 2. Level 2 (Moderate): BP in response to fluid shifts, normal blood flow distribution with redirection of blood to the brain and heart. Loss of skin color, coldness, and sweating.
• 3. Level 3 (Severe): Responds only to stimuli, decreased systemic tissue perfusion, ischemic heart dysfunction with hypoperfusion, increased capillary permeability, and sphincter relaxation.
• 4. Level 4 (Irreversible): Severe organ damage, refractory to treatment, profound hypotension, renal failure, multiple organ dysfunction syndrome, and imminent death.

Nursing Interventions

Investigation of patient history and assessment of jugular veins. Engorged veins indicate pump failure (treat for cause, scase liquids, avoid Trendelenburg). Empty veins indicate fluid loss, blood loss, or shock types (infusion of liquids, strong Trendelenburg). Common measures include: two large-bore peripheral IV lines, analytical blood tests, administration of fluids, serum bicarbonate and Ringer's lactate, oxygen therapy, optimal positioning, and diagnostic and etiologic support.

Sepsis

Occurs due to a disseminated infection, primarily normovolemic single gram-negative bacteria, leading to decreased oxygen. When microorganisms invade tissues, the immune system triggers a massive inflammatory response and chemical mediators are produced, resulting in vasodilation and increased capillary permeability.

Treatment: Eradicate the infection, collect blood cultures and other aggressive diagnostic samples. Identify the septic focus immediately and administer aggressive antibiotic therapy. Symptoms are similar to other forms of shock but present with a higher body temperature.

Cardiogenic Shock

Caused by deterioration of heart function. Decreased pumping capacity leads to reduced tissue perfusion, including the heart itself. Angina and arrhythmias frequently occur. Normovolemia is maintained. Causes can be coronary or non-coronary (most common in patients with AMI, stroke, and arrhythmias). In addition to decreased perfusion, pulmonary fluid accumulates due to systolic ventricular failure and increased left ventricular end-diastolic pressure.

Neurogenic Shock

Vasodilatation resulting from the loss of sympathetic tone, causing relative hypovolemia due to spinal cord damage. Skin is dry and warm, followed by tachycardia and sometimes bradycardia. Treatment includes vasoconstrictors and the Trendelenburg position.

Heart Failure (HF)

An abnormal cardiac condition where the heart pump fails. It is not a primary disease of the number of cardiopathies, but a consequence of conditions like hypertension or ischemic heart disease (IHD). Characterized by ventricular dysfunction, reduced exercise tolerance, clinical deterioration, and shortened life expectancy.

Compensatory Mechanisms

• Dilatation: Dilation due to volume overload. Heart chamber fibers and muscle stretch to increase force. Over time, dilation stops being effective and cardiac output decreases.
• Hypertrophy: Increases muscle mass and ventricular wall thickness. Persistent dilation and increased contractile potential initially increase cardiac output, but contractility eventually declines.
• Sympathetic Activation: Noradrenergic activation increases heart rate and peripheral vascular constriction. While it helps maintain pump function initially, it ultimately proves detrimental by increasing myocardial oxygen consumption and workload.
• Neurohormonal Response: Decreased blood flow to the active glomerular blood system activates the renin-angiotensin-aldosterone system (RAAS), causing vasoconstriction, sodium and water retention, and increased blood pressure.

Symptoms

• Respiratory Manifestations: Exertional dyspnea, orthopnea, paroxysmal nocturnal dyspnea, pulmonary edema, and cough.
• Low Cardiac Output Symptoms: Decreased peripheral and central tissue perfusion.
• Visceral Congestion Symptoms: Extremity edema, nocturia, sensation of abdominal heaviness, and gastric fullness.
• Mixed Origin Symptoms: Weight loss, muscle atrophy, cachexia, and low heart rate.

Nursing Interventions

Cardiac auscultation, vital signs assessment, functional alterations monitoring, presence of petechiae in mucous membranes, chest care, and administration of prescribed drugs to decrease preload and afterload. Oxygen administration, reduction of venous return via phlebotomy (white and red blood removal <400cc) if indicated.

Acute Pulmonary Edema (APE) Care Objectives

The main goals of treatment are to decrease intravascular volume, reduce intravascular preload and afterload, improve gas exchange and oxygenation, increase cardiac output, and reduce anxiety.

Valvular Heart Disease and Infarction

• Mitral Stenosis: Most cases stem from rheumatic fever, causing scarring of the valve leaflets and chordae tendineae. Obstructs mitral flow, increasing atrial pressure and pulmonary vessel pressure. Manifestations: dyspnea, hemoptysis, palpitations, diastolic murmur, and stroke.
• Mitral Regurgitation: Anomalies of the mitral leaflets, annulus, chordae, papillary muscles, left atrium, or left ventricle can lead to regurgitation. Causes include inflammatory, degenerative, infectious, structural, or congenital conditions. Leads to pulmonary edema, peripheral shock, thready pulse, cold extremities, fatigue, and dyspnea.
• Aortic Stenosis: Obstruction of flow during systole, increasing left ventricular workload and myocardial oxygen consumption, while decreasing pulmonary perfusion. Causes angina, syncope, and heart failure.
• Aortic Regurgitation: Result of primary disease of the leaflets, aortic root, or both. Acute causes include bacteria, trauma, or aortic dissection. Chronic causes include rheumatic heart disease or syphilis. Physiologically, retrograde flow into the left ventricle causes volume overload and ventricular dilation. Symptoms include weakness, dyspnea, hypotension, bounding pulse, paroxysmal nocturnal dyspnea, orthopnea, and nocturnal angina (initially asymptomatic).
• Dilated Cardiomyopathy: Most common form. Ventricular dilation and impaired contractile function with atrial enlargement, leading to heart failure.
• Hypertrophic Cardiomyopathy: Asymmetric hypertrophy. A frequent cause of sudden death in athletes. The ventricle becomes rigid and unable to fill or relax properly, decreasing cardiac output.

Heart Rhythms and Conduction Disorders

• Sinus Rhythm: P wave in lead II is positive, single-phase, and uniform. Normal PR interval and QRS duration (<0.11s). Heart rate 75-80 bpm.
• Nodal Rhythm: PR interval may be shortened or inverted before the QRS. Heart rate 50-60 bpm.
• Ventricular Rhythm: Originates in the ventricles without a preceding P wave. QRS duration >0.11s. Heart rate 15-30 bpm.
• AV Block (Second Degree):
  • Mobitz I (Wenckebach): Progressive PR elongation until a QRS is dropped.
  • Mobitz II: Constant PR interval with intermittently dropped QRS complexes.
• Ventricular Tachycardia: Wide QRS complexes, severely decreased cardiac output. Ventricular fibrillation results in zero cardiac output.
• Flutter and Atrial Tachycardia: Rapid, uncoordinated atrial contractions with sawtooth patterns, while ventricles respond with varying rates.

Angina Pectoris

Pathophysiology: Coronary blood flow decrease shifts myocardial metabolism from aerobic to anaerobic. Release of metabolites causes pain due to sympathetic stimulation.

Types of Angina

• Unstable Angina / Acute Coronary Syndrome (ACS): Pain occurs at rest or with minimal exertion. Often caused by atherosclerotic plaque rupture with superimposed platelet aggregation and local vasoconstriction leading to a partial thrombus. High risk of myocardial infarction. Treatment includes immediate rest, aspirin, and anticoagulation.
• Stable Angina: Predictable chest pain triggered by exertion, lasting 3 to 5 minutes, and relieved by rest or nitroglycerin. Electrocardiogram reveals ST-segment depression. Controlled with outpatient medications.

Assessment

Precordial pain rating (increased heart rate and retrosternal pain radiating to the jaw or left arm). Pain does not change with respiration, palpation, or movement. Physical signs include pallor and diaphoresis. Diagnostic support includes chest X-ray, lab work, and exercise stress testing.

Myocardial Infarction (AMI)

Assessment: Pain evaluation, physical signs (pallor, sweat, restlessness, tachycardia, hypotension, dyspnea), electrocardiogram (ST-segment elevation), cardiac enzyme concentrations (CPK, troponin), gamma camera imaging, and cardiac catheterization.

Complications: Ventricular dysfunction, arrhythmias (90%), heart failure (60%), cardiogenic shock, ventricular wall rupture (5%), and papillary muscle rupture.

Cardiac Rehabilitation

• Phase 1: Inpatient period (explanation of objectives, low-intensity exercise program, energy-saving techniques, correct body posture, home discharge recommendations).
• Phase 2: 1st month outpatient (medical evaluation, health surveillance, supervised exercise sessions on stationary bicycles, pulse and blood pressure monitoring, educational sessions).
• Phase 3: 2nd month outpatient (return to work, aerobic exercise, holistic effort testing with ECG).
• Phase 4: 3rd month outpatient (consolidating achieved goals).

Pericardial Diseases

Pericarditis

Acute inflammation with or without pericardial effusion. Etiologies include idiopathic infection and autoimmune conditions. Characteristics include chest pain, pericardial friction rub, low-grade fever, and generalized ST-segment elevation on ECG. Treatment: rest and NSAIDs.

Pericardial Effusion

Accumulation of more than 50 ml of fluid in the pericardial space. Rapid or large effusions compress adjacent structures. Etiologies include pericarditis, idiopathic, and autoimmune conditions. Diagnosed via echocardiography, chest X-ray, CT, MRI, ECG, and serology. Treatment targets the underlying cause.

Cardiac Tamponade

Severe hemodynamic compromise from elevated intraperintra-pericardial pressure impairing systolic function. Etiologies include trauma, tuberculosis, purulent infections, and neoplasia. Signs include tachycardia, tachypnea, chest pain, jugular venous distension, pericardial friction rub, and Beck's triad. Treatment: pericardiocentesis, surgical evacuation, or pericardial window. Diuretics are strictly contraindicated.

Constrictive Pericarditis

Limitation of diastolic relaxation and ventricular filling due to a rigid pericardium. Manifests as dyspnea, orthopnea, palpitations, and signs of heart failure (edema, ascites, jugular venous distension). Treatment: extensive pericardiectomy and treatment of the cause.

Basic Life Support (BLS)

Check for unresponsiveness, call for help, open airway, check for breathing, call emergency services (112), perform 30 chest compressions followed by 2 rescue breaths.

Hypertension (HTN)

A major global health problem known as a silent killer. Defined as blood pressure consistently above 160/90 mmHg. Depends on cardiac output and peripheral vascular resistance.

Physiological Factors: Vessel thickening decreases renal blood flow, triggering activation of the renin-angiotensin-aldosterone system.

Risk Factors: Genetic (family history, race, age, sex) and environmental (stress, occupation, socioeconomic level, obesity, alcohol, tobacco, sedentary lifestyle).

Buerger's Disease (Thromboangiitis Obliterans)

A non-atherosclerotic, segmental, inflammatory disorder affecting medium-sized arteries, veins, and nerves of the upper and lower extremities. Predominantly affects young males (25 to 40 years old). Strongly linked to tobacco use. Characterized by thrombosis and inflammatory cell infiltration rather than lipid buildup, leading to tissue ischemia.

Clinical Manifestations: Intermittent claudication in hands or feet, ischemic pain at rest, skin color and temperature changes, paresthesias, superficial thrombophlebitis, and cold sensitivity.

Treatment: Absolute cessation of tobacco use. Severe cases may require digital or distal amputations.

Raynaud's Syndrome

Vasospastic attacks causing transient ischemia in the fingers and toes, often triggered by cold or stress, categorized by vasospastic phases (pallor, cyanosis, and reactive hyperemia).

Chronic Ischemia Syndrome

Characterized by functional factors (vascular spasms) and organic factors (atherosclerosis, thrombosis, and collateral circulation failure). Manifests as intermittent claudication, rest pain, and ischemic gangrene (dry or wet). Surgical treatments include ganglionectomy, endarterectomy, and autologous vein bypass grafting.

Arterial Trauma

Hemorrhagic syndrome, external hematoma, or traumatic arteriovenous fistulas. Clinical signs include a continuous machinery murmur, thrills, distal ischemia, and signs of chronic venous insufficiency if a fistula is present. Treatment involves surgical repair of the vessel and closure of communication.

Varicose Veins

Permanent dilation of superficial veins with irreversible structural wall alterations. Manifests as leg heaviness, cramps, pruritus, malleolar edema, and tortuous venous dilations. Complications include ulcers, superficial thrombophlebitis, and hemorrhage. Treatments include lifestyle modifications, compression stockings, sclerotherapy, and surgical stripping (safenectomy).

Lymphedema

Chronic lymphatic edema of the extremities, classified as primary (congenital malformations) or secondary (acquired obstruction). Manifests as soft early edema progressing to firm, non-pitting, fibrotic tissue thickening ("elephantiasis"). Management includes physical deconstructive therapy, meticulous skin hygiene, postural drainage, compression, and surgical interventions if conservative measures fail.