Cardiovascular Disease Notes PDF

[Aging Effects in the CV System:] - **Decreased** *elasticity of blood vessels*, response to ANS, and *baroreceptor sensitivity* - **Increased** *Systolic blood pressure/SBP (widening pulse pressure),* connective tissue in SA and AV nodes - Heart valves stiffen, thickened atria and...

[Aging Effects in the CV System:] - **Decreased** *elasticity of blood vessels*, response to ANS, and *baroreceptor sensitivity* - **Increased** *Systolic blood pressure/SBP (widening pulse pressure),* connective tissue in SA and AV nodes - Heart valves stiffen, thickened atria and ventricles - Overall: decreased cardiac reserve (not able to pump enough blood to keep up with the body's needs) **[Hypertension]** Primary/essential unidentifiable cause Secondary narrowing of renal arteries, atherosclerosis, certain meds, pregnancy, coarctation of aorta (narrowing) BP Categories Category Systolic mmHg Diastolic mmHg --------------------- --------------- -------- ---------------- Normal \180 And/or \>120 Mechanisms that result in HTN: - *Vasoconstriction, Fluid retention* - RAAS system - Increased aldosterone - SNS Risk factors: age, gender, race, cigarette smoking, obesity, excessive alcohol intake, diabetes, vitamin D insufficiency, salt sensitivity Morbidity: atherosclerosis, heart disease/heart failure, stroke, chronic renal failure, PAD, retinopathy, dementia, targeted organ damage (TOD) to heart, brain and kidneys Management - Weight reduction - DASH diet (low salt, low fat) - Medications: diuretics, beta blockers, ACE inhibitors, ARBs, Ca Channel blockers, vasodilators - Stop smoking - Limit alcohol intake **[Myocardial Infarction (MI)]** - Blood flow to the heart is blocked myocardium necrosis - plaque rupture/thrombosis results in complete occlusion of the artery - ischemia and necrosis of myocardium - profound imbalance of oxygen supply and demand - ischemia injuryinfarction - decreased oxygen supply: atherosclerosis, vasospasm, hypovolemia, hypotension and anemia - increased oxygen demand: tachycardia, thyrotoxicosis (thyroid storm), cocaine *Most common etiology: atherosclerosis* - \#1 killer of men and women annually - 4-5 million assess for chest pain and 1.5 million diagnosed with AMI (50% will die within the first hour) - 40% increased risk of MI between 6am-12n Symptoms: - Chest pain (50%) - Indigestion, nausea - Cool, pain, moist skin - Tachycardia, palpitation, tachypnea, SOB - Atypical symptoms (diabetics, elderly, women): fatigue, N/V, SOB, weakness, dizziness Initial Goals of Treatment - Relieve symptoms: MONA *Morphine* *Oxygen\ Nitroglycerin\ Aspirin* - \*Thrombolytic therapy tPA - dissolves blood clots - PCI (percutaneous coronary intervention) -- angioplasty/stent - CABG -- coronary artery bypass graft - Pacemaker \*Administration of Thrombolytic Therapy Indications - Chest pain \> 20 minutes, unrelieved with nitroglycerin - ST segment elevation in at least 2 similar leads - \ - Active bleeding/known bleeding disorders - History of hemorrhagic stoke - Recent major surgery or trauma - Uncontrolled hypertension - pregnancy **Atherosclerosis** Endothelial injury (of blood vessels) prompts an inflammatory response. This activates macrophages and WBC which engulf lipids like LDL. This accumulates and creates plaques. The develops and can rupture. If it ruptures, the contents can be exposed to the bloodstream which can form a thrombus (blood clot) which can obstruct blood blow to the coronary arteries. The leads to ischemia in the myocardium which can manifest as angina or progress to acute coronary syndrome (ACS or MI) Endothelial injury inflammatory response macrophage activation lipid accumulation plaque formation plaque rupture and thrombosis ischemia *Angina (chest pain)* - Stable vs. Unstable - Associating factors: exposure to cold, physical exertion, eating a heavy meal, stress **Coronary Artery Disease (CAD)** - narrowing or blockage of coronary arteries Assessment: - skin color - capillary refill - JVD - *Xanthelasma* -- yellow plaques around eyes - Increased blood and pulse pressures Signs/Symptoms - *Angina* - L side pain (shoulder upper back, arm, jaw, neck) - SOB - Nausea/vomiting - *WOMEN: neck, shoulder blade, jaw pain and indigestion* Diagnostic Tests - *ECG* - Stress test - Blood work -- *troponin I or T levels* - Cardiac catheterization (cath lab) - Holter monitor General Management GOAL: decrease oxygen demand and increase oxygen supply - Decrease modifiable risk factors (weight loss, diet, smoking cessation) - Medications -- nitrates, beta-blockers, Ca channel blockers, antiplatelets and anticoagulants - subcategory of CAD that\'s almost always associated with a symptom, such as unstable angina or myocardial infarction - *12 Lead ECG* - Signs/symptoms of MI cannot be distinguished from unstable angina **Heart Failure** - Inability for heart to pump sufficient blood to meet the oxygen needs of the tissues and usually progressive Risk Factors: 1. CAD and MI 2. HTN 3. Diabetes, smoking, high sodium intake Valvular disease, cardiomyopathy, pericarditis/endocarditis, chemotherapy, alcohol, drugs Clinical Manifestations Left-Sided Right-Sided ---------------------------- -------------------------------------- *Dyspnea* *JVD* *Crackles/pulmonary edema* *Dependent edema and pitting* PND and DOE (types of SOB) *Weight gain due to fluid retention* anxiety Ascites (abdominal swelling) S3 (ventricular gallop) weakness orthopnea Anorexia and nausea Cough (dry moist) Hepatomegaly -- enlarged liver Diagnostics - *ECG* - *[ejection fraction (EF)]* - *Normal: 50-75%* - *Below Normal: 36-49%* - *Low: 35% and below* - *Brain natriuretic peptide (BNP) -- released when heart is stretched* - *CXR* - Cardiac stress test or cardiac catheterization Management - *Diuretics* - *Decreased sodium intake and fluid restriction* - *DAILY WEIGHTS* - ACE inhibitors - Beta blockers - Inotropes -- increase contraction force - Anticoagulants (A-fib heart not beating efficiently which can create small clots) - Oxygen Overall Goal: relieve symptoms, improve quality of life, extend survival Objectives: - Eliminate/reduce causative factors (HTN or A-fib) - Reduce workload of heart by reducing preload and afterload via pharmacologic and therapeutic regimens - Maximize cardiac health and lifestyle - Patient education **ARTERIES** **VEINS** ---------------------------------- ------------------------------ Oxygenated blood from heart De-oxygenated blood to heart Can change diameter Cannot change diameter High pressure Low pressure Thicker walls Thinner walls No valves valves Occlusion by plaques or thrombus Occlusion by thrombus pulsation No pulsation **Peripheral Artery Disease (PAD)** Assessment: Skin - Pallor - Dependent rubor - Cyanosis - Dry, cool, scaly skin - Paranesthesia - Ulcerations - brittle nails - hair loss - muscle atrophy [6 Ps] Pallor rubor, parenthesia, pulse reduced/absent, poikilothermal (cool), pitting edema, pain Symptoms: *Intermittent claudication* muscular cram pain in extremities caused by increased degree of activity and relieved by rest (chronic) *Critical limb ischemia* persistent pain in the forefoot at rest indicates severe ischemia (worse at night) *Acute limb ischemia* sudden ischemia to an extremity that threatens tissue viability and present with a cold, pulseless and mottled extremity Assessment: Pulse scales -- compare bilaterally Diagnostic Evaluation Ankle-brachial index (ABI) - Normal -- 1.4-1 - Claudication: 0.95-0.50 - Rest pain: \ - Invasive - Risks: dye allergy, bleeding, thrombosis, renal injury Treatment Options 1. Exercise 2. Percutaneous transluminal angioplasty (PTA) 3. Stents after angioplasty 4. Atherectomy 5. Bypass 6. Hyperbaric Oxygen therapy **Aortic Aneurysms** Localize sac or dilation formed at a weak point in the arterial wall Classifications Saccular -- projects from one side of vessel Fusiform -- entire segment dilated Symptoms - Vary on location/size - Most asymptomatic and SILENT - Acute abdominal pain impending rupture Risk Factors - *Smoking* - *HTN* - *Hyperlipidemia* - Family history - Advanced age - *Male gender* Etiology 1. ATHEROSCLEROSIS -- damage to media and intima 2. Genetics and congenital weakness 3. Disease 4. Trauma Management of Aneurysms - Antihypertensives (diuretics, beta blocks, ACE inhibitors, Angiotensin II Antagonists, Ca Channel blockers) - Surgical management - Endovascular grafting (stent) - Surgical repair **VENOUS DISEASE** Deep Vein thrombosis (DVT) - Venous Thromboembolism (VTE) - Post-thrombotic syndrome - Chronic venous insufficiency (CVI) Deep Vein Thrombosis (DVT) PATHOLOGY A venous thrombi forms (usually due to Virchow's triad) which consists of platelets, WBCs and RBCs. It attaches to a vein wall and propagates in the direction of blood flow. Fragmentation can occur with increased venous pressure and can cause venous obstruction. Virchow's triad (risk factors for thrombosis) 1. *[Stasis]* - Prolonged immobilization (post-op) - Spinal cord injury 2. *[Vessel wall injury]* - Thrombophlebitis - Trauma - Iatrogenic (catheters) 3. *[Hypercoagulability ]* - Injury - Tumor/cancer - Increased platelet count - Coagulation disorders \*Predisposing conditions are also risk factors: - ORAL CONTRACEPTIVES AND SMOKING - Advanced age, obesity, pregnancy, cancer, constrictive clothing Clinical Manifestations - *[Pain, tenderness]* - *[Erythema (warm to touch)]* - *[Unilateral edema ]* - Prominent superficial veins elsewhere on the extremity - Chronic venous insufficiency Complications - Pulmonary emboli - CVI - Varicosities - Venous ulcers - Edema - Venous gangrene Treatment - Anticoagulation (heparin, enoxaparin, apixaban/dabigatran, warfarin) - Thrombolytic therapy - Surgery and endovascular management - Thrombectomy - Vena cava filter Nursing Management - Monitor blood (tests) - PTT (Partial thromboplastin time is a blood test that measures how long it takes for a patient\'s blood to clot) - PT/INR -- how long it takes for blood to clot - H/H -- measures hemoglobin and hematocrit - Monitor bleeding and thrombocytopenia - Comfort Prevention - Identify high risk patients - Pneumatic compression devices - Proper body positioning - Exercise (pumping feet while in bed) - Anticoagulant therapy - SC heparin (15 seconds of direct pressure with gauze after injection) Chronic Venous Insufficiency A condition that occurs when the venous wall and/or valves in the leg veins are not working effectively which causes [impaired venous return.] - Defective valves allow for backflow of blood Risk factors - Blood clots (DVT) - Varicose veins - Cancer - Right heart failure - Obesity - leg trauma Signs - leg swelling - skin color and texture changes - venous ulcers Post-thrombotic syndrome *\*Develops after DVT* *\*Symptomatic CVI* Obstruction of venous valves resulting in reflux of blood and venous congestion - incompetent valves - venous hypertension - may affect 20-50% of patients with DTV (usually 1-2 years after) Signs - edema - stasis - dermatitis - redness - dependent cyanosis - varicose veins - hyperpigmentation - healed ulcer Symptoms - heaviness - cramps - pain - paresthesia - swelling - bursting pain - itching **Arterial and Venous Ulcer Comparison** Arterial Venous -------------------------------- ------------------------------ Intermittent claudication pain Dull achy pain No edema Lower leg edema No pulse or weak pulse Pulse present and drainage Punched out sores Sores with irregular borders Toes and feet Located on ankles Black eschar Yellow slough or ruddy skin