Nursing 302 Alterations in Cardiovascular Function PDF

Alterations of the Cardiovascular System Nursing 302: Week Six  Learning Objectives 1. Discuss modifiable and non-modifiable risk factors related to the development of cardiovascular disease. 2. Discuss diagnostic test(s) used to identify cardiovascular disorders. 3. Discuss the pa...

Alterations of the Cardiovascular System Nursing 302: Week Six  Learning Objectives 1. Discuss modifiable and non-modifiable risk factors related to the development of cardiovascular disease. 2. Discuss diagnostic test(s) used to identify cardiovascular disorders. 3. Discuss the pathophysiology of central and peripheral cardiovascular disorders. 4. Compare and contrast venous and arterial disorders. 5. Describe the causative factors, clinical manifestations, complications of cardiovascular disorders. 6. Identify effective medical treatments used for cardiac related disorders. 7. Differentiate the various types of shock. For each condition; know the "quick & dirty", including risk factors, clinical manifestations & presentation, treatment and education. Varicose Veins ► Vein in which blood has pooled ► Distended, tortuous and palpable ► Caused by trauma of valves in the vein; increased pressure influenced by gravity ► Venous distention develops overtime in people who stand for long periods of time, wear restricting garments, or cross the legs at the knees ► Risk factors o Age, female gender, family history, obesity, pregnancy, deep vein thrombosis (DVT), previous leg injury ► Can progress to chronic venous insufficiency (CVI) Chronic Venous Insufficiency (CVI) ► Inadequate venous return over a long period ► Venous hypertension, circulatory stasis and tissue hypoxia cause skin ulcerations (due to cell death) ► Infection can occur as poor circulation impairs the delivery of cells for immunity response ► Symptoms o Edema of the lower extremities and hyperpigmentation of the skin of the feet and ankles o Slow circulation (capillary refill >3 seconds) ► Treatment of varicose veins and CVI o Conservatively; elevating legs, compression stockings, exercise o Invasive management includes endovenous ablation, sclerotherapy, or surgical ligation and stripping Thrombus Formation in Veins Thrombus: a blood clot that remains attached to a vessel wall Embolism: travelled from the site of a thrombus (pulmonary embolism usually comes from DVT) Deep Vein Thrombosis (DVT): when a blood clot blocks veins; occurs primarily in the lower extremity VIRCHOW'S TRIAD: factors that promote venous thrombosis 1. Venous stasis (immobility) 2. Venous endothelial damage (trauma, IV meds) 3. Hypercoagulable states (inherited disorders, pregnancy, oral contraceptives) Symptoms include - Pain and swelling in one leg, chest pain (if emboli travels)  NORMAL ANATOMY DEEP VEIN THROMBOSIS Diagnosis & Treatment of ~ FEMORAL ~ ~- - - V E I N Thrombus Formation POPLITEAL. - - - - - VEIN Preventative Measures Early ambulation POSTERIOR TIBIAL Pneumatic devices (sequential compression devices, ---VEINS compression stockings) Prophylactic anticoagulation (enoxaparin) ANTERIOR TIBIAL ---VEINS Diagnosis CALF SWELLING, ERYTHEMA (SWELLING) D-dimer measurement, ultrasound of lower extremity AND LEG WARMTH ARE INDICATIONS THAT A PATIENT MAY HAVE DEEP VEIN THROMBOSIS. Treatment GREAT Anticoagulation (Heparin and Warfarin) SAPHENOUS - - - VEIN *Do not massage leg! This could cause the clot to break off! ANTERIOR VIEWS OF LOWER RIGHT LEG Thrombus Formation in Arteries Arterial thrombi are formed through stasis of blood (aneurysm, atrial fibrillation) Diagnosed by U/S and CT angiography (CT+ contrast dye) Treatment includes anticoagulants and thrombolytics, removal or compression with a balloon-tip catheter Hypertension Hypertension: consistent elevation of systemic blood pressure. Systolic BP >140mmHg or Diastolic BP >90mmHg Primary HTN: elevated BP with no medical cause, meaning its cause is idiopathic or caused by modifiable/non-modifiable risk factors Secondary HTN: elevated BP with specific underlying medical disorder Significant risk factor for cerebrovascular disease, coronary heart disease, heart failure, renal failure, and peripheral vascular disease. Risk Factors of Primary HTN Modifiable Non-Modifiable - Sedentary lifestyle - Advancing age - High dietary sodium intake - Diabetes - Elevated serum lipids - Gender - Substance abuse (alcohol, - Family history tobacco, caffeine) - Increased SNS activity (stress) - Diabetes - Obesity Pathophysiology of Secondary HTN Caused by a systemic disease process that raises peripheral vascular resistance or cardiac output o Renal vascular or parenchymal disease, adrenocortical tumours, adrenomedullary tumours o Medications (BC pill, corticosteroids, SNS stimulants (cocaine, caffeine)) o Pregnancy (eclampsia) o Neurological disorders (tumours) o Acute stress (hyperventilation, hypoglycemia, burns, ETOH withdrawal *once the cause is fixed, the hypertension should resolve Complicated HTN Chronic hypertensive damage to blood vessels and tissues leading to target organ damage in the heart, kidney, brain, and eyes; complications are due to CONSTRICTION o CV complications: LV hypertrophy, CHF, CAD, Ml o Vascular complications: aneurysms, intermittent claudication (numbness, tingling, pain with walking) o Renal complications: renal failure Malignant HTN (Hypertensive Crisis): rapidly progressive (SBP >140mmHg) o Medical emergency o Can cause encephalopathy (confusion, unsteady gait, asterixis Clinical Manifestations, Diagnosis & Treatment of Hypertension Diagnosis Clinical Manifestations At least two BP readings, taken 2 minutes apart. HTN is called "silent disease" as the early stages No caffeine or smoking within the last 30 minutes have no clinical manifestations 24hr BP monitoring, CBC, urinalysis, electrolytes Manifestations are usually caused by ECG complications of the damaged organs Treatment Evidence of heart disease If secondary, treating the underlying cause Renal insufficiency Lifestyle modification; exercise, smoking Impaired vision (blurred vision) cessation, losing weight, reducing salt intake Impaired mobility Pharmacological treatment of antihypertensives Vascular occlusion Follow up and monitoring of blood pressure Edema Headache Orthostatic (Postural) Hypotension Decrease in both systolic and diastolic blood pressure upon standing; lack of normal blood pressure compensation in response to gravitational changes on the circulation Can be acute or chronic Signs and Symptoms: dizziness, syncope, blurring or loss of vision Treatment Changing positions slowly Wearing waist-high compression stockings Getting plenty of fluids Avoiding alcohol Increasing salt in the diet Eating small meals Exercising Aneurysm Aneurysm: local dilation or outpouching of a vessel wall or cardiac chamber True aneurysms: involve all three layers of the arterial wall {/weakening of the vessel" False aneurysms: extravascular hematoma that communicates with the intravascular space Most commonly occur in the thoracic or abdominal aorta, and can lead to aortic dissection or rupture if not treated. Can also occur in the cerebrum (usually in the circle of Willis) Genetic & environmental (smoking, diet) are the biggest risk factors Causes include atherosclerosis and hypertension Clinical Manifestations, Diagnosis & Treatment of Aneurysms Clinical Manifestations (*depend on where its located!*) Diagnosis Aorta (no symptoms until they rupture) U/S, CT, MRI or angiography are used Severe pain & hypotension Treatment Dysphagia (difficulty swallowing) If it has not ruptured: Dyspnea (breathlessness) Cessation of smoking Cerebral Reduction of blood pressure and blood volume Increased intracranial pressure If rupture or still growing: s/s of stroke Surgical treatment (graft) Heart Dysrhythmias HF Embolism of clots  Fusiform , circumferential Fusiform, saccular Tunica media Adventitia Lumen False Dissecting, saccular Clot A  Arteriosclerosis/ Atherosclerosis Arteriosclerosis: thickening and hardening of a vessel wall Atherosclerosis: a form of arteriosclerosis that is caused by the accumulation of lipids within the arterial wall, which leads to formation of a plague; this plaque may break off and become a thrombus Injured endothelial cells - inflammation - fatty streak - plaque development * Leading cause of Coronary Artery Disease (CAD) and Cerebrovascular Disease * Risk Factors Causes of endothelial injury: smoking, HTN, diabetes, increased levels of low-density lipoprotein (LDL or 'bad" cholesterol), decreased levels of high-density lipoprotein (HDL or "good" cholesterol), autoimmunity Clinical Manifestations ATHEROSCLEROSIS Inadequate perfusion of tissues ; potentially leading to ischemia and infarction Plaque Grows, Plaque Forms in the Lining of Artery Blood Clot Forms Lining of Artery Damaged Plaque Ruptures Limited Blood Flow Diagnosis History of risk factors Lab tests; lipid panel, glucose reading Imaging such as X-ray, U/S, MRI, angiogram depending on signs/symptoms Treatment ~ V 2 Stabilizing/reversing plaques with medication VI CII.&I, If obstructed flow, primary goal is to restore that blood flow 0 "0 c( Lifestyle modification (exercise, diabetes & HTN control, reducing LDL cholesterol)  Peripheral Artery Disease (PAD) PAD refers to atherosclerotic disease of arteries that perfuse to the limbs, especially lower extremities; narrowed arteries reduce blood flow to the arms or legs; the extremities don 1t receive enough blood flow to keep up with demand Risk Factors: same as with atherosclerosis, but major links to diabetes & smoking SYMPTOMS OF PAD Clinical Manifestations MHVI..OIAMMNG OM Leg numbness, weakness, and pain when walking (claudication} Otl lOTH Hl,S,, THIGHS OR CAlf MUSCU.S WHCH WAUOIIIIQJIIIStAHtS No pulse or weak pulse in foot Shiny skin on legs, skin colour changes Slower growth of the toenails Coldness in the lower leg or foot Sores on toes, legs or feet that may lead to gangrenous lesions & potential amputations - - - - - - - - - - - HAIi.LOU OH ---- ,m Diagnosis IOOISONTOU, nffOILIGS History and physical focusing on artherosclerotic disease Ankle-brachia I index (BP difference}.,._.....,. _ _ Sl.OWU_,, Measuring blood flow with a Doppler Treatment Decreasing risk factors (smoking cessation & management of diabetes, HTN and dyslipidemia} Vasodilators, cholesterol lowering medications, and antiplatelet/antithrombotic therapy Surgical revascularization  Coronary Artery Disease (CAD) Any vascular disorder that narrows or occludes the coronary arteries (atherosclerosis is the most common cause) Risk Factors ► Modifiable: dyslipidemia, HTN, smoking, diabetes, obesity/sedentary lifestyle ► Non-Modifiable: increased age, family hx, male or female gender postmenopause CAD ~ myocardial ischemia ~ myocardial infarct Deprivation of oxygen & nutrients needed for the pumping ability of the heart; this is known as ischemia The cells remain alive, but cannot function properly Persistent ischemia or complete occlusion of a coronary artery will cause acute coronary syndromes, including infarction (cell death)  Coronary Artery Disease (CAD) ~ Myocardial lschemia Clinical Manifestations Coronary Artery Disease Angina (chest pain); described as burning, squeezing or crushing tightness in the substernal area which may radiate to arms, neck, jaw or shoulder blades Blood Chest heaviness or pressure (on exertion) clot Indigestion, nausea/vomiting, faiting, cool & clammy extremities Plaque Stable or Unstable Angina? If it is predictable and relieved by rest or nitroglycerin it is stable If it increases in frequency, duration and easily induced, it is unstable (classified as acute coronary syndrome and may progress into an Ml) Coronary arteries [J Cleveland Clinic «;) 2022 Myocardial lschemia (1/3) Deprivation of the coronary blood supply; where the supply does not meet the metabolic demand. Most commonly caused by formation of _ _ _ __ - Other causes may include hypotension, dysrhythmias, decreased oxygen-carrying capacity of the blood (ie. anemia, hypoxia) Cells become ischemic within 10 seconds of occlusion; anaerobic metabolism takes over which causes the accumulation of lactic acid (lactate is a lab test we use) Myocardial lschemia (2/3) Clinical Manifestations - Angina (stable, unstable, Prinzmetal) - Prinzmeta/ Angina: vasospasm of coronary vessels cause unpredictable chest pain, usually occurs at night; usually benign but may cause dysrhythmias Diagnosis - Rapid HR, extra heart sounds, and pulmonary congestion (chest sounds) - ECG (ST segment depression, T wave inversion, ST segment elevation) - Lab tests; lactate level, lipid panel, troponin Myocardial lschemia (3/3) Treatment (increase blood flow!) - Reducing risk factors - Medications (antiplatelet, statins (lipid control), beta-blockers & CCBs and nitrates) - Percutaneous Coronary Intervention {PC/}: procedure where narrowed vessels are dilated with a catheter, with placement of stents - Coronary Artery Bypass Grafting {CABG}: narrowing surgical treatment where they use a vein to bypass the blocked artery Acute Coronary Syndromes (ACS) ACS refers to a group of conditions that include unstable angina, ST-elevation myocardial infarction (STEMI) and non-ST-elevation myocardial infarction (NSTEMI) Unstable Angina: angina at rest, increasing in frequency or new-onset angina; "crushing" chest pain, increased dyspnea, diaphoresis, anxiety "impending doom" **important to recognize, as it signals that blood flow has become more compromised & infarction may follow!  Coronary artery Thrombus Acute Coronary Syndromes (ACS) Myocardial Infarction: when coronary artery Pericardium blood flow is interrupted for an extended 8 period of time and cell death occurs Coronary artery Non-STEMI: infarction of the Thrombus myocardium closest to the endocardium (not full thickness); no ST elevation on ECG! STEMI: infarction of the myocardium extending from the endocardium to the pericardium (full thickness); causes ST elevation on ECG! Myocardial Infarctions Clinical Manifestations ST - Sudden severe crushing chest pain , ' - Radiation of pain to neck, jaw, oas shoulder or left arm; back pain in women -- __,uc--~·"'=- -- ,__'_ _ - Indigestion, N/V - Cool & clammy skin - Increase in HR and BP - May result in cardiac arrest due to ischemia, left ventricular dysfunction and electrical instability  Treatment Myocardial Infarctions - Aspirin immediately - Pain relief (nitroglycerin & morphine) Diagnosis - Oxygen; if required - Position patient in high fowlers - History & physical examination - Telemetry monitoring - ECG results - Cardiac troponin elevations (lab NSTEMI & Unstable Angina value) - Antithrombotics & anticoagulation - Drawn as soon as possible, - PCI and then 4 hours after and monitored for a few days to STEMI see elevation in number (if - Emergent PCI and antithrombotics elevation, a Ml has occurred) - Thrombolytics if PCI not readily available Post Myocardial Infarction Care ► Cardiac monitoring ► Bed rest & gradual return to ADLs (reduce oxygen demand) ► DVT prophylaxis ► Stool softeners (no straining; can stimulate vagus nerve~ bradycardia) ► Education o Appropriate diet and caffeine intake o Smoking cessation o Exercise Disorders of the Heart Wall Disorders of the pericardium o Acute pericarditis o Pericardia! effusion Disorders of the myocardium o Cardiomyopathy (dilated, hypertrophic, restrictive) Disorders of the endocardium o Infective endocarditis o Valve dysfunctions (stenosis & regurgitation) Heart Failure (left-sided vs. right-sided) Rheumatic Fever & Rheumatic Heart Disease  Acute Pericarditis - Disorder of the Pericardium Inflammation of the pericardium! Most often idiopathic, but viral infections can also cause this Clinical Manifestations (need 2/4 to be diagnosed) - Chest pain that worsens with respiratory movements or laying in a recumbent position - Friction rub@ cardiac apex (membranes rubbing against each other) - ECG changes - New or worsening pericardia! effusion CT, US and MRI may be used Treatment - Anti-Inflammatory drugs and Colchicine - Aspiration of pericardia! effusion if present  Pericardia I Effusion & Cardiac Tamponade - Disorder of the Pericardium Accumulation of fluid in the pericardia I cavity Usually idiopathic, but may be caused by infection; ultimately it indicates an underlying disorder! Enough fluid can cause sufficient pressure to cause cardiac compression and develop into cardiac tamponade which can be life-threatening; the heart will be unable to fill and pump effectively Beck's Triad: low BP, distention of jugular veins, muffled or diminished heart sounds on auscultation Diagnosis: echocardiogram, CT Treatment: pericardiocentesis, pain management, potential sur Infective Endocarditis Inflammation of the endocardium Diagnosis: positive blood cultures, ECHO, CRP Cause: bacteria, viruses, fungi, parasites Clinical Manifestations Treatment: Fever - Antibiotics New or changed cardiac murmur Petechial lesions of the skin, conjunctiva, and Osler Nod oral mucosa Osler nodes (painful erythematous nodules on the pads of the fingers and toes) - Janeway lesions (nonpainful hemorrhagic lesions on the palms and soles) - Other: weight loss, back pain, night sweats, and heart failure Cardiomyopathies Conditions that affect the heart muscle; the heart can't efficiently pump blood to the rest of the body. Cardiomyopathy gets worse over time. Treatment can slow the progression and improve quality of life. Clinical Manifestations - Fatigue - Shortness of breath - Heart palpitations Types - Dilated cardiomyopathy (stretch of muscle fibres) *most co - Hypertrophic cardiomyopathy (thickening) - Restrictive cardiomyopathy (stiff ventricles) Cardiomyopathies Diagnosis - Chest X-ray - Echocardiogram - Cardiac catheterization - Lab value- BNP; higher the BNP the greater the stretch Treatment (variable depending on the type) - Dilated; reduce blood volume and increase contractility - Hypertrophic; pain mgmnt (may complain of chest pain) - Restrictive; treat underlying cause  ormal yper ,rophic R strictive Cardiomyopathies Valvular Dysfunctions Valvular stenosis; constricted and narrowed - Pressure rises to overcome resistance ~can lead to hypertrophic cardiomyopathy - Aortic or Mitral Treatment includes valve replacement! Valvular regurgitation; cusps fail to shut completely - Blood flows back (causing a murmur) ~increases volume of blood in the heart & increasing the workload of the heart~ hypertrophy - Eventually, ventricles fail from being overworked - Aortic, Mitra I or Tricuspid Heart Failure Heart Failure is when the heart is unable to generate an adequate cardiac output; usually occurs in the left ventricle, but may also happen in the right. Left-sided failure develops first. Risk Factors GON6£5TIVE HEART FAILUR£ (GHF) - CAD HEART CANNOT PUMP ----> FLUID ACCUMULATION or FILL PROPERL'i - HTN - Cardiomyopathies - Mi's - Age - Obesity - Diabetes - Renal failure - Valvular dysfunctions Left-Sided Heart Failure Dysfunction of the left ventricles ability to pump; decreased CO and perfusion to organs & back up into pulmonary circulation Less contractility-----► INCREASED preload-----► INCREASE afterload to compensate and provide adequate CO Clinical Manifestations (Left = Lungs) - Pulmonary vascular congestion (crackles on auscultation) - SOB, orthopnea, coughing w/ or w/o frothy sputum - Tachypnea - Decreased SpO2 Right-Sided Heart Failure Dysfunction of the right ventricles ability to pump; decreased pulmonary circulation & back up into systemic circulation Increased pulmonary vascular resistance ~ inhibits RV pump~ becomes dilated and fails Usually results from left-sided heart failure Clinical Manifestations (Right = Rest of body) - Peripheral edema - Increased JVD - Hepatomegaly - Weight gain - Ascites Diagnosis & Treatment of Heart Failure Diagnosis L F 51 D ILU Echo Serum BNP Higher the BNP, worse the HF Treatment Medications Decrease BP Decrease fluid backup Increase contraction Nursing Interventions Lungs: auscultate for crackles or wheeze, 02 or Fowler's position Fluid Volume: fluid restriction, low sodium diet, daily weights Education on lifestyle factors Acute Rheumatic Fever and Rheumatic Heart Disease Acute Rheumatic Fever: Systemic, inflammatory disease caused by a delayed immune response to pharyngeal infection by the group A beta-hemolytic streptococci. If left untreated may cause rheumatic heart disease Febrile illness Inflammation of the joints, skin, nervous system, and heart Clinical Manifestations: Diagnosis: Recent streptococcal infection Fever Nausea/vomiting Treatment: Tachycardia Antibiotics Abdominal pain Anti lnflammatories Epistaxis Chorea (uncontrollable jerky movements) Erythema marginatum (rash) Shock Cardiovascular system fails to perfuse the tissues adequately leading to impaired cellular metabolism ~impaired oxygen & glucose use~ can progress to organ failure and death Manifestations vary based on stage but often include hypotension, tachycardia, increased respiratory rate Treatment is to discover & correct underlying cause - Improve tissue perfusion - Administer IV fluids, use of vasopressors, supplemental 02 - Control glucose levels Types of Shock: cardiogenic, hypovolemic, neurogenic, anaphy Cardiogenic Shock ► Decreased CO and tissue hypoxia in the presence of adequate intravascular volume ► Usually follows Ml ► Clinical Manifestations o Impaired thought process o Dyspnea and tachypnea o Systemic and pulmonary edema o Dusky skin colour o Hypotension o Oliguria ► Treatment o Fluid & vasopressor administration o Angiography o Ventricular assist device (pacemaker) o Revascularization (PCI or CABG) Hypovolemic Shock ► Loss of whole blood (hemorrhage), plasma (burns), or interstitial fluid (diabetes, emesis/diarrhea) in large amounts ► Initially offset by compensatory mechanisms... increased HR and BP ► Eventually, compensation fails resulting in decreased tissue perfusion ► Clinical Manifestations o High BP then extremely low o Poor skin turgor o Thirst, oliguria o Rapid HR, thready pulse o Decreased LOC ► Treatment o Rapid fluid replacement Neurogenic Shock ► Result of widespread and massive vasodilation that results from parasympathetic overstimulation and sympathetic understimulation ► Caused usually by trauma to the spinal cord or medulla; or conditions that interrupt the supply of 02 or glucose to same. Other causes include depressive medications and anaesthetic agents. ► Clinical Manifestations o Relative hypovolemia (no fluid loss, but low BP) o Bradycardia ► Treatment o Fluids and vasopressors o Reversal of cause Anaphylactic Shock ► Results from hypersensitivity reaction (anaphylaxis) ► Begins with exposure to allergen ~ inflammatory response~ vasodilation & tissue edema~ constriction of smooth muscle (causing laryngospasm and bronchospasm) ► Clinical Manifestations o Anxiety o Dizziness o Difficulty breathing, stridor, wheezing o Pruritus, hives o Swollen lips and tongue o Hypotension ► Treatment o Removal of antigen o Epinephrine IM o IV fluids o Antihistamines & corticosteroids o Continuous monitoring even after the shock, as there could be "rebound Septic Shock ► Begins with an infection that progresses to bacteremia (in blood), then systemic inflammatory response syndrome {SIRS}, then severe sepsis, then septic shock, then multiorgan dysfunction syndrome (MODS} ► Clinical Manifestations o Decreased perfusion of tissues o Hypotension o Tachycardia o Temperature instability Sepsis guidelines as treatment; include IV fluids and vasopressors, antibiotics, and respiratory support