Chronic Cardiovascular Conditions PDF

Chronic Cardiovascular Conditions Sarah Nixon MN RN Created by Megan Keszler BA BN GradCertEd CNCC(C) Adapted f rom slides created by: Kara Sealock EdD MEd BN RN CNCC (C) CCNE L e a h Te l l i e r R N , M N , C C N E , CHSE  Topics and Objectives  Age Related Cardiovascular Chang...

Chronic Cardiovascular Conditions Sarah Nixon MN RN Created by Megan Keszler BA BN GradCertEd CNCC(C) Adapted f rom slides created by: Kara Sealock EdD MEd BN RN CNCC (C) CCNE L e a h Te l l i e r R N , M N , C C N E , CHSE  Topics and Objectives  Age Related Cardiovascular Changes  Complicated HTN, Pediatric HTN, Endocrine HTN  Metabolic syndrome  Long term effects on the body post-MI  Chronic heart failure  Cardiomyopathies  Valve dysfunction  Acute versus chronic pericarditis  Peripheral Arterial Disease ◦ Objectives: ◦ Reflect on Anatomy and Physiology of the cardiovascular system and look at how it relates to chronic illness ◦ Explain pathophysiology of the above conditions ◦ Examine relevant nursing assessments, clinical manifestations, and relevant lab values related to various conditions Age-Related Cardiovascular Changes  Age-Related Cardiovascular Changes Age-Related Changes in Vascular Age-Related Changes in Cardiovascular Function Function collagen, elastin and calcification systolic blood pressure and pulse pressure wall thickening and arterial stiffening left ventricular wall thickness Endothelial dysfunction promoting early diastolic filling vasoconstriction  Age-Related Cardiovascular Changes Age-Related Changes to Kidney Function Cardiovascular Function Renal function (continued) Impaired cardiac reserve Alterations in heart rate & rhythm Improper maintenance of extracellular fluid volume Prolonged cardiac action potential and composition Aging increases risk for HTN---HTN is not a normal part of the aging process Webb & Inscho, From Hypertension in the Elderly (2005) Fig 2, p. 14 Age-Related Differences in Cardiovascular Assessment Table 34.1, p. 757, Tyerman & Cobbett (2023) Primary and Secondary Hypertension  Hypertension (HTN) Definition sustained Associated with increased risk for target organ systolic pressure of >140 mmHg disease events such as: or  MI diastolic pressure > 90 mmHg  Kidney disease  Stroke Classification of Blood Pressure for Adults (> 18 years old) Isolated Systolic HTN Systolic > Secondary 140 mmHg Primary HTN HTN Normal diastolic Table 24-1, p.582, Power-Kean et al. (2023)  Primary Hypertension Increased HR CO Increased CO Cardiac The amount of blood pumped by Output each ventricle per minute Increased SV Increased Blood HTN Viscosity Increased Peripheral Vascular Resistance  Preload Decreased Vessel  Afterload Diameter  Contractility Both CO and Peripheral Vascular Resistance  Risk Factors Family History Advancing age Cigarette smoking Obesity Heavy alcohol consumption Gender African or Indigenous decent Increased dietary sodium intake Decreased dietary intake of potassium, magnesium, and calcium Socioeconomic status change related to immigration Glucose intolerance  Statistically First Nations, Inuit, and Métis people have higher rates of: High blood Type 2 Childhood Smoking pressure diabetes obesity Hypertension and the Heart rate disease rates are as much as 50% higher and death Indigenous rate due to stroke is twice as high as compared to the general population Population Poorer health outcomes in Indigenous communities linked to inequities in the social determinants of health (Tobe et al., 2019) Pathophysiology Changes in vascular tone and/or blood volume = sustained increase in blood pressure Pathogenesis: SNS- sympathetic nervous system RAAS (Renin angiotensin aldosterone system) Pressure natriuresis relationship (next slide) Inflammation- Endothelial injury and tissues ischemia Obesity Insulin resistance Fig 24-4, p. 584, Power-Kean et al., (2023)  Secondary Hypertension Caused by an Pathogenesis of secondary Fix the cause, fix underlying disease hypertension by cause: the hypertension process or medication that raises peripheral Renal Disorders vascular resistance or Endocrine Disorders cardiac output Vascular Disorders Pregnancy Induced Hypertension (PIH) Neurological Disorders Acute Stress Drugs and other Substances Complicated Hypertension  Complicated Hypertension Primary hypertension develops into complicated hypertension Organ damage to: Aorta and small arteries, heart, kidneys, retina, CNS Early hypertension Prehypertension Established Complicated (10-30 years; increased cardiac ( 20-40 Years; hypertension hypertension output) increased peripheral (30-50 years) (40-60 years) resistance)  Complicated Hypertension Chronic hypertension damages Cardiovascular complications: walls of systemic blood vessels LV CAD Hypertrophy Hypertrophy & hyperplasia with fibrosis of the tunica intima and media Angina MI Target organs for hypertension Pectoris include: kidney, brain, heart, extremities CHF and eyes Sudden (Left Death Ventricular)  Complicated Hypertension Most common: Ascending Aorta/ Usually deep, diffuse chest Aortic Arch: Vascular complications include: Asymptomatic pain extending to interscapular area hoarseness The formation, dissection and Distended neck rupture of aneurysms Dysphagia veins and edema of Dysrhythmias head and arms Intermittent claudication Embolism of clots Heart Failure to brain or other Pain upon rupture Gangrene results from vessel vital organs occlusion Dyspnea  Complicated Hypertension Renal complications include: Retinal complications include: Parenchymal damage Vascular sclerosis Nephrosclerosis Exudation Renal arteriosclerosis Hemorrhage Renal insufficiency or failure microalbuminuria  Complicated Hypertension Malignant Hypertension (Hypertensive Emergency)  Linked to dysfunction of renin and angiotensin Diastolic > 140  Can cause encephalopathy due to high arterial mmHg pressure  May also cause papilledema, cardiac failure, uremia, retinopathy and stroke  Considered hypertensive crisis requiring vasodilators to lower BP Hypertension in the Pediatric and Adolescent Population  Essential hypertension (no identifiable Divided into two cause) categories: Secondary hypertension (subsequent to an identifiable cause) Hypertension Hypertension in Stage I HTN includes patients with BP in the children and adolescents: readings between the ninety-fifth and Pediatric and systolic or diastolic BP ninety-ninth percentile Stage II HTN includes describes Adolescent that consistently falls at or over the ninety- patients with BP readings over the Population fifth percentile ninety-ninth percentile plus 5 mmHg Includes children and adolescents Another group: with prehypertension (or high- normal BP) Hypertension in the Pediatric and Adolescent Population Etiology: Occurs secondary to a structural abnormality of underlying pathological process Cause of essential hypertension is undetermined but likely genetic and environmental Most common cause of secondary hypertension is renal disease followed by cardiovascular, endocrine and some neurological disorders The younger the child and the more severe the hypertension, the more likely it is to be secondary  Hypertension in the Pediatric and Adolescent Population Diagnosis Clinical Manifestations < 3 years > 3 years Adolescents and Infants and with high risk of: Older Children Young Children Routine assessment for Family History Frequent healthy children Irritability headaches CHD Kidney Disease Head Malignancy Dizziness banging or Transplant head rubbing Neurological Those Issues known to Systemic Issues cause Waking up HTN Changes in screaming in vision the night Endocrine Hypertension HYPERALDOSTERONISM PHEOCHROMOCYTOMA  Endocrine Hypertension: Hyperaldosteronism Primary Hyperaldosteronism Secondary Hyperaldosteronism Overproduction of Aldosterone Causes: Eg: Activation of Renin-Angiotensin Eg: System  Adrenocortical Neoplasm Adrenocortical Low BP Tumour Causes:  Bilateral Idiopathic  Decreased renal perfusion  Familial  Arterial hypovolemia and edema  Pregnancy Aldosterone Activation of production RAAS Aldosterone Aldosterone HTN HTN Sodium Suppression of Sodium High Renin RAAS High Renin (Low Renin) Renin Aldosterone Potassium Potassium Image: Colourbox.com Image: Colourbox.com  Endocrine Hypertension: Pheochromocytoma  Adrenomedullary Due to vascular nature hyperfunction is caused of tumour Clinical Manifestations by tumors known as pheochromocytoma  Tumors produce excess norepinephrine Sudden low BP Hypermetabolism Persistent/severe with diaphoresis Unexplained HTN abdominal or Glucose chest pain lasting Severe pounding intolerance Tumour Sudden severe headache a few mins to Rupture abdominal pain Heat intolerance several hours Pallor Weight loss Tachycardia with palpitations Rigid Constipation Abdomen Metabolic Syndrome  Also called insulin resistance syndrome or Metabolic syndrome x Syndrome Associated with insulin resistance and modifiable risk factors such as Clustering of clinical traits that accelerate smoking, exercise and diet cardiovascular disease and type 2 diabetes mellitus Syndrome develops during childhood and is prevalent among overweight children and adolescents Must have 3 of 5 traits: Increased waist HDL for Risk factors: abdominal obesity, Plasma Fasting 102 cm in men or men/transgender BP inactive lifestyle, insulin resistance, triglycerides Plasma transgender females or 1.7 glucose ≥5.6 smoking (for heart disease) females; > 90 cm in mmol/L mmol/L for women mmHg mmol/L women or or transgender transgender males) males Post Myocardial Infarction  Coronary Atherosclerosis (Review) Abnormal accumulation of lipid, or fatty substances and fibrous tissue in lining of arterial blood vessel walls. Pathophysiology:  Begins as fatty streaks of lipids  Genetics and environmental factors are involved of the progression of the lesions  Inflammatory effects on the arterial wall attracts macrophages that infiltrate the injured endothelium  Ruptured plaque leads to thrombus formation that leads to MI Fig 24.08, p. 592, Power-Kean et al., (2023)  Angina (Review) Risk Factors: Long-Term Effects on Stable the Body Post-MI Elevated blood lipids Smoking Cardiogenic HTN Dysrhythmias Heart Failure Unstable Shock DM Obesity Family history of premature CV Papillary disease Ventricular Variant Muscle Pericarditis Age Aneurysm (prinzmetal) Dysfunction Metabolic syndrome Dressler’s Syndrome Living with Heart Failure and Cardiomyopathies  Heart Failure Basics  Preload  Afterload  Contractility Heart unable to Preload generate adequate CO Afterload Inadequate Pulmonary LV diastolic capillary tissue perfusion filling pressures pressures Contractility Fig 24-35, p. 618, Power- Kean et al., (2023)  Heart Failure Basics Risk Factors Left heart failure: Most cases Ischemic EF Heart HTN Cardio- myopathies HFrEF Ejection fraction (EF) < 40% = Disease CO Myocarditis Obesity Age HFpEF Valvular Renal Diabetes heart Failure Right heart failure: d/t pulmonary disease or disease secondary to left heart failure Congenital Excessive heart COVID disease alcohol use Forward failure: CO leads to cardiogenic shock Backward failure: preload leads CVP to systemic congestion  Living with Heart Failure Ejection Fraction: amount of blood ejected by ventricles per beat Determined by: Ejection Fraction What does it Measurement mean? Echocardiogram CT 50-70% Normal 41-49% Mild Heart Failure Nuclear Angiogram Medicine Scan < 40% Moderate Heart Failure < 35% Severe Heart Failure  Left Heart Failure Assessment Findings: Level of Consciousness (LOC), dizziness, light- headedness. Poor colour, poor pulse strength x 6, tachycardia, presence of S3, S4, cap refill > 3 sec. Coarse crackles, tachypnea, SOB, wet cough, could be persistent. GI: nil RENAL: Decreased urine output, nocturia, orthopnea, nocturnal dyspnea, 24-hour fluid balance MSK: Unsteady gait. Timby. 12th Edition. Chapter 28. Caring for the Clients with Heart Failure  Right Heart Failure (Cor Pulmonale) Same as left-sided failure RV-sided heaves, JVD, RUQ pain (hepatomegaly) Same as left-sided failure GI: Anorexia, nausea, GI bloating, ascites RENAL: same as left-sided failure Timby. 12th Edition. Chapter 28. Caring for the Clients with Heart Failure  Cardiac Asthma Left heart Medical emergency failure Tip: listen to the lower lobes for crackles in conjunction with wheeze in the upper lobes and other heart failure symptoms. Pulmonary edema Wheezing Unresponsive Coughing to Tanabe, T., Rozycki, H. J., Kanoh, S., & Rubin, B. K. (2012). Cardiac bronchodilators asthma: new insights into an old disease. Expert review of Orthopnea respiratory medicine, 6(6), 705–714. https://doi.org/10.1586/ers.12.67  Cardiomyopathy Types of Cardiomyopathy Dilated Hypertrophic Restrictive Most are a result of remodeling of the heart Secondary to: muscle, caused by the effects of 1. Infectious disease neurohormonal responses to: 2. Exposure to toxins 1. Ischemic heart disease 3. Systemic connective tissue disease 2. Hypertension 4. Infiltrative and proliferative disorders 5. Nutritional deficits  Cardiomyopathy: Dilated Cardiomyopathy Ventricular dilation and grossly impaired systolic function leading to dilated heart failure Diminished myocardial contractility, diminished ejection fraction, increased end-diastolic and residual volumes Dyspnea, fatigue, and pedal edema. Displaced Tyerman: Lewis's Medical-Surgical apical pulse, S3 gallop, Nursing in Canada, 5th Edition, Figure peripheral edema, jugular 39.12, p. 892 venous distension, and pulmonary congestion Fig 24.26, Fig 24.27, p. 609 Power-Kean et al., (2023)  Cardiomyopathy: Hypertrophic Cardiomyopathy Hypertrophic obstructive Hypertensive or valvular Fig 24.26, Fig 24.27, p. 609 cardiomyopathy hypertrophic Power-Kean et al., (2023) cardiomyopathy Most common of inherited cardiac disorders Hypertrophy of the myocytes to Thickening of septal wall which compensate for increased workload cause outflow obstruction to LV Increased resistance to ventricular Occurs when HR is increased, and ejection seen in hypertension or valvular volume is decreased stenosis (aortic) Diastolic relaxation is impaired Asymptomatic or: Assessment findings: Angina Extra heart sounds Syncope and murmurs Tyerman: Lewis's Dyspnea on exertion Medical-Surgical Palpitations Nursing in Canada, 5th Edition, Figure 39.12, p. 892  Cardiomyopathy: Restrictive Cardiomyopathy Idiopathic or as a manifestation of scleroderma, amyloidosis, sarcoidosis, lymphoma and hemochromatosis Restrictive filling and reduced diastolic volume of either or both the ventricles Myocardium becomes rigid and noncompliant, impeding ventricular filling and raising filling pressures during diastole Tyerman: Lewis's Medical-Surgical Right sided heart failure with systemic venous congestion Nursing in Canada, 5th Edition, Figure 39.12 , p 892 Cardiomegaly and dysrhythmias are common  Characteristics of Different Cardiomyopathies Normal Dilated Restrictive Hypertrophic Major None Fatigue, weakness, Dyspnea Dyspnea, angina, Symptoms palpitations fatigue, syncope, palpitations Ejection 50-70% < 30% when severe 25-50% >60% Fraction LV wall Normal Decreased Normal or Increased thickness increased Dysrhythmias None Ventricular Atrial fibrillation Ventricular Tachyarrhythmias or Ventricular in tachyarrhythmias, atrial fibrillation sarcoidosis atrial fibrillation Compliance Normal Increased Decreased Decreased Valve None Mitral Mitral Mitral incompetence Fig 24.25, p. 608 Contractility Normal Decreased Normal Increased Power-Kean et al, (2023) Eventual CV Left heart failure Right heart failure Left heart failure event  Heart Failure in Pregnancy: Peripartum Cardiomyopathy (PPCM) Difficult to diagnose: HF symptoms like third-trimester presentation of feet and legs swelling and shortness of breath Heart Clinical Manifestations Lab Tests chambers enlarge, Last month of pregnancy Electrolytes muscle to 5 months post Fatigue Palpitations CBC weakens (Na, K) EF < 45% Nocturia Orthopnea Kidney Liver SOBOE Function Function SOB Cardiac Markers Ankle Distended CO Peripheral Swelling Neck Veins BNP TNT, CK, CK- MB edema Low BP Thyroid Orthostatic Function Hypotension Valve Dysfunction  Valve Dysfunction AORTIC VALVE MITRAL VALVE Fig 34.01, p. 752. Tyerman: Lewis's Medical-Surgical Nursing in Canada, 5th Edition  Valve Dysfunction and Repair Congenital or Acquired Damage Acquired forms include: Most common cause of Structural alterations acquired dysfunction: caused by remodeling of the matrix and lead to: Inflammatory Ischemic Rheumatic heart Incompetence Stenosis disease (RHD) (regurgitation) Traumatic Degenerative Infectious Diagnosis by: alterations of the valve structure and function Echo Left-sided heart valves >> Right-sided  Acquired Valve Dysfunction: Rheumatic Fever Clinical Temperature of Tonsils that are red and swollen with Red rash Manifestations >38.3°C white patches Tender and Small, red spots swollen lymph Headache on the roof of the nodes mouth Nausea and Thick, bloody Difficulty vomiting discharge from swallowing nose  Acquired Valve Dysfunction: Endocarditis Splinter Hemorrhages Weakness Fever Osler Lesions Malaise Chills Janeway Lesions Fatigue Petechiae Heart Clinical Muscle & Night Failure Sweats Aortic valve Manifestations Joint Pain > Mitral Valve New or Changed Abdominal Discomfort Heart Murmur Anorexia Mitral > Weight Loss Tricuspid  Valve Dysfunction: Stenosis Aortic Clinical Manifestations Most common form of stenosis Angina Characterized by: Caused by: Fatigue Syncope SV HR Congenital bicuspid valve CO Degeneration with Narrowed Pulse aging Dyspnea Palpitations Pressure Inflammatory damages caused Murmur by RHD **Poor prognosis once patients become symptomatic  Valve Dysfunction: Stenosis Mitral Increased pressure in Murmur Decreased CO pulmonary circulation Leaflets become fibrous Atrial dilation Risk of atrial and fused Incomplete Scarring emptying of left and dysrhythmia Chordae tendinae become shortened atrium hypertrophy And thrombi If untreated may lead to pulmonary HTN, pulmonary edema, RV failure  Valve Dysfunction: Regurgitation Aortic Clinical  Widened pulse pressure  Turbulence produces a murmur Manifestations  Carotid pulsations and bounding peripheral pulses (Corrigan pulse)  Symptoms of Heart Failure Inability Compen- of leaflets Volume satory to close dilation to Ventricular Heart overload increase properly in SV and hypertrophy Failure during ventricle maintain diastole CO Causes:  Connective tissue  Idiopathic or: disorders  Rheumatic heart disease  Appetite-suppressing  Bacterial endocarditis medication  Syphilis  Trauma  HTN  Atherosclerosis Image: Colourbox.com  Valve Dysfunction: Regurgitation Tyerman: Lewis's Medical- Mitral Causes:  Mitral valve prolapse Surgical Nursing in Canada, 5th Edition, Figure 39-07, p 884  RHD  Infective endocarditis  MI  Connective tissue disease  Dilated cardiomyopathy Inability of leaflets to LV dilates & close Backflow LV Heart from LV to Hypertrophy properly to maintain failure failure during LA CO diastole  Valve Dysfunction: Regurgitation Associated with failure and dilation of RV secondary Tricuspid to pulmonary HTN Valve Volume Increased Right- overload in systemic sided incompetence RA venous BP HF Image: Colourbox.com Pulmonic valve dysfunction has the same consequences as tricuspid valve dysfunction Mitral Valve Prolapse One or both cusps of the mitral valve billow upward (prolapse) into the left atrium during systole. The most common cause of MVP is myxomatous degeneration of the leaflets in which the cusps are redundant, thickened, and scalloped because of changes in tissue proteoglycans, increased levels of proteinases, and infiltration by myofibroblasts. Mitral regurgitation occurs if the ballooning Fig 24.31, p. valve permits blood to leak into the atrium. 607, Power-Kean et al., (2023) Acute vs Chronic Pericarditis  Acute vs Chronic Pericarditis Acute Chronic inflammation of the pericardium, causing the pericardial membranes to become inflamed and roughened Etiology Etiology Trauma Viral Trauma Connective Infection: Neoplasm Surgery Infection Surgery tissue Bacterial disease (SLE Acute MI Complication Radiation Viral Disorders: of HIV and RA) Response to injury Therapy Fungal including: Metabolic Bacterial Neoplasm Rickettsial Acute pericarditis Immunologic Infection Post-MI Vascular (especially Idiopathic Parasitic Pericardial effusion TB) Constrictive Uremia pericarditis Fig 24.22, p. 607, Power-Kean et al., (2023)  Constrictive Pericarditis (Chronic Pericarditis) Form of pericardial disease Fig 24.24, p. 608 Power-Kean et al., (2023)  Idiopathic or associated with:  Radiation exposure  Rheumatoid arthritis  Uremia  CABG Lesions Compresses Fibrous Visceral Obliteration encase the the heart and scarring with and parietal of heart in a rigid reduces occasional layers pericardial shell cardiac output calcification adhere cavity Develops gradually  Constrictive Pericarditis (Chronic Pericarditis) Clinical Manifestations Assessment Findings Pulsus Exercise paradoxus intolerance Weight loss Edema Dyspnea on Hepatic Fatigue JVD exertion Congestion Anorexia Pericardial knock (early Atrial diastolic sound) Fibrillation  Aneurysms Most common cause of arterial aneurysms: An aneurysm could result in Atherosclerosis dissection, rupture, hemorrhage. Most commonly occur in the thoracic or abdominal aorta ***Surgical Emergency*** Risk Factors Clinical Manifestations: Aortic: Asymptomatic until Genetic Smoking rupture Rupture: severe pain and hypotension Diet HTN Thoracic: Dysphagia Collagen Dyspnea vascular Syphilis Chest pain radiating to disorders back Fig 24-7, p. 589, Power-Kean et al., (2023) Peripheral Arterial Disease  Peripheral Arterial Disease (PAD) Atherosclerotic narrowing of the noncardiac, noncranial peripheral arteries Modifiable Risk Factors Non-Modifiable Risk Factors Assessment Focus Often asymptomatic, undiagnosed, Advanced Smoking Age undertreated Bruit Diabetes Family Mellitus History Ankle Brachial Index Doppler Blood Flow Physical Obesity Occurs often in the lower extremities Inactivity Patients are at risk for: Hyper- HTN CV death lipidemia Stroke Diet high in fats and Kidney MI and worse cholesterol Disease Limb ischemia and lower limb amputation  PAD vs PVD PAD PVD Slow toenail growth Itchy, dry skin on the legs Leg pain or cramping while walking Swelling in the feet, ankles, or legs Presence of spider veins or Leg numbness or weakness varicose veins Image from Cumming, M. (2023) Sores on toes, feet, or legs that Clinical evaluation for Peripheral Tired feeling in the legs arterial disease. won’t heal https://www.drcumming.com/educa tional-musings/clinical-evaluation- for-peripheral-arterial-disease Coldness on the lower leg or foot Difficulty standing for very long Image from HMP Global (2023). Teaching proper treatment and Changes in the colour of legs, Burning, numbness, or tingling in the assessment of peripheral vascular texture, or temperature thighs or calves disease. https://www.woundsource.com/blo g/teaching-proper-treatment-and- assessment-peripheral-vascular- disease  Indigenous Populations and PAD Indigenous peoples across First Nations, Inuit and Metis populations have a higher incidence of risk factors associated with PAD increasing risk of developing this disease PAD is more likely to develop in Indigenous people with diabetes than in non-Indigenous people with diabetes, and the former also experience an increased burden of other diabetic complications, including hypertension, microvascular damage, diabetic foot, diabetic nephropathy and peripheral neuropathy  Key Points to Remember Can you perform a full head-to-toe assessment with knowledge of physiological landmarks and anatomy and physiology related to Neuro, CV, Resp, GI and GU assessment about chronic cardiac conditions? Explain the “why” associated with head-to-toe assessment and connections to other systems Identify and apply concepts of lab values related to alterations in chronic CV conditions  Do you understand the pathophysiology, clinical manifestations and nursing assessment related to:  Age Related Cardiovascular Changes  Acute versus chronic pericarditis  Complicated HTN, Pediatric HTN, Endocrine HTN  Cardiomyopathies  Metabolic syndrome  Chronic heart failure  Long term effects on the body post-MI  Valve dysfunction