Student.LECTURE.Cardiovascular.NOTES (1).pdf

Alterations in Cardiovascular System  Tell me what you know: About blood vessels? About the heart's anatomy How do the kidneys affect the heart? What is the conduction system?  Diseases of the Arteries Arteriosclerosis Abnormal thickening and hardening o...

Alterations in Cardiovascular System  Tell me what you know: About blood vessels? About the heart's anatomy How do the kidneys affect the heart? What is the conduction system?  Diseases of the Arteries Arteriosclerosis Abnormal thickening and hardening of the vessel walls Atherosclerosis- it’s the umbrella of it A form of arteriosclerosis Plaque build up on arterial wall  Diseases of the Arteries Progression of Atherosclerosis Damage & inflammation of endothelium Cellular proliferation & macrophage migration LDL oxidation & Foam cell accumulation Fatty streak appears on intima lining of vessel wall Fatty streaks produce free radicals and more damage Fibrous plaque forms that can obstruct lumen or can rupture and form a complicated plaque Complicated plaque & subsequent rupture hematoma can cause sudden thrombus formation, occlusion & tissue ischemia  Endothelium as Active Tissue Fluid filtration- it compensates when the body needs to Maintain blood vessel tone Semipermeable barrier Neutrophil chemotaxis Hormone secretion  Endothelial Injury Leads to arteriosclerosis and atherosclerosis Endothelial injury attracts WBCs ’ Initiates inflammation (autoimmunity involved) T lymphocytes: react against oxidized LDL B lymphocytes produce antibodies against oxLDL vWF released increasing platelet aggregation Foam cells (lipid-rich macrophages) form NO release inhibited: vasoconstriction Plaque formation - resorts in this stage  Blood Flow Regulation Blood flow Inversely related to diameter of vessel- if the vessel is larger, what should the pressure be- lower and vice versa Resistance- all of the factors below affect it Vessel diameter Vessel length Blood viscosity  Blood Flow Regulation Cardiac output (CO) Amount of blood from LV per minute- pumps blood to the rest of the body CO = BP/PVR BP = CO × PVR Factors can be adjusted independently To raise BP: Increase CO Increase PVR Cardiac Factors  Blood pressure is dependent on CO (cardiac ouput) X SVR (stroke value) Components of Blood CO = cardiac output Pressure SVR = systemic vascular resistance  Orthostatic (postural) hypotension- certainly feeling dizzy/bp drops when standing from a sitting position Baroreceptors Decrease in both systolic and diastolic blood pressure within 3 minutes of moving to a standing Diseases position Drop in SBP of 20 mm Hg or > of the OR Drop in DBP of 10 mm Hg or > Arteries Lack of normal blood pressure compensation in response to gravitational changes on the circulation Acute orthostatic hypotension – common in elderly Chronic orthostatic hypotension  Renin-Angiotensin-Aldosterone System (RAAS) Key role in BP regulation Renin From JG (juxtaglomerular) cells of kidneys Released in response to low pressure or perfusion Converts angiotensinogen (from liver) to angiotensin I Angiotensin I converted to angiotensin II ACE (angiotensin-converting enzyme) in the lungs  Renin-Angiotensin-Aldosterone System Angiotension II Potent Vasoconstrictor Activates aldosterone for adrenal cortex Aldosterone Stimulates sodium and water retention this increases value which in return increases BP Result Combination of vasoconstriction (angiotensin II) and fluid retention (aldosterone) serve to elevate BP  Antidiuretic Hormone (ADH) Released from- Posterior pituitary (in the brain) AKA: vasopressin Signal for release: Drop in BP and/or Decreased blood volume Increased blood osmolarity Response: Increases water reabsorption b/c we want to increase the blood valume Raises blood volume and blood pressure Blood Pressure Regulation Other Factors Affecting the Arteries  Hyperlipidemia Elevated levels of lipids Cholesterol (hypercholesterolemia) Triglycerides (hypertriglyceridemia) Dyslipidemia- they have all three of these Hypertriglyceridemia Elevated LDL cholesterol levels Decreased HDL levels  Elevated lipid risk factors Familial hypercholesterolemia (FH) Diabetes mellitus Obesity Hypothyroidism Sedentary lifestyle Diet high in saturated fats Medications: progestins, corticosteroids Hyperlipidemia: Signs and Symptoms Plaque formation Along vessel walls Lipid-filled WBC’s (foam cells) Overt signs and symptoms May be lacking Xanthoma: cholesterol deposits under skin Xanthelasma: cholesterol deposits around eyes Arcus senilis: yellow-white ring around cornea Review family history, risk factors for cardiovascular disease  Hyperlipidemia: Diagnosis Blood samples: lipoproteins, Chol, TGs 10-year atherosclerotic cardiovascular disease (ASCVD) risk ACC Risk Estimator App FH genetic testing 2018 AHA/ACC Expert Consensus Panel Recommends FH genetic testing standard of care Patients with probable or definite FH At-risk relatives Hyperlipidemia: Nonpharmacologic Treatment Lifestyle modifications Dietary cholesterol less than 300 mg/day Limit saturated fats Regular physical activity Raises “good” cholesterol  Hypertension General criteria: Two or more BP readings DBP > 80 or SBP > 130 mm Hg “Silent killer” Primary HTN: 95% Etiology unknown Combination of genetic and environmental factors Also called essential or idiopathic HTN 95% of cases are primary hypertension Secondary HTN: 5% Due to underlying disease Example: Cushing’s disease  Hypertension Risk Factors Gender Obesity- plaque Men > Women up to age Advancing age Family history 55 buildup Women > Men after age 55 Cigarette Smoking- High intake of Na, Low intake of K, causes Black race ETOH Ca, Mg vasoconstriction Glucose intolerance Pathophysiology of Primary Hypertension Pathological effects High shearing stress arterial walls LV hypertrophy (LVH) it can not fill up as much vs the othr side Hypertension: Signs and Symptoms Often no symptoms Target organ damage signs: Headaches Chest pain Vision disturbances Dizziness Check for disorders and medications known to elevate BP  Hypertension: Assessment BP measurement Seated for 5 minutes No caffeine, exercise, smoking within prior 30 minutes Two measurements: use average HTN: Two separate measurements of elevated BP on separate days Ambulatory BP monitoring may be used Hypertension: Assessment Hypertension: Nonpharmacologic Treatment  Stepped Care of Management of HTN ❖Step 1: Lifestyle modifications ❖Step 2: Drug therapy added ❖Step 3: Change in drug dose or class or addition of another drug ❖Step 4: Second or third agent or diuretic is added  Hypertension: Pharmacological Treatment ❖Work to alter normal reflexes that control BP ❖Not all patients respond in same way to antihypertensive drugs because of different factors and complicating conditions ❖Several different types of medication may need to be used in combination ❖Drugs include: o ACE inhibitors o Angiotensin II receptor blockers (ARBs) o Calcium-channel blockers o Vasodilators Other agents Hypertension: Complications  Electrocardiogram Standard waveforms P wave: Atrial depolarization QRS complex: Ventricular depolarization T wave: Ventricular repolarization 12-Lead ECG 12 different views of electrical activity of heart  Normal ECG Waveform Five main waves o P wave: formed as impulse originating in SA node (pacemaker of the heart) or pacemaker pass through arterial tissues o QRS complex: depolarization of the bundle of His (Q wave) and ventricles (R and S waves) o T wave: repolarization of ventricles SA node SA node  Dysrhythmias Disturbance of the heart Can be caused by an Examples: rhythm abnormal rate of impulse generation or abnormal impulse conduction Tachycardia Flutter Fibrillation Bradycardia Premature ventricular contractions (PVCs) Premature atrial contractions (PACs) Asystole  Heart Failure Left heart failure ( Formerly Etiology: MI, ischemic heart called “Congestive heart disease, hypertension, genetic failure”) Inadequate cardiac output. predisposition, obesity, DM, Systolic HF with reduced ejection Affects 10% of persons > 65 fraction RF, other heart disease, Diastolic HF with preserved ejection excessive alcohol use fraction High-output failure: Inability of Right heart failure: Most heart to supply adequate commonly caused by oxygenated blood despite pulmonary disease such as adequate blood volume and COPD which increases R cardiac function. Most ventricular after load (cor commonly caused by anemia, pulmonale) septicemia, hyperthyroidism, or beriberi.  Heart Failure Four stages o Stage A: High risk for HF but no structural heart disease or symptoms o Stage B: Structural heart disease but no signs or symptoms of HF o Stage C: Structural heart disease with prior or current symptoms of HF o Stage D: Refractory HF requiring specialized interventions  Heart Failure Functional classifications o Class I: No limitation of physical activity o Class II: Slight limitation of physical activity o Class III: Marked limitation of physical activity o Class IV: Unable to perform any physical activity without symptoms, or symptoms at rest Usually involves dysfunction of cardiac muscle Preload Afterload Left Heart Failure  Systolic HF or HFrEF ⬤ Ejection fraction < 40% ⬤ Decreased contractility of myocardium increases the LV end diastolic volume (preload) ⬤ This then leads to a stretching of myocardium & more decrease in contractility. AND/OR ⬤ Increased peripheral vascular resistance leads to increased afterload (force which LV has to contract to eject blood) ⬤ This then leads to LV remodeling (hypertrophy) & decreased compliance.  Diastolic HF or HFpEF ⬤ Impaired ventricular relaxation and filling during diastole ⬤ High filling pressures due to stiff ventricles. ⬤ This results in venous engorgement in both the pulmonary and systemic vascular systems ⬤ Usually a result of LV hypertrophy post MI and/or with HTN, valve disease. ⬤ Ejection fraction normal ⬤ Persons can also have mixed HF with features of both  HF – General Pathophysiology ⬤ Ventricular failure leads to: Low blood pressure- why? Low cardiac output (CO) ⬤ Abrupt or subtle onset ⬤ Compensatory mechanisms mobilized to maintain adequate CO: Dilation and hypertrophy Sympathetic nervous system (SNS) activation Neurohormonal responses: Renin, Aldosterone, ADH Neuropeptide responses: ANP & BNP  Heart Failure Acute Chronic Rapid, sudden More Common development of HF Gradual weakening of Substantial ventricular heart and can’t reverse muscle injury (MI) the damage that was already done Sudden severe shock