Cardiac Hypertension Notes
Cardiac Hypertension Notes NSG 335
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This 8 page Class Notes was uploaded by Brieanna Phipps on Monday February 29, 2016. The Class Notes belongs to NSG 335 at University of North Carolina - Wilmington taught by Dr. Sauer in Spring 2016. Since its upload, it has received 31 views. For similar materials see Pathology and Pharmacology in Nursing and Health Sciences at University of North Carolina - Wilmington.
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Date Created: 02/29/16
Systemic Circulation -Heart -Arteries -Arterioles -Capillaries -Venules -Veins Factors Affecting Blood Flow -Pressure -force exerted on a liquid unit per area -measured in mm of Hg -Resistance -opposition to force -diameter and length of the blood vessels contribute to resistance -inversely related to blood flow. Blood flow is measured in L/min (CO) -Velocity -Velocity is the distance blood travels in a unit of time (cm/sec) -Laminar vs. turbulent flow -Laminar straight ahead vs. turbulent flow obstructed flow causing whirls and eddys. Can hear murmur on auscultation -Vascular compliance -Vascular compliance is the ability of vessel to take on more value with increased pressure. -Stiffness is opposite of compliance. -Veins have more compliance than arteries Regulation of BP -Arterial Pressure -Mean Arterial Pressure (MAP) -Average pressure in the arteries throughout the cardiac cycle -MAP= [(2xDP) + SBP] divided by 3 -minimum is 60 to keep organs perfused -Effects of CO (HR x SV) -Effects of total peripheral resistance -vasoconstriction higher BP -vasodilation lower BP -Effect of hyperemia -Effects of hormones vasoconstriction -Epinephrine and Norepinephrine -ADH, RAAS, and natriuretic peptides -Adrenomedullin -secreted by adrenal medulla and smooth muscles of and mediates vasodilatation and sodium excretion -Insulin -increases vasodilation -Venous Pressure Diastole -heart is relaxed -ventricles filling -coronary perfusion occurs -2/3 of total cardiac cycle time -Early diastole -the ventricles fill passively -Late diastole -the atria contract and “top off” the ventricles with additional volume -AKA “atrial kick” (can equal 10-30% of blood in the ventricle) -HR increases, diastolic time decreases -filling time is shortened less blood in ventricles less blood pumped out -coronary perfusion time is decreased while myocardial O2 demand is increasing -valves are closed Systole -active contractile phase -blood is being pumped -right ventricle pulmonary artery lungs left ventricle aorta systemic circulation Cardiac Output (CO) -HR x SV (stroke volume) -normal CO is 4-6L -SV is how much blood is in the ventricle, affected by fluid in the body -dehydrated, lower SV Cardiac Performance -Preload -left ventricular end-diastolic volume -Afterload -load muscle must move after it starts to contract -determined by system vascular resistance in aorta, arteries, and arterioles Preload -degree of the stretch of the heart before contracting -volume in the ventricle increases preload -a stretch beyond their limits causes a decrease in contractility Afterload -arterial resistance during contraction -the force needed for the ventricle to push blood past the valves -Arterial BP -EF (Ejection Fraction): amount of fluid leaving the ventricle with contraction -55-75% is normal Contractility -measure of cardiac performance -degree to which muscle fibers can shorten to function and contract to push the blood around -decreased by diseases that impact myocyte activity -ischemia/MI -myocarditis -cardiomyopathies -drugs that increase contractility are called intropes Diseases of the Veins -Varicose Veins -a vein in which the blood has pooled; distorted, tortuous and palpable; valves don’t work as well -caused by trauma or gradual venous distention -risk factors -age -female -family hx -obesity -DVT -prior leg injury -Chronic Venous Insufficiency -inadequate venous return over a long period of time due to varicose veins or valvular incompetence -venous stasis ulcers -capillaries are enlarged -Deep Venous Thrombosis (DVT) -obstruction of venous flow which increases venous pressure -factors: -Virchow’s Triad -venous stasis -venous endothelial damage -hypercoagulable states -cancer, orthopedic surgery/trauma, HF, immobility -use Doppler to find DVT -Superior Vena Cava Syndrome (SVCS) -occlusion of the SVC that leads to venous distention of upper extremities and head -oncologic emergency Diseases of the Arteries and Veins -Hypertension (HTN) -isolated systolic HTN- becoming prevalent in all age groups -elevations of systolic are caused by inc CO, total peripheral resistance, or both -Primary HTN -essential or idiopathic -genetic and environmental factors -risk factors -high sodium -natriuretic peptide abnormalities -obesity -insulin resistance -Complicated HTN -chronic damage to the walls of the systemic blood vessels -smooth muscle cells undergo hypertrophy and hyperplasia -affects heart, kidneys, and retina -can result in transient ischemic attack/stroke, cerebral thrombosis, aneurysm, and dementia -Malignant HTN -rapidly progressive -diastolic pressure is usually >140 mm/Hg -life threatening organ damage -Orthostatic HTN -decrease in both systolic and diastolic BP upon standing -lack of normal blood pressure in response compensation in response to gravitational changes in the circulation -can be both acute or chronic -Thrombus formation -blood clot that remains attached to the vessel wall -Risk factors -intimal injury, inflammation, obstruction of flow, pooling (stasis) -thromboembolus: moving -thrombophlebitis: inflammation at vessel -arterial and venous thrombi -Embolism -bolus of matter that is circulating in bloodstream -dislodged thrombus, air bubble, amniotic fluid, aggregate of fat from a broken bone, bacteria, cancer cells, foreign substance -Peripheral Artery Disease -artherosclerotic disease of the arteries that perfuses the limbs Medications used to treat HTN -RAAS suppressants -Calcium Channel Blockers (CCBs) -Sympatholytic -Direct Vasodilators -Alpha/Beta Blockers Renin-Angiotensin Aldosterone System -ACE Inhibitors- block conversion of angiotensin I to angiotensin II -decreases BP by relaxing vessels and increasing venous compliance -ADR: cough, hyperkalemia, HA, dizziness, fatigue -CONTRAINDICATED IN PREGNANCY Pril’s -Enalapril- ACE used to treat HTN, HF -Captopril- ACE used to treat HF, post-MI left ventricular dysfunction, diabetic retinopathy -alter dose with decreased renal function RAAS -Losartan -Angiotensin II receptor blocker (ARB): prevents angiotensin II from binding to receptors -HTN, HF, post MI, CAD, CKD -has LESS side effects than ACE -ADR: hypotension, HA, dizziness Direct Renin Inhibitor (DRI) -Aliskiren- acts directly on renin, suppressing the RAAS -DO NOT take DRIs with ACE and ARB concurrently -ADR: hypotension, diarrhea, dizziness -CONTRAINDICATED IN PREGNANCY -very potent, used infrequently, strong SE Aldosterone Antagonists -Spironolactone -lowers BP by promoting excretion of Na and water -potassium sparing diuretic -ADR: hyperkalemia -used a lot in HF Calcium Channel Blockers (CCBs) -two categories 1. Dihydropyridines act only on arterioles- Nifidipine -lowers BP by vasodilation -angina, HTN -ADR: reflex tachycardia, flushing, HA, peripheral and gingival hyperplasia 2. Non-dihydropyridines act on arterioles and conduction- Verapamil and Diltiazem -lowers BP and decreases HR by vasodilation and blocks SA node -angina, HTN, dysrhythmias -ADR: constipation (only Verapamil), flushing, dizziness -prevents calcium ions from entering cells therefore affecting contractioin -relaxation of arterioles -used to treat HTN, angina, atrial cardiac dysrhythmias Sympatholytics (Anti-Adrenergic) Drugs 5 types: -Beta blockers -Alpha blockers -Alpha/Beta blockers -Centrally acting alpha agonist -Adrenergic neuron blockers Beta Blockers -Propanolol: non-selective BB -Metoprolol: cardio-selective BB, used after pts have MI -blocks the effects of epinephrine, decrease in HR and BP, suppress reflex tachycardia, reduce release of renin, reduces PVR (peripheral vascular resistance) over time -ADR: bradycardia, AV HB (heart block), HF, rebound excitation (with withdrawal), bronchoconstriction, altered glucose, fatigue, dizziness, loss of libido, SOB, depression -antidote for OD is epinephrine Alpha Agonist1 -Doxazosin- used to treat HTN and BPH (increases urine flow) -vasodilation from blocking alpha1 receptors on arterioles and veins -ADR: orthostatic hypotension, inhibit ejaculation, nasal congestion -DO NOT GIVE WITH VIAGRA Centrally-acting Alpha2 -Clonidine- act within brainstem to suppress sympathetic outflow to the heart and blood vessels -vasodilation, reduced CO -ADR: sedation, dry mouth, severe rebound HTN if treatment is stopped -usually people in renal failure Thiazide Diuretics -Hydrochlorothiazide (HCTZ)- first drug in line for HTN -reduces BP by decreasing blood volume and reducing arterial resistance -ADR: hypokalemia, dehydration, hyperglycemia, hyperuricemia (uric acid in urine) Loop Diuretics -Furosemide (Lasix)- not used routinely for HTN as it is more potent than needed. -reserved for pts who require greater diuresis and have a low GFR -ADR: hypokalemia, dehydration, hyperglycemia, hyperuricemia, hearing loss -IF POTASSIUM IS LESS THAM 3.5 HOLD IT Potassium Sparing Diuretics -Spironolactone -inhibits reabsorption of Na in kidneys -diuresis is small, can balance effects of other HTN therapies -ADR: hyperkalemia, dizziness HTN Emergency -Nitroprusside- Nipride (IV) -DBP >140 mm/Hg -severity is determined by end organ damage -relaxes smooth muscles of the heart -usual rate of infusion is 0.5-0.8 mcg/kg/min -continuous BO monitoring -prolonged infusion (72 hours) can result in toxic build up of thiocyanate Alpha/Beta Blockers -Carvedilol -decreases HR, BP, increases CO, decreased risk of death -HTN, HF, LVD after MI -ADR: bradycardia, pulmonary edema, dizziness, fatigue -Very potent, not given for HTN usually unless you have gone through a lot of drugs
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