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blood path
left side of heart-arteries-arterioles-capillaries-venules-veins-right side of the heart
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arteries
- walls composed of elastin connective tissue, fibrous connective tissue, and smooth muscle
- Elastic arteries located in aorta and major branches
- muscular arteries located in medium/small arteries
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Capillaries
- very thin walls, making exchange of substrates, metabolites, and other products possible
- products pass through via junctions, fenestration, vesicles of active transport, diffusion
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Veins
- More numerous than arteries
- thin walled fibrous, less elastic tissue, larger diameter, few smooth muscle fibers, valves to reduce back flow
- 60% of blood is in veins
- contains muscle pumps, skeletal muscle contraction compresses deep vein muscles to aid in flow of blood to heart
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Factors affecting blood flow
amount of blood moved per unit of time (mL/min)
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pressure
pressure: force exerted on the liquid per unit area (mm Hg)
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resistance
Resistance: the opposition of force (radius/length, viscosity (dehydrated vs hypotonic), arrangement (sequential vs parallel), cross sectional area)
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velocity
velocity: distance blood travels in unit of time (cm/sec)
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turbulent v laminar flow
smooth or bumby
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compliance
Compliance: increase in vessel volume to accommodate for increase in pressure
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total peripheral resistance
- total resistance in the systemic circulation
- determined primarily by changes in arterioles
- Reflex control: sympathetic (heart arterioles veins), parasympathetic (heart)
- autoregulation: smooth muscle activity by vasodilators and vasoconstrictors
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Reflex control in arteries
- smooth muscle layer innervated my sym nervous system
- a1adrenergic receptors: cause vasoconstriction of vessel
- b2 adrenergic receptors: induce smooth muscle relaxation
- vasodilators mainly act locally
- vasoconstrictors are systemic (raas)
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shunting
- shock: shut down everthing but heart and brain
- exercise after eating
- fight or flight
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arteriosclerosis
- chronic disease of arterial system
- abnormal thickening and hardening of vessel walls
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atherosclerosis
- soft deposits of intra-arterial fat and fibrin in vessels which harden over time
- the most common form af arteriosclerosis
- leading cause of coronary artery and cerebrovascular disease
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steps of atherosclerosis
- injury to arterial wall
- macrophages/immune cells bind to injury site
- inflammation releases oxygen radicals that oxidize ldl (foam cells)
- macrophages engulf foam cells which penetrates into intima
- lesion is created (fatty streak)
- collagen migrates over fatty streak, forming a fibrous plaque
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risk factors of atherosclerosis
- Standard american diet, Mcdonalds
- smoking
- cholesterol
- lack of exercise
- glucose intolerance
- htn
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partial obstruction
- due to narrowing caused by plaque
- wen severe enough to cause inadequate oxygenation-produces ischemia
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total obstruction
- stroke (cva), heart attack (myocardial infarction)
- may be due to thrombu, or embolus that follow flow of blood to eventually block an artery
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aneurysms
- outpouching or dilation of a vessel wall or cardiac chamber due to weakened area (changes in collagen and elastin that make the vessel more vulnerable to pressures)
- burst causes bleeding: often asymptomatic until rupture
- examples: abdominal aorta 3/4, brain (berry aneurysms)
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aneurysm risks
- atherosclerosis most common cause: formation erodes vessel wall
- htn increases wall stress
- collagen vascular disorders (marfans)
- infections that affect arterial walls (syphilis)
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chambers functions
- atria: collecting chambers that feed ventricles
- left arium: collects blood from lungs
- Right atrium: collects blood from body
- Ventricles: pump
- Left ventricle: directs blood to body
- Right ventricle: directs blood to lungs
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valves
- between atria and ventricles (tricuspid-right; mitral -left)
- semilunar valves between ventricles and arteries (pulmonic- right; aortic - left0
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cardiac cycle
- hearts contraction and relaxation that follows it
- systole: ventricular contraction that ejects blood into aorta
- diastole: muscle relaxation: filling of ventricles
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systole
- LUB
- ventricular contraction increasing pressure and forcing blood into aorta
- ventricle=aorta pressure
- semilunar valve opens
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Diastole
- DUB
- ventricle relaxes completely
- Ventricles < aorta pressure
- semilunar valve closes
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Cardiac Output
- CO=SV*HR
- normal adult: 5 L/min
- Factors: Preload, afterload and myocardial contractibility
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myocardial contractility
- inotopic state; force of contraction affected by
- changes in stretching of ventricular muscle due to volume of blood
- alterations in sympathetic activation of ventricles
- adequate oxygen supply
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inotropy
the force or energy of muscle contractions
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heart rate regulators
- neural humoral (body fluids)
- ANS: sympathetic increases hr, parasympathetic decrease hr (vasovagal, syncope)
- hormones and biochemicals: Norepinephrine increases hr, Growth hormone thyroid and adrenal hormones decreases hr
- atrial receptors: influence hr and volume retention
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Mean arterial pressure
- MAP=Pd+1/3(Ps-Pd)
- MAP=CO*SVR
- normal: 80-120 mmHg
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Baroreceptors
- location: Carotid sinus, atrial walls, vena cava, aortic arch
- Sense change in pressures
- when stretched it signals high pressure and decreases CO (HR and SV)
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arterial chemoreceptors
- location: carotid, aortic arteries
- sense changes in o2 co2 and ph
- \/ o2 ph ^ pressure
- ^ co2 ^ pressure
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SVR controls
- systemic vascular resistance
- a1 adrenergic receptors: vasoconstriction
- b2 adrenergic receptors: smooth muscle relaxation
- histamines prostaglandins and RAAS
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aldosterone
retains sodium and water in kidney
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osmoreceptors
neurons in hypothalamus: stimulate ADH
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ADH
- antidiuretic hormone
- retains free water, induce thirst and vasoconstriction
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natriuretic peptides
regulate sodium excretion, diuresis, vasodilation, and antagonize RAAS
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hypertension
- systolic > 120 or diastolic > 80
- increases risk for stroke, left vent hypertrophy, renal failure
- interventions ace inhibitors, diuretics, beta blockers, calcium channel blockers, nitrates
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hypotension
- cause: loss of blood volume, excessive demand (heat stroke/sepsis), heart failure
- response to hypotension: ^ hr via sns, ^ heart contractility via sns, ^ svr direct blood to essential areas (heart brain), increase preload
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orthostatic hypotension
- vasoconstricting slow/absent with change to position resulting in blood pooling
- altered body chemistry, drug action, prolonged immobility, starvation, phys exhaustion, volume depletion, venous pooling
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increase preload
- deep breaths to increase thoracic pump
- constriction of veins by activation of sns
- conserve and attempt to renew blood volume (thirst, water conservation by secreating adh)(decrease urine output via RAAS)
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atherosclerosis
- soft deposits of intra-arterial fat and fibrin in vessels whch harden over time
- most common form of arteriosclerosis
- leading cause of coronary artery and cerebrovascular disease
- ischemia/hypoxia
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ischemia
insufficient blood flow to tissues that may result in hypoxia (can result in cell injury and or death)
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Hypoxia
Insufficient oxygen levels
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atherosclerosis outcomes
angina, myocardial infarction, sudden cardiac death, heart failure, stroke, pvd
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atherosclerosis risk factors
age gender family history diabetes smoking hypertension cholesterol sedentary lifestyle obesity
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inflammatory response hypothesis of atherosclerosis
- 1. risk factors cause chronic injury of endo and result in endo dysfuntion
- 2. injured endo allow lipids to enter intima and elicits ongoing inflam response
- 3. inflam response attempts to repair damage but also contributes to plaque formation
- 4. dysfunctional endo secretes growth factors that promote plaque growth and vesssel remodeling
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complication (athero)
continued inflammatory response weakens fibrous cap/ leads to rupture at shoulder of plaque/ leads to rapid clot formation
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fatty streak
- macrophages engulf foam cells and penetrate into intima; smooth muscle cells also migrate into intima
- does not obstruct blood flow
- develops in more advanced lesions
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foam cells
oxidized lipids (mostly ldl chol)
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fatty plaque
- intermediate between fatty streak and fibrous plaque
- accumulations of lipids smooth muscle cells & collagen, macrophages, lymphocytes
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Fibrous plaque
- consists of an extracellular lipid core in addition to smooth muscle cells, macrophages, and extracellular matrix found in fatty streak
- lipid core covered by fibrous cap of collagen and smooth muscle cells
- calcification of plaque may occur which can invade the vessel lumen and obstruct blood flow
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vulnerable plaque
- thin cap more likely to rupture
- has increased conc of macrophages and tcells
- once ruptured clot cascade initiated and rapid clot formation occur
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steps of athero
damage, fatty streak, fatty plaque, fibrous plaque, complicated lesion
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partial obstruction vessels
transient ischemic events (exercise, stress)
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complicated lesion
may result in complete obstruction= tissue infarction (formation of tissue infarct (death/necrosis) due to lack of o2
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order of electrical activity
sinatrial node (pacemaker) - atrioventricular node, bundle of his, bundle branches, purkinje fibers
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fibrillation
small sections of heart acting independently
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3 main coronary arteries
- right coronary artery RCA supplies right ventricle: supplies the sinus node in 55%
- left anterior descending LAD branches off the left main, supplies the left ventricle
- Circumflex: branches off the left main, supplies posterior left ventricle: Supplies sinus node in 45%
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ischemia
demand 02 exceeds supply
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stable angina pectoris
- discomfort lasts 3-5 min (activities)
- no permanent change/damage if blood flow is restored
- caused by gradual narrowing and hardening of vessel (stable plaque) (cannot dilate when demand increases
- pain releived by rest and nitrates
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angina
chest pain caused by ischemia
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unstable angina pectoris
- discomfort lasts 15-20 min without cause and with increasing severity
- caused by unstable plaque, prone to rupture
- vessels become blocked with blood clots that dissolve within 20 min
- does not respond to nitrates
- increased risk for heart attacks
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acute coronary syndrome
- sudden obstruction causing ischemia, usually blood clot formation over unstable/vulnerable plaque
- can cause mi and death: prolonged ischemia
- symptoms: 1st=sudden severe chest pain (heavy crushing) radiating to neck back shoulder and left arm; nausea vomiting; soa; diaphoresis
- women symptoms: fatique, sleep distubance, soa, indigestion, anxiety
- treatment: clot busters, platelet inhibitors or angioplasty (balloon or stent)
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pathogenesis of acute coronary syndrome
- plaque ruptures, spontaneously, induced by PCL (percutaneous coronary interventions)
- platelet adhesion at site of rupture
- more platelet activation
- platelet aggregation
- activation of clotting cascade
- clot formation at site
- obstruction from clot
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myocardial infarction
- 90% caused by thrombus in coronary arteries
- 40% fatal (usually from ventricular fibrillation)
- 10% due to prolonged coronary vasospasm
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valve dysfunction
- can be congenital.. or acquired: inflammatory, ischemic, traumatic, degenerative, infectious, endocarditis
- stenosis: valve opening constricted and narrowed
- regurgitation: valve leaflets/cusps fail to close completely
- management: valve replacement, longterm anticoagulation, prophylaxis for endocarditis PRN
- murmurs are heard
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pericardium
sac enclosing heart
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pericarditis
- inflammation of pericardium causing membranes to become rough
- 90% due to viruses
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pericardial effusion
- accumulation of fluid in the pericardial cavity
- occur with paricarditis
- if fluid accumulation is rapid can cause cardiac compression (fluid in sac displaces preload)
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cardiac tamponade
rapid fluid accumulation causing cardiac compression
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cardiomyopathy
- heart wall muscle doesnt function well
- most due to ischemia and htn, some idiopathic, primary:genetics, secondary:diseases toxins infections
- 3 types: dilated (congestive): big boggy heart , Hypertrophic: so much muscle it blocks outflow , restrictive: stiff small venticles
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heart failure
- cardiac dysfunction resulting in inadequate perfusion of tissues
- 10% adults over 65
- commonly left vent: syst & diast heart failure
- right vent: pulmonary disease
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left heart failure
- congestive heart failure
- systolic heart failure: decreased cardiac output, affected contractility, preload/afterload
- diastolic heart failure: preserved systolic function, due to decreased compliance of left vent and abnormal diastolic relaxation (increased lvedp)
- fluid retention lungs
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right heart failure
- can result form left heart failure: because of back up of blood in pulmonary circulation
- can be due to pulmonary hypertension (from diffuse hypoxic pulmonary disease): copd, cystic fibrosis, ards
- fluid retention abdomen
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causes of heart failure
- atherosclerotic coronary artery disease
- untreated hypertension
- cardiomyopathy
- hypoxic pulmonary disease, causing pulmonary hypertension
- valvular disease
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physiology of heart failure
- decreased cardiac output due to decreased stroke volume
- activates sns to increase hr
- activates raas
- increased wall tension leads to myocardial hypertrophy
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left forward hearth failure
- affects systemic circulation
- results in inadequate oxygen supply to body which results in fatigue
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left backward heart failure
- affects lungs
- results in pulmonary congestion then increased rv afterload then eventually rv failure
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forward right heart failure
- affects lungs
- lungs with too little flow causes too little flow in lv
- decreased cardiac output results in fatigue
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backward right heart failure
- affects veins
- congestion in veins (jugular disention)
- abdominal bloating, anorexia, ascites
- peripheral edema
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Diuretics
- decrease fluid retention (K+ sparring or not)
- decreases blood volume, which decreases venous return and blood pressure
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ACE inhibitors
Decrease afterload via vasodilation (affecting systolic failure)
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B-adrenergic agonists
Stimulate SNS, increasing calcium flow into myocardial cells causing increased contraction (positive inotrope)
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Shock
- insufficient cardiac output to maintain a blood pressure adequate for functioning
- Body reacts by saving fluid, increase HR, if possible vasoconstriction, Kussmaul breathing (fast deeep)
- Signs from SNS: dilated pupils, cool clammy skin, decreased LOC, possible anxiety/panic
- Vital Signs: Low BP, narrow pulse pressure, Tachycardia, tachypnea, acute renal failure (oliguria, increased BUN and Cr)
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Cardiogenic Shock
- Decreased CO=tissue hypoxia
- in the presence of adequate intravascular volume
- MI, cardiomopathy
- Treatment: inotropic medications, limit infarct size (supply O2), Intra aortic balloon pumps in acute care
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Hypovolemic shock
- loss of whole blood (hemorrhage), plasma (burns), or interstitial fluid (diarrhea, diaphoresis, emesis, diuresis)
- Treatment: restore volume
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Anaphylactic shock
- A widespread hypersensitivity reaction
- Vasodilation, peripheral pooling, hypovolemia, causing decreased tissue perfusion, impaired cellular metabolism
- Treatment: EpiPen- a catecholamine that increases blood pressure and heart contractility and dilates the bronchi
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Neurogenic shock
- widespread and massive vasodilation
- due to parasympathetic overstimulation or sympathetic understimulation
- Treatment: remove or treat underlying cause (trauma, drug, stress, pain)
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Septic Shock
- One component of Systemic Inflammatory Response Syndrome SIRS
- begins with infection (gram- or gram+ bacteria, fungi, or viruses) that progresses to bacteremia, then sepsis
- 40% in US progress to Multiple Organ Dysfunction Syndrome (MODS) and death
- Treatment: multiple drug antibacterial therapy, removal of source of infection, fluid sesuscitation, vasoactive mediations to improve hemodynamics
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Acute respiratory distress syndrom
- ARDS: acute lung inflammation and diffuse alveolocapillary injury with pulmonary edema
- complication of shock
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Disseminated Intravascular Coagulation
- DIC: many micro blood clots form causing tissue dammage and using up the clotting factors (clotting and bleeding occur simultaneously)
- complication of shock
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Multiple Organ Dysfunction syndrome
- MODS/MOSF: High mortality (2 organs=50%, 3 organs=90%
- complication of shock
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B-adrenergic blockers
- -lols: propanolol
- decrease hr, contractility and excitability
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ACE inhibitors
- -prils: lisinopril
- Blocks ace; prevents vasoconstriction
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ARBs
- -artans: losartan
- angiotensin II receptor blockers; prevents vasocontriction/ h2o retention
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Ca2+ Channel Blockers
- -dipines: amlodipine
- block ca2+ from moving into cardiac cells; cause vasodilation and loss of smooth muscle tone
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Diuretics
- -ides: furosemide
- promote fluid excretion
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Nitrates
- Angina: nitroglycerin
- cardiac vasodilation
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anticoagulants
- ASA and clopidigrel
- Prevent clot formation, "thin" the blood
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Pressors
- Dopamine and epinephrine
- adrengeric effects; cause vasoconstriction
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