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85 Cards in this Set
- Front
- Back
the vagal response is part of the SNS or PNS?
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PNS; it's an inhibitor response
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chemoreceptors respond to what kind of chemical condition in the body?
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reduced arterial oxygen concentration, elevation of CO2 and reduced pH
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how does SNS response affect bodily function?
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increases CO, BP, blood flow, blood glucose; decreases digestion
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when HR increases, does the diastole time increase, decrease or stay the same?
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it decreases diastolic time
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when HR increases, does the systolic time increase, decrease or stay the same?
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stays the same regardless of HR
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what is the normal ejection fraction at rest
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60-70%
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what is the heart's reserve at rest
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30-40%
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where is the major site of resistance in the body
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arterioles
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what parameter determines a pt is in shock condition
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sustained systolic pressure of <80mmHg
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what common symptoms will you see in the following area if cardiac dysfunction is present: circulation, breathing, urination, mentation?
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circulation = CP, weight change, swelling, dizziness, fatigue, palpitations, cool hand/feet; breathing = SOB, cough; urination = amt, frequency; mentation = alteration in mental status
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if a pt coughs up pink sputum, what might this indicate?
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he/she has pulmonary edema
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liver engorgement is a result of what kind of HF
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RHF
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how do you assess arterial flow
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palpate rate, rhythm, amplitude, symmetry of peripheral pulses
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how do you assess venous flow
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assess type/degree of edema, varicosities, skin color changes
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swan ganz catheter measures which 5 lumens?
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1. CVP - central venous pressure
2. PAP - pulm artery pressure 3. CO - cardiac output 4. SV - pacemaker wire lumen 5. PCWP - pulm capillary wedge pressure |
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right heart cardiac catheterization checks patency in which valves?
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tricuspid and pulmonic
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left heart cardiac catheterization checks patency in which valves
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mitral and aortic
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the use of left heart catheterization usually invades which artery? (how is this procedure approached)
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via femoral artery into aorta
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how is coronary angiography done
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dye injected into right/left coronary arteries, flow of dye is filmed
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how do you prepare for cardiac catheterization
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written consent, VS for pulses, anxiety/pain, allergies, 6-8hrs prior NPO, verify with dr. of pre-op medications
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post catheterization care
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activity restriction, maintain pressure dressing, use of angio seal device, monitor bleeding, VS, pulses, pain; neuro checks; push fluids to flush out dye, monitor UO, instruct pt to avoid bending/lifting
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complications to catheterization
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bleeding, hematoma, dysrhythmias, MI, allergic rxn, infection, hypovolemia, arterial/pulmonary embolization,
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stimulation of SNS causes vasoconstriction or vasodilation
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vasoconstriction
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beta 2 (in the lungs) activated by SNS causes vasoconstriction or vasodilation
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vasodilation
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what is the parameter for stage I hypertension
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140-159/90-99
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how does stress contribute to the development of HTN
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stress causes prolonged SNS activity, which increase vasoconstriction, increased HR and increased renin release
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how does the renin assay test help determine underlying cause of HTN; what is the treatment
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HTN usually caused by either stress or salt. low renin reading indicates salt HTN (which can be treated with diuretic); high renin reading indicates stress/renin HTN (treat with b-blocker, ACE-i, ARB)
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why might a pt have resistant HTN
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NSAID, COX2 inhibitors, cocaine, decongestants, oral contraceptives, steroids, tobacco, ephedra
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how do you evaluate a pt for HTN? (what info do you look for in order to say a pt is hypertensive)
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accurate BP, assess lifestyle, CV risk factors, concomitant disorders, identifiable causes of HTN, target organ damage
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what parameters of BMI is considered obesity
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>30 kg/m2
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how does diabetes contribute to development of HTN?
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high insulin conc in blood simulates SNS activity and impairs nitric oxide-mediated vasodilation; vascular hypertrophy and renal sodium reabsorption
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why is monitoring potassium lvls important for a hypertensive pt?
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to detect hyperaldosteronism; too much aldosterone means H2O & Na+ is being excreted while retaining excessive amt of K+; cardiac muscle is intolerant of acute increase in K+
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what are the two main goals of using drugs to treat HTN
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decrease BV & SVR
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what are the 6 general drug types used to treat HTN
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1. diuretics 2. adrenergic inhibitor 3. direct vasodilators 4. ganglionic blockers 5.angiotensin inhibitors 6. CCB
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what should you monitor for in a pt when giving diuretics?
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orthostatic hypotension
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what are some common adverse effect of using adrenergic inhibitors
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sedation, dry mouth, impotence, rebound HTN (with sudden withdrawal)
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the use of alpha 1 adrenergic blocker can result in what common a/e
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postural hypotension
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what condition is indicated for the use of direct vasodilators
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hypertensive crises
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the use of direct vasodilators can result in what kind of a/e
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acute hypotension, tachycardia
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what should you monitor for when giving angiotensin inhibitor
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monitor hyperkalemia and decrease renal function/failure
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what are some precaution when giving CCB and why
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use with caution in pt with heart failure; it lowers HR, contractility and SVR
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what type of diuretics are usually recommended first-time therapy
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thiazide diuretic
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what type of drugs are not recommended for HF
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CCB
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CCB are used to treat what type of conditions
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high coronary disease risk, diabetes
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what drugs are used to treat CKD
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ACEi and ARB
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ARBs may be used for what types of conditions
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HF, DM, CKD
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what drug is considered universal in CVD
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ACEi
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what type of drug is used for stroke prevention
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diuretic and ACEi
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what two conditions are not treated with b-blocker
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CKD and stroke prevention
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metabolic syndrome is characterized by what types of conditions
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high BP, central obesity, insulin resistant, dyslipidemia
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what is the hallmark of metabolic syndrome
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vascular endothelium damage
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under what conditions does metabolic syndrome occur
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when the pt becomes insulin resistant and has changes associated with increased lvls of angiotensin II, aldosterone, norepinephrine, and epinephrine
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what is the pressure-natriuresis relationship
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individuals with HTN tends to have higher blood volume because.. increase vascular volume is related to decreased renal excretion of salt (salt is retained)
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how does cytokines affect vasculature
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endothelial injury and tissue ischemia cause the release of inflammatory cytokines, which has a vasodilatory action in acute inflammatory injury. but chronic inflammation contributes to vascular remodeling and smooth muscle contraction
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how does insulin resistance contribute to HTN
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insulin resistance overactivates the SNS and RAA; it is r/t decrease release of nitric oxide and endothelial vasodilators
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during diastole, which two valves open
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atrioventricular: tricuspid and mitral
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what stimulates the angiogenesis of the collateral arteries
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hypoxia and endothelial growth factors
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what is the pathway of the bachmann bundle conduction?
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from the SA node to left atrium
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how does increased SNS affect coronary vessels
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it dilates
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how does increases PNS affect coronary vessels
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with the release of acetylcholine, it dilates coronary vessels
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how does cardiac muscle differ from skeletal muscle?
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cardiac = single nuclei, arranged in branching networks. many mitochondria for ATP needs, more T tubules; skeletal = multi-nucleus, arranged in parallel units
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what is the difference between T type and L type ca+ channels?
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L type is long lasting. they predominate and are blocked by CCB. t type is transient, less abundant and not blocked by CCB
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what is a good index of afterload
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aortic systemic pressure
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what 3 factors determine force of contraction
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stretching by preload, activation of SNS, and O2 supply
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what are the most important positive inotropic agents
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norepinephrine and epinephrine
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how does the body respond to decrease in O2 or pH, or increase in CO2
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increases BP
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what are some factors that control renin release
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1. drop in BP (decrease flow to renal)
2. decrease in NaCl to renal 3. b-adrenergic simuli 4. angiotensin II (reduces renin) 5. low plasma K+ (increase renin) |
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does angiotensin II increase or reduce renin release
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reduce renin release
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what simulates the secretion of aldosterone
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angio II
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how does angio II contribute to HTN
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it is considered a growth promoter in CV tissues, resulting in myocyte and vascular hypertrophy; angio II stimulates aldosterone secretion and activates SNS.. all these leads to HTN
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under what condition is the right atrium stimulated to release ANP?
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when it sense an increase in BP
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what kind of activity does adrenomedullin produce
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secreted by endothelial and smooth muscle cells; vasodilation, limiting endothelial injury, reducing oxidative stress and promoting angiogenesis, mediates na+ excretion
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how does insulin resistance contribute to development of HTN
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reduces NO and increases vasoconstrictors; promotes inflammation; increase clot formation; contributes to endothelial damage; contributes to lipid changes
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what two mechanisms increase venous pressure and return to the heart
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1. muscle pump - muscle contraction compresses vein, decreased venous capacity increases return to heart
2. respiratory pump - downward movement of diaphragm during inspiration compress ab vein, moving blood towards heart |
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what is the role of adenosine
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a vasodilator, it is released in response to a decrease in myocardial oxygenation
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how, or through what mechanism does inherited defects cause HTN
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renal na+ excretion, RAA, SNS, insulin resistance, cell membrane na/ca transport
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what is the pressure natriuresis relationship
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ppl with HTN tend to retain more salt
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isolated systolic HTN tends to occur in what type of population
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elderly, over 65
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what does an increase in pulse pressure indicates
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reduced vascular compliance of large arteries
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what are some complications of HTN
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MI, LVHypertrophy, angina, LHF, CAD, sudden death
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how does HTN contribute to HF
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catecholamines from SNS and angio II causes vascular remodeling, deposition in cardiac muscle.. hypertrophy then leads to increase O2 demand and impaired contractility
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what are early s/s of HTN
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there is none! only high BP
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what are later s/s of HTN
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depends on which organ HTN damages; HA (due to constriction of cerebral vessels) may be the only symptom
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elderly are more prone to which type of orthostatic hypotension: acute or chronic
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acute
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what are some nontraditional risk factors for CAD
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CRP markers (inflammation), hyperhomocysteinemia, infection
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