Cv Exam 1

Front 1

the vagal response is part of the SNS or PNS?

Back 1

PNS; it's an inhibitor response

Front 2

chemoreceptors respond to what kind of chemical condition in the body?

Back 2

reduced arterial oxygen concentration, elevation of CO2 and reduced pH

Front 3

how does SNS response affect bodily function?

Back 3

increases CO, BP, blood flow, blood glucose; decreases digestion

Front 4

when HR increases, does the diastole time increase, decrease or stay the same?

Back 4

it decreases diastolic time

Front 5

when HR increases, does the systolic time increase, decrease or stay the same?

Back 5

stays the same regardless of HR

Front 6

what is the normal ejection fraction at rest

Back 6

60-70%

Front 7

what is the heart's reserve at rest

Back 7

30-40%

Front 8

where is the major site of resistance in the body

Back 8

arterioles

Front 9

what parameter determines a pt is in shock condition

Back 9

sustained systolic pressure of <80mmHg

Front 10

what common symptoms will you see in the following area if cardiac dysfunction is present: circulation, breathing, urination, mentation?

Back 10

circulation = CP, weight change, swelling, dizziness, fatigue, palpitations, cool hand/feet; breathing = SOB, cough; urination = amt, frequency; mentation = alteration in mental status

Front 11

if a pt coughs up pink sputum, what might this indicate?

Back 11

he/she has pulmonary edema

Front 12

liver engorgement is a result of what kind of HF

Back 12

RHF

Front 13

how do you assess arterial flow

Back 13

palpate rate, rhythm, amplitude, symmetry of peripheral pulses

Front 14

how do you assess venous flow

Back 14

assess type/degree of edema, varicosities, skin color changes

Front 15

swan ganz catheter measures which 5 lumens?

Back 15

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

Front 16

right heart cardiac catheterization checks patency in which valves?

Back 16

tricuspid and pulmonic

Front 17

left heart cardiac catheterization checks patency in which valves

Back 17

mitral and aortic

Front 18

the use of left heart catheterization usually invades which artery? (how is this procedure approached)

Back 18

via femoral artery into aorta

Front 19

how is coronary angiography done

Back 19

dye injected into right/left coronary arteries, flow of dye is filmed

Front 20

how do you prepare for cardiac catheterization

Back 20

written consent, VS for pulses, anxiety/pain, allergies, 6-8hrs prior NPO, verify with dr. of pre-op medications

Front 21

post catheterization care

Back 21

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

Front 22

complications to catheterization

Back 22

bleeding, hematoma, dysrhythmias, MI, allergic rxn, infection, hypovolemia, arterial/pulmonary embolization,

Front 23

stimulation of SNS causes vasoconstriction or vasodilation

Back 23

vasoconstriction

Front 24

beta 2 (in the lungs) activated by SNS causes vasoconstriction or vasodilation

Back 24

vasodilation

Front 25

what is the parameter for stage I hypertension

Back 25

140-159/90-99

Front 26

how does stress contribute to the development of HTN

Back 26

stress causes prolonged SNS activity, which increase vasoconstriction, increased HR and increased renin release

Front 27

how does the renin assay test help determine underlying cause of HTN; what is the treatment

Back 27

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)

Front 28

why might a pt have resistant HTN

Back 28

NSAID, COX2 inhibitors, cocaine, decongestants, oral contraceptives, steroids, tobacco, ephedra

Front 29

how do you evaluate a pt for HTN? (what info do you look for in order to say a pt is hypertensive)

Back 29

accurate BP, assess lifestyle, CV risk factors, concomitant disorders, identifiable causes of HTN, target organ damage

Front 30

what parameters of BMI is considered obesity

Back 30

>30 kg/m2

Front 31

how does diabetes contribute to development of HTN?

Back 31

high insulin conc in blood simulates SNS activity and impairs nitric oxide-mediated vasodilation; vascular hypertrophy and renal sodium reabsorption

Front 32

why is monitoring potassium lvls important for a hypertensive pt?

Back 32

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+

Front 33

what are the two main goals of using drugs to treat HTN

Back 33

decrease BV & SVR

Front 34

what are the 6 general drug types used to treat HTN

Back 34

1. diuretics 2. adrenergic inhibitor 3. direct vasodilators 4. ganglionic blockers 5.angiotensin inhibitors 6. CCB

Front 35

what should you monitor for in a pt when giving diuretics?

Back 35

orthostatic hypotension

Front 36

what are some common adverse effect of using adrenergic inhibitors

Back 36

sedation, dry mouth, impotence, rebound HTN (with sudden withdrawal)

Front 37

the use of alpha 1 adrenergic blocker can result in what common a/e

Back 37

postural hypotension

Front 38

what condition is indicated for the use of direct vasodilators

Back 38

hypertensive crises

Front 39

the use of direct vasodilators can result in what kind of a/e

Back 39

acute hypotension, tachycardia

Front 40

what should you monitor for when giving angiotensin inhibitor

Back 40

monitor hyperkalemia and decrease renal function/failure

Front 41

what are some precaution when giving CCB and why

Back 41

use with caution in pt with heart failure; it lowers HR, contractility and SVR

Front 42

what type of diuretics are usually recommended first-time therapy

Back 42

thiazide diuretic

Front 43

what type of drugs are not recommended for HF

Back 43

CCB

Front 44

CCB are used to treat what type of conditions

Back 44

high coronary disease risk, diabetes

Front 45

what drugs are used to treat CKD

Back 45

ACEi and ARB

Front 46

ARBs may be used for what types of conditions

Back 46

HF, DM, CKD

Front 47

what drug is considered universal in CVD

Back 47

ACEi

Front 48

what type of drug is used for stroke prevention

Back 48

diuretic and ACEi

Front 49

what two conditions are not treated with b-blocker

Back 49

CKD and stroke prevention

Front 50

metabolic syndrome is characterized by what types of conditions

Back 50

high BP, central obesity, insulin resistant, dyslipidemia

Front 51

what is the hallmark of metabolic syndrome

Back 51

vascular endothelium damage

Front 52

under what conditions does metabolic syndrome occur

Back 52

when the pt becomes insulin resistant and has changes associated with increased lvls of angiotensin II, aldosterone, norepinephrine, and epinephrine

Front 53

what is the pressure-natriuresis relationship

Back 53

individuals with HTN tends to have higher blood volume because.. increase vascular volume is related to decreased renal excretion of salt (salt is retained)

Front 54

how does cytokines affect vasculature

Back 54

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

Front 55

how does insulin resistance contribute to HTN

Back 55

insulin resistance overactivates the SNS and RAA; it is r/t decrease release of nitric oxide and endothelial vasodilators

Front 56

during diastole, which two valves open

Back 56

atrioventricular: tricuspid and mitral

Front 57

what stimulates the angiogenesis of the collateral arteries

Back 57

hypoxia and endothelial growth factors

Front 58

what is the pathway of the bachmann bundle conduction?

Back 58

from the SA node to left atrium

Front 59

how does increased SNS affect coronary vessels

Back 59

it dilates

Front 60

how does increases PNS affect coronary vessels

Back 60

with the release of acetylcholine, it dilates coronary vessels

Front 61

how does cardiac muscle differ from skeletal muscle?

Back 61

cardiac = single nuclei, arranged in branching networks. many mitochondria for ATP needs, more T tubules; skeletal = multi-nucleus, arranged in parallel units

Front 62

what is the difference between T type and L type ca+ channels?

Back 62

L type is long lasting. they predominate and are blocked by CCB. t type is transient, less abundant and not blocked by CCB

Front 63

what is a good index of afterload

Back 63

aortic systemic pressure

Front 64

what 3 factors determine force of contraction

Back 64

stretching by preload, activation of SNS, and O2 supply

Front 65

what are the most important positive inotropic agents

Back 65

norepinephrine and epinephrine

Front 66

how does the body respond to decrease in O2 or pH, or increase in CO2

Back 66

increases BP

Front 67

what are some factors that control renin release

Back 67

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)

Front 68

does angiotensin II increase or reduce renin release

Back 68

reduce renin release

Front 69

what simulates the secretion of aldosterone

Back 69

angio II

Front 70

how does angio II contribute to HTN

Back 70

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

Front 71

under what condition is the right atrium stimulated to release ANP?

Back 71

when it sense an increase in BP

Front 72

what kind of activity does adrenomedullin produce

Back 72

secreted by endothelial and smooth muscle cells; vasodilation, limiting endothelial injury, reducing oxidative stress and promoting angiogenesis, mediates na+ excretion

Front 73

how does insulin resistance contribute to development of HTN

Back 73

reduces NO and increases vasoconstrictors; promotes inflammation; increase clot formation; contributes to endothelial damage; contributes to lipid changes

Front 74

what two mechanisms increase venous pressure and return to the heart

Back 74

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

Front 75

what is the role of adenosine

Back 75

a vasodilator, it is released in response to a decrease in myocardial oxygenation

Front 76

how, or through what mechanism does inherited defects cause HTN

Back 76

renal na+ excretion, RAA, SNS, insulin resistance, cell membrane na/ca transport

Front 77

what is the pressure natriuresis relationship

Back 77

ppl with HTN tend to retain more salt

Front 78

isolated systolic HTN tends to occur in what type of population

Back 78

elderly, over 65

Front 79

what does an increase in pulse pressure indicates

Back 79

reduced vascular compliance of large arteries

Front 80

what are some complications of HTN

Back 80

MI, LVHypertrophy, angina, LHF, CAD, sudden death

Front 81

how does HTN contribute to HF

Back 81

catecholamines from SNS and angio II causes vascular remodeling, deposition in cardiac muscle.. hypertrophy then leads to increase O2 demand and impaired contractility

Front 82

what are early s/s of HTN

Back 82

there is none! only high BP

Front 83

what are later s/s of HTN

Back 83

depends on which organ HTN damages; HA (due to constriction of cerebral vessels) may be the only symptom

Front 84

elderly are more prone to which type of orthostatic hypotension: acute or chronic

Back 84

acute

Front 85

what are some nontraditional risk factors for CAD

Back 85

CRP markers (inflammation), hyperhomocysteinemia, infection