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312 Patho > EXAM 4 > Flashcards

EXAM 4 Flashcards

WEEKS 8-9 CARDIAC AND CARDIOVASCULAR DISORDERS

1
Q

PRIMARY FUNCTION OF THE CIRCULATORY SYSTEM IS?

A

TO TRANSPORT OXYGEN AND NUTRIENTS TO THE TISSUES

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2
Q

WHAT IS THE CIRCULATORY SYSTEMS PARTICIPATION IN WASTE?

A

CARRIES WASTE FROM THE TISSUES TO THE KIDNEYS FOR ELIMINATIONS

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3
Q

HOW DOES THE CIRCULATORY SYSTEM CONTRIBUTE TO THE REGULATION OF BODY TEMP

A

THROUGH EITHER VASOCONSTRICTION OR VASODILATION TO TRANSPORT HEAT TO PERIPHERAL TISSUES WHERE IT CAN DISSIPATE INTO THE ATMOSPHERE

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4
Q

WHAT IS THE SIZE OF THE HEART

A

ABOUT THE SIZE OF YOUR FIST

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5
Q

HOW MUCH BLOOD DOES THE HEART TRANSPORT THROUGH THE BODY EVERY DAY

A

ABOUT 1800 GALLONS

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6
Q

WHERE IS THE HEART LOCATED

A

WITHIN OUR MEDIASTINUM

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7
Q

WHERE IS THE MEDIASTINUM LOCATED

A

THORACIC CAVITY

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8
Q

WHAT IS THE PERICARDIUM

A

THE LITTLE SAC THAT ENCLOSES THE HEART

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9
Q

2 LAYERS OF THE PERICARDIUM

A

VISCERAL- CLOSER TO THE HEART
PARIETAL- OUTSIDE LAYER

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10
Q

PERICARDIAL CAVITY

A

IN BETWEEN THE PERICARDIUM LAYERS
HOLDS PERICARDIAL FLUID

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11
Q

PERICARDIAL FLUID

A

SEROUS FLUID
30-50 ML

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12
Q

FUNCTION OF PERICARDIAL FLUID

A

MINIMIZE FRICTION AS THE HEART CONTRACTS AND RELAXES

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13
Q

PERICARDIAL EFFUSION

A

TOO MUCH FLUID OR FLUID BUILDUP IN THE PERICARDIAL SPACE

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14
Q

THE WALL (AKA MUSCLE) OF THE HEART CONSISTS OF HOW MANY LAYERS

A

3

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15
Q

ENDOCARDIUM

A

INNER LAYER OF THE HEART WALL INSIDE OF THE CHAMBERS OF THE HEART

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16
Q

3 LAYERS OF THE HEART WALL

A

ENDOCARDIUM
MYOCARDIUM
EPICARDIUM

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17
Q

MYOCARDIUM

A

MIDDLE LAYER OF THE HEART WALL
THICKEST/LARGEST LAYER
ACTUAL MUSCULAR LAYER OF THE HEART

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18
Q

EPICARDIUM

A

OUTER LAYER OF THE HEART

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19
Q

HOW MANY CHAMBERS IN THE HEART

A

4

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20
Q

WHAT ARE THE TOP CHAMBERS OF THE HEART

A

ATRIA (SINGULAR IS ATRIUM)

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21
Q

WHAT ARE THE LOWER CHAMBERS OF THE HEART CALLED

A

VENTRICLES

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22
Q

CARDIAC MUSCLE FUNCTION IS VOLUNTARY OR INVOLUNTARY

A

INVOLUNTARY

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23
Q

WHAT DOES THE CARDIAC MUSCLE RELY ON FOR CONTRACTION AND WHY

A

RELIANT ON EXTRACELLULAR CALCIUM FOR CONTRACTION. CARDIAC CELLS DON’T HAVE THE CAPACITY TO STORE CALCIUM WELL

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24
Q

HOW WOULD YOU DESCRIBE THE SKELETON OF THE HEART

A

LIKE A CONNECTIVE TISSUE SKELETON

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25
Q

SEPTUM

A

DIVIDES THE RIGHT AND LEFT SIDES OF THE HEART FROM ATRIA TO VENTRICLES

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26
Q

WHAT DOES THE CONNECTIVE SKELETON OF THE HEART PROVIDE

A

SUPPORT FOR THE VALVES TO HAVE SOMEWHERE TO ATTACH TO

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27
Q

HOW MANY VALVES ARE IN THE HEART AND WHY ARE THEY IMPORTANT

A

4 MAIN VALVES
HELP TO PROMOTE PROPER BLOOD FLOW DIRECTION

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28
Q

4 VALVES OF THE HEART

A

ATRIOVENTRICULAR OR AV VALVES (2)
(MITRAL VALVE AKA BICUSPID VALVE
TRICUSPID VALVE)
AND THE SEMILUNAR VALVES- AORTIC AND PULMONIC

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29
Q

WHAT DOES BI AND TRI DESCRIBE IN THE BICUSPID AND TRICUSPID VALVES

A

THE NUMBER OF CUSPS OR LEAVES THEY HAVE WHEN YOU LOOK DOWN AT THEM DIRECTLY

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30
Q

WHAT SUPPORTS THE VALVES IN THE HEART

A

PAPILLARY MUSCLES

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31
Q

CORDAE TENDONAE (SP?)

A

LONG FIBERS THAT HELP SECURE AND HOLD VALVES IN PLACE

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32
Q

ATRIOVENTRICULAR OR AV VALVES PREVENT BACKFLOW OF BLOOD WHEN

A

DURING THE SYSTOLE OR CONTRACTION OF THE HEART

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33
Q

SEMILUNAR VALVES

A

AORTIC AND PULMONIC VALVES THAT PREVENT BACKFLOW OF BLOOD FROM THE AORTA AND PULMONARY ARTERIES INTO THE VENTRICLES DURING THE DIASTOLE OR RELAXATION OF THE HEART

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34
Q

HOW MANY CUSPS DO THE AORTIC AND PULMONIC VALVES HAVE

A

3

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35
Q

DO WE HAVE VALVES IN OUR ATRIA WHERE BLOOD ENTERS THE HEART

A

NO

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36
Q

BECAUSE THE ATRIA HAVE NO VALVES, WHAT HAPPENS TO THE BLOOD IF THESE TOP CHAMBERS BECOME DISTENDED OR OVERFILLED WITH FLUID

A

IT GETS PUSHED BACK INTO THE VEINS
SPECIFICALLY PUSHED BACK INTO THE SUPERIOR VENA CAVA, INFERIOR VENA CAVA, AND POSSIBLY INTO THE JUGULAR VEINS

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37
Q

WHAT WILL WE SEE WHEN BLOOD BACKS UP FROM THE ATRIA

A

JUGULAR VEIN DISTENSION
PERIPHERAL EDEMA

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38
Q

SYSTOLE

A

PERIOD IN WHICH VENTRICLES CONTRACT

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39
Q

DIASTOLE

A

PERIOD IN WHICH VENTRICLES RELAX AND FILL

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40
Q

PHASES OF THE CARDIAC CYCLE

A
  1. ATRIOLE SYSTOLE BEGINS
  2. VENTRICULAR SYSTOLE- 1ST PHASE
  3. VENTRICULAR SYSTOLE- 2ND PHASE
  4. VENTRICULAR DIASTOLE- EARLY
  5. VENTRICULAR DIASTOLE- LATE
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41
Q

ATRIOLE SYSTOLE BEGINS

A

ATRIAL CONTRACTION FORCES BLOOD INTO VENTRICLES

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42
Q

VENTRICULAR SYSTOLE
FIRST PHASE

A

VENTRICULAR CONTRACTION PUSHES AV VALVES CLOSED

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43
Q

VENTRICULAR SYSTOLE
SECOND PHASE

A

SEMILUNAR VALVES OPEN AND BLOOD IS EJECTED

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44
Q

VENTRICULAR DIASTOLE
EARLY

A

SEMILUNAR VALVES CLOSE AND BLOOD FLOWS INTO ATRIA

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45
Q

VENTRICULAR DIASTOLE
LATE

A

CHAMBERS RELAX AND BLOOD FILLS VENTRICLES PASSIVELY

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46
Q

WHAT DOES THE CARDIAC CYCLE TELL US WHEN LOOKING AT THE SYSTOLIC AND DIASTOLIC VALUES OF BP?

A

DIRECT CORRELATION

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47
Q

ELEVATED SYSTOLIC BP INDICATES?

A

VENTRICLES CAN’T CONTRACT WELL BECAUSE THEY ARE HAVING TO PUSH OUT AGAINST SO MUCH PRESSURE TO PUSH THE BLOOD OUT

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48
Q

WHAT DOES THE ELECTRICLE CURRENT OF THE HEART ON THE EKG LINE CORRELATE TO

A

THE MUSCULAR CONTRACTION. THE ELECTRICAL ACTIVITY OF THE HEART GUIDES THE MUSCULAR FUNCTION OF THE HEART

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48
Q

ELEVATED DIASTOLIC PRESSURE INDICATES?

A

VENTRICLES AREN’T FULLY RELAXING SO THEY AREN’T ADEQUATELY FILLING WITH BLOOD

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48
Q

HOW DO WE VIEW AND MONITOR THE EKG ON A CONTINUOUS BASIS

A

VIA TELEMETRY OR A HARDWIRED CARDIAC MONITOR

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49
Q

WHAT DOES AN EKG SNAPSHOT WITH A 12 LEAD SHOW

A

ALLOWS YOU TO SEE IN ALL DIFFERENT AREAS OF THE HEART WHAT THE ELECTRICAL ACTIVITY IS DOING

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50
Q

WHERE DOES THE S1 HEART SOUND COME FROM

A

CLOSURE OF THE AV VALVE- SO OUR MITRAL AND TRICUSPID VALVES AT THE ONSET OF SYSTOLE

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51
Q

WHERE DOES THE S2 SOUND COME FROM

A

CLOSURE OF THE AORTIC AND PULMONIC VALVES AND MARKS THE ONSET OF DIASTOLE

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52
Q

IS THE HEART EVER EMPTY?

A

NO

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53
Q

AS ONE CHAMBER EMPTIES AND PUSHES BLOOD OUT, WHAT HAPPENS

A

MORE BLOOD IS BEING PUSHED BACK INTO IT ON THE NEXT SQUEEZE FROM A DIFFERENT CHAMBER

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54
Q

SVC

A

SUPERIOR VENA CAVA

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55
Q

IVC

A

INFERIOR VENA CAVA

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56
Q

HOW IS VENOUS BLOOD RETURNED TO THE HEART

A

FROM OUR SVC AND IVC THAT DUMPS INTO THE RIGHT ATRIUM

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57
Q

FROM THE RIGHT ATRIUM, WHERE DOES THE BLOOD GO

A

THROUGH THE TRICUSPID VALVE TO THE RIGHT VENTRICLE

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58
Q

WHERE DOES BLOOD GO WHEN IT LEAVES THE RIGHT VENTRICLE?

A

THROUGH THE PULMONARY VALVE –> THROUGH THE PULMONARY ARTERY

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59
Q

WHAT DOES THE PULMONARY ARTERY CARRY

A

DEOXYGENATED BLOOD

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60
Q

WHERE DOES THE PULMONARY ARTERY TAKE THE BLOOD

A

TO THE LUNGS

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61
Q

WHAT HAPPENS WHEN THE BLOOD REACHES THE LUNGS

A

ON A MICROSCOPIC LEVEL, THERE IS THE GAS EXCHANGE IN THE CAPILLARY NETWORK AROUND THE AVEOLI

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62
Q

WHAT HAPPENS WHEN BLOOD BECOMES OXYGENATED IN THE LUNGS THROUGH GAS EXCHANGE

A

IT COMES BACK THROUGH THE PULMONARY VEINS TO THE LEFT ATRIUM

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63
Q

WHAT DOES THE PULMONARY VEIN CARRY

A

OXYGENATED BLOOD

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64
Q

WHERE DOES BLOOD GO WHEN LEAVING THE LEFT ATRIUM

A

THROUGH THE MITRAL VALVE INTO THE LEFT VENTRICLE

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65
Q

WHERE DOES BLOOD GO WHEN IT LEAVES THE LEFT VENTRICLES

A

PASSES THROUGH THE AORTIC VALVE OUT TO THE AORTA

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66
Q

WHERE DOES BLOOD GO WHEN LEAVING THE AORTA

A

IT BRANCHES OFF INTO THE REST OF THE CIRCULATORY SYSTEM TO PERFUSE ALL TISSUES AND ORGANS OF THE BODY

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67
Q

WHAT DOES IT MEAN THAT THE HEART IS SELF SUFFUSING

A

IT ALSO HAS TO SUPPLY ITSELF WITH BLOOD

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68
Q

HOW DOES OUR CORONARY CIRCULATION WORK

A

DEOXYGENATED BLOOD FROM THE HEART COLLECTS W/IN THE CORONARY SINUS AND IS DUMPED INTO OUR SVC TO FOLLOW THE NORMAL PATHWAY

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69
Q

WHERE IS THE CORONARY SINUS LOCATED

A

THE POSTERIOR SIDE OF THE HEART

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70
Q

WHERE DO THE CORONARY ARTERIES BRANCH

A

OFF THE AORTA

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71
Q

HOW DOES THE HEART GET ITS BLOOD SUPPLY

A

BLOOD IS PUSHED THROUGH THE LEFT VENTRICLE, THROUGH THE AORTA TO SUPPLY ALL THE TISSUES, IT ALSO FEEDS ITSELF AND SUPPLIES THE CORONARY ARTERIES

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72
Q

LEFT MAIN CORONARY ARTERY WILL BRANCH OUT INTO WHAT

A

BRANCH OUT INTO THE LEFT ANTERIOR DESCENDING (LAD) AND THEN YOUR CIRCUMFLEX

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73
Q

CIRCUMFLEX

A

CURVES AROUND THE POSTERIOR SIDE OF THE HEART

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74
Q

LEFT CORONARY ARTERY PERFUSES WHAT

A

A HUGE CHUNK OF THE HEART

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75
Q

IF SOMEBODY HAS A CORONARY BLOCKAGE OR A MYOCARDIAL INFARCTION TO THE LEFT CORONARY ARTERY, WHAT HAS HAPPENED

A

CALLED A WIDOWMAKER
THERE IS A BLOCKAGE IN THE LARGE AREA SO IT ISN’T GETTING PERFUSED AND IS FATAL FOR MANY

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76
Q

RIGHT CORONARY ARTERY AKA RCA BRANCHES INTO WHAT

A

POSTERIOR DESCENDING ARTERY

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77
Q

WHAT IS A COMPENSATORY MECHANISM OF THE HEART IF IT REQUIRING MORE PERFUSION AND OXYGEN

A

THERE IS DEVELOPMENT OF COLLATERAL CIRCULATION SO OUR BODY AND OUR HEART WILL GROW ADDITIONAL VEINS AND CIRCULATION TO COMPENSATE

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78
Q

WHAT HAPPENS IF A PATIENT HAS A SLOW CHRONIC TYPE OCCLUSIONS

A

COLLATERAL CIRCULATION OVER TIME

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79
Q

CARDIAC OUTPUT

A

AMOUNT OF BLOOD PUMPED BY THE HEAERT EACH MINUTE

THE EFFICIENCY OF THE HEART

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80
Q

EQUATION OF CARDIAC OUTPUT

A

CO = SV X HR

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81
Q

SV AKA STROKE VOLUME

A

AMOUNT OF BLOOD PUMPED BY THE LEFT VENTRICLE WITH EACH CONTRACTION

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82
Q

NORMAL SV

A

60-70 ML

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83
Q

NORMAL CO

A

4-6 L/MIN

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84
Q

FACTORS THAT INFLUENCE CO

A

PRELOAD
AFTERLOAD
CONTRACTILITY
HEART RATE

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85
Q

PRELOAD

A

AMOUNT OF TENSION/STRETCH APPLIED TO HEART MUSCLE BEFORE CONTRACTION

SPECIFICALLY THE MEASURE OF FORCE ON THE ATRIA THAT ARE BEING FILLED

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86
Q

AFTERLOAD

A

AMOUNT OF FORCE/WORK THE HEART MUSCLE HAS TO APPLY TO MOVE BLOOD INTO THE AORTA

ALSO CALLED SYSTEMIC VASCULAR RESISTANCE BECAUSE PRIMARILY INFLUENCED BY BP

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87
Q

CONTRACTILITY

A

FORCE AT WHICH THE HEART CONTRACTS (HOW STRONG IS THE SQUEEZE)

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88
Q

HEART RATE

A

HOW MANY TIMES THE HEART CONTRACTS OR BEATS PER MINUTE

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89
Q

NORMAL EJECTION FRACTION (EF)

A

55-75%

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90
Q

WHAT DO WE SEE WITH DECREASED CARDIAC OUTPUT

A

S/S OF HYPOPERFUSION THAT CAN LEAD TO ORGAN DECLINE

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91
Q

WHY DO WE THINK OF VENOUS RETURN VOLUME WHEN WE TALK ABOUT PRELOAD

A

IF PATIENT IS IN FLUID OVERLOAD, THEN WE HAVE INCREASED PRELOAD BECAUSE THE ATRIA IS FILLING WITH MUCH MORE BLOOD AND THE HEART IS HAVING TO STRETCH MORE

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92
Q
A
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93
Q

HOW IS EJECTION FRACTION CALCULATED

A

SV DIVIDED BY END DISTOLIC VOLUME TO GET PERCENTAGE OF BLOOD EJECTED DURING SYSTOLE DURING THE CONTRACTION OF THE HEART

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94
Q

WHAT IS EF TELLING US

A

WHAT PERCENTAGE OF BLOOD IN THE LEFT VENTRICLE IS EJECTED AND PUSHED OUT INTO THE AORTA WITH EACH BEAT

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95
Q

WHEN DO WE LOOK AT EF

A

WHEN Tx PATIENTS WITH HEART FAILURE BECAUSE IT INDICATES FUNCTION OF THE HEART

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96
Q

WHAT MAKES THE HEART MUSCLE SPECIAL

A

IT CAN GENERATE AND RAPIDLY CONDUCT ITS OWN ELECTRICLE IMPULSES OR ACTION POTENTIALS TO EXCITE MUSCLE FIBERS AND GENERATE THE MUSCLE CONTRACTIONS

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97
Q

WHAT DOES CAPTURING ELECTRICAL ACTIVITY OF THE HEART IN WAVE FORM HELP DIAGNOSE

A

MYOCARDIAL INFARCTIONS
DYSRHYTHMIAS
OTHER CARDIAC PROBLEMS

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98
Q

SA NODE
SINO ATRIAL NODE

A

PACEMAKER OF THE HEART
PRIMARY FUNCTION: ENSURE ELECTRICAL ACTIVITY IN THE HEART IS GENERATED TO MAINTAIN 60-100 BPM

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99
Q

WHERE DOES ELECTRICAL ACTIVITY TRAVEL AFTER LEAVING THE SA NODE

A
  1. AV NODE (ATRIOVENTRICULAR NODE)
  2. DOWN TO THE FIBERS IN THE LEFT VENTRICLES
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100
Q

IF THERE ARE CONDUCTION ISSUES IN THE HEART, WHAT MIGHT WE SEE

A

FAILURE OF THE SA NODE DUE TO MYOCARDIAL INFARCTION OR OTHER REASONS

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101
Q

WHAT HAPPENS IF THERE IS A SA NODE DYSFUNCTION

A

WE HAVE A BACKUP PACEMAKER CALLED THE AV NODE BUT IT DOESN’T SEND IMPULSES AS RAPIDLY AS THE SA NODE

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102
Q

WHAT IS THE RATE FOR THE AV NODE

A

40-60 BPM
SO HEART DOESN’T BEAT AS FAST AS IT SHOULD

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103
Q

PERKINJE FIBERS

A

BACK UP TO THE BACKUP PACEMAKER
CAN GENERATE THEIR OWN ELECTRICAL IMPULSES AT 15-40 BPM (SEVERE BRADYCARDIA)

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104
Q

MINOR ISSUES OF CARDIAC CONDUCTION

A

PREMATURE BEATS
LATE BEATS
LITTLE PALPITATIONS
RAPID RHYTHMS

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105
Q

TACHYDYSRHYTHMIAS

A

FAST HEART RHYTHM

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106
Q

BRADYDISRHYTHMIAS

A

SLOW HEART RHYTHM

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107
Q

DISORGANIZED ELECTRICAL ACTIVITY

A

TOP CHAMBERS ARE NOT BEATING EFFECTIVELY WITH THE BOTTOM CHAMBERS SO THEY ARE NOT IN TIME

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108
Q

TO HAVE ADEQUATE BLOOD FLOW, WE HAVE TO HAVE A GOOD SYSTEM OF WHAT

A

PATENT BLOOD VESSELS AND ADEQUATE PERFUSION PRESSURE

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109
Q

HOW MANY LAYERS ARE IN THE WALLS OF BLOOD VESSELS (WITH EXCEPTION OF THE CAPILLARIES)

A

3

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110
Q

3 LAYERS OF BLOOD VESSELS

A

TUNICA EXTERNA-OUTER
TUNICA MEDIA-MIDDLE
TUNICA INTIMA-INNER

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111
Q

HOW ARE CAPILLARY LAYERS DIFFERENT THAT BLOOD VESSELS

A

HAVE VERY THIN LAYERS OF ENDOTHELIAL CELLS BECAUSE THIS ALLOWS FLUID/GASES/NUTRIENTS TO PASS

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112
Q

WHAT ARE BLOOD VESSELS COMPOSED OF

A

ENDOTHELIAL CELLS THAT ALLOW FOR THEM TO HAVE A SEMI PERMEABLE MEMBRANE

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113
Q

WHAT IS THE TUNICA MEDIA COMPOSED OF

A

SOME VASCULAR SMOOTH MUSCLE CELLS WHICH GIVES THE ABILITY TO CONSTRICT OR DILATE IN RESPONSE TO OUR SYMPATHETRIC NERVOUS SYSTEM ACTIVATION AND OTHER HOMEOSTATIC MECHANISMS

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114
Q

WHAT ARE MOST DIFFERENCES OF ARTERIAL AND VENOUS CIRCULATION DUE TO

A

STRUCTURE OF THE VESSELS
WHAT THEY ARE CARRYING
AMOUNT OF PRESSURE

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115
Q

CHARACTERISTICS OF ARTERIAL CIRCULATION

A
  1. THICKER VESSELS
  2. ELASTIC
  3. OXYGENATED BLOOD
  4. HIGH PRESSURE SYSTEM
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116
Q

CHARACTERISTICS OF VENOUS CIRCULATION

A
  1. THIN WALLED VESSELS
  2. DISTENSIBLE
  3. COLLAPSIBLE
  4. DEOXYGENATED BLOOD
  5. LOW PRESSURE SYSTEM
  6. VALVES
  7. MUST OPPOSE GRAVITY
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117
Q

DO YOU BLEED OUT FASTER IF A CUT IS ARTERIAL OR VENOUS

A

ARTERIAL BECAUSE OF HIGH PRESSURE

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118
Q

PULSATILE

A

VERY HIGH PRESSURE

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119
Q

IS VENOUS BLOOD COMPLETELY DEOXYGENATED

A

NO

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120
Q

DO VEINS HAVE A PULSE

A

NO

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121
Q

FACTORS AFFECTING BLOOD FLOW

A
  1. ADEQUATE BLOOD VOLUME
  2. PRESSURE/RESISTANCE IN VASCULATURE
  3. RADIUS OF BLOOD VESSEL
  4. VELOCITY OF FLOW
  5. LAMINAR/TURBULENT FLOW
  6. DISTENTION AND COMPLIANCE
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122
Q

ATHEROSCLEROSIS AND BLOOD FLOW

A

IT IS HARDENING OF THE ARTERIES SO MORE PRESSURE AND RESISTANCE RESULTING IN LOW BLOOD FLOW

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123
Q

ATHEROSCLEROTIC PLAGUES AND BLOOD FLOW

A

IS A BUILDUP OF FATTY PLAQUES WITHIN THE BLOOD VESSEL (OR COULD EVEN HAVE VASOCONSTRICTION) CAUSING VESSEL SHRINKING AND LESS FLOW

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124
Q

VELOCITY OF BLOOD FLOW

A

DEPENDS ON HR AND FORCES THAT ARE ACTING ON THE VESSEL. LOW VELOCITY = LOW FLOW

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125
Q

LAMINAR FLOW

A

NORMAL FLOW: THIN LAYER OF PLASMA ADHERES TO VESSEL WALL AND LAYERS OF BLOOD CELLS AND PLATELETS SHEAR AGAINST IT. EACH LAYER TOWARDS THE MIDDLE MOVES FASTER THAN PREVIOUS LAYER.

IF WE DON’T HAVE BLOOD FLOWING IN THE CORRECT DIRECTION, IT DECREASES SPEED AND FLOW

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126
Q

HOW MUCH MORE DISTENDABLE ARE VEINS THAN ARTERIES

A

ABOUT 24 TIMES

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127
Q

MECHANISMS THAT REGULATE BP

A

SYMPATHETIC NS
RAAS
INFLAMMATORY RESPONSE
CLOTTING

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128
Q

SYMPATHETIC NS

A

EPINEPHRINE AND NOREPINEPHRINE (NEUROTRANSMITTERS) REGULATE BY SEVERAL MECHANISMS

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129
Q

HOW DO EPINEPHRINE AND NOREPINEPHRINE REGULATE BP

A
  1. CONTROL RELEASE OF RENIN FROM KIDNEYS TO ACTIVATE RAAS TO INCREASE BP
  2. CAUSE VASOCONSTRICTION THAT INCREASES BP
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130
Q

RAAS AKA RENIN ANGIOTENSIN ALDOSTERONE SYSTEM

A

ANGIOTENSIN II (MOST POWERFUL VASOCONSTRICTOR IN BODY) THAT INCREASES BP
ANGIOTENSIN II ALSO STIMULATE ADRENAL GLANDS (LOCATED ON TOP OF KIDNEY) TO RELEASE ALDOSTERONE

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131
Q

ALDOSTERONE

A
  1. CAUSES KIDNEYS TO REABSORB SODIUM
  2. REABSORBTION OF SODIUM MEANS REABSORBTION OF WATER WHICH CAUSES EXCRETION OF POTASSIUM
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132
Q

INFLAMMATORY RESPONSE AND REGULATION OF BP

A

HISTAMINE, BRADYKININ, PROSTAGLANDINS ALL CAUSE VASODILATION TO DECREASE BP

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133
Q

CLOTTING AND BP REGULATION

A

SEROTONIN THAT IS TRANSPORTED BY PLATELETS AND AIDS IN CLOTTING AND CAUSES VASOCONSTRICTION AS WELL AS AIDING PLATELET AGGREGATION WHICH INCREASES BP

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134
Q

VASOPRESSIN AND BP REGULATION

A

AKA ADH
STIMULATES BODY TO HOLD ONTO OUR VOLUME VS RELEASING FLUID. MORE VOLUME = HIGHER BP

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135
Q

ADEQUATE PERFUSION REQUIRES 4 KEY ELEMENTS

A
  1. PUMPING ABILITY OF THE HEART
  2. INTACT VASCULAR SYSTEM TO TRANSPORT BLOOD
  3. SUFFICIENT BLOOD TO FILL THE VASCULAR SYSTEM
  4. TISSUES THAT CAN EXTRACT O2 AND NUTRIENTS
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136
Q

WHAT HAPPENS WHEN THERE IS DYSFUNCTION IN THE CIRCULATORY SYSTEM

A
  1. INTERRUPTION OF CORONARY CIRCULATION
  2. BP CHANGES
  3. ELECTRICAL CONDUCTION PROBLEMS
  4. VALVE PROBLEMS
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137
Q

S/S OF INTERRUPTION OF CORONARY CIRCULATION

A

MYOCARDIAL INFARCTION
CHEST PAIN/ANGINA

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138
Q

THE ____ IS THE MAIN ORGAN OF THE CARDIOVASCULAR SYSTEM

A

HEART

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139
Q

WHAT IS THE MEDICAL TERM FOR HIGH BP

A

HYPERTENSION

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140
Q

WHICH IS RESPONSIBLE FOR REGULATING HEART RATE?
A. PURKINJE FIBERS
B. SA NODE
C. BUNDLE OF HIS
D. AV NODE

A

B

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141
Q

THE ________ ARE THE LOWER CHAMBERS OF THE HEART

A

VENTRICLES

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142
Q

THE _______ IS THE LARGEST ARTERY IN THE BODY

A

AORTA

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143
Q

THE CARDIOVASCULAR SYSTEM IS RESPONSIBLE FOR TRANSPORTING O2, NUTRIENTS, AND HORMONES THROUGHOUT THE BODY.

T/F

A

TRUE

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144
Q

WHAT IS THE AVERAGE RESTING HEART RATE FOR ADULTS

A

60-100 BPM

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145
Q

CARRIES OXYGENATED BLOOD FROM THE HEART TO THE REST OF THE BODY

A

AORTA

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146
Q

CARRIES DEOXYGENATED BLOOD FROM THE HEART TO THE LUNGS

A

PULMONARY ARTERY

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147
Q

MICROSCOPIC BLOOD VESSELS WHERE GAS EXCHANGE OCCURS

A

CAPILLARIES

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148
Q

CARRIES BLOOD BACK TO THE HEART

A

VEINS

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149
Q

WHICH CHAMBER OF THE HEART RECEIVES OXYGENATED BLOOD FROM THE LUNGS

A

LEFT ATRIUM

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150
Q

WHAT IS THE ROLE OF VALVES IN THE CARDIOVASCULAR SYSTEM

A

TO PREVENT BACKWARD FLOW OF BLOOD

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151
Q

SYSTOLIC PRESSURE

A

VENTRICULAR CONTRACTION

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152
Q

DIASTOLIC PRESSURE

A

VENTRICULAR RELAXATION

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153
Q

MEAN ARTERIAL PRESSURE

A

TISSUE PERFUSION

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154
Q

PULSE PRESSURE FORMULA

A

SYSTOLIC - DIASTOLIC

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155
Q

CARDIAC OUTPUT FORMULA

A

HR X SV

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156
Q

MAP FORMULA

A

DIASTOLIC + (PULSE PRESSURE/3)

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157
Q

BLOOD PRESSURE FORMULA

A

CO X TOTAL PERIPHERAL RESISTANCE

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158
Q

CARDIOVASCULAR CENTER

MECHANISMS FOR BP REGULATION

A

MEDULLA
PONS

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159
Q

NEURAL MECHANISMS

MECHANISMS FOR BP REGULATION

A
  1. ANS–> SYMPATHETIC, PARASYMPATHETIC
  2. BARORECEPTOR AND CHEMORECEPTOR REFLEXES
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160
Q

HUMORAL MECHANISMS

MECHANISMS FOR BP REGULATION

A

NATRIURETIC PEPTIDES
RAAS
SYMPATHETIC NS
ADH

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161
Q

PRIMARY/ESSENTIAL HYPERTENSION

A

90-95% OF CASES
NO CAUSE CAN BE IDENTIFIED

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162
Q

SECONDARY HYPERTENSION

A

ELEVATION IN BP DUE TO ANOTHER DISEASE LIKE RENAL DISEASE, DISORDERS OF ADRENAL HORMONES, PHEOCHROMOCYTOMA

5-10% OF CASES

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163
Q

HYPERTENSIVE CRISIS

A

SYSTOLIC > 180
AND/OR
DIASTOLIC >120

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164
Q

ORTHOSTATIC (POSTURAL) HYPOTENSION

A

DROP IN BP WHEN MOVING FROM A SEATED OR SUPINE POSITION

DROP IS 20MMHG SYSTOLIC OR 10 MMHG DIASTOLIC OR MORE

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165
Q

RISK FACTORS OF BP ISSUES

A

AGE, GENDER, RACE, FAMILY Hx, DIET, DYSLIPIDEMIAS, TOBACCO, ETOH, FITNESS, OBESITY, METABOLIC ABNORMALITIES, SLEEP APNEA

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166
Q

If I move too quickly from a reclining to standing position,what does my baroreceptor reflex do

A

Your baroreceptor reflex is a series of quick actions your body takes to keep your blood pressure in a normal range in response to an abrupt change in position

IF YOU MOVE FASTER THAN THIS HOMEOSTATIC MECHANISM CAN RESPOND, YOUR BP WILL DROP

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167
Q

If natriuretic peptide is released, what will happens to B/P?

A

THERE IS A FALL IN BP

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168
Q

What two actions occur in response to the release of angiotensin II?

A

VASOCONSTRICTION AND STIMULATION OF THE SYMPATHETIC NS TO RAISE BP

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169
Q

If cardiac output increases what happens to blood pressure?

A

BP RISES

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170
Q

If I infuse fluids or blood what happens to venous volume?
What determinant of cardiac output is affected?

A

THERE IS AN INCREASE IN VENOUS VOLUME. THIS AFFECTS PRELOAD, AND VENOUS RETURN, AS WELL AS HEART RATE AND STROKE VOLUME

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171
Q

What happens to blood pressure in response to massive vasodilation?

A

DECREASED BP BECAUSE VASODILATION CAUSES DECREASE IN SVR AND INCREASE IN BLOOD FLOW

172
Q

What effect does arterial vasoconstriction have on blood pressure?

A

IT REDUCES VOLUME IN THE BLOOD VESSEL, SO FLOW IS REDUCED CAUSING HIGHER RESISTANCE AND HIGHER BP

173
Q

NORMAL BP

A

LESS THAN 120/ LESS THAN 80

174
Q

ELEVATED BP

A

120-129/LESS THAN 80

175
Q

HYPERTENSION STAGE 1

A

130-139/80-89
ONLY NEED ONE

176
Q

HYPERTENSION STAGE 2

A

> 140/>90
ONLY NEED ONE

177
Q

HYPERTENSIVE CRISIS

A

> 180/>120
CAN BE ONE OR BOTH

178
Q

WHAT IS THE GOAL OF HYPERTENSION Tx

A

BP LESS THAN 130/80

179
Q

HYPERTENSION Tx

A

WEIGHT
SODIUM
DASH DIET
ETOH
EXERCISE
SMOKING CESSATION
MAINTAIN Ca AND K INTAKE
MEDICATIONS

180
Q

DASH DIET

A

DIETARY APPROACHES TO STOP HYPERTENSION
FLEXIBLE AND BALANCED EATING PLAN THAT HELPS CREATE A HEART HEALTHY EATING STYLE FOR LIFE

181
Q

ETOH

A

ETHYL ALCOHOL
ALCOHOL CONSUMPTION

182
Q

EFFECTS OF HYPERTENSION ON THE HEART

A

HYPERTROPHY
ANGINA
MI
HEART FAILURE

183
Q

EFFECTS OF HIGH BP ON THE BRAIN

A

STROKE
TIA

184
Q

OTHER EFFECTS OF HYPERTENSION

A

CHRONIC KIDNEY DISEASE
PERIPHERAL VASCULAR DISEASE
RETINOPATHY
SEXUAL DYSFUNCTION

185
Q

A patient complains of dizziness andlightheadedness upon getting up in the morningWhat problem does the nurse suspect?

A

ORTHOSTATIC HYPOTENSION

186
Q

Give three examples of target organ damage thatcan occur in association with uncontrolledhypertension?

A

CHRONIC KIDNEY DISEASE
BRAIN-STROKE, TIA
HEART- HEART FAILURE, MI, ANGINA

187
Q

A client has had repeated B/P ranging from 140-159/90-99. What is the B/P classification?

A

HYPERTENSION STAGE 2

188
Q

A client presents to the Emergency Room with a B/P of 210/110 and complaints of a headache. What problem is represented?

A

HYPERTENSIVE CRISIS

189
Q

What is the treatment for hypertension?

A

SMOKING CESSATION
WEIGHT LOSS
MEDS
DASH DIET
Na, Ca, AND K CONTROL
CONTROL ALCOHOL CONSUMPTION

190
Q

FUNCTIONS OF THE ENDOTHELIUM

PART 1

A

Selectively permeable barrier
Modulates blood flow and vascular reactivity
Regulates thrombosis
Regulates cell growth

191
Q

FUNCTIONS OF THE ENDOTHELIUM

PART 2

A

Regulates inflammatory/immune response
Maintains extracellular matrix
Involved in the metabolism of lipoproteins

192
Q

ENDOTHELIAL DYSFUNCTION

A

changes inthe normal function in response to smoking, dys/hyperlipidemia, diabetes and obesity

193
Q

What are lipids?

A

Cholesterol, triglycerides

any of a class of organic compounds that are fatty acids or their derivatives and are insoluble in water but soluble in organic solvents. They include many natural oils, waxes, and steroids.

194
Q

What are lipoproteins?

A

any of a group of soluble proteins that combine with and transport fat or other lipids in the blood plasma.

Carriers of lipids in the blood

195
Q

WHAT ARE APOLIPOPROTEINS

A

Protein combines with a lipid toform a lipoprotein. Promotesmovement of lipids in bloodand between cells

A is a protein carried in HDL (“good”) cholesterol. It helps start the process for HDL to remove bad types of cholesterol from your body

196
Q

What are the five types of lipids?

A

Chylomicrons, VLDL, IDL,HDL, LDL

197
Q

Dyslipidemia

A

Dyslipidemia is the imbalance of lipids such as cholesterol, low-density lipoprotein cholesterol, (LDL-C), triglycerides, and high-density lipoprotein (HDL)

198
Q

Lipoprotein Structure

A

Lipoproteins are complex particles that have a central hydrophobic core of non-polar lipids, primarily cholesterol esters and triglycerides. This hydrophobic core is surrounded by a hydrophilic membrane consisting of phospholipids, free cholesterol, and apolipoproteins

199
Q

HDL AND LDL AFFECT ON ATHEROSCLEROSIS

A

HDL lowers risk of atherosclerosis, LDL increases risk

200
Q

CORE LIPID OF VLDL

A

TRIGLYCERIDE

201
Q

CORE LIPID OF LDL AND HDL

A

CHOLESTEROL

202
Q

APOLIPOPROTEIN OF VLDL

A

B-100
E
OTHERS

203
Q

APOLIPOPROTEIN OF LDL

A

B-100

204
Q

APOLIPOPROTEIN OF HDL

A

A-I
A-II
A-IV

205
Q

TRANSPORT FUNCTION OF VLDL

A

DELIVERS TRIGLYCERIDES TO NON-HEPATIC TISSUES

206
Q

TRANSPORT FUNCTION OF LDL

A

DELIVERS CHOLESTEROL TO NON-HEPATIC TISSUES

207
Q

TRANSPORT FUNCTION OF HDL

A

TRANSPORTS CHOLESTEROL FROM NON-HEPATIC TISSUES AND BACK TO LIVER

208
Q

INFLUENCE OF VLDL ON ATHEROSCLEROSIS

A

PROBABLE CONTRIBUTOR

209
Q

INFLUENCE OF LDL ON ATHEROSCLEROSIS

A

DEFINITE CONTRIBUTOR

210
Q

INFLUENCE OF HDL ON ATHEROSCLEROSIS

A

PROTECTS AGAINST

211
Q

LDL CHOLESTEROL LABS

A

<100 = OPTIMAL
100-129 = NEAR/ABOVE OPTIMAL
130-159 = BORDERLINE HIGH
160-189 = HIGH
>190 = VERY HIGH

212
Q

TOTAL CHOLESTEROL LABS

A

LESS THAN 200 = DESIRABLE
200-239 = BORDERLINE HIGH
240 OR HIGHER = HIGH

213
Q

HDL CHOLESTEROL LABS

A

LESS THAN 40 = LOW
HIGHER THAN 60 = HIGH

214
Q

HYPERCHOLESTEROLEMIA

A

HIGH CHOLESTEROL

215
Q

Atherosclerosis

A

Accumulation of fibrofatty material in intimal artery wall (large, medium arteries)

216
Q

ATHEROSCLEROSIS CAN LEAD TO WHAT

A

PERFUSION PROBLEMS
CAD
PAD
STROKE

217
Q

ATHEROSCLEROSIS PROGRESSION

A
  1. endothelial injury monocytes, inflammatory cells migrate
  2. inflammation, foam cell formation, lipid deposits, fibrous caps
  3. plaque with a lipid core, calcified lesion- susceptible to rupture, bleeding, thrombus formation

PROGRESSES WITH AGE

218
Q

common sites of Atherosclerosis

A

Atherosclerosis can affect most of the arteries in the body, including arteries in the heart, brain, arms, legs, pelvis, and kidneys.

219
Q

risk factors of Atherosclerosis

A

High cholesterol and triglyceride levels.
High blood pressure.
Smoking.
Type 1 diabetes.
Obesity.
Physical inactivity.
High saturated fat diet

220
Q

Clinical manifestations of atherosclerosis

A

Usually none until severe narrowing, blocking of the artery, decreased perfusion

221
Q

complications of atherosclerosis

A

Rupture, thrombus formation –> ischemia, injury, infarction of cells (peripheral, brain, coronary arteries)
Aneurysm

222
Q

3 lesions of atherosclerosis

A

fatty streaks
fibrous plaques
complicated lesions

223
Q

fatty streak Atherosclerosis

A

Fatty streaks appear when the presence of foam cells at the site of plaque formation expands. At this stage, a lipid core has been formed that will progress into a mature atherosclerotic plaque following additional influx of different inflammatory cell types and extracellular lipids.

224
Q

complicated lesions of Atherosclerosis

A

complex plaque referred to as complicated fibroatheromatous plaques or complex lesions. Characterized by possible surface defect, hemorrhage with or without bleeding, and visible lipid and collagen deposits plus thrombotic materials.

225
Q

fibrous plaque atherosclerosis

A

Atherosclerotic plaque begins as fibrous plaque. This consists of an amorphous central lipid core of cellular debris, cholesterol, cholesterol esters, and foam cells. A fibrous cap surrounds the fibrous plaque, consisting mainly of smooth-muscle cells in a matrix of collagen and proteoglycans.

226
Q

What are the risk factors for endothelial dysfunction?

A

diabetes, dyslipidemia, hypertension, smoking, aging, and obesity

227
Q

What are the five types of lipoproteins?

A

chylomicrons
very-low-density lipoproteins (VLDL)
intermediate-density lipoproteins (IDL)
low-density lipoproteins (LDL),
high-density lipoproteins (HDL)

228
Q

Which lipoprotein primarily carries cholesterol?

A

LDL

229
Q

which lipoprotein primarily carries triglycerides

A

VLDL

230
Q

Which lipoprotein carries cholesterol from the tissues to the liver?

A

HDL

231
Q

What is an optimal LDL, HDL, total cholesterol?

A

our HDL (“good” cholesterol) is the one number you want to be high (ideally above 60). Your LDL (“bad” cholesterol) should be below 100. Your total should be below 200.

232
Q

What are the three types of atherosclerotic lesions?

A

FATTY STREAKS
FIBROUS PLAQUES
COMPLICATED LESIONS

233
Q

How can I modify hypertension and diabetes and reduce the risk of atherosclerosis?

A

SMOKING CESSATION
EXERCISE
MAINTAIN HEALTHY WEIGHT
EAT HEALTHY
MANAGE STRESS

234
Q

Arterial Disease - Extremities

A

PERIPHERAL ARTERY DISEASE
THROMBOANGIITIS OBLITERANS AKA BEURGER DISEASE
RAYNAUD PHENOMENON

235
Q

PERIPHERAL ARTERY DISEASE

A

ATHEROSCLEROTIC BLOCKAGES
LARGE ARTERIES (NOT HEART, BRAIN, AORTIC ARCH)

236
Q

Thromboangiitis obliterans (Buerger disease)

A

non-sclerotic inflammation and thrombosis
small and medium sized arteries and veins in foot and lower leg

237
Q

RAYNAUD PHENOMENON

A

intense vasospasm
arteries and arterioles in fingers and occassionally. toes

238
Q

Patho of Peripheral Artery Disease

A

Patho: atherosclerosis, or inflammatory process

239
Q

risks of peripheral artery disease

A

advancing age
smoking
diabetes

240
Q

onset of peripheral artery disease

A

gradual

241
Q

clinical manifestations of peripheral artery disease

A

ntermittent claudication (calf pain with walking), thinning of skin, decrease in size of leg muscles, numbness, leg color- dependent rubor, blanches with elevation, cool, weak or absent pulses, ulceration, gangrene

242
Q

diagnosis of peripheral artery disease

A

physical exam
us
mri
angiography
bp

243
Q

Tx of peripheral artery disease

A

decrease risk and symptoms

244
Q

Thromboangiitis Obliterans (Buerger Disease)

basic info

A

Non-sclerotic, inflammatory disorder —> thrombosis of small and medium sized arteries and veins usually in feet, lower legs

245
Q

cause of Thromboangiitis Obliterans (Buerger Disease)

A

unknown

246
Q

risk factors of Thromboangiitis Obliterans (Buerger Disease)

A

less than 35 yo
heavy smoker
genetics

247
Q

Tx of Thromboangiitis Obliterans (Buerger Disease)

A

smoking cessation
meds
surgery

248
Q

diagnosis of Thromboangiitis Obliterans (Buerger Disease)

A

ankle/arm ratio
us
mri
ct
arteriography

249
Q

clinical manifestations of Thromboangiitis Obliterans (Buerger Disease)

A

pain (arch of foot), intermittent claudication, increased sensitivity to cold, decreased pulses, thin shiny skin, with impaired hair/nail growth, tissue

250
Q

Raynaud Phenomenon

basic info

A

Vasospasm – arteries, arterioles, usuallyoccurs in hands/fingers

251
Q

Raynaud Phenomenon

cause

A

unknown

252
Q

Raynaud Phenomenon

risk factors

A

young women
cold exposure
strong emotions

253
Q

Raynaud Phenomenon

clinical manifestations

A

pallor
cyanosis
hyperemia
normal color
cold
numbness
paresthesias

254
Q

Raynaud Phenomenon

diagnosis

A

cold water immersion of hands
doppler studies

255
Q

Raynaud Phenomenon

treatment

A

eliminate cause
meds
surgery

256
Q

aneurysms

basic info

A

Localized area of vessel dilation caused by weakness in arterial wall

257
Q

types of aneurysms

A

berry
fusiform
dissecting (life threatening)

258
Q

aneurysms

clinical manifestations

A

depends on location and size

259
Q

aneurysms

diagnosis

A

mri
ct
us

260
Q

aneurysms

treatment

A

reduce risk of rupture
surgical intervention

261
Q

aaa size (cm) compared to annual risk of rupture (%)

A

less than 3.0 = 0%
3.0-3.9 = 0.4%
4.0-4.9 = 1.1%
5.0-5.9 = 3.3%
6.0-6.9 = 9.4%
7..0-7.9 = 24%

262
Q

endovascular aortic repair
evar

A

an important advance in the treatment of abdominal aortic aneurysm (AAA). EVAR is performed by inserting graft components that are folded and compressed within a delivery sheath through the lumen of an access vessel, usually the common femoral artery.

263
Q

A client complains of pain in the calf when walking. The nurse understands this to be a symptom of what disorder?

A

claudication is a symptom of PAD

264
Q

what causes claudication in PAD

A

The pain is caused by too little blood flow to the legs or arms.

265
Q

What arterial disorder primarily manifests in the hands and fingers?

A

raynaud’s phenomenon

266
Q

What advice to reduce the risk of Raynaud’s phenomenon would you provide to a client?

A

avoid prolonged exposure to cold
avoid sudden temp changes
smoking cessation
treat secondary diseases

267
Q

What advice to reduce the risk of Buerger’s disease would you provide to a client?

A

avoid nicotine
smoking cessation
meds usually don’t work

268
Q

Where do berry aneurysms commonly occur?

A

on arteries at the base of the brain
most common type of aneurysm

269
Q

What is the risk of an aneurysm that is increasing in size

A

they are at high risk for rupture

270
Q

venous disorders

A

varicose veins
chronic venous insufficiency
venous thrombosis

271
Q

varicose veins

location

A

Primary (superficial veins), secondary disorders (deep veins)

272
Q

varicose veins

risk factors

A

prolonged standing, gender, age, obesity, increased intra-abdominal pressure, heavy lifting, pregnancy

273
Q

vericose veins and prolonged increased venous pressure

A

leads to venous dilation and valve incompetence

274
Q

varicose veins

clinical manifestations

A

aching, edema, warmth, physical look –redness, ropiness of veins

275
Q

varicose veins

complications

A

can lead to venous insufficiency

276
Q

varicose veins

diagnosis

A

physical exam
doppler studies
angiographic venous studies

277
Q

varicose veins

treatment

A

improve flow, prevent injury
– Compression/support stockings
– Sclerotherapy - superficial
– Surgical treatment

278
Q

venous insufficiency

clinical manifestations

A

venous hypertension
edema
varicose veins
skin changes and discoloration
skin ulceration

279
Q

Venous Thrombosis - Thrombophlebitis

basics

A

virchow’s triad- risks
1. venous stasis
2. increased blood coagulability
3. vascular wall injury

*immobilization

280
Q

Venous Thrombosis - Thrombophlebitis

clinical manifestations

A

pain (calf, distal thigh, popliteal areas), swelling, deep muscle tenderness, some are asymptomatic

281
Q

Venous Thrombosis - Thrombophlebitis

diagnosis

A

us
venography
labs- d dimer

282
Q

Venous Thrombosis - Thrombophlebitis

complications

A

pulmonary embolism

283
Q

Venous Thrombosis - Thrombophlebitis

treatment

A

Prevention
Thrombolytics, anticoagulation,
Bedrest – gradual ambulation with support stockings (avoid standing, sitting)

284
Q

What are the three elements of Virchow’s triad?

A

These are endothelial injury, venous stasis, and hypercoagulability

285
Q

With venous disorders will clients lack a pulse?

A

possibly

286
Q

Why are nurses at risk for the development of varicose veins?

A

long shift
heavy lifting
constantly on feet

287
Q

Why do venous stasis ulcers develop?

A

Venous ulcers typically occur because of damage to the valves inside the leg veins. These valves control the blood pressure inside the veins. They allow it to drop when you walk. If the blood pressure inside your leg veins doesn’t fall as you’re walking, the condition is called sustained venous hypertension.

288
Q

What complication is a client with a deep vein thrombosis at risk for?

A

pulmonary embolism (PE)

289
Q

Tests Used in Assessment of Coronary Blood Flow and Perfusion

A

ekg
stress test
echocardiography
cardiac catheterization and arteriography

290
Q

Electrocardiography (EKG) –

A

measures electrical activity of the heart-

291
Q

ambulatory EKG monitoring –

A

Holter monitor

292
Q

stress testing

A

monitors cardiac function under stress (exercise, pharmacologic)

293
Q

echocardiography

A

assessment of structure, function of the heart using ultrasound

294
Q

Cardiac catheterization and arteriography –

A

catheter advanced into the heart
– Right heart – vein  views great vessels,chambers
– Left heart – artery uses dye to viewcoronary vessels

295
Q

Acute Pericarditis

A

Inflammation of the pericardium

296
Q

Acute Pericarditis

causes

A

infectious, non-infectious process

297
Q

Acute Pericarditis

patho

A

vasodilation, increased capillary permeability, WBC’s, exudate in pericardial space

298
Q

Acute Pericarditis

clinical manifestations

A

chest pain – pleuritic/positional fever, pericardial friction rub, EKG changes

299
Q

Acute Pericarditis

diagnosis

A

ekg
echo
cxr
labs

300
Q

Acute Pericarditis

treatment

A

based on cause

301
Q

Acute Pericarditis

complications

A

recurrence, pericardia leffusion, pericardial tamponade, adhesions/scar tissue

302
Q

Pericardial effusion

A

– accumulation of fluid in pericardialcavity

303
Q

Pericardial tamponade

A

– life threatening compression of the heart due to blood/fluid in pericardial space

304
Q

Pericardial Effusion/Tamponade

diagnosis

A

echo
ekg

305
Q

Pericardial Effusion/Tamponade

treatment

A

pericardiocentesis

306
Q

Pericardial Effusion/Tamponade

clinical manifestations

A

jugular vein distention, narrowing of pulse pressure, muffled heart sounds, tachycardia, pulsus paradoxus (fall in B/P with inspiration)

307
Q

Coronary Artery Disease

A

Disease of heart as a result of impaired coronary blood flow
* Two main coronary arteries branch off the aortic root
* Most common cause of CAD is atherosclerosis.

308
Q

coronary artery disease

complications

A

myocardial ischemia, angina, MI, arrhythmias, heart failure, sudden death

309
Q

What normally happens in a blood vessel when oxygen demand exceeds supply

A

A mismatch between myocardial oxygen supply and demand can result in myocardial ischemia or infarct. Unfortunately, infarct results in irreversible damage to the myocardium

310
Q

What normally happens in a blood vessel when oxygen supply cant meet demand

A

If your blood has low levels of oxygen, it can’t deliver enough oxygen to your organs and tissues that need it to keep working (hypoxia). This can damage your heart or brain if it persists over time

311
Q
  • Chronic ischemic heart disease

cad

A

arrowing of artery –> atherosclerosis or vasospasm –>Recurrent, transient

312
Q
  • Acute coronary syndrome

CAD

A

Disruption of atherosclerotic plaque –> unstable angina, MI

313
Q

plaque

CAD

A

– Stable, fixed – obstructs flow
– Unstable – obstructs flow, risk for rupture, seen in ACS

314
Q
  • Thrombosis, vessel occlusion

CAD

A

Platelet aggregation, thrombus formation

315
Q

Atherosclerotic Plaque – Stable,

A

Stable atherosclerotic plaque builds up over time and causes arteries to become hardened. It can lead to narrowing of the arteries over time, so much so that eventually blood flow to the heart and other organs is restricted. This obstructive stable plaque can be detected and treated.

316
Q

Atherosclerotic Plaque – unstable

A

Instability of coronary atherosclerotic plaque culminates in abrupt vascular thrombus formation that impedes blood flow and leads to critical myocardial ischemia. Clinically, this often manifests as life-threatening Acute Coronary Syndromes (ACS)

317
Q

Chronic Ischemic Heart Disease

A

Blood supply does not meet demand
* Causes: Atherosclerosis, vasospasm

318
Q

Chronic Ischemic Heart Disease

types

A

– Chronic stable angina/exertional
– Variant (vasospastic)
– Silent ischemia
– Chest pain with normal coronary angiography
– Ischemic cardiomyopathy

319
Q

Chronic Ischemic Heart Disease –Chronic Stable Angina

A

Fixed plague – disparity between supply/demand*

Angina = pain- not all cad patients have pain

320
Q

Chronic Ischemic Heart Disease –Chronic Stable Angina

causes

A

ncreased demand – cold, exertion, stress

321
Q

Chronic Ischemic Heart Disease –Chronic Stable Angina

location of pain

A

Substernal area, may radiate to back, left shoulder, jaw, arms

322
Q

Chronic Ischemic Heart Disease –Chronic Stable Angina

Tx

A

relieved with rest
nitroglycerin

323
Q

Silent myocardial ischemia

Chronic Ischemic Heart Disease -

A

impaired blood flow in the absence of pain

324
Q

Variant (vasospastic) angina –

Chronic Ischemic Heart Disease -

A

hypercontractility of vascular smooth muscle, occurs at rest with minimal exercise, frequently during night, EKG changes and dysrhythmias

325
Q

Chest pain with normal coronary angiography –

A

cardiac syndrome X, ?? Cause

326
Q

Ischemic cardiomyopathy

A

– CAD from myocardial dysfunction

327
Q

Diagnosis/Treatment: Chronic Ischemic Disease

part 1

A

History/physical – risk factors, pain -characteristics
* Lab studies – lipid panel, biomarkers are normal
* Diagnostic tests – EKG, echo, stress testing, CT, MRI, cardiac cath

328
Q

Diagnosis/Treatment: Chronic Ischemic Disease

part 2

A

reduce symptoms,
prevent MI
– Pharmacologic – meds
– Coronary interventions – PCI (angioplasty, stent placement), CABG
– Non-pharmacologic – reduce risk factors

329
Q

What are two modifiable risk factors associated with coronaryartery disease?

A

smoking
diabetes
obesity
diet
stress

330
Q

What are two unmodifiable risk factors associated with coronaryartery disease?

A

gender
race
family Hx
advancing age

331
Q

Which type of angina is caused by vasospasm?

A

Prinzmetal angina (vasospastic angina or variant angina) is a known clinical condition characterized by chest discomfort or pain at rest with transient electrocardiographic changes in the ST segment, and with a prompt response to nitrates. These symptoms occur due to abnormal coronary artery spasm.

332
Q

What would you advise a client who experiences angina while walking to do?

A

stop and rest

333
Q

What problem other than atherosclerosis can cause chronic ischemic heart disease?

A

Obesity, limited physical activity, psychosocial factors such as stress and depression, as well as co-existing chronic kidney disease or another atherosclerotic cardiovascular disease (ASCVD) such as stroke, or peripheral vascular disease (PVD) are also associated with ischemic heart disease.

334
Q

What medication is commonly used to reduce the symptoms of angina?

A

sublingual nitroglycerin

335
Q

Acute Coronary Syndrome (ACS) -

types

A

unstable angina
non st segment elevation (non q wave) mi
st segment elevation MI (STEMI)

336
Q

unstable angina

acs

A
  • Ischemia
  • No elevation in biomarkers, some EKG changes
337
Q
  • Non-ST segment elevation (non-Q wave) MI

Acute Coronary Syndrome (ACS) -

A
  • Severe ischemia with myocardial damage
  • Biomarker elevation, no ST elevation on EKG, some changes
338
Q
  • ST segment elevation MI (STEMI)

Acute Coronary Syndrome (ACS) -

A
  • Ischemic death of myocardial tissue
  • Biomarker elevation, ST elevation on EKG
339
Q

ACS Unstable Angina/Non-ST MI

patho

A
  • Development of unstable plaque
    – Rupture, non-occlusive thrombus formation
  • Obstruction by spasm, constriction
  • Severe narrowing of the coronary lumen
  • Inflammation
  • Physiologic state causing ischemia related to decreased O2 supply
340
Q

ACS - Unstable Angina, Non ST MI Pain in Contrast to Stable Angina

A
  • Pain with UA, Non ST MI
    – Occurs at rest or with minimal exertion
    – Lasts more than 20 minutes if untreated
    – Severe – described as frank pain, of new onset
    – More severe, prolonged, or frequent than previously experienced.
341
Q

ACS - STEMI

patho part 1

A
  • Lack of blood flow to heart* Aerobic to anaerobic metabolism–>inadequate energy to sustain cell function
  • Loss of contractile function
  • Cell changes in minutes
342
Q

ACS-STEMI

PATHO PART 2

A
  • Loss of function of ischemic area
  • Irreversible damage-40 minutes of severei schemia
  • Necrosis 20-40 minutes following severe ischemia
  • Recover related to size, location of MI
343
Q

Evaluation of ACS (UA, Non-ST, STEMI)

- Diagnostics

A
  • EKG changes – electrical conduction changes through damaged tissue
  • ECHO –wall motion abnormalities
  • Serum biomarkers (labs)
344
Q

Evaluation of ACS (UA, Non-ST, STEMI)

DIAGNOSTICS-SERUM BIOMARKERS LABS

A
  • Troponin I (TnI)
  • Troponin T (TnT)
  • Creatine kinase (CK-MB)
  • Myoglobin
345
Q

STEMI (ACS)

Clinical Manifestations –

A
  • Chest pain – abrupt onset, or progression from UA/NSTEMI
    – Severe, unrelieved, may radiate to jaw, shoulder, upper back, arm
  • Nervous system responses
  • Hypotension, shock (cardiogenic – pump failure) ,dysrhythmias
346
Q

STEMI (ACS)

NERVOUS SYSTEM RESPONSES

A

– GI distress, nausea, vomiting
– Tachycardia, vasoconstriction
– Anxiety, restlessness, impending doom

347
Q

ACS

TREATMENT

A
  • Symptom recognition, prompt treatment – “time is muscle - myocardium”
  • Oxygen, antiplatelet- aspirin, nitrates, pain meds, beta blockers, anticoagulation therapy
  • Reperfusion – reestablish blood flow
  • Cardiac rehabilitation programs
348
Q

ACS

TREATMENT- REPERFUSION

A

– Thrombolytic drugs
– Percutaneous coronary intervention (PCI) balloon angioplasty, stenting, artherectomy
– Coronary artery bypass graft (CABG) -surgical revascularization

349
Q

post infarction

A

acute inflammatory response (area of necrosis) – 2-3 days
* Necrotic cells replaced with granulation and scar tissue
* Necrotic area soft, yellow – 4-7 days
* Necrotic tissue replacement – 7 weeks

350
Q

3 zones of tissue damage

post infarction

A

– Necrotic zone
– Surrounding zone of injured/hypoxic cells , some recovery
– Outer zone ischemic – salvageable cells

351
Q

Complications - MI

part 1

A
  • Dysrhythmias
  • Sudden cardiac death
  • Cardiogenic shock
  • Heart failure
  • Arrhythmias
352
Q

Complications - MI

part 2

A
  • Ventricular, valve, interventricular septal rupture
  • Pericarditis
  • Aneurysms
  • Stroke
353
Q

Cardiomyopathy

A
  • Disorders of myocardium – (mechanical and/or electrical)
  • Primary or secondary
354
Q

cardiomyopathy

types

A

– Genetic – Hypertrophic, Arrhythmogenic, Ion channelopathies
– Mixed – Dilated, Restrictive
– Acquired – Myocarditis, Peripartum, Takotsubo
– Idiopathic

355
Q

Hypertrophic Cardiomyopathy

patho

A

Left ventricular hypertrophy, disproportionate thickening of the ventricular septum –> abnormal diastolic filling, cardiac dysrhythmias, intermittent outflow obstruction (left ventricle-in 25%)

  • Genetic disorder: autosomal dominant
356
Q

Hypertrophic Cardiomyopathy

clinical manifestations

A

asymptomatic, dyspnea, chest pain, exercise intolerance, syncope, dysrhythmias

357
Q

Hypertrophic Cardiomyopathy

diagnosis

A

echocardiogram, EKG, continuous ambulatory monitoring (Holter monitor), MRI, genetic testing, physical exam may be normal

358
Q

Hypertrophic Cardiomyopathy

treatment

A

medical management, medications, pacemakers, AICD; surgical - myectomy/ablation of septum

359
Q

Acute Infective Endocarditis

patho

A

infection of the inner surface of the heart and valves
* Bacterial invasion–> valvular vegetation/debris lesions –> emboli –> bacteremia –> destruction of cardiac valves –> valve dysfunction/perforation, abcesses, pericarditis

360
Q

Acute Infective Endocarditis

risks

A

ETOH/IV drug use, diabetes, neutropenia, damaged endocardial surface (valvular disease), implantable devices

361
Q

Acute Infective Endocarditis

common infecting organisms and sites

A

Common infecting organisms – staphylococcal, enterococci

  • Common site – aortic, mitral valves
362
Q

Acute Infective Endocarditis

clinical manifestations

A

fever, heart murmur, petechial hemorrhages in skin, nailbeds, mucous membranes, cough arthralgia/arthritis (emboli)

363
Q

Acute Infective Endocarditis

diagnosis

A

blood culture
echo

364
Q

Acute Infective Endocarditis

treatment

A

eliminate cause - antibiotics, minimize cardiac effects - may require valve replacement, treat effect of the emboli

365
Q

Valvular Disease – Stenosis, Regurgitation

A

Heart valves promote unidirectional flow of blood through the heart

Most common: Mitral, aortic

Disturbances in blood flow, turbulence

366
Q

Valvular Disease – Stenosis, Regurgitation

causes

A

congenital, trauma, ischemia, infection, inflammation

367
Q

Valvular Disease – Stenosis, Regurgitation

stenosis

A

narrowing of orifice, failure of leaflets to open normally –> decreased blood flow –> impaired emptying, increased work demands on heart

368
Q

Valvular Disease – Stenosis, Regurgitation

regurgitation

A

Regurgitant valve – does not close properly –> blood flow continues despite valve closure and/or backward flow

369
Q

valvular disease

heart murmur

A

– Stenosis – hear murmur when blood shoots through the narrow opening when valve opens
– Regurgitation – when blood leaks back through a valve that should be closed

370
Q

valvular disease

heart murmur part 2

A

Mitral regurgitation, stenosis, aortic regurgitation – pulmonary symptoms
* Aortic stenosis – angina, syncope and heart failure

371
Q

What two tests are used to diagnose infective endocarditis?

A

blood culture
cbc
echo
ekg
cxr
ct
mri

372
Q

Abnormal turbulent blood flow through a diseased valve produces what clinical manifestation?

A

heart murmur

373
Q

What happens to blood flow in diastole in mitral valve stenosis

A

in mitral valve stenosis, the valve opening narrows. The heart now must work harder to force blood through the smaller valve opening. Blood flow between the upper left and lower left heart chambers may decrease.

374
Q

What happens to the left ventricle in aortic valve stenosis?

A

Over time, aortic valve stenosis causes your heart’s left ventricle to pump harder to push blood through the narrowed aortic valve. The extra effort may cause the left ventricle to thicken, enlarge and weaken. If not addressed, this form of heart valve disease may lead to heart failure

375
Q

Does mitral valve regurgitation result in a decreased stroke volume?

A

The physiologic consequences of mitral regurgitation include reduced forward stroke volume

376
Q

What valvular problem does the nurse anticipate if the chordae tendinae rupture as a complication of MI?

A

CTR is characterised by sudden onset, rapid progression of pulmonary edema, hypotension, and left-sided heart failure which may finally lead to severe cardiac shock or pulmonary hypertension and acute right-sided heart failure

377
Q

Adequate Perfusion

A
  • Pumping ability of the heart
  • Intact vascular system to transport blood
  • Sufficient blood to fill the vascular system
  • Tissues that can extract O2 and nutrients
378
Q

Heart Failure in Adults

A

Failure of the heart to deliver sufficient blood to meet the metabolic needs of tissues/cells
* Decrease in cardiac output and the body’s attempt to compensate
Major causes: MI, HPT
* Chronic disorder –> requires continuous treatment with medications

379
Q

heart failure in adults

characteristics

A

– Ventricular dysfunction – pump doesn’t work, or a filling problem
– Can reduce ejection fraction
– Reduced cardiac output
* Signs of inadequate tissue perfusion
* Signs of fluid volume overload

380
Q

aca/aha stage vs nyha functional classification

stage a = n/a classification

A

high risk for hf
no structural heart disease
no symptoms of hf

381
Q

acc/aha stage vs nyha functional classification

stage b = class i

A

b. structural heart disease without symptoms of hf

i. asymptomatic

382
Q

acc/aha stage vs nyha functional classification

stage c = class ii and iii

A

c. structural heart disease with prior or current hf symptoms

class ii. symptomatic w/ moderate exertion

class iii. symptomatic with minimal exertion

383
Q

acc/aha stage vs nyha functional classification

stage d = class iv

A

d. advanced structural heart disease with marked symptoms of hf at rest despite maximal medical therapy requiring specialized interventions like heart transplant or mechanical assist device

iv. symptomatic at rest

384
Q

What are signs of inadequate tissue perfusion?

A

pallor
pain/discomfort
diminished/absent pulse
delayed capillary refill
cyanosis
numbness
loss of motor function

385
Q

What are signs of fluid retention/volume overload?

A

Rapid weight gain.
Noticeable swelling (edema) in your arms, legs and face.
Swelling in your abdomen.
Cramping, headache, and stomach bloating.
Shortness of breath.
High blood pressure.
Heart problems, including congestive heart failure

386
Q

compensatory mechanisms of the heart

A

frank starling mechanism
myocardial hypertrophy and remodeling
sympathetic reflexes
renin angiotensin aldosterone mechanism

387
Q

higher levels of natriuretic peptide indicate what

A

worsening hf

388
Q

frank starling mechanism

A

the heart’s physiological ability to change its contraction force, and therefore stroke volume, in response to changes in venous return

389
Q

myocardial hypertrophy and remodeling mechanism

A

Cardiac hypertrophy is a common type of cardiac remodeling that occurs when the heart experiences elevated workload. The heart and individual myocytes enlarge as a means of reducing ventricular wall and septal stress when faced with increased workload or injury.

390
Q

sympathetic reflexes mechanism

A

Sympathetic vasoconstrictor reflexes are essential for the maintenance of arterial blood pressure in upright position. It has been generally believed that supraspinal sympathetic vasoconstrictor reflexes elicited by changes in baroreceptor activity play an important role.

391
Q

renin angiotensin aldosterone mechanism

A

The RAAS is a complex multi-organ endocrine (hormone) system involved in the regulation of blood pressure by balancing fluid and electrolyte levels, as well as regulating vascular resistance & tone. RAAS regulates sodium and water absorption in the kidney thus directly having an impact on systemic blood pressure.

392
Q

cardiac remodeling post MI

A

After myocardial infarction (MI), the heart undergoes extensive myocardial remodeling through the accumulation of fibrous tissue in both the infarcted and noninfarcted myocardium, which distorts tissue structure, increases tissue stiffness, and accounts for ventricular dysfunction.

393
Q

expansion of infarct

A

hours to days

394
Q

global remodeling

A

days to months

395
Q

right ventricular failure

clinical manifestations

A

congestion of peripheral tissues
dependent edema and ascites
liver congestion
signs related to impaired liver function
gi congestion
anorexia
gi disease
weight loss

396
Q

left ventricular failure

clinical manifestations

A

decreased cardiac output
activity intolerance
signs of decreased tissue perfusion
pulmonary congestion
impaired gas exchange
cyanosis
signs of hypoxia
pulmonary edema
cough with frothy sputum
orthopnea
paroxysmal nocturnal dyspnea

397
Q

heart failure

diagnosis

A

h and p
labs
ekg
cxr
echo

398
Q

heart failure

labs

A

b type natriuretic peptide

399
Q

heart failure

treatment goals

A

recting cause, improving cardiac function, maintaining fluid volume, developing activities within individual limitations of cardiac reserve

400
Q

heart failure

treatment

A

meds
o2
ventilator support
aicd
ventricular assist devices
heart transplant (end stage failure)

401
Q

What are two common causes of heart failure?

A

cad
diabetes
high bp
obesity

402
Q

Where does blood back up in right sided heart failure?

A

veins

403
Q

Where does blood back up in left sided heart failure?

A

pulmonary veins toward the organs

404
Q

Left sided heart failure will primarily present with symptoms related to what system

A

respiratory

405
Q

what might an increase in dyspnea on exertion tell you about heart failure

A

it is progressing and that co does not increase sufficiently

406
Q

What tests are used in the diagnosis of heart failure?

A

blood work
cxr
ecg
ekg
echo
ef
stress test
ct
mri

407
Q

Why would the nurse instruct a client with heart failure to weigh themselves daily

A

to detect worsening HF early and avoid complications.

408
Q

What causes pulmonary edema?

A

too much fluid accumulates in the lungs, interfering with a person’s ability to breathe normally

409
Q

hemodynamics

A

how your blood flows through your arteries and veins and the forces that affect your blood flow. Normally, your blood flows in a laminar (streamlined) pattern. It flows fastest in the middle of a blood vessel, where there’s no friction with blood vessel walls

410
Q

dvt

A

condition that occurs when a blood clot forms in a deep vein. These clots usually develop in the lower leg, thigh, or pelvis, but they can also occur in the arm

411
Q
A
412
Q

The Heart, Part 1 - Under Pressure: Crash Course Anatomy & Physiology #25

A

https://www.youtube.com/watch?v=X9ZZ6tcxArI

413
Q

The Heart, Part 2 - Heart Throbs: Crash Course Anatomy & Physiology #26

A

https://www.youtube.com/watch?v=FLBMwcvOaEo

414
Q

The (BLANK) is the largest artery in the body.

A

AORTA

415
Q

The cardiovascular system is responsible for transporting oxygen, nutrients, and hormones throughout the body.
TRUE OR FALSE

A

TRUE

416
Q

Which of the following is responsible for regulating heart rate?

Purkinje fibers

SA node (sinoatrial node)

Bundle of His

AV node (atrioventricular node)

A

SA NODE (SINOATRIAL NODE)

417
Q

What is the average resting heart rate for adults?

More than 200 beats per minute

100-150 beats per minute

60-100 beats per minute

30-60 beats per minute

A

60-100 BEATS PER MINUTE

418
Q

The (BLANK) are the lower chambers of the heart.

A

VENTRICLES

419
Q

The (BLANK) is the main organ of the cardiovascular system.

A

HEART

420
Q

What is the role of valves in the cardiovascular system?

To create blood cells

To control heart rate

To regulate blood pressure

To prevent backward flow of blood

A

To prevent backward flow of blood

421
Q

Which chamber of the heart receives oxygenated blood from the lungs?

Left atrium

Left ventricle

Right atrium

Right ventricle

A

LEFT ATRIUM

422
Q

PULMONARY ARTERY

A

Carries deoxygenated blood from the heart to the lungs

423
Q

AORTA

A

Carries oxygenated blood from the heart to the rest of the body

424
Q

CAPILLARIES

A

Microscopic blood vessels where gas exchange occurs

425
Q

VEINS

A

Carry blood back to the heart

426
Q

What is the medical term for high blood pressure?

Hypotension

Atherosclerosis

Arrhythmia

Hypertension

A

HYPERTENSION

427
Q

MEDICAL - How cholesterol clogs your arteries (atherosclerosis)

A

https://www.youtube.com/watch?v=fLonh7ZesKs

428
Q
A

312 Patho (3 decks)

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