Exam 2 Flashcards
1
Q
Central Venous Pressure (CVP) measures what
A
Pressure in the right atrium
2
Q
Normal value for CVP
A
2-6 mmHg
3
Q
When is CVP recorded
A
At the end of exhalation
4
Q
Normal systolic and diastolic pulmonary artery (PA) pressures
A
PA Systolic: 15-25 mmHg
PA Diastolic: 5-15 mmHg
5
Q
What are PAOP/PCWP
A
Pulmonary artery occlusion pressure and pulmonary artery capillary wedge pressure
6
Q
What does PAOP and PCWP measure
A
End diastole left ventricular pressure
7
Q
What is the maximum inflation of balloon for PAOP/PCWP
A
1.5 mL
8
Q
Normal Values for PAOP/PCWP
A
4-12 mmHg
9
Q
Normal Cardiac Output
A
4-8 L/min
10
Q
Normal ejection fraction
A
50-75%
11
Q
What does cardiac index measure. How to find it. Normal range
A
The cardiac output value based on patient size. Cardiac output/body surface area. 2.8-4.2 L/min/m2
12
Q
Normal Systemic Vascular Resistance (SVR)
A
800-1400
13
Q
What do values outside of the normal SVR indicate
A
Below 800 = vasodilation
Above 1400 = vasoconstriction
14
Q
What does nitroglycerin do?
A
Arterial and venous vasodilator (primarily venous)
Dilates coronary arteries, reduces cardiac filling pressures, relieves pulmonary congestion, reduces cardiac workload and O2 consumption
15
Q
What is the door to balloon time for STEMI?
A
90 minutes
16
Q
Order of MI treatment
A
Oxygen, aspirin, nitroglycerine, morphine
17
Q
Manifestations of pericarditis
A
Sharp substernal pain, DIFFUSE ECG CHANGES, PAIN ON INSPIRATION, fever, shortness of breath, tachycardia, tropinin, cough, ST elevations on all leads
18
Q
Treatment of pericarditis
A
Sit forward, ECG, NSAIDs, colchicine to lower inflammation
19
Q
Cause of pericarditis
A
Trauma, myocardial injury, respiratory infection, rheumatic fever, autoimmune
20
Q
Cause of endocarditis
A
Staph, bacterial migration from dental work, invasive devices, IV drugs
21
Q
Manifestations of endocarditis
A
Muscle aches, petechiae, fever, tachycardia, dyspnea, night sweats, flu like symptoms
22
Q
Treatment of endocarditis
A
Management of infection, strict aseptic technique, prophylactic medications before all invasive procedures
23
Q
Causes of myocarditis
A
Viral infections, fungal infections, bacterial, lyme disease, autoimmune, burns, drugs
24
Q
Manifestations of myocarditis
A
Stabbing pain, tachycardia, dysrhythmias, dyspnea, fatigue, fever, NO ECG CHANGES
25
Treatment of myocarditis
Supportive treatment (VAD), antiarrhythmics, time to self heal
26
What classifies a hypertensive crisis
Systolic over 180 mmHg and/or diastolic over 110 mmHg
27
Signs and symptoms of hypertensive crisis
Severe headache, blurred vision, epistaxis, SOB, increased anxiety, worsened angina
28
Causes of hypertensive crisis
Pheochromocytoma, thyroid storm, lack of medication adherence
29
Tx of hypertensive crisis
Oxygen, Get IV access (PO meds take too long), Prevent falls
Meds: nitroprusside, nicardipine, labetalol
30
When is surgery recommended for aortic aneurysm
When aneurysm is greater than 5.5cm
31
Activation of alpha receptors causes what
Vasoconstriction of smooth muscle in the heart, skin, resp, GI, kidneys
32
Activation of beta I receptors does what
Increases heart rate and cardiac contractility
33
Activation of beta II receptors does
Vasodilation, bronchial relaxation
34
Important thing to monitor for beta drugs
Glucose
35
What does digoxin do
Slows heartrate but increases strength and force of cardiac contraction by blocking the sodium potassium pump.
36
Important nursing considerations with digoxin
Cannot be given if hypokalemic because it allows more dig to enter the cells. Digoxin can cause hyperkalemia
37
Symptoms of digoxin toxicity
Yellow green halo, blurred vision, headache, dizziness, confusion, bradycardia, nausea, vomiting, anorexia, SA/AV block
38
What does dopamine do
Low: 0.5-3.0 (mcg/kg/min): increase renal and mesenteric blood flow
Medium: 4-8 (mcg/kg/min): Stimulates B1 receptors -> improves contractility, increasing heart rate and cardiac output
High: 8-10 (mcg/kg/min): pure alpha agonist (negates all beta and dopaminergic effects)
Increases cardiac workload, increases afterload through vasoconstriction
39
Nursing considerations for dopamine
Should be administered through central line as peripheral line infiltration causes necrosis. Have Regitine (Phentolamine) on hand
40
What is the antidote for dopamine
Regitine (Phentolamine)
41
What does dobutamine do
Primarily a beta I agonist which increases myocardial contractility. Has some beta II traits which promotes vasodilation in the pulmonary bed
42
What does milrinone do
Inodilator which increases cardiac output by decreasing SVR and PVR. Decreases O2 demand of the heart and has less influence on heart rate compared to dopamine and dobutamine. Great emptying of the pulmonary bed
43
What does epinephrine do
Beta I agonist which increases heart rate, heart contractility, and cardiac output. Higher doses cause alpha stimulation. Activates automaticity of pacemaker cells
44
What should be monitored after giving epinephrine
BP, HR, glucose
45
What does norepinephrine do
Stimulates alpha and beta I receptors. More severe vasoconstrictor than epinephrine.
46
Nursing considerations for norephinephrine
Causes major peripheral vasoconstriction which can lead to peripheral tissue ischemia/necrosis. Been shown to perfuse GUT better and decrease chance of intestinal necrosis
47
What does vasopressin do
Synthetic ADH. Increases blood pressure through vasoconstriction and water retention
48
What does phenylephrine (NEO-synephrine) do
Causes vasoconstriction through being a pure alpha agonist. Increases BP but usually not HR
49
Side effects of nitroglycerine
Flushing and profound headache, hypotension
50
Nursing considerations with teaching for a patient using nitroglycerine
Keep with patient at all times, check expiration, rotate patch sites, after 3 doses (one every 5 minutes) of unrelieved chest pain call 911
51
What does sodium nitroprusside (SNP) do
Potent rapid acting venous and arterial vasodilator (primarily arterial). Given for hypertensive crisis
52
Nursing considerations for sodium nitroprusside
Needs to be given through arterial line.
Prolonged administration results in thiocyanate toxicity: SNP is metabolized down to Cyanide. Toxicity indicators: nausea, confusion, tinnitus
53
Considerations for smooth muscle relaxants (Nitroglycerine, hydralazine, sodium nitroprusside)
Relaxes smooth muscle, peripheral vasodilation (decreases BP), cerebral vasodilation (headaches), compensatory (reflex tachycardia, Na+ and H20 retention due to RAAS activation)
54
Considerations for calcium channel blockers (Diltiazem, Nicardipine, Verapamil)
Decreases O2 demand on heart. Decreases BP, relaxes smooth muscle as well
55
Considerations for ACE inhibitors (Captopril, Vasotec, Enalapril)
Causes both venous and arterial vasodilation by blocking the production of ACE impeding the conversion of angiotensin I to angiotensin II
56
Considerations for ARBs (Losartan, Diovan)
Decreases blood pressure by preventing angiotensin II mediated vasoconstriction and release of aldosterone (block action of angiotensin II
57
Considerations for B-Type Natriuretic Peptide (Natrecor)
Decreases preload, decreases vascular resistance, decreases BP
58
Considerations for alpha adrenergic blockers (Cadura)
Peripheral adrenergic blockers inhibit alpha receptors in the peripheral vasculature
Results are opposite of a stimulation and cause vasodilation, decreased peripheral vascular resistance, reduced venous return to the heart
59
When is amiodarone used
Ventricular dysrhythmias, supraventricular tachycardia (SVT), atrial fibrillation
60
What does amiodarone do
Prolongs action potential, increases QT and PR intervals, decreases peripheral vascular resistance, decrease sinus rate
61
Nursing considerations for amiodarone
Monitor ECG (PR and QT intervals), decrease BP and HR.
Can cause pulmonary fibrosis.
Watch for ARDS, respiratory failure
Monitor K+ Na+ ALT/AST
Can effect warfarin so watch for s/s of bleeding
62
When is lidocaine used
Ventricular arrhythmias, frequent PVCs, ventricular tachycardia, ventricular fibrillation
63
What does lidocaine do
Reduces cardiac excitability, delays cardiac conduction in ventricle
64
Nursing considerations for lidocaine
Monitor ECG, lowers BP and HR. Watch for circulatory depression (Dopamine). Watch electrolytes. Only IV
Monitor lidocaine levels to prevent lidocaine Toxicity: Can build up toxic levels in body which cause: hypotension bradycardia bradypnea, seizures
65
When is adenosine used
Conversion of paroxysmal supraventricular tachycardia (PSVT) to sinus rhythm
66
What does adenosine do
Slows conduction through AV node, can interrupt pathways upon reentry (will cause a brief period of asystole while heart resets)
67
Nursing considerations for adenosine
Rapid IV push, very fast acting with a very short half life. ECG monitor while administering. Monitor electrolytes. Monitor BP pulse and respirations
Have code cart available
68
When is atropine used
Symptomatic bradycardia and heart block
69
What does atropine do
Anticholinergic which decreases response to acetylcholine
70
Nursing considerations for atropine
Monitor ECG, increases HR, can cause CNS stimulation (confusion, excitement), I and O, can cause severe constipation due to decrease GI motility
71
Normal length of PR interval
0.12-0.20 seconds
72
Normal length of QRS complex
0.06-0.10 seconds
73
Normal length or QT interval
0.38-0.42
74
Causes of premature atrial contractions (PACs)
Stimulants, myocardial ischemia, potassium or magnesium abnormalities, myocardial hypertrophy or dilation
75
PAC nursing interventions
Treat the cause and avoid triggers. Can be a signal for impending atrial fibrillation
76
What happens with atrial flutter and what is the atrial rate
One irritable foci in the heart cause rapid regular atrial rate (240-320bpm). Loss of atrial kick. Ventricular response is regular and not fast.
77
Causes of atrial flutter
Lung disease, ischemic heart disease, hyperthyroidism, hypoxemia, heart failure, ETOH abuse, potassium and magnesium abnormalities
78
Interventions for atrial flutter
Anticoagulation, prevention of hypovolemia from atrial kick loss, synchronized cardioversion (requires anticoagulation before and after), MAZE procedure
79
What happens with atrial fibrillation
Multiple ectopic foci in the heart cause chaotic quivering of the atria leading to loss of atrial kick and no effective atrial output.
80
What are causes of atrial fibrillation
Ischemia, heart disease, valvular heart disease, hyperthyroidism, hypoxemia, heart failure, potassium and magnesium abnormalities
81
Medication treatments for atrial flutter and atrial fibrillation
Amiodarone, beta blocker, diltiazem
82
Nursing interventions for atrial fibrillation
Anticoagulation, prevent hypovolemia, synchronized cardioversion (with anticoagulation before and after), MAZE procedure
83
What junctional rhythm
When the AV node pacemakes for the heart
84
What's the heart rate and what does a junctional rhythm look like on the ECG strip
40-60bpm. P waves are either inverted or absent
85
What can be a cause of junctional rhythm
Surgery, sick sinus syndrome, inflammation disorders, valvular related causes (damage, surgery related), ischemic heart disease, digoxin
86
What are interventions for junctional rhythm
Monitor VS, monitor for s/s of cardiac ischemia, monitor for low cardiac output.
No treatment unless patients become symptomatic. If symptomatic: Atropine, transcutaneous pacing, dopamine
87
What is paroxysmal supraventricular tachycardia
Supraventricular triggering of the ventricles to beat at 150-250 bpm. PSVT has sudden onset and termination
88
What causes PSVT
Stimulants, Catecholamines, Electrolyte Abnormalities, Heart Disease
89
What are interventions for PSVT
Monitor vital signs and monitor for cardiac ischemia and decreased cardiac output. Can sometimes be fixed by vagal maneuvers. Providers can give carotid massage. Heart rate above 150 with symptoms calls for immediate cardioversion. Medication for PSVT is adenosine
90
What does the ECG look like for PVCs and VT
Widened QRS complex, multifocal QRS complexes (up and down). Predictable and follow a pattern
91
Classifications of PVCs
More than 3 consecutive is referred to as non-sustained ventricular tachycardia
92
Causes of PVCs
Hypoxemia, Ischemic heart disease, Hypokalemia, Hypomagnesemia, Acid-base imbalances, Increased catecholamines
93
Interventions for PVCs
Correct the underlying cause (electrolyte, acid-base).
94
Important considerations with ventricular tachycardia
Heart rate is over 100 but is usually 150-250 beats per minute. Patient may or may not have a pulse
95
Causes of ventricular tachycardia
Hypoxemia
Acid-base imbalance
Exacerbation of heart failure
Ischemic heart disease
Cardiomyopathy
Valvular heart disease
Electrolyte Abnormalities (K+ and Mg+)
96
Nursing interventions for ventricular tachycardia
DETERMINE A PULSE. Monitor patient. Correct electrolyte or acid base imbalance if present. Medications: amiodarone, lidocaine.
97
What causes torsades de pointes and whats the treatment
Magnesium or potassium imbalance, hypoxemia, or acid base balance
Treated with magnesium, amiodarone, or lidocaine. Cardioversion can be done after
98
Causes of ventricular fibrillation
Hypoxemia
Acid-base imbalance
Exacerbation of heart failure
Ischemic heart disease
Valvular heart disease
Electrolyte Abnormalities (K+ and Mg+)
99
What medications are given for ventricular fibrillation
Epinephrine, Atropine, Amiodarone, Sodium Bicarbonate
100
What is a first degree heart block. What does the ECG look like
Consistent delayed conduction through the A/V node or Atrial tissue
EKG: Prolonged PR interval-greater than .20
101
Causes of first degree heart block
Aging
Ischemic valvular related
Ischemic Heart Disease
102
Nursing considerations for first degree heart block
Monitor for elongation of PR interval
103
What is second degree type 1 (Morbitz 1 or Wenckebach) and what is seen on ECG
Progressive elongation of PR interval until there is no QRS complex. No QRS restarts cycle
104
Causes of second degree type I block
Drugs
Aging
Acute Inferior Wall MI
Ischemic Heart Disease
Digitalis
Toxicity Right ventricular infarct
105
What is 2nd Degree A/V Block Type II (MOBITZ II) and what is seen on ECG
Occurs lower in the bundle of HIS or bundle branches. P wave present BUT QRS is sometimes absent. Can progress to 3rd Degree
106
Causes of second degree type II block
Heart Disease
Acute Inferior Wall MI
Ischemic Heart Disease
Increased Vagal Tone
Right ventricular infarct
107
Nursing interventions for second degree type II block
Find and treat cause
Trend P & QRS complex interval
May require pacemaker or transcutaneous pacing in emergency if patient symptomatic
Medications: Atropine if symptomatic or slow
108
What is a 3rd degree heart block and what is seen on the ECG
No atrial impulses are conducted through the A/V node
The Atria and Ventricles are beating independently of one another.
P and QRS do not synchronize with one-another
109
Causes of third degree heart block
Heart Disease
Acute Myocardial Infarction
Ischemic Heart Disease
Conduction system disorder
110
Nursing interventions for third degree heart block
Find and treat cause
REQUIRES temporary pacemaker or transcutaneous pacing
Permanent pacemaker needed!
Trend P & QRS complex interval
111
What is sinus pause/sinus arrest (atrial standstill)
> 2 second pause without heart beat.
SA Node does not generate ANY signal. Rate prior to pause/arrest is typically regular, however, A-fib/flutter can break and cause a pause
AV Node is not stimulated, and fails to back up
112
Causes of sinus pause/arrest
Acute Infection
SA Node Fibrosis
Increase Vagal Tone
Dixogin & Salicylates Toxicity
Beta-Blocker Excess Dose
Ca+ Channel Blockers
Myocarditis
MI
Sick Sinus Syndrome
113
What is done for sinus pause/arrest
Watch Patient!
Fall Risk, Syncope, Safety Digoxin or Salicylate levels
Reduce or eliminate Beta-Blockers or Ca+ Channel Blockers
Atropine or Epinephrine along with temporary or transcutaneous pacing if pause causes circulatory collapse/patient is symptomatic
May require permanent pacemaker
Trend P & QRS complex interval
114
Difference of millivolts and milliamperes
Electrical Output: Amount of energy delivered in order for depolarization to happen. Millamperes(mA)
Sensitivity: The ability for the pacemaker to recognize the intrinsic rate of the body. Millivolts (mV)
115
What happens when a pacemaker fails to pace? What is seen on ECG? Causes? Fixes?
Pacemaker does not fire and initiate a response when it should
No pacer spikes present on EKG
Caused by: Generator malfunction, Wire problems, Battery issues
Fix: turn up milliamperes to try to stimulate responses, change battery
Support patient until fix can be done
116
What happens when a pacemaker fails to capture? What is seen on the ECG? Causes? Fixes?
Pacemaker generates an impulse, but no response from chamber occurs
Pacer spike present, no subsequent EKG wave
Causes: Not adequate mA, displacement of wires from myocardium, increased pacing threshold (meds, or electrolyte imbalance), battery issue or fractured pacer wires
Troubleshoot: check the medications patient is on, turn up the amperage
117
What happens when a pacemaker fails to sense? What is seen on ECG? What's the danger? What are causes?
Pacemaker does not sense the intrinsic rate of the heart (millivolt problem) and fires anyway
Pacer spikes present, but fall too close or in EKG complexes
Can initiate lethal arrhythmias (R on T phenomenon)
Causes: Displacement of pacemaker wire, or pacemaker not set to sense at adequate mV
118
What is the acronym for caring for someone post pacemaker insertion
PACER
119
What is the care for a patient post pacemaker insertion
P= Pulse, monitor and teach patient to take pulse each day. Notify provider if <5 BPM below preset rate of pacemaker. Pain meds for incision site pain.
A= Assess insertion site for: redness, swelling, drainage or hematoma.
C= Control shoulder movement. Do no lift arm above head. Put in sling. No heavy lifting for up to 2 month, maybe more.
E= Evaluate rhythm strip for proper pacing spikes
R= Record device, date and time of insertion, programmed mode, rhythm strip, and patient response to procedure. Recommend medic alert bracelet and carry pacemaker ID. Relate all pacemaker to providers before tests (MRI), or procedures.
120
What should the nurse always do with pulses and ECG
Comparision
121
When working with temporary pacemakers what is essential for patient safety
Wear gloves at all times
122
Normal PT level (coagulation)
10-15 seconds
123
Normal INR and what will people have on anticoagulants
Less than 1.1 for healthy people. 2-3.5 for those on anticoagulants
124
Normal PTT level
60-70 seconds
125
What are classifications and risks for platelet values
Less than 150,000/microliter is classified as thrombocytopenia.
People are at risk for spontaneous hemorrhage when platelet counts are below 30,000/mcl
People are at risk for fatal hemorrhage when platelets fall below 10,000
126
What is ITP
Decreased platelet formation by bone marrow, increased destruction of platelets, abnormal distribution of platelets
127
Signs and symptoms of ITP
Ecchymosis, oozing from sites, petechiae
128
Treatment of ITP
Infusion of platelets
129
What is heparin induced thrombocytopenia
Heparin binds to platelet producing PF4. Some can develop antibodies which can attach to PF4 causing macrophages to attack the platelets. This creates sticky microparticles that cause platelets to clot together. Patients have hypercoagulability and thrombosis rather than bleeding
130
Diagnosis of HIT
50% decrease in platelet count after 5-10 days from start of heparin therapy
131
Risks for HIT
Unfractionated heparin followed by low molecular weight heparin. Recent major surgery
132
Treatment of HIT
DISCONTINUE HEPARIN, argatroban / danaparoid / bivalirudin are all medications that can be given but are ineffective in some and very expensive. Do not give platelets until heparin is out of body
133
What are causes of DIC
Vessel injury caused by disease states, tissue injury, or a foreign body in the bloodstream
134
What is the priority with DIC
Tissue perfusion
135
Diagnosis of DIC is made through
ELEVATED FIBRINOGEN DEGRADATION PRODUCTS(FDP) OR FIBRINOGEN SPLIT PRODUCTS (FSP) : (NORMAL <10 MCG/ML)
INCREASED D-DIMER : (NORMAL <100 MCG/L)
DECREASE ANTITHROMBIN III: (NORMAL >50% OF PLASMA)
136
Medications that can be given for DIC
Heparin, antithrombin III, amicar (prevents fibrinolysis)
137
What are risks for patients getting coronary bypass graft surgery
stroke and PE from blood stasis, bleeding from platelet destruction, electrolyte abnormalities from pleashge, hemodilution
138
What is a valvuloplasty
Repair of a cardiac valve. Most valvuloplasties require general anesthesia and cardiopulmonary bypass
139
What is a commissurotomy
Repair to the commissures between the valve leaflets (where the leaflets meet). Indicated for stenosis or regurgitation
140
What is an annuloplasty
Repair of the valve annulus (junction of the valve leaflets and the muscular heart wall)
141
What are the 4 types of shock
Hypovolemic, distributive, cardiogenic, obstructive
142
What are the 4 stages of shock
Initial (hypoperfusion), compensatory, progressive (failure of compensatory mechanisms), refractory (unresponsive to therapy)
143
What happens in progressive stage of shock
Profound cardiovascular effects
Continued Hypoperfusion -> Profound Vasoconstriction:
Extremity ischemia, Cellular hypoxia, Anaerobic metabolism
Lactic acid production continues (metabolic acidosis takes over), Failure Na+/K+ pump
Increased capillary hydrostatic pressure -> Fluid leaks to peripheral tissues resulting in profound EDEMA
Continued decreased circulating intravascular volume
Decreased coronary perfusion
Decreased myocardial contractility
144
Initial and late neurologic changes with shock
Initial stage: Anxiety/restlessness
Late stage: LOC/Coma
145
Initial and late cardiovascular changes with shock
Blood pressure
Initial -> Compensatory stage: Fight of flight initiation = BP Slightly elevated & C/O elevated
Late Compensatory -> Refractory stage: Low B/P & Low C/O
Pulses: Elevated throughout
146
Pulmonary system initial and late changes with shock
Early stages: Rapid, deep respirations trying to offset hypoxia. Counteracting acidosis
Late stages: Shallow respirations
Poor gas exchange
147
Renal system initial and late changes with shock
Initial: Decreased glomerular filtration -> Oliguria. Increase BUN
Activated renin-angiotensin aldosterone system. Sodium retention Water reabsorption Vasoconstriction
Late Stages:
AKI -> Anuria, increasing metabolic acidosis, edema, lethal electrolyte levels
148
GI system initial and late changes with shock
Slowing intestinal activity
Decreased bowel sounds, distension, nausea, and constipation
Of critical importance is damage to the intestinal microvilli, allowing intestinal bacteria to translocate from the gut to other areas, increasing the patient’s risk for SEPSIS
149
Hepatic initial and late changes with shock
Altered liver enzymes
Clotting disorders -> Risk for bleeding
Increased susceptibility to infection
Inability to detoxify medications
Hepatic encephalopathy
Poor glucose control
150
Hematological initial and late changes with shock
Consumptive coagulopathy or Disseminated Intravascular Coagulation (DIC):
Enhanced clotting/inhibited fibrinolysis
Depletion of clotting factors
Clotting in the microcirculation
151
Integumentary initial and late changes with shock
Skin color, temperature, texture, and turgor
Cyanosis-late/unreliable sign
Skin turgor taut from edema
Pooling of blood causes mottling
Cool, clammy skin from massive vasoconstriction
152
General management for shock
Treat underlying cause:
Reverse altered circulatory component
Maintain circulatory volume
Combination therapy:
Fluids: Bolus and continuous
Pharmacotherapy
Mechanical therapy
Minimize oxygen consumption
153
Normal PVR
20-120 mmHg
154
