Exam2 Flashcards
Pulmonary Embolism
Collection of particulate matter(air,solid,or liquid) that enters venous circulation and lodges in pulmonary vessel
Pulmonary Embolism Risk Factors
Prolonged immobility Central Venous Factors Surgery Obesity Advancing Age Conditions that increase blood clotting History of thromboembolism Pregnancy/Estrogen therapy Cancer Trauma Smoking
PE physical assessment
Dyspnea Pleuritic chest pain on inspiration Auscultation (crackles, wheezes, rubs) Dry or productive cough Tachycardia Low grade fever JVD Cyanosis, diaphoresis Hypotension Abnormally HR sounds Shock & or death
PE Lab Assessment
Early-Respiratory alkalosis(low PaCO2) Late- Respiratory acidosis followed by metabolic acidosis. Pulmonary Angiography CT-PA Chest X-Ray
PE nursing diagnosis
Hypoxemia related to mismatch of lung perfusion and alveolar gas exchange.
Hypotension related to inadequate circulation to left ventricle
Potential for inadequate clotting or bleeding related to anticoagulation
Anxiety related to hypoxemia and life threatening illness
Pain related to work of breathing
Fluid-volume deficient
Low cardiac output
Full risk
Skin breakdown
PE interventions
Elevate HOB/ Apply oxygen/ Call rapid response
Reassurance
Telemetry and continuous pulsOX
Maintain adequate venous access
Assess respitory and cardiac stratus AT LEAST q30min
Ensure that radiology and laboratory studies are completed and reported
Administer anticoagulants
APTT and PTT (partial thromboplastin time)
Measures heparin therapy
Common range 30-20sec
Therapeutic range 1.5-2.5
PT (prothrombin time/pro time)
Measures effectiveness of Coumadin therapy
Normal range 11-12.5sec
Therapeutic range 1.5-2 times normal range
INR international normalized ratio
Common range 0.8-1.1
Therapeutic for PE 2.3-3.0 to 4.5 for recurrent PE
Managing Hypotension w/PE
IV fluid therapy (crystalloid solution-isotonic-close to blood)
ECG monitoring & hemodynamic monitoring (CVP)
Monitor effectiveness of fluid therapy: urine output, skin turgor, moisture of mucous membranes
Drug therapy and vasopressors: dopamine, levophed, doubutamine, nitroprusside
Frequent physical assessment and VS
Minimizing bleeding
Thoracic Trauma
First emergency approach to all chest injuries is BAC( Breathing/Airway/Circulation) a rapid assessment and treatment of life-threatening conditions
Pulmonary contusion
Most common- Rapid d-cel during car crashes
Potentially life threatening
Respiratory failure can develop
Hemorrhage and edema in&between alveoli reducing lung movement and available area for gas exchange
Can develop dyspnea or hypoxia over time
Bruising over chest/cough/tachycardia/tachypnea
Breath sounds
Chest x-Ray will develop transparency
Rib fractures
Blunt force trauma to chest.
Increase risk for deep chest injury (pulmonary contusion/pneumothorax/ hemothorax
Pain on movement and splints affected area
Pre-existing lung condition ^risk of pneumonia&atelectasis
Treatment: analgesics of pain and promote normal ventilation
Flail Chest
Result of blunt chest trauma (high speed car crashes)
Cardiopulmonary resuscitation
Fractures at least two neighboring ribs in two or more places causing PaRDOXICAL chest wall movement- injuries to underlying tissue and structures-impairs gas exchange
Assess for ^/ tachycardia/ cyanosis/ SOB/hypotension
Flail Chest interventions
Humidified oxygen Pain management Cough&Deep breathing Tracheal suctioning Mechanical PEEP ABGs VS fluid and electrolyte imbalances Pain/ SaO2
Pneumothorax
Injury that allows air to enter pleural space. (Increases chest pressure and reduces vital capacity)(lung collapse)
Blunt chest trauma or medical procedure
Assessment:
Reduced breath sounds on affected sign
Hyperresonance on percussion
Lack of chest wall movement on affected side
Deviation of trachea away from side of injury (tension pneumothorax)
Pleuritic pain/tachypnea/ subQ emphysema
Pneumothorax interventions
Chest x-Ray Chest tubes Pain control Pulmonary hygiene Continuous assessment for respiratory failure
Tension Pneumothorax
Rapidly developing and life threatening complication of blunt chest trauma resulting from an air leak in the lung or chest wall
Causes compete collapse of affected lung
Air entering pleural space upon inspiration does not exist upon expiration
Air under pressure collapse blood vessels and decrease blood return
Can quickly become fatal
Assessment findings of Tension Pneumothorax
Asymmetry of the thorax
Tracheal movement away from midline towards the unaffected side
Extreme respiratory distress
Absence of breath sounds
Distended neck veins
Cyanosis
Hypertympanic sound on percussion over affected side
Hemodynamic instability
ABGs reveal hypoxia and respiratory alkalosis
Chest x-Ray reveals collapsed lung and shifting of internal organs away from affected side.
Management of tension pneumothorax
Needle thoracostomy with large-bore needle inserted in 2nd intercostal space midclavicular line of affected space.
Chest tube in forth intercostal space to water seal drainage system
Pain control
Pulmonary hygiene
Psychosocial interventions
Hemothorax &assessment findings
Common after blunt trauma or penetrating injuries
-simple or massive
-bleeding from injury to lung tissue, or fractured ribs/sternum
-bleeding from trauma to heart/great vessels/intercostal arteries
Assessment
Respiratory distress with decreased breath sounds on affected side
Percussion on affected side is dull
Chest X-ray reveals blood on pleural space
Hemothorax interventions
Focused on removing blood to improve breathing and prevent infection Chest tube to drain pleural cavity Serial chest X-rays Aggressive pain management Frequent VS I&O Transfusions and and fluid replacement Surgical management Open thoractomy for large initial blood or persistent bleeding Mechanical ventilation
Chest tubes
- Drain air/blood/or fluid from pleural space or thoracic cavity.
- Used after thoracic surgery, pneumothorax, hemothorax, palliative treatment of lung cancer of heart failure.
- placed in pleural space to allow lung re-expansion and prevention of air and fluid moving back into chest cavity
- may or may not be attached to suction
- has water seal compartment to ensure no air gets back to pt
Placement and care of chest tubes.
- tip of tube is placed near the front lung apex when draining air
- tip of tube is placed on side near base
- insertion sight is protected with airtight dressings
- approx 6ft of tubing from end of chest tube to closed container placed below pt chest (allows pt movement)
- Three parts on Pleur-Vac: collection chamber/water seal chamber/suction regulator
Chamber #1
Cheeks fluid draining from the pt and is checked hourly.
If end of tubing is under fluid level in collection chamber, pt can develop pneumo.
Chamber #2
Water seal that prevents air from reentering the pt pleural space.
Air from pt pleural space travels through collection chamber where it is trapped under water and causes gentle bubbling (tidaling) in the chamber as air escapes. KEEP FILLED WITH 2CM.
Bubbling will stop once air is removed from pt chest cavity.
Blocked or kinked tubing can also cause bubbling to stop.
EXCESSIVE bubbling indicates air leak.
Chamber #3
Suction control system. Wet or dry suction available; amount of suction in system is determined by manufacturer. NOT wall suction amount.
Management of Chest tube Drainage system
- maintain patency and sterility of drainage system
- keep manipulation of tubing to a minimum
- frequent respiratory assessment of pt
- frequent check of device
- pain management
- respiratory management
- TCDB&A (turn/cough/deep breath/ambulate)
Coronary Artery Disease
Single largest killer of American Men and Women in all ethnic groups.
Causes decreased function of the myocardium resulting in decreased perfusion to vital organs and tissues
Results in ischemia and infarction of myocardial tissue
Includes stable and unstable angina
Acute coronary syndrome
- Describes unstable angina and acute myocardial infarction
- Atherosclerosis plaque in coronary artery ruptures causing platelet aggregation, thrombus formation, and vasoconstriction
Three categories of acute coronary syndrome
Classified according to ST-segment elevation on ECG and serum troponin markers
ST-elevation MI (STEMI) traditional manifestation
Non-ST elevation MI (NSTEMI) common in women
Unstable angina pectoris
Unstable angina
Chest pain or discomfort that occurs at rest or with exertion and causes severe activity intolerance.
May last longer than 15min or not relieved by rest or NTG.
May have ECG changes (ST elevation) but NOT troponin or CK-MB changes.
Untreated may lead to a MI
Acute Myocardial Infarction
Myocardial tissue abruptly and severely deprived of oxygen; BF
NSTEMI
WILL NOT HAVE ST elevation. Will have ST segment and T wave changes on 12 lead indicating myocardial ischemia; enzymes elevate over 3-12hrs
STEMI
WILL HAVE ST elevation in TWO contiugous leads on 12 lead ECG; caused by plaque rupture and complete occlusion of coronary artery
Acute MI manifestations
Dynamic process-evolves over several hours
Hypoxemia from ischemia
Acidosis and electrolyte imbalances: catecholamine release causes ^HR/contractility/and after load
^O2 demand may cause life threatening ventricular dysrhythmias
Extent of infarction depends on what three things?
1) collateral circulation (build more vessels)
2) metabolism
3) workload demands on myocardium
Timeframe of what heart muscle will look like
6hrs-tissue blue&swollen
48hrs-infarction gray area and yellow striped
8-10days- granulation tissue develops
3months- thin firm scar formation causes ventricular remodeling
LAD
Left anterior or Septal MI
HIGHEST mortality rate
Ventricular dysrhythmias
Circumflex
Left lateral ventricle/possible posterior wall
SA node and AV node
Sinus dysrhythmias
RCA
SA&AV nodes
Right ventricle and inferior portion of LV
RIGHT SIDED MI
Atherosclerosis Risk Factors Non-modifiable vs Modifiable
NON: Age/gender/family history/ethnic background
MODIFIABLE: ^serum lipid levels/smoking&tobacco use/limited physical activity/HTN/Diabetes mellitus/Obesity/Excessive alcohol/excessive stress/poor coping skills
Metabolic Syndrome (Syndrome X) Risk factors
Additional risk factor for cardiovascular disease.
HTN:BP^130/85 OR HTN meds
160men >135women) OR anti cholesterol MEDS
^FBS 100 or higher OR anti diabetic MEDS
Large waist size (Men:40in/102cm Women:35in/89cm) central obesity
Pt centered collaborative care
History: dependent on presenting symptoms
Physical assessment: RAPID: VS/Pain/Symptoms
Psychological: denial/fear/anger/depression (include family)
LAB: troponin/ CK-MB
Radiology: chest X-Ray
12lead ECG w/in 10 minutes
Immediate assessment for ACS
Labs
ECG
Time tissues/minutes muscle
Managing pain?
MORPHINE
OXYGEN
NTG
ASPRIN
IV access X2
Improving Cardiopulmonary Tissue Perfusion
Adequate cardiac output
Normal sinus rhythm
VS WNL
ALL within 90min from door
Aspirin for ACS
Aspirin: 4baby (81mg x 4 = 325mg)
Calcium Channel Blockers for ACS
Promotes vasodilation and MI perfusion
Only for angina or HTN
Glycoproteins inhibitors for ACS
Glycoprotein inhibitors: Aggrastat/abciximab/eptibatide IV to prevent fibrinogen from attaching to activated platelets @site of thrombus.
Beta-adrenergic agents for ACS
Beta-adrenergic agents: metoprolol/carvedilol decrease the size of infarct/ occurrence of Ventricular dysrhythmias/&mortality rates. Heart can perform more work w/o ischemia
AECIs&ARBs for ACS
AECIs & ARBs: given within 48hrs if EF
Thrombolytic therapy for ACS
Fibrinolytics dissolve thrombi in coronary arteries and restore myocardial blood flow.
Tissue plasminogen activator: (t-PA/ alteplase (activate)) IV
Reteplace (retavase): IV
Tenectaplace (TNK) IV
Percutaneous Coronary Intervention
Used to reopen clotted coronary artery and restore perfusion preferably w/in 2-3hrs of on test of symptoms
Indications that artery has re-perfused
1) abrupt cessation of pain or discomfort
2) sudden onset of ventricular dysrhythmias
3) resolution ST-segment depression/elevation or T-wave inversion
4) a peak at 12hrs of markers of myocardial damage
Post thrombolytics
Heparin infusion 3-5days to maintain coronary patency due to large amount of thrombin released into system potentially causing rare-occlusion
- aPTT usually 1.5-2.5 times control sample
- Enoxaparin(lovenox) IV 1mg
Coronary Artery BYpass Graftt
Open heart surgical procedure to replace occluded artery with earth pt vessel or synthetic graft substance (Internal Mammary Artery vessel of choice)
IABP
Intra Aortic Balloon Bypass machine
Maintain as perfusion of coronary arteries in HF or post procedure
Arterectomy or Stent Placement
Use of angiography to remove plaque and maintain patency of coronary artery
Hemodynamic Monitoring
Swan Gauze Catheters/CVP(central venous pressure)/PAWP(pulmonary artery wedge pressure) /RAP(right atria pressure)
Cardiogenic Shock
is a condition in which your heart suddenly can’t pump enough blood to meet your body’s needs. The condition is most often caused by a severe heart attack. Cardiogenic shock is rare, but it’s often fatal if not treated immediately.
Cardiogenic Shock S/Sx
Confusion or lack of alertness. Loss of consciousness. A sudden and ongoing rapid heartbeat. Sweating. Pale skin. A weak pulse. Rapid breathing. Decreased or no urine output. Cool hands&feet
Cardio genie shock treatment
Assessment
Fluid
Drugs
Oxygen
Pt centered collaborative care
History: dependent on presenting symptoms
Physical assessment: RAPID: VS/Pain/Symptoms
Psychological: denial/fear/anger/depression (include family)
LAB: troponin/ CK-MB
Radiology: chest X-Ray
12lead ECG w/in 10 minutes
Immediate assessment for ACS
Labs
ECG
Time tissues/minutes muscle
Managing pain?
MORPHINE
OXYGEN
NTG
ASPRIN
IV access X2
Improving Cardiopulmonary Tissue Perfusion
Adequate cardiac output
Normal sinus rhythm
VS WNL
ALL within 90min from door
Aspirin for ACS
Aspirin: 4baby (81mg x 4 = 325mg)
Calcium Channel Blockers for ACS
Promotes vasodilation and MI perfusion
Only for angina or HTN
Glycoproteins inhibitors for ACS
Glycoprotein inhibitors: Aggrastat/abciximab/eptibatide IV to prevent fibrinogen from attaching to activated platelets @site of thrombus.
Beta-adrenergic agents for ACS
Beta-adrenergic agents: metoprolol/carvedilol decrease the size of infarct/ occurrence of Ventricular dysrhythmias/&mortality rates. Heart can perform more work w/o ischemia
AECIs&ARBs for ACS
AECIs & ARBs: given within 48hrs if EF
Thrombolytic therapy for ACS
Fibrinolytics dissolve thrombi in coronary arteries and restore myocardial blood flow.
Tissue plasminogen activator: (t-PA/ alteplase (activate)) IV
Reteplace (retavase): IV
Tenectaplace (TNK) IV
Percutaneous Coronary Intervention
Used to reopen clotted coronary artery and restore perfusion preferably w/in 2-3hrs of on test of symptoms
Indications that artery has re-perfused
1) abrupt cessation of pain or discomfort
2) sudden onset of ventricular dysrhythmias
3) resolution ST-segment depression/elevation or T-wave inversion
4) a peak at 12hrs of markers of myocardial damage
Post thrombolytics
Heparin infusion 3-5days to maintain coronary patency due to large amount of thrombin released into system potentially causing rare-occlusion
- aPTT usually 1.5-2.5 times control sample
- Enoxaparin(lovenox) IV 1mg
Coronary Artery BYpass Graftt
Open heart surgical procedure to replace occluded artery with earth pt vessel or synthetic graft substance (Internal Mammary Artery vessel of choice)
IABP
Intra Aortic Balloon Bypass machine
Maintain as perfusion of coronary arteries in HF or post procedure
Arterectomy or Stent Placement
Use of angiography to remove plaque and maintain patency of coronary artery
Hemodynamic Monitoring
Swan Gauze Catheters/CVP(central venous pressure)/PAWP(pulmonary artery wedge pressure) /RAP(right atria pressure)
Cardiogenic Shock
is a condition in which your heart suddenly can’t pump enough blood to meet your body’s needs. The condition is most often caused by a severe heart attack. Cardiogenic shock is rare, but it’s often fatal if not treated immediately.
Cardiogenic Shock S/Sx
Confusion or lack of alertness. Loss of consciousness. A sudden and ongoing rapid heartbeat. Sweating. Pale skin. A weak pulse. Rapid breathing. Decreased or no urine output. Cool hands&feet
Cardio genie shock treatment
Assessment
Fluid
Drugs
Oxygen
5 lead ECG placement
Sky+/grass(ground) DIRT- Smoke+/fire+
White+/green(ground) Brown- Black+/red+
Automaticity
the ability of cardiac cells to generate
an electrical impulse spontaneously and repetitively
Excitability
is the ability of non-pacemaker heart cells to respond to an
electrical impulse that begins in pacemaker cells and to depolarize.
Conductivity
is the ability to send an electrical stimulus from cell
membrane to cell membrane. As a result, excitable cells depolarize in
rapid succession from cell to cell until all cells have depolarized
Contractility
is the ability of atrial and ventricular muscle cells to
shorten their fiber length in response to electrical stimulation, causing
sufficient pressure to push blood forward through the heart. In other
words, contractility is the mechanical activity of the heart
Sinoatrial node
Electrical impulses 60-100bpm
P wave on ECG
Depolarization of atrium
Atrioventricular junction
AV node itself PR segment on ECG-Here T-cells (transitional cells) cause impulses to slow down or to be delayed in the AV node before proceeding to the ventricles Contraction known as "atrial kick" 30-40% of cardiac output
Purkinje cells
make up the
bundle of His, bundle branches, and terminal Purkinje fibers. These cellsare responsible for the rapid conduction of electrical impulses throughout the ventricles, leading to ventricular depolarization and the subsequent ventricular muscle contraction
Action potential of Cardiac Muscle cell
A slow influx of NA+ into the cell, once it reaches a threshold CA+ RUSHES into the cell causing DEPOLARIZATION and muscle contraction, as the CA+ rushes in the K- rushes out.
Cell slowly returns to a REPOLARIZED state as CA+ and NA+ leave the cell and K- renter the cell.
How many seconds does each tiny box equal?
0.4 seconds
How many seconds does FIVE tiny boxes equal?
How many TINY boxes equal a LARGE box?
0.2 seconds
5 tiny boxes = 1 Large box
How many seconds does 15 large boxes equal? 30?
3 seconds
6 seconds
What is the P wave on a ECG
Atrial depolarization
PR segment on the ECG?
Represents the time required for the impulse to travel through the the AV node, where it is delayed and then through the bundle of his, bundle branches, and purkinje fiber networks, just before ventricular depolarization.
PR interval?
Represents the time required for atrial depolarization as well as impulse travel through the conduction system and the purkinje fiber network, inclusive of the P wave and PR segment. It is measured from the beginning of the P wave to the end of the PR segment.
QRS complex?
Represents ventricular depolarization and is measured from the beginning of the Q wave to the end of the S wave.
ST segment?
Represents early ventricular depolarization.
T wave?
Represents ventricular repolarization.
U wave?
Represents late ventricular repolarization.
QT interval?
Represents the total time required for ventricular depolarization and repolarization.
Measured from the begging of the QRS complex to the end of the T wave.
How do you determine a HR using an ECG?
Measure the number of QRS complexes in 6 seconds(30 boxes) and multiply by 10.
What is Norma PR interval time?
0.12-0.2 seconds (3-5 TINY boxes)
What is normal time for QRS complex?
0.04-0.10 (ONE to TWO and a HALF tiny boxes)
What does A-fib look like on an ECG?
Absence of P waves. Or the look of multiple or NO P waves.
The P wave kind of flutters before the QRS complex.
Atrial Fibrillation
Most common
Associated with atrial fibrosis and loss f muscle mass
Common in heart disease: COPD/ HF/ Coronary artery disease/ HTN
Cardiac output can decrease by 20-30%
Atrial rate can be 350-400bpm
What does April flutter look like on an ECG?
Saw tooth pattern.
What is Atrial flutter? How do you fix it?
Re-entrant tachydysrythmia that produces flutter waves at rates between 220 and 350BPM
Typically 1/2 of atrial beats are stopped at the AV node.
Atrial rate of 300 would have ventricular rate of 150.
Cardioversion and Calcium channel blockers.
Cardioversion?
Synchronized countershock.
Used in emergencies for unstable ventricular/supra ventricular tachydysrythmias
Ventricular Tachycardia or Vtach
Look like?
How do you fix?
Causes?
FAST Wide blizzard QRS complex
EMERGENCY
VERY fast ventricular beats.
Normal
What is SVT Supraventricular tachycardia?
How do you fix?
Look like?
Rapid stimulation of atrial tissue occurs at rate of 100-280 BPM
Vagal maneuvers/carotid massage/Adenosine 12mg FAST repeat 6mg x2. Stimulates parasympathetic system
Narrow QRS
