3. PCCN REVIEW PART 1
OBJECTIVES
1. Understand the different types of acute coronary syndromes.
2. Identify basic coronary circulation and how it relates to different types
of myocardial infarctions.
3. Anticipate potential complications associated with an AMI.
4. Identify the standard treatment of an AMI.
5. Distinguish between various AV blocks.
6. Recognize the signs & symptoms of heart failure.
7. Identify the treatment of heart failure.
8. Recognize the general definition and classifications of aortic
aneurysms.
9. Understand the different types of aortic dissections.
10. Recognize the signs & symptoms of cardiomyopathy.
11. Differentiate between the different types of cardiomyopathy.
12. Identify the treatment for the different types of cardiomyopathy.
4. PCCN REVIEW PART 1
OBJECTIVES
13. Understand the different stages of shock.
14. Differentiate between different types of shock.
15. Distinguish between arterial and venous peripheral vascular disease.
16. Identify the various treatments for peripheral vascular disease.
17. Define respiratory failure.
18. Identify the various treatments for acute respiratory failure.
19. Recognize the signs & symptoms and causes of various respiratory
alterations.
20. Identify the standard treatment for various respiratory alterations.
21. Explain the common causes of gastrointestinal bleeding.
22. Describe the most commonly seen treatments for GI bleeding.
23. Describe the signs & symptoms of acute pancreatitis and available
treatments.
6. Acute Coronary Syndrome
DEFINITIONS
– Term used to cover a group of symptoms
compatible with acute myocardial ischemia
– Acute myocardial ischemia is insufficient blood
supply to the heart muscle usually resulting from
coronary artery disease
7. Acute Myocardial Infarction
DEFINITION
– Infarction occurs due to mechanical obstruction
of a coronary artery (or branch) caused by a
thrombus, plaque rupture, coronary spasm
and/or dissection.
– STEMI vs. NSTEMI (non-STEMI)
8. Acute Myocardial Infarction
SIGNS & SYMPTOMS
– Complains Vary
May include crushing chest pain (which may or may
not radiate), back, neck, jaw, teeth and/or epigastric
pain, SOB, nausea/vomiting and dizziness
– ST elevations on ECG
– Elevated cardiac enzymes
9. Acute Myocardial Infarction
SIGNS & SYMPTOMS
↑ PAWP, ↓ CO, ↑ SVR, dysrhythmias, S4,
cardiac failure, cardiogenic shock
– Diaphoresis, pallor, referred pains
– Diabetics and women often present abnormal
symptoms
11. 12 Lead ECG
I AVR V1
V4
II AVL V2 V5
III AVF V3 V6
II
V
12. Acute Myocardial Infarction
ST ELEVATIONS
– Anterior Wall MI
Leads V1-V4
Reciprocal changes in leads II, III, and aVF
Area supplied by the LAD
– Inferior Wall MI
Leads II, III and aVF
Reciprocal changes in leads I, and aVL
Area usually supplied by the RCA
13. Acute Myocardial Infarction
ST ELEVATIONS
– Lateral Wall MI
I, aVL, V5 and V6
Area supplied by the Circumflex artery
– Posterior Wall MI
Reflected on the opposite walls
Opposite deflections
18. Acute Myocardial Infarction
NURSING INTERVENTIONS
– O2
– Bedrest
– Serial ECG’s
– Serial cardiac enzymes
– Keep pain free (NTG. MSO4)
– MONA (Morphine, O2, Nitroglycerin, Aspirin),
Heparin, beta-blockers, and ace inhibitors. May also
include thrombolytics or Gp2b3a inhibitors
– PCI, PTCA, IABP, CABG
19. Acute Myocardial Infarction
TREATMENT
– Time Is Heart Muscle
– Prompt ECG
– Goals: Relieve pain, limit the size of the
infarction and to prevent complications
(primarily lethal dysrhythmias)
20. Acute Myocardial Infarction
TREATMENT
– MONA (Morphine, O2, Nitroglycerin, Aspirin),
Heparin, beta-blockers, and ace inhibitors.
May also include thrombolytics or Gp2b3a
inhibitors
– Cardiac Catheterization (with angioplasty,
atherectomy and/or stent)
– IABP, CABG, education
25. Aortic Aneurysms
DEFINITION
– A bulge or ballooning of the aorta
When the walls of the aneurysm include all three
layers of the artery, they are called true aneurysms
When the wall of the aneurysm include only the
outer layer, it is called a pseudo-aneurysm
– May be thoracic or abdominal
27. Aortic Aneurysms Rupture
An aortic aneurysm, depending on its size, may
rupture, causing life-threatening internal bleeding
The risk of an aneurysm rupturing increases as the
aneurysm gets larger
The risk of rupture also depends on the location of
the aneurysm
Each year, approximately 15,000 Americans die of a
ruptured aortic aneurysm.
28. Aortic Aneurysms
CLASSIFICATIONS
– Classified by shape, location along the aorta,
and how they are formed
– May be symmetrical in shape (fusiform) or a
localized weakness of the arterial wall (saccular)
30. Aortic Aneurysms
SIGNS & SYMPTOMS
– Often produces no symptoms
– If an aortic aneurysm suddenly ruptures it presents
with extreme abdominal or back pain, a pulsating
mass in the abdomen, and a drastic drop in blood
pressure
– An increase in the size of an aneurysm means an
increased in the risk of rupture
31. Aortic Aneurysms
THORACIC SIGNS & SYMPTOMS
– Back, shoulder or neck pain
– Cough, due to pressure placed on the trachea
– Hoarseness
– Strider, dyspnea
– Difficulty swallowing
– Swelling in the neck or arms
32. Aortic Dissections
DEFINITION
– Tearing of the inner layer of the aortic wall, which
allows blood to leak into the wall itself and causes
the separation of the inner and outer layers
– Usually associated with severe chest pain radiating
to the back
33. Aortic Dissections
A. Dissection B. Whenever the
beginning in the ascending aorta
ascending aorta is not involved
34. Aortic Dissections
A. Dissection B. Whenever the
beginning in the ascending aorta
ascending aorta is not involved
38. Aortic Aneurysms
TREATMENT
Medical management
– Controlled BP (within specific range)
Surgical repair
> 4.5 cm in Marfan patients or > 5 cm in non-
Marfan patients will require surgical
correction or endovascular stent placement
39. Cardiomyopathy
DEFINITION
– Diseases of the heart muscle that
cause deterioration of the function of
the myocardium
40. Cardiomyopathy
CLASSIFICATIONS
– Primary / Idiopathic (intrinsic)
Heart disease of unknown cause, although viral
infection and autoimmunity are suspected causes
– Secondary (extrinsic)
Heart disease as a result of other systemic diseases,
such as autoimmune diseases, CAD, valvular
disease, severe hypertension, or alcohol abuse
42. Hypertropic Cardiomyopathy
Bizarre hypertrophy of the septum
– Previously called IHSS
Idiopathic Hypertropic Subaortic Stenosis
– Known as HOCM
Hypertropic Obstructive Cardiomyopathy
Positive inotropic drugs Should Not Be Used
↑ Contractility will ↑ outflow tract obstruction
Nitroglycerin Should Not Be Used
– Dilation Will Worsen The Problem
44. Hypertropic Cardiomyopathy
TREATMENT
– Relax the ventricles
Beta Blockers
Calcium Channel Blockers
– Slow the Heart Rate
Increase filling time
– Use Negative Inotropes
Optimize diastolic filling
– Do Not use NTG
Dilation will worsen the problem
45. Restrictive Cardiomyopathy
Rigid Ventricular Wall
– Due to endomyocardial fibrosis
– Obstructs ventricular filling
Least common form
47. Dilated Cardiomyopathy
Grossly dilated ventricles without hypertrophy
– Global left ventricular dysfunction
– Leads to pooling of blood and embolic episodes
– Leads to refractory heart failure
– Leads to papillary muscle dysfunction secondary to
LV dilation
52. Conduction Defects
STABLE VS UNSTABLE
– Stable
Start with medications
– Unstable
Shock (cardioversion or defibrillation)
53. Normal Sinus Rhythm
Heart Rate 60 - 100 bpm
Rhythm Regular
P Wave Before each QRS & identical
PR Interval (in seconds) 0.12 to 0.20
QRS (in seconds) < 0.12
54. Atrial Fibrillation
AFib
– Multifocal atrial impulses at rate 300-600/min
– Irregular conduction to ventricles
55. Atrial Flutter
AFL
– Atrial impulses at rate of 250-350/min
– Regularly blocked impulses at the AV node
– Saw tooth flutter waves
56. Wandering Atrial Pacemaker
WAP
– Multiple ectopic foci in the atria
– Three or more p wave morphologies
– Rate < 100
57. Supraventricular Tachycardia
SVT
– Supraventricular rhythm at rate 150-250
– P waves cannot be positively identified
Atrial Tach = supraventricular rhythm with p wave morphology
that is noticeably different from the sinus p wave
59. Torsades de Pointes
Polymorphic VT
– VT with alternating ventricular focus
– Often associated with prolonged QT Rate < 100
60. Heart Blocks (AV Blocks)
Sinus Rhythm with First Degree AV Block
Sinus Rhythm with Second Degree AV Block, Type 1
Sinus Rhythm with Second Degree AV Block, Type 2
Third Degree AV Block
61. Heart Failure
DEFINITION
– A condition in which the heart cannot pump
sufficient blood to meet the metabolic needs of
the body
– Pulmonary (LVF) and/or systemic (RVF)
congestion is present.
62. Heart Failure
DEFINITION
– Pulmonary Edema
Fluid in the alveolus that impairs gas exchange by
altering the diffusion between alveolus and capillary
Acute left ventricular failure causes cardiogenic
pulmonary edema
Non-cardiogenic pulmonary edema is a synonym for
Adult Respiratory Distress Syndrome (ARDS)
63. Heart Failure
COMPENSATORY MECHANISMS
– Sympaththetic nervous system stimulation
Tachycardia
Vasoconstriction and increased SVR
– Renin-angiotensin-aldosterone system
activation
Hypo perfusion to the kidneys (renin)
Vasoconstriction (angiotension)
Sodium and water retention (kidneys)
Ventricular dilation
64. Heart Failure
FUNCTIONAL CLASSIFICATIONS
–(without noticeable limitations)
Class I
– Class II upon activity)
(symptoms
– Class III
(severe symptoms upon activity)
– Class IV
(symptoms at rest)
67. Shock States
DEFINITION
– Inadequate perfusion to the body tissues
– Low blood pressure with impaired perfusion
to the end organs
– May result in multiple organ dysfunction
68. Shock States
TYPES OF SHOCK
– Hypovolemic Shock
– Cardiogenic Shock
– Distributive Shock
– Obstructive Shock
69. Shock States
SIGNS & SYMPTOMS
The body attempts to compensate for shock:
1. Tachycardia
Attempts to deliver more blood to the tissues
2. Vasoconstriction
Attempts to maintain adequate BP in order to
adequately perfuse the body tissues
3. Increased ADH Secretion
ADH makes the body hold onto water in an effort to
maintain volume and thus enough blood pressure to
perfuse the body tissues
80. Peripheral Vascular Disease
SYMPTOMS ARTERIAL VENOUS
PAIN Upon walking While standing
PAIN RELIEF On resting, standing or Elevation of extremities
dependent position of lower limbs
EDEMA None Present, edematous
PULSES Decreased or absent May be difficult to palpate
INTEGUMENT Hair loss Brownish pigmentation
Skin shiny May be cyanotic when
CHANGES Nail thickening extremities are dependent
Pallor when elevated
Red when dependent
Ulcers located on toes, lateral Ulcers located on ankles,
ULCERS areas or site of trauma medial or pre-tibial areas
Gangrene possible
SKIN TEMPERATURE Cool Normal or warm
SEXUAL ISSUES Impotency Not present
Sexual dysfunction
81. Peripheral Vascular Disease
TREATMENTS
– Medical
Are they taking ASA, Coumadin, Ticlid, Plavix,
Oral Contraceptives, Hormones?
– Invasive
PTA, atherectomy, stents
– Surgical
Grafts
85. ARDS
DEFINITIONS
– Severe respiratory failure associated with pulmonary
infiltrates (similar to infant hyaline membrane disease)
– Pulmonary edema in the absence of fluid overload or
depressed LV function (Non-cardiogenic pulmonary edema)
– Originates from a number of insults involving damage to the
alveolar-capillary membrane
87. ARDS
PATHOPHYSIOLOGY
– Inflammatory mediators are released causing extensive
structural damage
– Increased permeability of pulmonary microvasculature
causes leakage of proteinaceous fluid across the alveolar–
capillary membrane
– Also causes damage to the surfactant-producing type II cells
88. ARDS
CXR CHARACTERISTICS
– Normal size heart
– No pleural effusion
– Ground Glass appearance
– Often normal early in the disease but may rapidly
progress to complete whiteout
92. ARDS
TREATMENT
– Respiratory Support
– PEEP, CPAP
93. Chronic Lung Disease
COPD
– Presents with hyper-inflated lung fields
Due to chronic air trapping
May be barrel chested
– May lead to cor pulmonale (right-sided heart failure)
Due to chronic high pulmonary pressures
– Often hypercarbic (high pCO2)
Often dependent upon hypoxic drive
95. Near Drowning
Salt Water
– Causes body fluids to shift into lungs
Osmosis: From low to high concentration
Results in hemoconcentration & hypovolemia
– Results in acute pulmonary edema
Fresh Water
– Fluids shift into body tissues
Results in hemodilution & hypervolemia
Can result in gross edema
– Damaged alveoli fill with proteinaceous fluid
May lead to pulmonary edema
96. Pneumonia
Lung infection (bacterial, viral, or fungal)
– Most commonly caused by Streptococcus
pneumoniae
Symptoms include fever, pleuretic chest
pain, productive cough, and tachypnea
– Often presents bronchial breath sounds over the
lung area
Treatment involves giving the right antibiotic
97. Pneumothorax
DEFINITIONS
– Simple pneumothorax
Results from buildup of air or pressure in the pleural space
– Spontaneous pneumothorax
May be due to blebs that rupture
The 2 key risk factors are increased chest length and
cigarette smoking
– Tension pneumothorax
Involves a buildup of air in the pleural space due to
one-way movement of air
Progressively worsens
Requires immediate intervention
101. Pneumothorax
SIGNS & SYMPTOMS
– Standard Pneumothorax
Sharp "pleuritic" chest pain, worse on breathing
Sudden shortness of breath
Dry, hacking cough (may occur due to irritation
of the diaphragm)
May cause mediastinal shift
– Tension pneumothorax
Signs of standard pneumothorax with signs of
cardiovascular collapse
Immediately life threatening
May cause mediastinal shift
102. Pneumothorax
TREATMENT
Spontaneous pneumothorax
– Depends on symptoms & size of pneumothorax
– Provide respiratory support
– May need chest tube or needle decompression
Some resolve without intervention
Tension pneumothorax
– Requires immediate intervention
– May cause cardiovascular collapse
– May need chest tube or needle decompression
2nd intercostal space
103. Pneumothorax
TREATMENT
– Pleurodesis
Chemical or surgical adhesion of the lung
to the chest wall
Used for multiple collapsed lungs or
persistent collapse
107. Pulmonary Embolism
Treatment
– Requires immediate intervention
– Provide respiratory support
– Treat pain & comfort
– Usually includes intravenous heparin
Heparin reduces risk of secondary
thrombus formation while clot is reabsorbed
– May require embolectomy
– May require thrombolysis
– May need umbrella filter
– May need long term anticoagulants
108. Respiratory Failure
DEFINITIONS
– Failure to maintain adequate gas exchange
– Inadequate blood oxygenation or CO2
removal
– PaO2 < 50 mmHg
and/or PaCO2 > 50 mmHg
and/or pH <
7.35
on Room Air
115. Respiratory Failure
TREATMENT
– Ensure Adequate Ventilation
↑ FiO2
Ineffective with shunting
Prolonged O2 > 40% causes O2 toxicity
Must use caution with CO2 retainers
– Chronic hypercapnia causes CO2 retainers
to use hypoxic drive
– Too much O2 can depress respirations
120. Gastrointestinal Bleeding
Hematemesis – vomiting of blood (or coffee ground
material) (indicates bleeding above the duodenum )
Melena – passage of black tarry stools > 50ml (indicates
degradation of blood in the bowel)
Hematochezia – passage of red blood (rectal bleeding)
Occult Bleeding – bleeding that is not apparent to the
patient and results from small amounts of blood
Obscure Bleeding – occult or obvious but source not
identified
121. Gastrointestinal Bleeding
Hematemesis – always UGI source
Melana – indicates blood has been in GI tract
for extended periods
– Mostly UGI
– Small bowel
– Rt colon (if bleeding relatively slow)
Hematochezia
– Mostly colon
– Massive UGI bleeding (not enough time for degradation)
122. Gastrointestinal Bleeding
TREATMENT
– Find the underlying cause
– Fluid volume replacement
– Endoscopy or colonoscopy
– Medical and /or surgical therapy
Somatostatin
IV or intra-arterial vasopressin
Sclerotherpay
Angiography with embolization
Electrocoagulation
Band ligation
Balloon tamponade (Sengstaken-Blackmore tube)
123. The Pancreas
The Pancreas secretes digestive enzymes,
bicarbonate, water, and some electrolytes into
the duodenum via the pancreatic duct
– Lipase, Amylase, Trypsin
The Pancreas also produces
and secretes insulin
124. Pancreatitis
DEFINITION
– An autodigestive process resulting
from premature activation of
pancreatic enzymes
125. Pancreatitis
PATHOSHYSIOLOGY
• Inactive pancreatic enzymes are activated outside
of the duodenum
• The swelling pancreas causes fluids to shift into
the retro peritoneum and bowel
• Fluid shifts can cause severe hypovolemia and
hypotension
• Inflammation cause commotion around pancreas
126. Pancreatitis
MANY CAUSES
– Alcoholism – Hypercalcemia
– Biliary Disease – Peptic Ulcer Disease
– Gallstones – Cystic Fibrosis
– Infections – Vascular Disease
– Hyperparathyroidism – Multiple Drugs
– Hypertriglyceridemia – Much Much More
129. Pancreatitis
TREATMENT
– Stabilization – Monitor For Complications
Correct Fluid And – Monitor Blood Sugar
Electrolyte Status
– Respiratory Support – Drug Therapies
– Control Pain Somatostatin,
Demerol Anticholinergics
– NG Tube – Watch For Signs Of
NPO Infection
– TPN – Pray
Restricted Diet
130. Pancreatitis
FULMINATING PANCREATITIS
• Overwhelming form
• Necrotizing form
• Extreme symptoms
• Seen with ESRF patients
• May lead to ARDS & DIC
131. Pancreatitis
FULMINATING PANCREATITIS
• Signs & Symptoms
Tachycardia & low BP (may be the only sign)
Pulmonary & cerebral insufficiency
Acute diabetic ketosis or oliguria
Hemorrhagic pancreatitis may appear
134. Resources
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131-142.
American Heart Association. (2005). Guidelines 2005 for Cardiopulmonary Resuscitation and
Emergency Cardiovascular Care. Available at: www.americanheart.org.
www.americanheart.org.
Anderson, L. (July 2001). Abdominal Aortic Aneurysm, Journal of Cardiovascular Nursing:15(4):1–14,
July 2001.
Chulay, M., Burns S. M. (2006). AACN Essentials of Critical Care Nursing. McGraw-Hill Companies,
Inc., Chapter 23.
Finkelmeier, B., Marolda, D. Aortic Dissection, Journal of Cardiovascular Nursing: 15(4):15–24.
Hughes E. (2004). Understanding the care of patients with acute pancreatitis. Nurs Standard: (18) pgs
45-54.
Irwin, R. S.; Rippe, J. M. (January 2003). Intensive Care Medicine. Lippincott Williams & Wilkins,
Philadelphia: pgs. 35-548.
Sole, M. L., Hartshorn, J., & Lamborne, M. L. (2001). Introduction to Critical Care Nursing (3rd ed).
Philadelphia: W. B. Saunders/Elsevier.
Thelan, L. A., Urden, L. D., Lough, M. E. (2006). Critical care: Diagnosis and Treatment for repair of
abdominal aortic aneurysm. St. Louis, Mo.: Mosby/Elsevier. pg 145-188.
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Management (5th ed). St. Louis, Mo.: Mosby/Elsevier.
Woods, S., Motzer, S. U. (2004). Cardiac Nursing (4th ed): Philadelphia: Lippincott Williams &
Wilkins.
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1751–1803.
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242-266.
Notes de l'éditeur
As plaque develops and the coronary arteries become increasingly narrower, collateral branches form to help supply those areas of heart muscle. MI’s with no collateral circulation tend to suffer more severe infarctions and more hemodynamic compromise. Edema and color changes (within the heart) are evident 6 hours after an MI. LV function is altered immediately in ischemic states as well as in infarctions. Wall thickness decreases 8 to 10 days later due to a natural physiological cleanup and/or necrotic tissue removal. Scar tissue and tissue remodeling occur later and may lead to cardiac failure. Transmural MI involves full thickness of the myocardium whereas subendocardial MI (non-Q wave) involves partial thickness.
Cardiac Enzymes: Troponin The troponin level rises within 4-6 hours after an AMI, peaks in 24 hours, and returns to baseline within 7-10 days. CK or CPK MB-CK is the cardiac specific isoenzyme MB-CK is normally less then 5% of the CK The CK level rises within 4-8 hours, peaks in 8-58 hours (with an average of 24 hours), and returns to baseline within 3-4 days. LDH LDH 1 is the cardiac specific isoenzyme When LDH 1 > LDH 2 , an AMI is probably occurring The LDH level rises within 24-48 hours, peaks within 3-6 days, and returns to baseline within 8-14 days. False positives enzyme levels may be seen in conditions that involve muscle injury (trauma, disease, vigorous exercise or rhabdomyolysis)
Coronary Circulation: RCA Supplies the SA node, AV node, bundle of his, posterior papillary muscles, inferior wall of the left ventricle, and the posterior third of the septum The RCA supplies most of the blood supply to the inferior wall of the left ventricle for most people A person is said to be right dominant when the RCA supplies most of the blood supply to the inferior wall (of the left ventricle) IWMI usually due to RCA occlusion Watch for problems associated with the SA node (tachycardia, bradycardia, sick sinus or sinus arrest), the AV node (AV blocks), the right ventricle (RV involvement), and the posterior papillary muscles (MR or papillary muscle rupture). LAD (branches off left main artery) Supplies the anterior wall of the left ventricle, some of the lateral wall, and most of the intra-ventricular septum (including it’s conduction system) AWMI usually due to LAD occlusion Watch for problems involving large areas of the anterior left ventricle (cardiogenic shock) and problems involving the septum (blocks and VSD). Circumflex (branches off left main artery) Supplies the lateral and posterior walls of the left ventricle A small percentage of people have a short RCA and the circumflex artery then wraps around and supplies most of the inferior wall A person is said to be left dominant when the circumflex artery supplies most of the blood supply to the inferior wall (of the left ventricle) Lateral and/or posterior wall MI usually due to circumflex occlusion
Two or more leads of a group: IWMI Leads II, III and aVF view the inferior wall (of the left ventricle) Reciprocal changes are seen in leads I, and aVL AWMI Leads V 1 -V 4 view the anterior-septal wall (left ventricle) Reciprocal changes are seen in leads II, III, and AVF Lateral wall MI Leads I, aVL, V 5 and V 6 view the lateral wall (left ventricle) Reciprocal changes are seen in leads II, III, and aVF Posterior wall MI Posterior MI’s are difficult to detect on a 12 lead EKG because no leads are placed directly over the posterior Changes are reflected on the opposite walls (Instead of ST elevations, you will see ST depression. Instead of Q waves, you will see tall R waves. Instead of T wave inversions, you will see upright T waves) Reciprocal changes may be seen in leads V 1 and V 2 Right Ventricle Leads V 6 R - V 3 R view the RV
Two or more leads of a group: IWMI Leads II, III and aVF view the inferior wall (of the left ventricle) Reciprocal changes are seen in leads I, and aVL AWMI Leads V 1 -V 4 view the anterior-septal wall (left ventricle) Reciprocal changes are seen in leads II, III, and AVF Lateral wall MI Leads I, aVL, V 5 and V 6 view the lateral wall (left ventricle) Reciprocal changes are seen in leads II, III, and aVF Posterior wall MI Posterior MI’s are difficult to detect on a 12 lead EKG because no leads are placed directly over the posterior Changes are reflected on the opposite walls (Instead of ST elevations, you will see ST depression. Instead of Q waves, you will see tall R waves. Instead of T wave inversions, you will see upright T waves) Reciprocal changes may be seen in leads V 1 and V 2 Right Ventricle Leads V 6 R - V 3 R view the RV
NTG Dilates coronary arteries Decreases preload (decreases afterload some) MSO 4 Morphine is the analgesic of choice with AMI because it also reduces preload and decreases myocardial oxygen demand. Morphine decreases anxiety, restlessness, and autonomic nervous system activity. Aspirin Inhibits platelet aggregation Heparin Prevents further extension of existing thrombi and/or new clot formation (blocks conversion of prothrombin to thrombin and fibrinogen to fibrin) Beta Blockers Slow heart rate and lower BP Encourages electrical stability Improves mortality ACE Inhibitors Reduce afterload (vasodilatation) Reduces work of heart Decreases remolding effects GP IIb IIIa Inhibitors (anti-thrombolytics) Integrilin Reopro Thrombolytics Given up to 12 hours from the onset of an AMI Contraindicated in patients with active bleeding, BP>200/120, major surgery within 2 weeks, CPR >10 min, recent head trauma, suspected aortic dissection, pregnancy, CVA within 1 year, history of a hemorrhagic CVA, of major illnesses or cancers Anti-Lipidemics HDH is associated with risk LDH is associated with risk Look at the HDL : LDL ratio
Increased incidence of sudden death or blood clots
Increased incidence of sudden death or blood clots
Generalized Treatment of Cardiomyopathy: Treat Symptoms Monitor For Signs of Worsening Heart Failure Daily Weights Prone To Digoxin Toxicity Due To Renal Perfusion Monitor Digoxin Levels Give Positive Inotropic Drugs (Except With Hypertropic Cardiomyopathy) Give Vasodilators (Except With Hypertropic Cardiomyopathy) Reduce Preload & Afterload Diuretics Calcium Channel Blockers As Indicated Beta Blockers As Indicated IABP Vasodilators As Indicated Fluid Restriction Give O2 With Exacerbations & As Needed Give Antidysrhythmic Agents As Needed Restrict Sodium Decrease Activity, Plan Activities & Rest Consider Heart Transplant Educate Patient & Family Give Emotional Support
AFib TREATMENT O2 and monitor. Slow rate when necessary. ECG Attempt to convert with medications if relatively new rhythm and hemodynamically stable. Prepare for synchronized cardioversion if hemodynamically unstable. Chronic atrial fibrillation usually treated with coumadin, ASA, etc.
AFL TREATMENT O2 and monitor. ECG Attempt to convert with medications if relatively new rhythm and hemodynamically stable (beta-blockers, calcium channel blockers, digoxin). Prepare for synchronized cardioversion if hemodynamically unstable.
WAP TREATMENT O2 and monitor ECG
SVT TREATMENT O2 and monitor. ECG May attempt vagal maneuvers. May require beta-blockers, calcium channel blockers, etc. Prepare for synchronized cardioversion if hemodynamically unstable.
VT TREATMENT Immediate defibrillation or cardioversion. CPR and ACLS
Torsades TREATMENT MgSO4 Immediate defibrillation. CPR and ACLS.
Pulmonary (LVF) and/or systemic (RVF) congestion is present. The weakened LV doesn’t empty properly and backs up toward the pulmonary vasculature. The increased pressures allow fluid to leak back into the pulmonary interstitial spaces and into the alveolus. Back pressure form the RV to the systemic venous system leads to increased venous pressures with engorgement of the liver and spleen and third-spacing of fluid into interstitial spaces, causing peripheral edema and ascites.
Class I: Patient with cardiac disease without resulting limitation of physical activity. Ordinary physical activity does not cause undue fatigue, palpitations, dyspnea or angina. Class II: Patient with cardiac disease resulting in slight limitation of physical activity. They are comfortable at rest but ordinary physical activity results in fatigue, palpitations, dyspnea or angina. Class III: Patient with cardiac disease resulting in marked limitations of physical activity. They are comfortable at rest but, less than ordinary activity causes fatigue, palpitations, dyspnea or angina. Class IV: Patient with cardiac disease resulting in inability to do any physical activity without discomfort. Symptoms of cardiac insufficiency or angina are increased when any activity is attempted.
Improve Oxygenation O 2 Intubation PEEP Diuretics Decrease Myocardial Oxygen Consumption Bedrest (HOB elevated) Physical comfort (temperature control) Emotional control (keep informed, sedative prn) Gradually increase activity as tolerated, rest between activities Decrease Preload Diuretics (usually loop diuretics such as furosemide) High fowler’s position (legs dependent) Venous vasodilator (NTG, MSO 4 ) Sodium and fluid restriction Increase Contractility Cardiac glycosides (digoxin) Positive Inotropics (dopamine, dobutamine) Decrease Afterload Ace Inhibitors (captopril, enalapril) Nitroprusside (if hypertensive) Calcium channel blockers Dobutamine, Primacor Pulmonary vasodilators (aminophylline) IABP Prevent Valsalva Maneuvers Stool softeners Exhaling when turning Manage Dysrhythmias Atrial: Digoxin may be used to decrease ventricular rate by increasing refractoriness of the AV node. Ventricular: Lidocaine or amiodarone if necessary (procainamide and bretlium may significantly decrease contractility) Beta Blockers Used for mild CHF Protects heart form excessive catecholamines Cor Pulmonale (RVF) O 2 Therapy Pulmonary Vasodilators RVF Due to Pulmonary Embolus O 2 Therapy Anticoagulants Thrombolytics (if significant RVF or hypoxia)
Hypovolemic Shock Inadequate perfusion to the tissues due to insufficient intravascular volume. Cardiogenic Shock Inadequate perfusion to the tissues due to heart failure. Distributive Shock (Anaphylactic, Septic, and Spinal Shock) Inadequate perfusion to the tissues due to maldistribution of blood flow out of the intravascular space causing insufficient intravascular volume. Obstructive Shock Inadequate perfusion to the tissues due to obstruction of blood flow. Causes: Pulmonary Embolus Tamponade Tension Pneumothorax Aortic Aneurysm
Self destructive form of shock High mortality rate (75-100%) Occurs in 10% of AMI’s Usually means loss of at least 40% LV function Ventricular gallop = S3
Somatostatin Somatostatin is classified as an inhibitory hormone, whose main actions are to: Inhibit the release of growth hormone (GH) Inhibit the release of thyroid-stimulating hormone (TSH) Suppress the release of gastrointestinal hormones Gastrin Cholecystokinin (CCK) Secretin Motilin Vasoactive intestinal peptide (VIP) Gastric inhibitory polypeptide (GIP) Enteroglucagon (GIP) Lowers the rate of gastric emptying, and reduces smooth muscle contractions and blood flow within the intestine. Suppress the release of pancreatic hormones Inhibit the release of insulin Inhibit the release of glucagon Suppress the exocrine secretory action of pancreas. Somatostatin opposes the effects of Growth Hormone-Releasing Hormone (GHRH)