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Nursing Care of the Adult (or anyone) experiencing shock

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1 Nursing Care of the Adult (or anyone) experiencing shock
Donna Roberson, PhD, APRN, BC Sharon Cherry,MPH,CNE Assistant Lecturer

2 Four Classes of Shock as proposed by Dr. Alfred Blalock in 1934
Hypovolemic Vasogenic (Septic) Cardiogenic Neurogenic Hypovolemic most common type resulting from a loss of circulating blood volume Hallmark Clinical Indicators of shock are hypotension, tachycardia, decreased urine output and altered mental status

3 What is shock? Syndrome of low blood flow and/or abnormal blood flow patterns Results in imbalance between oxygen and nutrient delivery and consumption on the cellular level Five types Low blood flow Mal-distribution of flow

4 Low Blood Flow Shock Hypovolemic Cardiogenic

5 Maldistribution of Blood Flow
Septic Neurogenic Anaphylactic

6 Shock Key factor in any type of Shock is inadequate tissue perfusion
Adequate fluid replacement in shock victims should be indicated by urine outputs of 0.5 to 1ml/kg/hour Watch liver failure for increasing acidosis when LR fluids are utilized. The liver may not be able to convert lactate to bicarbonate thus increasing lactic acidosis

7 Clicker Question Prepare Clickers

8 Stages of Shock Initial Compensatory May not have signs and symptoms
Lactic acid accumulates due to anaerobic metabolism, liver cannot excrete (no oxygen) Compensatory Neural, hormonal and biochemical mechanisms Signs and symptoms seen Reversible stage with treatment

9 Compensatory Stage of Shock
Increased Heart Rate Slightly decreased Blood Pressure Pale cool skin Increased Blood Glucose

10 Second Stage of Shock Progressive stage
Compensatory mechanisms fail Third spacing seen – to the extreme Without aggressive treatment, MODS Respiratory – increased work, crackles, tachypneic Cardiac – output falls, ischemia (distal first), dysrrhythmias, MI, complete failure

11 Refractory Stage Third stage can be irreversible
Profound Hypotension and Hypoxemia Accumulation of waste products throughout system Cerebral ischemia occurs Total, multiple organ failure Recovery unlikely

12 Hypovolemic Shock Medical Stressors leading to Hypovolemic Shock
Hemorrhage Burns Severe vomiting and diarrhea Peritonitis Nursing Interventions Initiate Intravenous therapy with NS or Lactated Ringers Be prepared to administer Blood products PRBC’s and Platelets Prepare patient for Surgery

13 Burns can lead to Hypovolemic Shock

14 Hypovolemic Shock Blood Replacement
Crystalloids eg, 0.9% Saline or Ringers Lactate Colloids eg, Albumin Positive indicators urine output > 0.5 to 1mL/kg/hr, heart rate and mental status WNL

15 Hypovolemic Shock Patient has bleeding in lung
Knife removed in surgery

16 Hypovolemic Shock Loss of circulating vascular volume
Compounding problem Decreased circulating volume – decreased venous return – decreased stroke volume – decreased cardiac output – decreased oxygen and nutrients to cells – decreased tissue perfusion – impaired metabolism

17 Hypovolemic Shock GSW to chest Hemothorax
Note bleeding and collapsed lung

18 Hypovolemic Shock This young women was in a high speed collision
Stop sign impaled into abdomen Patient survived with removal of stop sign and right colon

19 Clicker Question

20 Hypovolemic Shock GSW to chest Hemothorax
Note bleeding and collapsed lung

21 Tissue Perfusion altered
Children playing with a machete Patient taken to OR Do you see the possibilities of more that one type of shock Patient survived

22 Open Chest CPR Patient Died in the Emergency Department

23 Blount Abdominal Trauma
Bleeding of liver and laceration of liver is noted on the right side of this CT scan Emergent surgery What type of shock is this patient at risk for? What nursing interventions are needed prior to surgery?

24 TENSION PNEUMOTHORAX Chest Trauma High speed air bag deployed
Pt with low BP and Sats of 91% on 100% nonrebreather bag Combative and agitated Can lead to Cardiogenic Shock of a noncoronary nature

25 Hemodynamic criteria for Cardiogenic Shock
Sustained hypotension systolic pressure less than 90 for 30 min Reduced cardiac index less than 2.2 L/min/m2 Pulmonary capillary pressure greater than 15 mm Hg

26 Cardiogenic Shock: Patient with enlarged heart (echocardiogram)
Myocardial Infarction End-stage Heart Failure Cardiac Tamponade Pulmonary Embolism Cardiomyopathy Dysrhythmias

27 Clicker Question

28 Cardiogenic Shock from Myocardial Ischemia

29 Cardiogenic shock: EKG Presentation note ST segment elevation This was a result of Pericarditis and pericardial tamonade

30 Clicker Question

31 Septic Shock Systemic inflammatory response to infection (usually bacterial) that has moved into the blood stream High mortality rate Bacteria release endotoxins Systemic Inflammatory Response Syndrome (SIRS)

32 Patients at risk for Sepsis
Immunocomprised ( AIDS, Cancer, Alcoholism, Diabetes) Invasive procedures Indwelling medical devices Increased number of resistant organisms Increased older population

33 Septic Shock Medical Stressors leading to Septic shock
Blood Stream Rank 1st Lungs 2nd Urinary tract infections 3rd Gram Negative Organisms Most common cause of septic shock eg,pseudomonas, acetobacter, E coli, Salmonella Gram Positive Organisms Fluid rescuitation with CVP of 15 is adequate Antimicrobial agents Inotropic agents Vasopressors Watch for bleeding abnormalities decreased platelets Assess for DIC

34 Other Gram Negative Bacteria
There are many groups of Gram-Negative bacteria such as Cyanobacteria, Spirochaetes, Green-Sulphur and Green Non-Sulphur Bacteria and Proteobacteria etc. Out of which, proteobacteria is one of the major group of known Gram-Negative bacteria (it includes bacteria like E-coli, Salmonella, Pseudomonas, Moraxella, Helicobacter, Stenotrophomonas, Legionella, Acetic Acid Bacteria etc.).

35 Systemic Inflammatory Response Syndrome (SIRS) in response to Sepsis
Temperature greater than 38 or less than 36 Heart rate greater than 90 Respiratory rate greater than 30 PaCO2 less than 32 WBC count greater than or less than 4000 or greater than 10% immature bands

36 Multiple organ dysfunction syndrome in response to Sepsis
Cardiovascular Hypotension Respiratory Hypoxemia Renal Increased Creatinine Hematologic Thrombocytopenia Metabolic lactic acidemia Neurologic Altered LOC Hepatic elevated liver function tests

37 Septic shock 6-10 liters of crystalloids, 2-4 liters of colloids
Invasive monitoring (ICU patient) Vasopressors and inotropics added if fluid fails Ventilator ANTIBIOTICS – broad spectrum until cultures back, then specific agents Xigris – administered over 96 hours, boosts activated protein C (unknown action – possibly anti-inflammatory)

38 Clicker question

39 Specifics to Type Cardiogenic
Diagnostic tests (caths) and supportive pumps (IABP or VAD) Medications – diuretics, ACEI, Beta-blockers, nitrates, (+) inotropes

40 Cardiogenic Shock Angioplasty Left Descending Coronary Artery Stenosis

41 Neurogenic Shock Medical Stressors leading to Neurogenic shock
Spinal Cord injury Severe Pain Epidural Block Spinal Anesthetics Treat hypotension and bradycardia Administer medications as ordered Ephedrine and possible need for Vaspressin if patient has used ACE inhibitors Keep HOB elevated 30 after spinal or epidural anesthesia Immobilize spine with injury Lovenox needed during period of inactivity and SCD’s

42 Neurogenic Shock Occurs after spinal cord injury at T5 or above
Massive vasodilation without sympathetic nervous system compensation (ex. SCI) Pooling with bradycardia and hypotension Also may have hypothalmic dsyfunction Temperature deregulated poikilothermia

43 Neurogenic Shock Usually begins within 30 minutes of injury and can last weeks Also caused by spinal anesthesia and BZDs Diagnosed based on cause and VS Treatment

44 Distributive Shock or Neurogenic Shock C-5 Burst Fracture Before and after repair

45 Distributive Shock (Neurogenic Shock)
Cervical Spine disk 2 fracture Hangman Fracture from look of a hanging Caused by fall or MVA Type of Shock nurse would assess for?

46 Neurogenic shock Stabilize spine
Support hypotension – volume, neo-synephrine (alpha adrenergic agonist) Keep warm Methylprednisolone (Solu-medrol) prevents secondary cord injury from inflammatory mediators

47 Clicker question

48 Anaphylactic Shock Medical Stressors leading to Anaphylactic shock
Insect bites Vaccines Adverse reactions to medications or foods Intravenous Epinephrine Inhalation bronchodilators Colloidal fluid replacement eg, Albumin Benadryl Corticosteroids H2 blockers eg, Tagamet Assess for Respiratory failure

49 Anaphylactic Shock Medical Stressors leading to Anaphylactic shock
Insect bites Vaccines Adverse reactions to medications or foods Intravenous Epinephrine Inhalation bronchodilators Colloidal fluid replacement eg, Albumin Benadryl Corticosteroids H2 blockers eg, Tagamet Assess for Respiratory failure

50 Anaphylactic Shock Life-threatening hypersensitivity to a substance (bee stings, medications, food) Massive vasodilation, vasoactive mediators released and increased capillary membrane permeability Laryngeal edema, hypotension, wheezing/stridor, skin changes – death! c/o dizziness, chest pain, difficulty swallowing or breathing, anxiety

51 Clicker Question Prepare Clickers

52 Presentation Young, healthy people can compensate up to a point
HR elevated, narrowed pulse pressure, hypotensive Tachypneic, decreased UO, increased specific gravity, pallor, cool/clammy Confused, anxious

53 Presentation Hypotension despite fluid support
Cardiac dysfunction, respiratory failure, oliguria, confusion, GI bleeds Systolic BP <90 or more than 40mmHg below baseline (inadequate for perfusion of major organs) One or more organs fail – multiple organ dysfunction syndrome (MODS)

54 Typical Interventions (collaborative)
Oxygen/airway (have intubation tray ready) Stabilize spine (as indicated) IV – at least 2 #18 or bigger bore Prepare to give crytalloids like NS or LR Stop obvious bleeding Assess for worsening cardiac and respiratory function

55 Collaborative Management
Requires immediate action by nurse (or family, or rescue, etc.) Protocols are established in areas that see this type of shock Usually administer epinephrine (subq, IV, IM). Benadryl (IV, IM, PO), steroids also given Anti-venom for insect stings IV support and monitoring

56 Anaphylactic shock Prevention Epinephrine #1, Benadryl, Tagamet
Airway preservation Nebulizers with Alupent or Albuterol Fluid replacement with colloids (prevent 3rd spacing)

57 Diagnostic Interventions
Monitor dropping hemoglobin and hematocrit, electrolytes FAST(Focused abdominal sonographic technique) can be done at the bedside of the trauma pt CT scans (Computed tomography scan) EGD Chest Radiographs Angiography Nuclear Medicine Scanning ABG’s Coagulation studies Electrolyte Studies Treatment Interventions Preserve and replace volume Blood, plasma expanders, albumin Crystalloid’s first choice of fluid for resuscitation (Normal Saline or Lactated Ringers

58 Diagnostics Treatment Cardiac enzymes – troponin levels
EKG, Chest Xray and echocardiogram See page 1800! Treatment Correct underlying cause

59 Hypovolemic Fluid replacement
Crystalloids – NS, LR (used for most shock) Blood- PRBC (all if Hgb <12) and as indicated Colloids- AKA plasma expanders hespan (all) Albumin – Dextran –

60 Renal – acute failure, increased BUN/crt, requires hemodialysis
GI – ulcers, bleeding, paralytic ileus Hematologic – DIC Hepatic – liver failure, enzymes increase

61 Clicker Question Prepare Clickers

62 Clicker question

63 Clicker question

64 Prepare to administer vasopressives
Prepare to insert Foley and NG Monitor and use protocols to treat dysrrhthmias Keep warm (septic may use cooling blankets) Daily weights – TPN after enteral feedings fail

65 A word about positioning
Pay attention to research studies Consider sample size, methods to measure Most agree, positioning does not impair tissue perfusion. Old-timers – firmly believe in Trendelenburg positioning to increase cerebral blood flow Not used with cord injuries Shock position– flat on back, elevate legs 12 inches (not for cord injuries), cover

66 Clicker question Prepare Clickers End of Shock Lecture

67 How can the nurse assess for Heart Failure?
Listen for Heart sounds and Lung Sounds Assess pulses Assess BP

68 Heart Failure: The heart’s inability to pump enough blood through the body

69 DRG Heart Failure DRG 127 - Substantiating Congestive Heart Failure
SIGNS/SYMPTOMS/CONDITIONS Shortness of breath Fatigue with exertion Orthopnea Paroxysmal nocturnal dyspnea Tachycardia Tachypnea Pulmonary rales (fine crackles) Edema of lower extremities Jugular vein distention Gallop on cardiac auscultation

70 Heart Failure COMMON TREATMENT
Medical treatment includes oxygen, nitroglycerin, diuretics, vasodilators, ACE inhibitors, ARB (Angiotensin receptor blocker), hydralazine, digoxin, beta-blockers or anticoagulation. Patients are educated and encouraged to restrict dietary salt and fluid intake.

71 Heart Failure Systolic dysfunction – inability to move blood forward through the heart Diastolic dysfunction – inability to move blood out of heart (poor right or left ventricular filling) Physiologic state in which inadequate tissue perfusion results from cardiac dysfunction

72 Heart Failure TESTS Chest x-rays may indicate presence of alveolar edema, interstitial infiltrates, pleural effusion or congestive heart failure Echocardiogram shows left ventricle dysfunction, diastolic dysfunction or ejection fraction of <50% Gated pool studies reveal moderate-to-severe left ventricular dysfunction or ejection fraction of <50% Cardiac Catheterization findings reveal left ventricular dysfunction or ejection fraction of <50%

73 Diagnostic test for Heart Failure
Chest x-rays may indicate presence of alveolar edema, interstitial infiltrates, pleural effusion or congestive heart failure Echocardiogram shows left ventricle dysfunction, diastolic dysfunction or ejection fraction of <50% Gated pool studies reveal moderate-to-severe left ventricular dysfunction or ejection fraction of <50% Cardiac Catheterization findings reveal left ventricular dysfunction or ejection fraction

74 Presentation Tachycardia, hypotension and narrow pulse pressure
Tachypneic, adventitious breath sounds Cyanosis, pallor, cool/clammy skin, decreased capillary refill time Increased central venous pressures Decreased cardiac output Oliguria Altered Mentation

75 Assessment findings: The patient’s heart is weaker
Blood and fluid back up into the lungs Fluid builds up into the feet, ankles and legs Patients experience tiredness and SOB

76 Nursing Care of the Adult with Cardiovascular Complications
Donna W. Roberson, PhD(c), APRN, BC

77 Anemias Deficiency in red blood cell mass and hemoglobin content.
Deficiency occurs from blood loss reduced production excessive hemolysis

78 Manifestations Mild (Hgb 10-14 g/dL) – Moderate (Hbg 6-10g/dL) –
none, slight fatigue, pale mucous membranes, DOE Moderate (Hbg 6-10g/dL) – increased fatigue, palpitations, dyspnea, diaphoresis Severe (Hbg <6 g/dL) – pallor, jaundice, glossitis, tachycardia, murmurs, cardiac symptoms, HA, vertigo, decreased concentration, organomegaly, bone pain, cold intolerance, lethargy

79 Etiology Decreased Erythrocyte Production Iron deficiency anemia (IDA)
Thalassemia and thalassemia trait Pernicious anemia (vitamin B12 deficiency) Folic acid deficiency anemia Aplastic anemia Anemias of leukemia/cancer Anemia of chronic disease (ACD)

80 Blood Loss – trauma, hemorrhage, GI, menstrual
Increased Erythrocyte Destruction Hemoglobin abnormalities (SSC, G6PD deficiency) Trauma – prosthetic valve, hemodialysis and other extracorporeal circulation, autoimmune disorder, infections and toxins

81 Morphology Size – consider diameter of cell
RDW Weight – how heavy the cell is MCV Chromicity – how pretty and red the cell is MCH, MCHC Normochromic, normocytic – normal color, size and weight

82 Normal Red Blood Cell Production
Erythropoietin produced by the kidney regulates cell production. Mature erythrocytes form from adequate caloric intake Iron folic acid vitamin B12 erythropoietin

83 Normal laboratory values
Reticulocyte count 0.5-2% Hgb Hct 37-52% MCV MCH MCHC RDW % Serum Ferritin >10 TIBC

84 The normal adult requires 20 mg of iron per day to produce HgB.
About 10 mg comes from degraded HgB. Most can absorb 1mg of iron per 10mg ingested (in duodenum)

85 IDA Most common anemia Very young, poor diet, women, absorption problems (lactose intolerance, celiac sprue), cancer *repeated blood draws (decreases recycling of iron from Hbg) Microcytic, hypochromic

86 Presentation Diagnosis Fatigue, pallor, glossitis
Worsens as stored iron is depleted Diagnosis History and physical CBC with differential, serum ferritin, serum iron, TIBC, hemoccult, hemoglobin electrophoresis (peripheral smear)

87 Thalassemia and Thalassemia Trait
Genetic disorder of decreased erythrocyte production Common in Mediterranean ancestry, equatorial Asia and Africa AKA Thalassemia major and minor (trait) Microcytic, hypochromic Thalessemia results in severe deficiencies and death

88 Megaloblastic Anemias
Cobalamin (B12 deficiency) dietary deficits, loss of intrinsic factor, hyperactive gut disorders Folic Acid deficiency Inadequate oral intake of folate-rich foods (ETOH abusers, pregnancy) Impaired absorption

89 Macrocytic normochromic cells
Pernicious anemia – intrinsic factor is not secreted by the gastric mucosa Erroneously used for all Cobalamin deficiency Anemias prolonged use of PPI in high doses (atrophy) Destroyed parietal cells (autoimmune)

90 Presentation Fatigue Sore tongue Anorexia, N/V Abd pain
Peripheral paresthesias Confusion Death if not corrected

91 Diagnosis CBC with diff, peripheral smear B12 and folate levels
Gastric exam (r/o cancer, check for atrophy)

92 Schilling test NPO 8-12 hrs, no B vitamins 3d before, no laxatives 1d before Collect small urine sample Radioactive B12 (po capsule) in radiology May eat RN gives 1mg B12 IM 1-2hrs after radioactive dose (saturates liver so capsule can be absorbed in sm. intestines) 24 hour urine (lab decides if iced or not)

93 Anemia of Chronic Disease
microcytic to normocytic and normochromic cells chronic depletion of RBC (none for recycling) Chronic state of over-iron utilization or bone marrow failure (cancers/chemo, infections, rheumatoid arthritis, lupus, diabetes, COPD, etc.)

94 Aplastic Anemia All blood components are low
Congenital (Fanconi syndrome) Acquired Idiopathic Chemical exposure Meds Pregnancy Radiation Infections

95 Care regimens – Medical and Nursing
Diet and nutrition Based on deficiency, encourage foods high in need (tends to be the same foods for iron and folate) Examples: spinach, liver, raisins, cast iron cooking pots, green leafy vegetables, yeast, dried beans, nuts

96 Absorptive disorders interfering
Educate and support restrictive diet Examples: assist in determining irritating foods - limit diary, teach label reading to avoid glutens

97 Supplementation - IRON
Expect improved S&S 5-7d ½ labs corrected labs in 3 weeks normal by 2 months. Iron stores refilled 4-6 months (if successful.) Biggest complaint – constipation and heartburn Normal – tarry, dark looking stools

98 Iron ferrous sulfate – 300 -325mg body absorbs 65mg
ferrous gluconate – 325mg body absorbs 38mg ferrous fumarate – 325mg body absorbs 106mg iron dextran –IV or IM monthly – use Z-track to prevent skin staining (test dose)

99 Cobalamin and Folic Acid
Vitamin B12 1000mg IM daily for 2 weeks Then weekly until normal hematocrit Then monthly for life Folic acid – usually give with multivitamin since malnutrition typical root of problem 1-5mg daily

100 Erythropoietin ACD (not BM cancers) EPO, Procrit, Epogen Refrigerated
Never shaken Subq at room temperature Monitor labs

101 Preventative care Balanced diet – particularly menstruating women
Use of COC for planned amenorrhea (also called chemical menopause) Substance abuse counseling Care for those with chronic illnesses or prolonged infections Management includes nutritional counseling

102 Protective care Support use of supplements – problem shooting for GI c/o Allow ventilation of concerns, offer support groups- use of the internet Encourage routine health screens by age new onset of anemia over age 50 presumed cancer until proven otherwise!

103 Anemia due to blood loss
Volume replacement and PRBCs Correct underlying cause Pressure, cautery COC Chronic losses – iron, diet

104 Hemolytic Anemia Overdestruction of RBCs
Defects of cell causes destruction by spleen and liver (Sickle Cell) Autoimmune disorder Jaundice from elevated bilirubin as RBCs destroyed In all cases, ensure renal protection from large RBC bits (ATN)

105 Polycythemia Overproduction of RBCs Causes thickened blood – problems?
Blood letting, hydration, BM suppression

106 Coagulation disorders
platelets nl 150k-400k excess - thrombocytosis deficit - thrombocytopenia 10k-20k results in hemorrhage from minor trauma < 10k results in spontaneous hemorrhage

107 Immune thrombocytopenia purpura (ITP)
acute - usually children/young adults follows a viral event chronic - usually women (20-50), unknown precipitating factor Platelets coated with antibodies and destroyed as an immune response by spleen after only 1-3 days

108 Manifestations of ITP Purpura, ecchymoses and petechiae Epistaxis
Menorrhagia Hematuria GI bleeds

109 Secondary thrombocytopenia
anemias, ETOH abuse, viral infections (Mono), AIDS, heparin, Coumadin, sulfonamides, digoxin, Lasix, MSO4, Tagamet ASA and NSAIDS interfere with platelet function but not production

110 Diagnostics and treatment
CBC - H/H and plt count bleeding times prolonged in ITP treat with plt transfusion - warming increase counts by 28% expect a rise in count by 8-10k per unit given. Can recheck plt count in 15 mins. after tx

111 Disseminated intravascular coagulation
state of both clotting and hemorrhage inappropriate thrombin response causes diffuse clotting, clotting factors are consumed and the fibrinolytic system is activated. Clots are dissolved, but no clotting factors are available, therefore hemorrhage occurs.

112 Clinical picture causes include trauma, obstetrics complications, hemolytic reactions, shock, sickle cell crisis, MI, PE, and others Skin - purpura, ecchymoses, petechiae, cyanosis of extremities, bleeding from wounds

113 More GI- ABD distention, blood in stool and vomitus, frank hemorrhage
Resp/CV – shock symptoms GU - hematuria, oliguria, renal failure CNS - confusion, coma, seizures

114 Diagnostics PT & INR/PTT increased Plt decreased
plasma fibrinogen decreased decreased clotting factors

115 Treatment heparin used when organ function is impaired
Heparin contraindicated in shock/active bleeding nursing care - promote hemostasis, tissue perfusion, manage pain, gas exchange and anxiety

116 Heart failure Many still call it Congestive Heart Failure (CHF)
Systolic failure -pump fails Decreased ejection fraction (EF) Decreased contractility Increased afterload cardiomyopathy

117 Diastolic heart failure (DHF) – ventricles fail to fill
Venous engorgement with S&S (criterion 1) Normal EF (criterion 2) Abnormal diastolic function (criterion 3) Can have both! To distinguish between SHF & DHF – must have measure of EF

118 Treatment Similar medications, different doses and reasons
SHF – improve inotropic function and improve remodeling of LV with Beta blockers. Digoxin still used. No use for calcium channel blockers DHF – Beta blockers used to decrease HR, increase diastole, improve response to exercise *smaller doses than SHF

119 DHF – improve venous congestion
Fluid and sodium restriction Dialysis Nitrates (nitroprusside, long acting oral agents) Diuretics- spironolactone, loops ACEI and ARBs

120 DHF – increasing diastole
Beta blockers, calcium channel blockers Digoxin only used in those with atrial fibrillation or very short term in the acute period

121 Cardiomyopathy Disease of the myocardium resulting in impaired function Primary Unknown Secondary Dilated, hypertrophic, or restrictive

122 Dilated Myopathies ETOH, cocaine, doxorubicin, genetic, HTN, idiopathic, ischemia, etc. c/o fatigue, palpitations, SOB/DOE, cough PE enlarged heart, decreased contractility, valve failure, arrhythmias, decreased CO Diagnostics – Xray, EKG, cath

123 Dilated Management Treat underlying cause
ACEI, diuretics, anticoagulants, cardiac transplant Teach family CPR, how to access EMS No ETOH, limited sodium

124 Hypertrophic Myopathies
Asymmetric enlargement without dilation Genetic, stenosis or HTN cause c/o exertional dyspnea, fatigue, angina Syncope seen in those with aortic outflow obstruction PE SVT, fib, tachy, S3 or S4 Primary diagnostic tool – EKG with increased QRS, also may get cath

125 Hypertrophic Management
Improve ventricular filling Support patient/family Relieve symptoms

126 Restrictive Myopathies
Fibrotic changes in the myocardium prevent ventricular filling c/o angina, syncope, fatigue, DOE *hallmark sign PE DHF signs and symptoms Diagnosis – EKG shows tachy at rest, CT or MRI

127 Restrictive management
No treatment other than DHF therapies Nursing supportive Cardiac transplant Recipient/donor matching based on body size, heart size and ABO type Maximum out-of-body time 6 hours Place recipient on cardiopulmonary bypass Start immunosuppressives in OR

128 Nursing care focused on Acute
Operative recovery Teaching about medications and diet Long term Ongoing support of lifestyle changes Monitor for rejection, lymphoma and vasculopathy

129 Heart Blocks 1st degree AV Prolonged PR interval 2nd degree AV
Type I (Wenckebach) AV node problem Lengthened PR, some P have no QRS Type II (Bundle Branch Block) His-Purkinje problem Ratios of Ps with QRS 3:1, 2:1 Poorer prognosis, requires temporary pacemaker 3rd degree AV complete No relation between P and QRS Junctional rhythm common with HR 20-40

130 Ventricular disturbance
PVCs – indicates electrical irritation across myocardium Bigeminy, Trigeminy possible Couplets lead to v-tach Ventricular Tachycardia – run of 3 or more PVCs Wide, aberrant QRS pattern Rate Leads to v-fib if not interrupted

131 Ventricular fibrillation
Asystole – flat line or occasional P, assess in different leads to make sure not V-fib

132 Treatment for AV Block Internal pacemaker – takes the place of the SA node Wide variety available – on demand, preset, responsive to exercise, etc. Complications – infection, bleeding, failure to capture, failure to sense, battery failure

133 Nursing care of pacemakers
Administer pre-pacer antibiotic Monitor for infection – small incision anterior chest or abdomen Reassurance – fear big problem Teach how to assess pulse *family too Avoid magnetic fields and electrical generators (Microwaves are safe) Medic alert

134 Treatment of Ventricular Dsyrhthmias
Automatic Internal Cardio-Defibrillator (AICD) also ICD Lead inserted through subclavian vein to endocardium. Pulse generator – upper chest or abdomen Lead senses v-tach or v-fib, cues pulse generator 25-joule shock delivered Recycles and can continue to work

135 Nursing Care Similar to pacers
Reassurance – fear of arrest, fear ICD won’t work properly Sexuality Anxiety – patient and family

136 Revascularization of the Myocardium
Treats post-MI ischemia and failed medication management of CAD CABG, RIMA, LIMA, saphenous veins Traditional method Open sternum incision, bypass, heart stopped Long leg(s) incision Chest tubes External pacing wires Cordis

137 Requires at least 2 days ICU in specialty care unit.
Usually hrs ventilator support Pain management Monitor CT drainage (2-4 CTs usual) EKG, cardiac output, pulmonary pressures

138 Robotics! Minimally Invasive Direct CABG
MIDCAB for short Used for LAD or single vessel bypass Several, small intercostal incisions Harvested LIMA used on heart slowed by calcium channel blockers or beta blockers

139 Nursing Care of MIDCABG
Usually 2 CTs Nitro drip Pain management No bypass used, so quicker recovery, shorter LOS *Teaching for both centers on lifestyle changes

140 Reduce Risk of Coronary Artery Disease and Heart Failure
In This Topic Mechanism of Loss Site of Fluid Loss Hypovolemic Shock Caused by Body Fluid Loss Skin Thermal or chemical burn, sweating from excessive heat exposure Diabetes mellitus or insipidus, adrenal insufficiency, “salt-losing” nephritis, the polyuric phase after acute tubular damage, and use of potent diuretics Kidneys Vomiting or diarrhea GI tract Shock is a state of organ hypoperfusion with resultant cellular dysfunction and death. Mechanisms may involve decreased circulating volume, decreased cardiac output, and vasodilation, sometimes with shunting of blood to bypass capillary exchange beds. Symptoms include altered mental status, tachycardia, hypotension, and oliguria. Diagnosis is clinical, including BP measurement. Treatment is with IV fluids, correction of underlying disorder, and sometimes vasopressors. Pathophysiology The fundamental defect in shock is reduced perfusion of vital tissues. Once perfusion declines so that O2 is inadequate for aerobic metabolism, cells shift to anaerobic metabolism with increased production of CO2 and accumulation of lactic acid. Cellular function declines, and if shock persists, irreversible cell damage and death occur. During shock, both the inflammatory and clotting cascades may be triggered in areas of hypoperfusion. Hypoxic vascular endothelial cells activate WBCs, which bind to the endothelium and release directly damaging substances (eg, reactive O2 species, proteolytic enzymes) and inflammatory mediators (eg, cytokines, leukotrienes, tumor necrosis factor [TNF]). Some of these mediators bind to cell surface receptors and activate nuclear factor kappa B (NFκB), which leads to production of additional cytokines and also nitric oxide (NO), a potent vasodilator. Septic shock (see Sepsis and Septic Shock) may be more proinflammatory than other forms because of the actions of bacterial toxins, especially endotoxin. Vasodilation of capacitance vessels leads to pooling of blood and hypotension because of “relative” hypovolemia (ie, too much volume to be filled by the existing amount of blood). Localized vasodilation may shunt blood past the capillary exchange beds, causing focal hypoperfusion despite normal cardiac output and BP. Additionally, excess NO is converted to peroxynitrite, a free radical that damages mitochondria and decreases ATP production. Blood flow to microvessels including capillaries is reduced even though large-vessel blood flow is preserved in settings of septic shock. Mechanical microvascular obstruction may, at least in part, account for such limiting of substrate delivery. Leukocytes and platelets adhere to the endothelium, and the clotting system is activated with fibrin deposition. Multiple mediators, along with endothelial cell dysfunction, markedly increase microvascular permeability, allowing fluid and sometimes plasma proteins to escape into the interstitial space. In the GI tract, increased permeability possibly allows translocation of the enteric bacteria from the lumen to the blood stream, potentially leading to sepsis or metastatic infection. Neutrophil apoptosis may be inhibited, enhancing the release of inflammatory mediators. In other cells, apoptosis may be augmented, increasing cell death and thus worsening organ function. BP is not always low in the early stages of shock (although hypotension eventually occurs if shock is not reversed). Similarly, not all patients with “low” BP have shock. The degree and consequences of hypotension vary with the adequacy of physiologic compensation and the patient's underlying diseases. Thus, a modest degree of hypotension that is well tolerated by a young, relatively healthy person might result in severe cerebral, cardiac, or renal dysfunction in a patient with significant arteriosclerosis. Compensation: Initially, when O2 delivery (DO2) is decreased, tissues compensate by extracting a greater percentage of delivered O2. Current guidelines provide for interventions that will maintain mixed-venous O2 saturation above 30%. Additionally, low arterial pressure triggers an adrenergic response with sympathetic-mediated vasoconstriction and often increased heart rate. Initially, vasoconstriction is selective, shunting blood to the heart and brain. Circulating β-adrenergic amines ( epinephrine ADRENALIN PRIMATENE MIST Click for Drug Monograph , norepinephrine LEVOPHED Click for Drug Monograph ) also increase cardiac contractility and trigger release of corticosteroids from the adrenal gland, renin from the kidney, and glucose from the liver. Increased glucose may overwhelm ailing mitochondria, causing further lactate production. Reperfusion: Reperfusion of ischemic cells can cause further injury. As substrate is reintroduced, neutrophil activity may heighten, increasing production of damaging superoxide and hydroxyl radicals. After blood flow is restored, inflammatory mediators may be circulated to other organs. Multiple organ dysfunction syndrome (MODS): The combination of direct and reperfusion injury may cause MODS—the progressive dysfunction of 2 or more organs consequent to life-threatening illness or injury. MODS can follow any type of shock but is most common when infection is involved; organ failure is one of the defining features of septic shock (see Sepsis and Septic Shock). MODS also occurs in > 10% of patients with severe traumatic injury and is the primary cause of death in those surviving > 24 h. Any organ system can be affected, but the most frequent target organ is the lung, in which increased membrane permeability leads to flooding of alveoli due to capillary leaks. Progressive hypoxia may be increasingly resistant to supplemental O2 therapy. This condition is termed acute lung injury or, if severe, acute respiratory distress syndrome (ARDS—see Acute Lung Injury and Acute Respiratory Distress Syndrome (ARDS)). The kidneys are injured when renal perfusion is critically reduced, leading to acute tubular necrosis and renal insufficiency manifested by oliguria and progressive rise in serum creatinine. In the heart, reduced coronary perfusion and mediators (including TNF and IL-1) may depress contractility, worsen myocardial compliance, and down-regulate β-receptors. These factors decrease cardiac output, further worsening both myocardial and systemic perfusion and causing a vicious circle often culminating in death. The GI tract can develop ileus and submucosal hemorrhage. Liver hypoperfusion can produce focal or extensive hepatocellular necrosis, transaminase elevation, and decreased production of clotting factors. Etiology and Classification There are several mechanisms of organ hypoperfusion and shock. Shock may be due to low circulating volume (hypovolemic shock), vasodilation (distributive shock), primary decrease in cardiac output (both cardiogenic and obstructive shock), or a combination. Hypovolemic shock: Hypovolemic shock is caused by a critical decrease in intravascular volume. Diminished venous return (preload) results in decreased ventricular filling and reduced stroke volume. Unless compensated for by increased heart rate, cardiac output decreases. A common cause is bleeding (hemorrhagic shock), typically from trauma, surgical interventions, peptic ulcer, esophageal varices, or aortic aneurysm. Bleeding may be overt (eg, hematemesis or melena) or concealed (eg, ruptured ectopic pregnancy). Hypovolemic shock may also follow increased losses of body fluids other than blood (see Table 1: Shock and Fluid Resuscitation: Hypovolemic Shock Caused by Body Fluid Loss     ). This Topic Cardiogenic shock Hemorrhagic shock General management Prognosis and Treatment Buy the Book PDA Download Print This Topic The Merck Manual Minute alerts Update Me Intravascular fluid lost to the extravascular space Increased capillary permeability secondary to inflammation or traumatic injury (eg, crush), anoxia, cardiac arrest, sepsis, bowel ischemia, acute pancreatitis Hypovolemic shock may be due to inadequate fluid intake (with or without increased fluid loss). Water may be unavailable, neurologic disability may impair the thirst mechanism, or physical disability may impair access. In hospitalized patients, hypovolemia can be compounded if early signs of circulatory insufficiency are incorrectly ascribed to heart failure and fluids are withheld or diuretics are given. Distributive shock: Distributive shock results from a relative inadequacy of intravascular volume caused by arterial or venous vasodilation; circulating blood volume is normal. In some cases, cardiac output (and DO2) is high, but increased blood flow through arteriovenous shunts bypasses capillary beds, causing cellular hypoperfusion (demonstrated by decreased O2 consumption). In other situations, blood pools in venous capacitance beds and cardiac output falls. Distributive shock may be caused by anaphylaxis (anaphylactic shock—see Allergic and Other Hypersensitivity Disorders: Anaphylaxis); bacterial infection with endotoxin release (septic shock—see Sepsis and Septic Shock); severe injury to the brain or spinal cord (neurogenic shock); and ingestion of certain drugs or poisons, such as nitrates, opioids, and adrenergic blockers. Anaphylactic shock and septic shock often have a component of hypovolemia as well. Cardiogenic and obstructive shock: Cardiogenic shock is a relative or absolute reduction in cardiac output due to a primary cardiac disorder. Mechanical factors that interfere with filling or emptying of the heart or great vessels explain obstructive shock. Causes are listed in Table 2: Shock and Fluid Resuscitation: Mechanisms of Cardiogenic and Obstructive Shock     . Abnormalities of cardiac rhythm Myocardial ischemia or MI, myocarditis, drugs Impaired myocardial contractility Tachycardia, bradycardia Back to Top      Audio Figures Photographs Sidebars Tables Videos Acute mitral or aortic regurgitation, ruptured interventricular septum, prosthetic valve malfunction Symptoms and Signs Lethargy, confusion, and somnolence are common. The hands and feet are pale, cool, clammy, and often cyanotic, as are the earlobes, nose, and nail beds. Capillary filling time is prolonged, and except in distributive shock, the skin appears grayish or dusky and moist. Overt diaphoresis may occur. Peripheral pulses are weak and typically rapid; often, only femoral or carotid pulses are palpable. Tachypnea and hyperventilation may be present. BP tends to be low (< 90 mm Hg systolic) or unobtainable; direct measurement by intra-arterial catheter, if done, often gives higher and more accurate values. Urine output is low. Distributive shock produces similar symptoms, except the skin may appear warm or flushed, especially during sepsis. The pulse may be bounding rather than weak. In septic shock, fever, usually preceded by chills, is generally present. Some patients with anaphylactic shock have urticaria or wheezing. Numerous other symptoms (eg, chest pain, dyspnea, abdominal pain) may occur due to the underlying disease or secondary organ failure. Diagnosis Diagnosis is mostly clinical, based on evidence of insufficient tissue perfusion (obtundation, oliguria, peripheral cyanosis) and signs of compensatory mechanisms (tachycardia, tachypnea, diaphoresis). Specific criteria include obtundation, heart rate > 100, respiratory rate > 22, hypotension (systolic BP < 90 mm Hg) or a 30 mm Hg fall in baseline BP, and urine output < 0.5 mL/kg/h. Laboratory findings that support the diagnosis include lactate > 3 mmol/L, base deficit < −5 mEq/L, and Paco2 < 32 mm Hg. However, none of these findings alone is diagnostic, and each is evaluated in the overall clinical context, including physical signs. Recently, measurement of sublingual PCO2 has been introduced as a noninvasive and rapid measurement of the severity of shock. Diagnosis of cause: Recognizing the underlying cause of shock is more important than categorizing the type. Often, the cause is obvious or can be recognized quickly by history and physical examination, aided by simple testing. Chest pain (with or without dyspnea) suggests MI, aortic dissection, or pulmonary embolism. A systolic murmur may indicate ventricular septal rupture or mitral insufficiency from acute MI. A diastolic murmur may indicate aortic regurgitation from aortic dissection involving the aortic root. Cardiac tamponade is suggested by jugular venous distention, muffled heart sounds, and a paradoxical pulse. Pulmonary embolism severe enough to produce shock typically produces decreased O2 saturation and occurs more often in special settings, including prolonged bed rest and after a surgical procedure. Tests include ECG, troponin I, chest x-ray, ABG measurements, lung scan, helical CT, and/or echocardiography. Abdominal or back pain or a tender abdomen suggests pancreatitis, ruptured abdominal aortic aneurysm, peritonitis, and, in women of childbearing age, ruptured ectopic pregnancy. A pulsatile midline mass suggests ruptured abdominal aortic aneurysm. A tender adnexal mass suggests ectopic pregnancy. Testing typically includes abdominal CT (if the patient is unstable, bedside ultrasound can be helpful), CBC, amylase, and lipase, and, for women of childbearing age, urine pregnancy test. Fever, chills, and focal signs of infection suggest septic shock, particularly in immunocompromised patients. Isolated fever, contingent on history and clinical settings, may point to heat stroke. Tests include chest x-ray; urinalysis; CBC; and cultures of wounds, blood, urine, and other relevant body fluids. In a few patients, the cause is occult. Patients with no focal signs or symptoms indicative of cause should have ECG, cardiac enzymes, chest x-ray, and ABG. If results of these tests are normal, the most likely causes include drug overdose, occult infection (including toxic shock), and obstructive shock. Ancillary testing: If not already obtained, ECG, chest x-ray, CBC, serum electrolytes, BUN, creatinine, PT, PTT, liver function tests, and fibrinogen and fibrin split products are done to monitor patient status and serve as a baseline. If the patient's volume status is difficult to determine, monitoring of central venous pressure (CVP) or pulmonary artery occlusion pressure (PAOP) may be useful. CVP < 5 mm Hg (< 7 cm H2O) or PAOP < 8 mm Hg may indicate hypovolemia, although CVP may be greater in hypovolemic patients with preexisting pulmonary hypertension. Prognosis and Treatment Untreated shock is usually fatal. Even when treated, mortality from cardiogenic shock after MI and from septic shock is high (60 to 65%). Prognosis depends on the cause, preexisting or complicating illness, time between onset and diagnosis, and promptness and adequacy of therapy. General management: First aid involves keeping the patient warm. Hemorrhage is controlled, airway and ventilation checked, and respiratory assistance given if necessary. Nothing is given by mouth, and the patient's head is turned to one side to avoid aspiration if emesis occurs. Treatment begins simultaneously with evaluation. Supplemental O2 by face mask is provided. In severe shock or if ventilation is inadequate, airway intubation with mechanical ventilation is necessary. Two large (16- to 18-gauge) IV catheters are inserted into separate peripheral veins. A central venous line or an intraosseous needle, especially in children, provides an alternative when peripheral veins cannot promptly be accessed (see also Approach to the Critically Ill Patient: Intraosseous Infusion). Typically, 1 L (or 20 mL/kg in children) of 0.9% saline is infused over 15 min. In major hemorrhage, Ringer's lactate is commonly used. Unless clinical parameters return to normal, the infusion is repeated. Smaller volumes (eg, 250 to 500 mL) are used for patients with signs of high right-sided pressure (eg, distention of neck veins) or acute MI. A fluid challenge should probably not be given to a patient with signs of pulmonary edema. Further fluid therapy is based on the underlying condition and may require monitoring of CVP or PAOP. Patients in shock are critically ill and should be admitted to an ICU. Monitoring includes ECG; systolic, diastolic, and mean BP, preferably by intra-arterial catheter; respiratory rate and depth; pulse oximetry; urine flow by indwelling bladder catheter; body temperature; and clinical status, including sensorium (eg, Glasgow Coma Scale—see Table 4: Coma and Impaired Consciousness: Glasgow Coma Scale*     ), pulse volume, skin temperature, and color. Measurement of CVP, PAOP, and thermodilution cardiac output using a balloon-tipped pulmonary arterial catheter may be helpful for diagnosis and initial management of patients with shock of uncertain or mixed etiology or with severe shock, especially when accompanied by oliguria or pulmonary edema. Echocardiography (bedside or transesophageal) is a less invasive alternative. Serial measurements of ABGs, Hct, electrolytes, serum creatinine, and blood lactate are obtained. Sublingual CO2 measurement (see Approach to the Critically Ill Patient: Other Types of Monitoring), if available, is a noninvasive monitor of visceral perfusion. A well-designed flow sheet is helpful. Because tissue hypoperfusion makes intramuscular absorption unreliable, all parenteral drugs are given IV. Opioids generally are avoided because they may cause vasodilation, but severe pain may be treated with morphine DURAMORPH MS CONTIN MSIR ROXANOL Click for Drug Monograph 1 to 4 mg IV given over 2 min and repeated q 10 to 15 min if necessary. Although cerebral hypoperfusion may cause anxiety, sedatives or tranquilizers are not routinely given. After initial resuscitation, specific treatment is directed at the underlying condition. Additional supportive care is guided by the type of shock. Hemorrhagic shock: In hemorrhagic shock, surgical control of bleeding is primary. Vigorous volume replacement (see also Shock and Fluid Resuscitation: Intravenous Fluid Resuscitation) accompanies rather than precedes surgical control. Blood transfusion is used for hemorrhagic shock unresponsive to 2 L (or 40 mL/kg in children) of crystalloid. Failure to respond usually indicates insufficient volume administration or unrecognized ongoing hemorrhage. Vasopressor agents are not indicated for treatment of hemorrhagic shock unless cardiogenic, obstructive, or distributive causes are also present. Distributive shock: Distributive shock with profound hypotension after initial fluid replacement with 0.9% saline may be treated with inotropic or vasopressor agents (eg, dopamine INTROPIN Click for Drug Monograph , norepinephrine LEVOPHED Click for Drug Monograph —see Table 3: Shock and Fluid Resuscitation: Inotropic and Vasoactive Catecholamines     ). Patients with septic shock also receive at least two broad-spectrum antibiotics (see Sepsis and Septic Shock: Treatment). Patients with anaphylactic shock unresponsive to fluid challenge (especially if accompanied by bronchoconstriction) receive epinephrine ADRENALIN PRIMATENE MIST Click for Drug Monograph to 0.1 mg IV, followed by epinephrine ADRENALIN PRIMATENE MIST Click for Drug Monograph infusion of 5 mg in 500 mL 5% D/W at 10 mL/h or 0.02 μg/kg/min (see also Allergic and Other Hypersensitivity Disorders: Treatment). Cardiac structural disorder Cardiogenic Pulmonary embolism Cause Mechanism Type Mechanisms of Cardiogenic and Obstructive Shock Obstructive Mechanical interference with ventricular filling Interference with ventricular emptying Tension pneumothorax, cava compression, cardiac tamponade, atrial tumor or clot Ancillary testing Distributive shock Reperfusion Multiple organ dysfunction syndrome (MODS) Compensation Pathophysiology Diagnosis of cause Shock Etiology and Classification Search Diagnosis Hypovolemic shock Symptoms and Signs Distributive shock Cardiogenic and obstructive shock Table 2 Table 1 SECTION Critical Care Medicine SUBJECT Shock and Fluid Resuscitation TOPICS Introduction· Intravenous Fluid Resuscitation·Shock O G M W Q J H C A K B D E F N V X Y L U T P Z R S I Symptoms Sections Index Shock       Table 3 Inotropic and Vasoactive Catecholamines Drug Dosage Hemodynamic Actions Norepinephrine LEVOPHED Click for Drug Monograph 4 mg/250 mL or 500 mL 5% D/W continuous IV infusion at 8–12 μg/min initially, then at 2–4 μg/min as maintenance, with wide variations α-Adrenergic: vasoconstriction β-Adrenergic: inotropic and chronotropic effects* Dopamine INTROPIN Click for Drug Monograph 400 mg/500 mL 5% D/W continuous IV infusion at 0.3 mL (0.25 mg)–1.25 mL (1 mg)/min 2–10 μg/kg/min for low dose 20 μg/kg/min for high dose α-Adrenergic: vasoconstriction† β-Adrenergic: inotropic and chronotropic effects and vasodilation† Nonadrenergic: renal and splanchnic vasodilation Dobutamine DOBUTREX Click for Drug Monograph 250 mg/250 mL 5% D/W continuous IV infusions at 2.5–10 μg/kg/min β-Adrenergic: inotropic effects‡ *Effects not apparent if arterial pressure is elevated too much. †Effects depend on dosage and underlying pathophysiology. ‡Chronotropic, arrhythmogenic, and direct vascular effects are minimal at lower doses. Cardiogenic shock: In cardiogenic shock, structural disorders (eg, valvular dysfunction, septal rupture) are repaired surgically. Coronary thrombosis is treated either by percutaneous interventions (angioplasty, stenting), coronary artery bypass surgery, or thrombolysis (see also Coronary Artery Disease). Tachydysrhythmia (eg, rapid atrial fibrillation, ventricular tachycardia) is slowed by cardioversion or with drugs. Bradycardia is treated with a transcutaneous or transvenous pacemaker; atropine ATROPEN ATROPINE-CARE SAL-TROPINE Click for Drug Monograph 0.5 mg IV up to 4 doses q 5 min may be given pending pacemaker placement. Isoproterenol ISUPREL Click for Drug Monograph (2 mg/500 mL 5% D/W at 1 to 4 μg/min [0.25 to 1 mL/min]) may occasionally be useful if atropine ATROPEN ATROPINE-CARE SAL-TROPINE Click for Drug Monograph is ineffective, but it is not advised in patients with myocardial ischemia due to coronary artery disease. Shock after acute MI is treated with volume expansion if PAOP is low or normal; 15 to 18 mm Hg is considered optimal. If a pulmonary artery catheter is not in place, cautious volume infusion (250- to 500-mL bolus of 0.9% saline) may be tried while auscultating the chest frequently for signs of fluid overload. Shock after right ventricular MI will usually respond partially to volume expansion; however, vasopressor agents may be needed. If hypotension is moderate (eg, mean arterial pressure [MAP] 70 to 90 mm Hg), dobutamine DOBUTREX Click for Drug Monograph infusion may be used to improve cardiac output and reduce left ventricular filling pressure. Tachycardia and arrhythmias occasionally occur during dobutamine DOBUTREX Click for Drug Monograph administration, particularly at higher doses, necessitating dose reduction. Vasodilators (eg, nitroprusside NIPRIDE Click for Drug Monograph , nitroglycerin NITRO-BID NITRO-DUR NITROL NITROQUICK Click for Drug Monograph ), which increase venous capacitance or lower systemic vascular resistance, reduce the workload on the damaged myocardium and may increase cardiac output in patients without severe hypotension. Combination therapy (eg, dopamine INTROPIN Click for Drug Monograph or dobutamine DOBUTREX Click for Drug Monograph with nitroprusside NIPRIDE Click for Drug Monograph or nitroglycerin NITRO-BID NITRO-DUR NITROL NITROQUICK Click for Drug Monograph ) may be particularly useful but requires close ECG and pulmonary and systemic hemodynamic monitoring. For more serious hypotension (MAP < 70 mm Hg), norepinephrine LEVOPHED Click for Drug Monograph or dopamine INTROPIN Click for Drug Monograph may be given, with a target systolic pressure of 80 to 90 mm Hg (and not > 110 mm Hg). Intra-aortic balloon counterpulsation is valuable for temporarily reversing shock in patients with acute MI. This procedure should be considered as a bridge to permit cardiac catheterization and coronary angiography before possible surgical intervention in patients with acute MI complicated by ventricular septal rupture or severe acute mitral regurgitation who require vasopressor support for > 30 min. In obstructive shock, cardiac tamponade requires immediate pericardiocentesis, which can be done at the bedside. Tension pneumothorax should be immediately decompressed with a catheter inserted into the second intercostal space, midclavicular line. Massive pulmonary embolism resulting in shock is treated with thrombolysis or surgical embolectomy. Last full review/revision May 2007 by Max Harry Weil, MD, PhD Content last modified May 2007 Back to Top          Previous: Intravenous Fluid Resuscitation                                                                                                                                                                                                          Reduce Risk of Coronary Artery Disease and Heart Failure Keep LDL cholesterol below 100 Keep HDL Cholesterol above 40 in men and above 50 in women Keep Triglycerides another fat in the blood below 150 Keep BP 130/80 or below Keep Blood Glucose under control Limit alcohol intake and quit smoking Dietary mg Foods low in saturated fats and low in salt                                                                                                                                                                                                                                                                    

141 General Care Principles
Identify patients at risk Careful history and examination Report early signs, prepare to act with supportive measures (IV, blood, medications, etc) Protect and support function


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