Exam 2 Flashcards
Pulmonary Edema
abnormal accumulation of fluid in the alveoli and intersititial spaces of the lungs. Life threatening emergency
Most common cause is Left sided heart failure
Ischemic Non-ischemic cardiomyopathy Valvular Heart disease
end inspiratory crackles (early), frothy sputum (late)
Pulmonary Emboli (PE)
Blockage of the pulmonary artery by a thrombus, fat or air embolus, bacterial vegitation, or tumor tissue.
Embolus lodges at a narrow part of the circulatory system and in this case it is in the pulmonary vasculature
More than 90% arise from DVT
Venous Thromboembolism (VTE)
is the term to describe the process of DVT to PE
Pulmonary Emboli clinical manifestations
Dyspnea
Mild to moderate hypoxemia
Tachypnea, cough, chest pain, hemoptysis, crackles
Pulmonary Emboli complications
Pulmonary infarction
Death
Pulmonary Hypertension
D-Dimer
diagnostic test for PE measures the cross-linked fibrin fragments found as a result of clot degradation and are rarely found in healthy individuals. increase= clot
Spiral CT
diagnostic test for PE Contrast media is injected into person and scanner illuminates pulmonary vasculature. Contraindicated in patients with Dye allergy or renal dysfunction
Ventilation/ Perfusion Scan (V/Q)
Used if CT is contraindicated.
If ventilation is normal and Perfusion is abnormal there is a high probability of a PE.
DVT Prophylaxis
LMWH
Compression devices
Early Ambulation
For Patient’s identified as having PE
Anticoagulants
Fibrinolytic Therapy
Surgical Therapy – pulmonary embolectomy
Cardiomyopathy (CMP)
Group of diseases that affect the structural or functional ability of the myocardium.
Primary (idiopathic)
Secondary (ischemic, ETOH, cardio toxicity)
CMP can lead to heart failure and cardiomegaly- leading cause of heart transplantation
Types of CMP
dilated, hypertrophic and restrictive Takotsubo Cardiomyopathy (Broken heart syndrome)
Dilated Cardiomyopathy
most common type
Etiology – infection, autoimmune, ETOH
Fibrosis of myocardium and endocardium
Ventricular dilation , impaired systolic function, atrial enlargement, stasis of blood (mural wall thrombi prevalent) .
Leading cause of death for DCM – sudden cardiac death
Dilated Cardiomyopathy Clinical Manifestations
DOE, Fatigue, dyspnea at rest, PND, orthopnea, cough, increased abdominal girth, anorexia, nausea vomiting, S3 and or S4, JVD, pulmonary crackles, hepatomegaly (HJR), displaced PMI, dysrhythmias, heart block, emboli
Diagnostic studies for Cardiomyopathy
ECHO, Chest x-ray, b-type naturetic peptide, cardiac cath, multiple gated acquisition (MUGA) nuclear scan, endometrial biopsy.
Determine EF <20% has a mortality rate of 50% within the next year.
Treatment for Cardiomyopathy
Heart Failure cocktail – ACEI or ARB, BB, nitrates, diuretics, KCL, aldosterone antagonist, antidysrhythmics if necessary and possibly anticoagulation. Remove cause if secondary Recurrent and multiple episodes common Inotropic therapy – milronone, dobutrex Statin therapy – decreases inflammation Ventricular assist devices Heart Transplant Hospice
Hypertrophic Cardiomyopathy pathophysiology
Nonobstructed-
Hypertrophy of the walls
Hypertrophied septum and relatively small chamber size
Obstructed-
Hypertrophy of the walls
Hypertrophied septum and relatively small chamber size
The hypertrophied septum creates an outflow track obstruction
Mital valve incompetence
Young athletes
Hypertrophic Cardiomyopathy 4 main characteristics
massive ventricular hypertrophy
rapid, forceful, contraction of the left ventricle
impaired relaxation(diastole)
obstruction to aortic outflow (not in all patients)
–Thickened intraventricular septum
diastolic dysfunction with RV stiffness
Hypertrophic Cardiomyopathy Clinical Manifestations
fatigue,DOE,angina, syncope, palpitations, dysrrthymias (SVT) AF, VT, VF), SCD, Heart failure
Hypertrophic Cardiomyopathy Diagnostic Studies
Assessment – exaggerated apical impulse and laterally displaced, S4, systolic murmur, ECG changes, ECHO, Nuclear testing.
Hypertrophic Cardiomyopathy treatment
BB, CCB, Dig(only for AF), antidysrhythmics, ICD, PPM, surgery, PTSMA (percutaneous transluminal septal myocardial ablation with Alcohol)
Digoxin, nitrates and other vasodilators contraindicated with the obstructed form.
Restrictive Cardiomyopathy Pathophysiology
Fibrosed walls cannot expand or contract. Chambers narrowed: emboli common
Disease of myocardium that impairs diastolic filling and stretch.
Systolic function normal
Myocardial fibrosis, amyolidosis, scarcoidosis, secondary to radiation therapy
Restrictive Cardiomyopathy Diagnostic studies
Diagnostic studies the same as others
may need endometrial biopsy for diagnosis
Pericarditis
a condition caused by inflammation of the pericardial sac (the pericardium).
The pericardial space is the cavity between these two layers. Normally it contains 10 to 15 mL of serous fluid.
Causes- Infectious or Non-Infectious, Hypersensitive or Autoimmune
Pericarditis associated with MI
Acute Pericarditis after MI
-48-72 hrs after MI
Late Pericarditis (Dressler syndrome)
-4-6 weeks after MI
Pericarditis: Clinical Manifestations
Severe sharp pleuritic chest pain Worse with deep inspiration, cough Unrelieved with NTG and many times Morphine Different dyspnea worse when lying down improves with sitting up and leaning forward Diffuse ECG changes (ST elevation) Pericardial Friction Rub Heard with diaphragm (LLSB)
Pericarditis: Complications
Pericardial Effusion
Tamponade – compression of heart (emergency)
-decreased LA filling
-decreased cardiac output
Manifestations of tampanode
- tachypnea and tachycardia
- muffled heart sounds and narrow pulse pressure
- increased pulsus paradoxus
- dyspnea
Pericarditis Diagnostic studies
ECG, ECHO, Labs
Pericarditis Collaborative Care
Identify are treatment of underlying problem
Bacterial – antibiotics
Acute Inflammation – NSAIDS (in some cases corticosteroids)
Colchicine (Colsalide) for recurrent pericarditis
Pericardiocentesis
Pericardial Biopsy
Pericarditis Nursing Management
Assessment Pain management elevate HOB NSAIDS with food or milk to decrease GI distress Anxiety management Monitor for signs of tamponade
Chronic Pericarditis
Etiology – scaring and loss of elasticity of pericardial sac.
Manifestations vague
-dysnea, peripheral edema, fatigue, anorexia weight loss
Diagnostic studies
-Chest x-ray, ECHO, MRI, CT scan
Collaborative Management
-Pericardiectomy (Pericardial Window)
Pericardial Tampanode
Increased fluid accumulation in pericardial space
Signs and symptoms-
Becks triad (rarely occur all together), JVD, Distant Heart Sounds, Hypotension, Pulses Paradoxus of >10mmHg (Abnormal fall in BP with inspiration)
Patients present with dyspnea and tachypnea
Treatment Pericardiocentesis
CXR that shows a widened mediastinum
Myocarditis
Acute or chronic inflammation of the myocardium as a result of pericarditis, systemic infection or allergic response
causes include viruses, bacteria, fungi, radiation therapy, and pharmacologic and chemical factors.
Coxsackie A and B viruses are the most common etiologic agents
Myocarditis Pathophysiology
The causative agent invades the myocytes and causes cellular damage and necrosis
Activation of the immune response
Autoimmune response is activated with destruction of myocytes
Results in- cardiac dysfunction, linked to DCM, associated with SCD
Myocarditis Clinical Manifestations
Variable from benign to heart failure and death.
Fever, fatigue, malaise, myalgias, pharyngitis, dyspnea, lymphadenopathy, and nausea and vomiting are early systemic manifestations of the viral illness.
cardiac signs appear 7 to 10 days after viral infection.
pleuritic chest pain with a pericardial friction rub and effusion. (Pericarditis)
S3 heart sound, crackles, JVD, syncope, peripheral edema, and angina. (Heart Failure)
Myocarditis Diagnostic studies
ECG, Lab Studies, Endometrial biopsy, Echocardiography, Nuclear Scans, MRI
Myocarditis Collaborative Care
Medication Therapy
-Analgesics, salicylates, NSAIDS
-Cautious use of Digoxin
-ACE inhibitors,BB,Diuretics, Afterload reducers
-Positive chronotropic agents, Anticoagulation, Immunosupressants, antidysrhythmics, antibiotics
oxygen therapy, bed rest, and restricted activity. In cases of severe HF, the use of intra-aortic balloon pump therapy and ventricular assist devices may be required
Myocarditis Nursing Management
assessment for the signs and symptoms of HF (decompensation)
decrease cardiac workload
monitoring.
assess the level of anxiety, institute measures to decrease anxiety, and keep the patient and caregiver informed about the therapeutic plan.
Infective Endocarditis
Infection of the inner most layer of the heart (Endocardium) and the heart valves.
Subacute (SBE)- involves those with pre-existing valve disease and may last months.
Acute – affects those with healthy valves and manifest as rapidly progressive disease.
Etiologies include: rheumatic heart disease, bacterial (vegetation), viral and fungal infections, IV drug use, and others
Vegitations
a clump of fibrin, leukocytes, platelets, and microbes that stick to the valve surface or endocardium.
Vegitations can break loose and become emboli
Infective Endocarditis Clinical Manifestations:
Low grade fever, chills, weakness, myalgias, weightloss, clubbing of fingers
Splinter hemorrhages – nailbeds
Petechiae – conjunctivae, lips, buccal mucosa and palate
Osler’s nodes – painful tender red or purple pea sized lesions on finger tips or toes
Janeway’s Lesions – flat painless red spots on palms and soles
New or changing murmur
Infective Endocarditis Diagnostic Studies
Blood Cultures
Echocardiography (TTE and TEE)
IE: collaborative Care
Prophylactic Treatment Drug Therapy Based on Culture and Sensitivity Requires weeks of therapy Valve replacement
IE : Nursing Management
Assess vital signs and heart sounds (murmur)
Examine patient for clinical evidence of IE
Goal
Normal or baseline cardiac function
Performance of ADLs
Knowledge of therapy and prevention of IE
transducer has to be at the level of the
right atrium, 4th intercoastal midaxillary line
Volume
Preload
Afterload
SVR
Cardiac Output
rate, contractility
Pump
cardiac output and contractility
Hemodynamic Monitoring
Direct system of measuring pressures (heart, blood pressure), Pulmonary artery pressure (PA), Central venous pressure (CVP, RA), Intra-arterial pressure, Wedge pressure
Must be in critical care unit
Called invasive monitoring
CVP (Volume)
The pressure within the superior vena cava; it reflects the pressure under which the blood is returned to the superior vena cava and right atrium (preload)
The CVP is measured with a central venous catheter in the superior vena cava
Normal CVP is 3-8 mm Hg
Elevated CVP indicates
An increase volume (sodium and water retention)
Decreased contractility
Excessive IVF
Kidney failure
Decreased CVP indicates
Decrease in intravascular volume
Hemorrhage
Severe vasodilation
Pooling of blood in the extremities
Measuring CVP
Identifying level of the right atrium Patient supine Zero the transducer to the right atrium Patient relaxed If on ventilator reading is taken at the point of end expiration
inflate PA catheter balloon with
1-1.5 mL of air
balloon inflated only
on insertion or to do wedge reading
Right atrial pressure (RA)
Assesses right ventricular function and venous return to the right side of heart
Proximal port of the pulmonary artery catheter (in RA)
Direct method of measuring right ventricular filling pressure (preload)
Increase in RA due to
right ventricular failure, hypervolemia or decreased contractility
Decreased CVP
usually hypovolemia
Pulmonary Artery Pressure
Assesses LV function
Diagnosis of etiology of shock
Assesses response to interventions such as administration of volume and medications that are vasoactive
PAS/PAD (PA Mean)
Normal 15-26/5-15
PAWP or PCWP (pulmonary artery wedge pressure or pulmonary capillary wedge pressure)
Wedge is achieved by momentary inflation of the balloon and watching the waveform dampen, Wedge pressure is normally 4-12 mm Hg and is reflective of the LV function
Increased wedge
Decreased wedge
Increased wedge
LV failure, hypervolemia, mitral regurgitation
Decreased wedge
Hypovolemia, afterload reduction
Cardiac Outputs
temperature probe (thermistor) at the end of the PA catheter and in the pressure tubing. The cardiac output monitor measures the difference in the two temperatures and calculates the cardiac output
Normal 4-7 liters per minute
Cardiac index: calculated using BSA (CO/BSA)
Normal is 2.5-4 L/min/m2
CABG - coronary artery bypass graft
Candidates determined by angiogram (stent or surgery)
Surgical decision depends on the extent of the disease and the location of the lesions
Purpose is to increase blood flow to the myocardium
Use saphenous (leg) vein graft(SVG), internal mammary artery (IMA), or radial artery
** keep BP low to prevent popping
SVG
Recurrence of atherosclerotic disease after surgery within 5-10 years
SVG is anastomosed to the ascending aorta and to the coronary artery beyond the blockage
IMA
Arterial grafts are preferred as they do not develop atherosclerotic changes as quickly as SVG
Proximal IMA is left intact and the distal end is moved from the chest wall to the coronary beyond the blockage
PRE-OP TEACHING Cardiac Surgery
Visit the ICU (patient and family)
Some medications will be discontinued prior to surgery (diuretics, digoxin, aspirin, anticoagulants)
Emotional support
Discussion of monitors, lines, tubes, ET tube (patient cannot speak with ETT), ventilator
ROM, CTs, pain control
Meticulous pulmonary care (splinting chest, TCDB, IS)
Post operative activity- Shoulder ROM
Post op equipment Cardiac Surgery
CTs, Epicardial pacing wires, ET tube, Mechanical ventilator, NG tube, Heart monitor, Foley, Swan, Arterial line, Dressings to sternal and leg incisions, O2 monitor, TEDs or pneumatic boots
Post op care Cardiac Surgery
VS q 15 minutes X4, q 30 minutes X 4 and then hourly
Hemodynamic monitoring- PA catheter to measure RA, PA, PCWP, CO, CI at same frequency as vital signs
Assess for hypothermia (vessels may be constricted). Rewarm no faster than 1.8 degrees F per hour to prevent shivering.
Assess for postoperative bleeding, peripheral circulation
Assess lab values (CBC, BMP, CK, troponins, coagulation studies)
ECG and CXR
Arterial line measures BP and site for drawing ABGs
Correlate the arterial blood pressure with the cuff blood pressure at least once per shift
incision care
Surgical dressing in place for 48 hours
After 48 hours, open to air
Clean daily with antiseptic (chlorohexidine, betadine)
Patient should be taught to shower daily and use antibacterial soap, pat dry and then use antiseptic
Chest tubes to drain the mediastinum and/or the pleural space
Assess for amount (should be less than 100/hr for the first few hours with a gradual decrease in the amount of chest tube drainage)
Assess for color
Assess for air leak
Usually kept in place for 24 to 48 hours and are taken out when drainage meets parameters and when there is no air leak
Assess chest tube dressing
Ventilator and respiratory care
ABGs, O2 Sats
Long anesthesia time (at least 4 hours)
Atelectasis r/t surgery
Usually on ventilator 4-12 hours postoperatively
Suction as needed as evidenced by breath sound assessment Q1-2 HOURS
After extubation T, C, DB, IS q2h
Pain must be controlled postoperatively so the client can breathe effectively and for the maintenance of effective respiratory care
Up in the chair ASAP
Control of fluid balance
Determine if too much or too little with Swan and labs
Maintain renal output at least 30 mL/hour
Assess electrolytes. Potassium should be replaced to keep level WNL.
May need volume replacement with colloids if H and H is normal, with PRBC if H and H is low
May need platelets or fresh frozen plasma if the client is bleeding too much
complication of cardiac surgery heart failure
Decreased BP, oliguria, poor peripheral vascular checks, decreased level of consciousness, crackles, chest pain
All are signs of decreased cardiac output
Client may be fluid overloaded but CO is diminished because the pump has failed
Valvular Disorders
Valves direct the flow of blood
When damaged, blood backs up and pressures in the system increase
Chordae tendineae anchor the valve leaflets to the papillary muscles and the ventricular wall
Semilunar valves between the ventricles and the arteries (pulmonic and aortic)
Anatomic Location of Tricuspid Valve
Fifth intercostal space to left of sternum
Anatomic Location of Pulmonic valve
Second intercostal space to the left of the sternum
Anatomic Location of Mitral Valve
Left midclavicular line at 5th intercostal space
Mitral area also apex and PMI (point of maximal impulse
Anatomic Location of Aortic Valve
Second intercostal space to the right of the sternum
S1 is heard when the
AV valves close and is heard loudest at the apex of the heart
S2 is heard when the
semilunar valves close and is heard best at the base of the heart
Mitral Valve Prolapse
Usually no symptoms
More likely with women
Portion of mitral valve prolapses back into atrium during systole
Blood regurgitates into LA from LV
If symptoms, may be fatigue, SOB, dizziness, syncope, palpitations, CP, anxiety
Eliminate caffeine, smoking and alcohol
Mitral Regurgitation
May be problem with valve leaflets, chordae tendineae, or papillary muscle
Blood flows LV to LA and leads to hypertrophy and dilation
Decreased CO
Systolic murmur
May be asymptomatic to severe HF symptoms depending on rapidity of development
Dyspnea, fatigue, weakness, palpitations, DOE, cough from pulmonary congestion, dizziness
Mitral Stenosis
Restricts blood flow LA to LV
Can be caused by rheumatic endocarditis
Hypertrophy and dilation
Backflow of blood into the pulmonary circulation
DOE, fatigue due to decreased CO, hemoptysis, cough, wheezing, palpitations, orthopnea, PND, and respiratory infections
Atrial fibrillation is common due to the strain on the atrium and therefore pulse is weak and irregular
Diastolic murmur
Atrial dysrhythmias
Aortic Regurgitation
Backflow of blood from the aorta to the LV during diastole
Leaflets do not close (Endocarditis, Congenital problem, Dissecting aorta)
LV dilates and hypertrophies
SBP increases due to increased force of myocardial contraction
DBP decreases due to arteries reflexively relaxing
Widened pulse pressure
Diastolic murmur
Aortic Regurgitation S&S
Symptoms of LV failure (orthopnea, paroxysmal nocturnal dyspnea)
Client may be able to feel the stronger pulse from the increased contractility
May be able to see pulsations in the carotids and temporal arteries
Fatigue, DOE
Prophylactic antibiotics are needed for invasive or dental procedures
Avoid strenuous activities (due to LV dysfunction)
Treat with valvuloplasty or AVR
Must preserve the LV
Aortic Stenosis
Narrowing of the valve between the LV and the aorta
Can be congenital
Can be due to rheumatic endocarditis or calcification
LV increases the force of contraction to compensate
LV hypertrophy
DOE, dizziness, syncope (decreased CO to the brain)
Orthopnea, PND, pulmonary edema
CP (increased myocardial oxygen demand)
Systolic murmur
Valve Replacement
Usually a mediastinal approach
Abrupt correction of long standing blood flow issues
Sudden changes in intra-cardiac pressures
Postoperative risk of thrombo-embolism, infection, bleeding, HF, HPTN, dysrhythmias
Mechanical (St. Jude) Valve Replacement
Last longer
Need to be on coumadin for life due to the risk of thromboembolism
Tissue or biologic valves (Pig valve, porcine, Synthetic)
Do not last as long
Do not need to be on coumadin
7-10 year viability
Post-operative care of the Valvular Surgery Client
ICU for 24-72 hours Hemodynamic monitoring VS frequent Medications for BP, HR, CP In hospital up to 7 days
Rheumatic Endocarditis
Beta hemolytic strep is the usual culprit of rheumatic fever
Can cause endocarditis (usually of the mitral valve)
Would hear a murmur
Prevent with prompt treatment of strep throat
Two criteria must be met before shock can be diagnosed:
There must be a reduction in mean systemic B/P
Clinical evidence of hypoperfusion of vital organs
This results in:
Decreased tissue perfusion and
Impaired cellular metabolism
Shock Initial Stage (Early Stage)-
Occurs at a cellular level and is usually not clinically apparent.
Increased sympathetic stimulation occurs (compensation)- mild vasoconstriction & increase in heart rate
Metabolism begins to change from aerobic to anaerobic.
Lactic acid begins to build.
Compensatory Shock-
Compensatory Mechanisms including neural, hormonal and biochemical are activated to maintain perfusion of Vital organs
Classic sign of shock (decreased blood pressure) is minimized by compensatory mechanisms, oxygen supply and demand mismatch
Compensatory Shock clinical manifestations
Neurologic System – barrorecptors activated – stimulate SNS. SNS releases epi and nore. Vasoconstriction results. Blood flow to heart and brain maintained but shunted away from non vital organs
Cardiovascular System – heart rate increases and coronary arteries dilate
Respiratory System – decreased blood flow to lungs increases physiologic dead space (VQ mismatch). O2 levels decrease and patient will compensate with increased depth and rate of respirations
Gastrointestinal System – shunting of blood decreases gastric motility, increased risk for paralytic ileus.
Renal System – activation of RAAS, and ADA released in response to increased osmolality
Decompensated or Progressive Shock-
Compensatory mechanisms Fail
Vital organs become underperfused
Overall metabolism is anaerobic- the small amount of energy created by anaerobic metabolism is not enough to keep the cell functional and irreversible damage begins to occur.
progressive stage clinical manifestations
Neuro – decreased mental status
Cardiovascular – CO falls resulting in decreased perfusion. Altered capillary permeability allows protein to leak out of vascular space resulting in decreased circulating volume and intersitial edema. (Anasarca may develop).
Pulmonary – increased VQ mismatch due to constricted arterioles. Pulmonary edema.
GI – protective mucosa becomes ishemic and sets the stage for PUD, and GI Bleeding.
Renal – tubular necrosis – renal failure - elevated BUN, Creatinine.
Liver – elevated liver enzymes
Hematologic system – DIC – results in bleeding from multiple sites.
Disseminated Intravascular Coagulation (DIC)
Serious bleeding and thrombotic disorder
Shock can predispose patient to DIC.
Blood pooling can lead to clotting.
This uses up clotting factors and results in bleeding
Irreversible or Refractory Shock-
anerobic metabolism accumulation of lactic acid causes increased capillary permeability – edema Decreased coronary blood flow Cerebral ischemia Severe tissue hypoxia with ischemia and necrosis Profound hypotension and hypoxemia Multiple organ dysfunction (MOD) Death
MAP=
(dx2)+s/3
Hypovolemic Shock
Occurs as a result of a loss of intravascular blood volume Volume is inadequate to fill the vascular space The volume loss may be either an absolute (d/v bleeding) or relative (internal fluid shift) volume loss class 1-4 of blood loss
Class I blood loss
a fluid volume loss up to 15 % or an actual volume loss up to 750 ml.
May be asymptomatic,restlessness or anxiety
Class II blood loss
patient has an intravascular volume deficit of 15 to 30% (actual blood loss of 750-1500ml)
decreased preload CO and BP, pallor apprehension, prolonged cap refill, increase HR and RR
Class III blood loss
occurs when blood volume loss reaches 30 to 40%(actual volume loss of 1500 to 2000 ml)
(All compensatory mechanisms are in full action and beginning to fail)
decrease BP cap refill UO, anxious, confused, increase HR RR
Class IV blood loss
blood volume deficit is greater than 40% (actual volume loss of more than 2000 ml)
(Compensatory mechanisms are exhausted)
impaired organ function, organ failure, irreversable shock
Collaborative Management(Hypovolemic Shock)
Give isotonic fluids while waiting for blood (packed red blood cells) ,IV crystalloids
Cardiogenic Shock
The result of failure of the heart to pump blood forward effectively
Etiology- systolic dysfunction (decrease contraction), diastolic (decreased filling), dysrhythmias (tachy or brady), structural factors (valve disease)
Can be defined as a low CO and hypotension with clinical signs of inadequate blood flow to tissues
Low urine output
Changes in mental status
Decreased peripheral pulses- Cool & clammy skin
most common event leading to cardiogenic shock
Acute myocardial infarction (AMI)
The risk of cardiogenic shock increases as the area of myocardial necrosis increases
When more than 40% of the left ventricle is destroyed in the AMI process, cardiogenic shock is likely within 48 hours of the acute event
Clinical Manifestations of Cardiogenic Shock
tachycardia, hypotension, narrowed pulse pressure, increased SVR, decreased cardiac output (less than 4L/min), Cardiac Index (less than 2.5L/min), Pulmonary crackles on auscultation, Cyanosis, pallor, mottling, Edema, decreased U/o, Anxiety, restlessness, confusion
Cardiogenic Shock Assessment
Left ventricular ejection fraction is usually less than 30%
Other S&S- hypotension, reduced CO, increase in respiratory rate, development of crackles (secondary to pulmonary congestion), urine output decreased, restlessness, agitation, confusion
Cardiogenic Shock Collaborative Management
restore the balance between oxygen supply and demand.
Definitive measures to restore blood flow include: thrombolytics, angioplasty, or coronary revascularization
IV fluids may be administered (if needed) to obtain maximal stretch of the myocardial fibers and optimal contraction
Positive inotropic agents-dobutamine (Dobutrex) increase MAP, dopamine (Intropin)
Vasoactive drugs-sodium nitroprusside (Nipride) decrease MAP, nitroglycerin (Tridil)
Intra-aortic balloon counterpulsation (IABC) is a treatment used to stabilize the patient with cardiogenic shock
Intra-aortic balloon counterpulsation
IABP decreases myocardial workload by improving myocardial supply and decreasing myocardial demand
IABP achieves this by improving coronary artery perfusion and reducing left ventricular afterload
Distributive Shock
Results in inadequate perfusion of the tissues through a maldistribution of blood flow
Intravascular volume and heart function are both normal, but blood is not reaching the tissues
It develops when acute vasodilation occurs without an increase in intravascular volume
3 types- septic shock, anaphylactic shock, & neurogenic shock
Sepsis
A documented infection with at least 2 of the 4 systemic inflammatory response criteria caused by infection
Sepsis is most commonly caused by Gram-negative bacteria (E. coli, Pseudomonas, Klebsiella)
Gram-positive bacteria represents the second most common causative organisms (Staphylococcus, Streptococcus)
Systemic Inflammatory Response Syndrome
Manifested by 2 or more of the following:
Temp higher than 38 C (100.4 F) or lower than 36 ° C (96.8 F)
HR more than 90 beats per min
Respiratory rate greater than 20 breaths per min or Paco2 less than 32 mm Hg
WBC count more than 12,000 cells/mm3, less than 4000 cells/mm3, or more than 10% immature (bands) forms
Findings to support sepsis indicating organ dysfunction
Creatinine > 2.0 Urine output ,0.5 ml/Kg/hr for 2 hours Bilirubin >2 mg/dl INR >1.5 (nl 1.0) PTT > 60 (nl 25-35 sec) Lactate (Lactic Acid) > 2mmol/L Platelets < 100,000 Acute respiratory failure
Procalcitonin (PCT)
Help differentiate infectious from non infectious causes of systemic inflammatory response syndrome.
PCT is increased in bacterial sepsis and decreased in most patients who progressed favorably.
PCT mean levels were 3.0 ng/mL in SIRS
PCT mean levels were 16.8 ng/ml in patients with Sepsis
PCT may be used to determine antibiotic utilization
Sepic Shock
Sepsis with hypotension (systolic B/P less than 90 mm Hg or a reduction of 40 mm Hg from baseline) despite adequate fluid resuscitation along with the presence of perfusion abnormalities, that may include lactic acidosis, scant urination, or an acute alteration in mental status
Tissue hypo-perfusion after crystalloid fluid resuscitation SBP < 90 MAP < 65
Or
Lactate (Lactic Acid) level > or equal to 4 mmol/L
Three major pathophysiologic effects of septic shock
vasodilation – resulting and relative hypovolumia
maldistribution of blood flow
myocardial depression
give alpha to constrict
Septic shock and respiratory failure
May also be accompanied by respiratory failure.
initial hyperventilation results in alkalosis then as compensatory mechanism fail acidosis occurs.
85% will develop respiratory failure
40% will develop adult respiratory distress syndrome
Septic Shock Assessment
Patient’s with septic shock can present in 2 states: An early (hyperdynamic) state, or A late (hypodynamic) state
Septic Shock Hyperdynamic Phase
Decreased vascular resistance, while B/P is barely maintained Peripheral vasodilation Normal to high CO Hypotension or normotension Fever Slight alterations in sensorium Moderate tachycardia Tachypnea Normal urine output
Septic Shock Hypodynamic Phase
Profoundly impaired perfusion Decreased CO Mental status changes (lethargy & coma) Clammy, pale skin Tachycardia, dysrhythmias, hypotension Pulmonary congestion Central cyanosis
Treatment of septic shock
IV fluids (normal saline, Ringer’s lactate solution)
Vasoconstrictors (Dopamine)
Eliminating the source of infection
Administering appropriate antibiotics
Anaphylactic Shock
due to an antigen-antibody reaction that occurs in blood vessels throughout the body in response to contact with a substance to which the person has a severe allergy
S&S can include skin rash/flushing, pruritis, sneezing/coughing, wheezing, urticaria, dizziness, chest pain, incontinence, angioedema, and restlessness, confusion, sense of doom
Life-threatening S&S can include respiratory stridor, bronchospasm and laryngeal edema
Anaphylactic Shock Assessment
The peripheral vasodilation and increased capillary permeability produce pooling of blood in the periphery and a decrease in preload
Can be severe enough to decrease CO and B/P
Will see a decrease in SVR (dilation of peripheral vessels)
Anaphylactic Shock Collaborative Management
ABCs of emergency care (ensure patent airway)
Volume expansion
Vasoconstricting agents
Epinephrine- first-line agent
Antihistamines, bronchodilators and corticosteroids
Neurogenic Shock
Causes: spinal cord injury, spinal anesthesia, depressant action of drugs
These conditions result in the loss of sympathetic vasoconstrictor tone
This results in massive vasodilation with severe hypotension
Bradycardia develops due to the unopposed activation of the parasympathetic nervous system.
Develop impaired thermoregulation because of the loss of vasomotor tone in the cutaneous blood vessels (that dilate and constrict to maintain body temp)
Become poikilothermic (assume the temperature of the environment)
Neurogenic Shock Pathophysiology
Disruption of sympathetic nervous system Loss of sympathetic tone Venous & arterial vasodilation (pooling of blood in the periphery) Decreased venous return Decreased stroke volume Decreased cardiac output Decreased cellular oxygen supply Decreased tissue perfusion
Neurogenic Shock Assessment
Presenting S&S include hypotension, HR less than 60, warm, dry skin, and hypothermia
Additional signs of hypoperfusion can include a decrease in urine output, changes in LOC, decrease in peripheral pulses, and a capillary refill of more than or equal to 3 seconds
Respiratory patterns need to be assessed (rate, rhythm, depth)
Neurogenic Shock Collaborative Management
For patients with spinal cord injuries, early and proper stabilization of the spinal cord is critical to preventing or limiting neurogenic shock
Treatment goals include the ABCs, fluid resuscitation and vasoconstrictors to increase B/P
Bradycardia may be treated with atropine
Hypothermia is treated with warming measures and environmental temperature regulation
Obstructive Shock
A physical obstruction to outflow of the heart such as
-Cardiac tamponade, tension pneumothorax, Pulmonary embolism.
S&S depend on obstruction. May include; JVD, pulsus paradoxus
Treatment of Anaphylactic, Septic and Neurogenic
“Fill up the tank”
fluid resuscitation (crystalloids and possibly colloids)
serial measurement of blood pressure and temp.
treatment of shock- Hypotension
fill up the tank first
-Vasopressor (goal to achieve and maintain MAP greater than 65 mmHg)
-norepinephrine (Levophed) dopamine (Intropin) phenylephrine (Neosynephrine) Vasopressin (Pitressin)
-Inotropic Agent
-Vasodilators – to reduce afterload, decreases myocardial workload and O2 requirements, Keep MAP greater than 65 mmHg
nitroglycerine (Tridil) Nitroprusside (Nipride)
-Diuretics may be needed in Cardiogenic shock
-Parenteral Nutrition
Epidermis
outermost layer of skin
Protective barrier
Regenerates every 28 days
Dermis
this is the layer where new skin is created.
Vascular connective tissue
Nerves, lymphatic tissue, hair follicles and sebaceous glands
Subcutaneous Tissue
Not part of the skin but attaches to the skin
Loose connective tissue and fat cells
Insulation, regulates temperature and provides shock absorption.
Burn size
Small burn – localized response
Large burns
25% or more of BSA for adult , 10% or more for child
Thermal Injury or Burn
An Injury to the tissue caused by Heat, Chemicals, Electric Current, Radiation Associated injury= Smoke Inhalation The result of a burn depends on Temperature of the burning agent Duration of Contact time. Type of tissue exposed
priority nursing action with burn
Assess for airway patency
Administer oxygen as needed
Obtain vital signs
Initiate IV access and fluid administration
Elevated extremities if no fractures are obvious
Maintain body heat
NPO
Smoke Inhalation Injuries
Result from inhalation of hot air or noxious chemicals
Cause damage to respiratory tract
Airway is a priority concern
Major predictor of mortality in burn victims
Of the 12,000 fire deaths each year in the U.S., 50% - 60% are due to inhalation injuries
Need to be treated quickly
Carbon monoxide (CO) poisoning
Treat with 100% humidified oxygen.
CO poisoning may occur in the absence of burn injury to the skin.
Skin color may be described as “cherry red” in appearance.
Electrical burn
caused by heat generated by electrical energy as it passes through the body, Results in internal tissue damage
Voltage, type of current, contact site and duration of contact are important to identify
most damage occurs beneath the skin- Iceberg effect
Patients are at risk for dysrhythmias, severe metabolic acidosis, and myoglobinuria.
May cause muscle contraction that is strong enough to fracture bones
Release of Myoglobin and Hemoglobin can result in ATN and Renal Failure
Chemical burn
Alkali, Acid, Organic compounds
Time/Temperature Relationshipto Full-Thickness Injury
ADULTS
30 sec=130 15 sec=135 5 sec= 140 1.8 sec= 150
CHILD
10 sec= 130 4 sec=135 1 sec=140 0.5 sec=149
Superficial partial-thickness burn
1st degree
epidermis only, mild swelling, local pain, erythema, blanches with pressure, no vesicles or bullae (sunburn)
Deep Partial Thickness Burn
2nd degree
Epidermis & dermis (not entirely) vesicles or bullae present moist- pink or red very painful Mild to moderate edema
Full- Thickness Burn
Involves entire dermis & epidermis, possibly SQ tissues
Color varies: waxy white, red, brown, black, tan, yellow
Dry & leathery
Thrombosed vessels may be visible
Pain insensitivity
rule of nines
front of leg-9 back of leg nine, chest- 18, back- 18, front of arm-4.5, back of arm- 4.5, face- 4.5, back of head- 4.5
Emergent (resuscitative) phase of burn management
Pre-Hospital Care and Emergency Department
Airway, oxygenfluids
Usually lasts up to 72 hours
concerns of hypovolemic shock and edema.
begins with fluid loss and edema formation and continues until fluid mobilization and diuresis begin (decreased BP increase Pulse)
Acute (wound healing) phase of burn management
time in hospital- for each 1% burn is about 1 day (without complications)
Begins when hemodynamically stable.
mobilization of extracellular fluid and subsequent diuresis.
The acute phase is concluded when the burned area is completely covered by skin grafts, or when the wounds are healed.
Bowel sounds return.
Rehabilitative (restorative) phase of burn management
after grafting, 6-12 months at home
The rehabilitation phase begins when Burn wounds are healed and Patient is able to resume a level of self-care activity
Monitor Three Areas: Positioning Contractures Hypertrophic Scaring (From not wearing garments or facemask)
Fluid Replacement
Large bore angiocath
Crystalloid Solutions (Lactated Ringer’s, Saline)
Colloid solutions (Albumin)
Begin as soon as possible
Fluid replacement calculation
4ml X % burnX wt (Kg)
give half in first 8hrs, give 1/4 next two 8 hour
Initial Debridement
Removes debris and loosens necrotic tissue
Reduces surface bacteria
Makes it easier to estimate the size and depth of injury
Begins preparation of area for grafting if indicated
Silvadene
for full thickness burns
Bacitracin
for partial thickness burns
Eucerin
are used as the burns and grafts are healing
Methods of debridement
Mechanical- Hydrotherapy, washcloths, scissors and forcepts
Enzymatic- Application of topical enzymes
Surgical- Excision of tissue in surgery
-Tangential Technique- Thin layers excised until bleeding occurs
-Fascial Technique- Wound excised to the level of the superficial facia. Only used for deep and extensive burns
mesh grafts
used on not visible skin, net to cover more SA
Sheet grafts
used on hands and face
nutrition and burns
Hypermetabolic state
Resting metabolic expenditure may be increased by 50% to 100% above normal.
Core temperature is elevated.
Caloric needs are about 5000 kcal/day.
Early, continuous enteral feeding promotes optimal conditions for wound healing.
Supplemental vitamins and iron may be given.
Patients should be weighed regularly.
Hemodynamic resuscitation goals
CVP greater than 12 mmHg (Filling the tank)
MAP greater than or equal to 65 mm Hg
Crystalloids
Isotonic (0.9% NS)
Hypotonic (0.45% NS) rarely used in shock
Hypertonic (3% NS) given slowly
Colloids
Large proteins:
Albumen
Hespan
Dextran
Alpha 1 receptor agonist
work on smooth muscle to cause vasoconstriction and increase SVR
Beta 1 receptor agonist
stimulate myocardial cells resulting in increased myocardial contractility (inotropy) and heart rate (chronotropy)
V1 receptors
in the vascular smooth muscle leads to vasoconstriciton of peripheral arterial beds
Norepinephrine (Levophed)
Mechanism of action: Vasopressor Stimulation of alpha receptors cause vasoconstriction and subsequent increase in SVR Dose: 0.05-1 mcg/kg/min Adverse Events Tachycardia Peripheral and GI ischemia
Epinephrine (Adrenalin)
Mechanism of action:
Stimulation of beta 1 receptors increase heart rate and contractility of the heart (inotropic and chronotropic effect)
Stimulation of alpha receptors cause vasoconstriction and subsequent increase in SVR
Dose:
0.05-0.5 mcg/kg/min
Adverse Events
Tachycardia Peripheral and GI ischemia
Dopamine (Intropin)
Mechanism of action:
stimulation of dopaminergic receptors cause renal mesenteric, coronary and cerebral arteries to dilate and increase the flow of blood.
Stimulation of beta 1 receptors increase heart rate and contractility of the heart (inotropic and chronotropic effect)
Stimulation of alpha receptors cause vasoconstriction and subsequent increase in SVR
Dose:
2-20 mcg/kg/min
Adverse Events
Tachycardia Arrhythmias
Dopaminergic doses should not be used for treatment of shock.
Phenylephrine (Neosynephrine)
Mechanism of action: Stimulation of alpha receptors cause vasoconstriction and subsequent increase in SVR Dose: 0.5-5 mcg/kg/min Adverse Events: Reflex Bradycardia
Vasopressin (Pitressin)
Mechanism of action:
Augments the effects of the other vasopressor agents
V1 receptors in the vascular smooth muscle leads to vasoconstriction of peripheral arterial beds
Dose:
0.04 units/min
Not titrated
Used in addition to other vasopressors (norepinephrine)
Adverse Events
Higher doses is associated with cardiac ischemia
Dobutamine (Dobutrex)
Mechanism of action: Stimulation of beta 1 and 2 receptors Dobutamine is a synthetic catecholamine with strong affinity for both beta1 and beta2 receptors in a 3:1 ratio. “Stimulation of cardiac beta1 receptors, resulting in potent inotropic activity with weaker chronotropic activity. On vascular smooth muscles, dobutamine (at lower doses) can decrease SVR as a result of reflex vasodilation and beta2 receptor activation leading to significant hypotension “ (2. Department of Surgical Education, Orlando Regional Medical Center) Dose: 5-20 mcg/kg/min Adverse Events Arrhythmias Hypotension
