SHOCK. SHOCK. ADULT HEALTH II SUMMER, 2010. Jerry Carley MSN, MA, RN, CNE. What’s on your mind?????. Hopefully, Learning About S-H-O-C-K !. “….it’s just a urinary tract infection….”.
ADULT HEALTH II
MSN, MA, RN, CNE
--December 30: Presented with complaint of dysuria---diagnosed as kidney stones & sent home on pain medications
--Presented again on January 3rd in septic shock.
--Developed dissiminated intravascular coagulopathy (DIC)
--partial gastrectomy (necrotic tissue)
--January 23rd, hands and feet amputated
--Comatose & on a ventilator
*****Died January 23rd
January 2009:Headline: Brazilian Super Model Dies
Mariana Bridida Costa, 20 y.o.
1. Your client has multi-trauma & just arrived in the ER. The client’s urinary output is normal, whereas respiratory rate and heart rate are slightly elevated from baseline. Which of the following should the nurse suspect?
2. A client has been admitted with a gastrointestinal ulcer. The client is NPO and has a nasogastric tube in place connected to low intermittent suction. What form of shock should the nurse suspect / monitor this client for?
3. A client in hypovolemic shock has been placed on a dopamine hydrochloride drip. Which parameter would indicate a desired client response to this drug?
4. A nurse is monitoring a client who is receiving a dopamine hydrochloride drip for the treatment of shock. What symptom would indicate a possible overdose of this medication?
5. What assessment is most appropriate for the client receiving sodium nitroprusside?
6. Which manifestations should the nurse expect when caring for the client with distributive shock resulting from an anaphylactic event?
7. The client has all the following clinical manifestations. Which one alerts the nurse to the probability of septic shock?
Insufficient oxygenation of tissues related to a sustained decrease in mean arterial pressure (MAP)
Cardiac / Pump Effectiveness
Seth, 17 y.o.
Decreased PO2 (+)
Capillary Refill > 3 sec
Kidney / Urinary:
Output < 30 mL/hr
SG > 1.035
Change in level of consciousness
Deformity, ecchymosis and edema, both thighs
Deformity, ecchymosis, crepitancebilat lower rib cage
*Chief Complaint: S/P MVC
Fractured lower two ribs, bilateral
Medical History: Negative
Pulse Ox 85%
Immobilization / Pain Medications
Boyd, 17 y.o.
Roseline, 36 y.o. w/ hx
Aortic Stenosis, CHF
Frank 32 y.o.
Ian, 26 y.o.
THE CAUSE OF SHOCK,
CATEGORY OF SHOCK,
AND STAGE OF SHOCK
DIRECT THE SPECIFIC TREATMENT
“Pump Failure” or “Heart Failure”
Decrease in intravascular volume
of 10-15% or more
Widespread vasodilation and capillary
permeability (3 types…)
(septic, neurogenic, anaphylactic)
Mechanical blockage in the heart or
No visible changes in client parameters, changes are now
occurring on the cellular level only
Body is mounting measures to increase cardiac output to
restore tissue perfusion and oxygenation.
Compensatory mechanisms begin to fail
TOTAL BODY FAILURE
Pump failure due to myocardial infarction, heart failure,
Cardiomyopathy, dysrhythmias, cardiac tamponade,
valvular rupture or valvular stenosis
Excessive fluid loss from diuresis, vomiting & diarrhea;
Blood loss secondary to surgery, trauma, ob-gyn causes;
Burns; Diabetic Ketoacidosis
Endotoxins and other mediators causing massive
vasodilation. Most common is gram-negative bacteria.
Loss of sympathetic tone causing massive
vasodilation. Trauma, spinal shock, and epidural
anesthesia are among the causes.
Antigen-antibody reaction causing massive vasodilation.
Blockage of great vessels. Cardiac valve stenosis, pulmonary
Embolism, and aortic dissection are among the causes.
-Miscellaneous: May see rashes with septic or anaphylactic shock.
-May see angioedema with anaphylactic shock.
-Rales (coarse crackles) are possible with cardiogenic shock.
-SEIZURES MAY OCCUR WITH ALL FORMS OF SHOCK.
-FEVER MAY OCCUR WITH ALL FORMS OF SHOCK—
BUT ESPECIALLY SEPTIC SHOCK
Evidence-Based Practice Update:
PT’s BP = 100/60 mm Hg
EBL 10% - 15%
Yields Hypovolemic Shock
0.10 x 5625 = 560 mL
0.15 x 5625 = 844 ml
Classified by site of action
-Venodilators: reduce preload - Nitroglycerin
-Arteriolar dilators: reduce afterload
Minoxidil and Hydralazine
-Combined: act on both arterial and venous beds and reduce both pre- and afterload Sodium Nitroprusside (Nipride)
-Vasodilator that acts directly on arterial and venous vascular smooth muscle.
-Indicated in hypertension and low cardiac output states with increased SVR.
-Also used in post-operative cardiac surgery to decrease afterload on an injured heart.
-Action is immediate; half-life is short; titratable action.
-Toxicity is with cyanide, one of the metabolites of the breakdown of nipride.
-Severe, unexplained metabolic acidosis might suggest cyanide toxicity.
-Dose starts at 0.5 mcg/kg/min and titrate to 5 mcg/kg/min to desired effect. May go higher (up to 10 mcg/kg/min) for short periods of time.
-Used to improve myocardial perfusion following cardiac surgery
-Dose ranges from 0.5 to 8 mcg/kg/min. Typical dose is 2 mcg/kg/min for 24 to 48 hours post-operatively
-Methemoglobinemia is potential side effect
-Non-specific beta agonist with minimal alpha-adrenergic effects.
-Causes inotropy, chronotropy, and systemic and pulmonary vasodilatation.
-Indications: bradycardia, decreased cardiac output, bronchospasm (bronchodilator).
-No longer available in some markets
-Occasionally used to maintain heart rate following heart transplantation.
-Dose starts at 0.01 mcg/kg/min and is increased to 1.0 mcg/kg/min for desired effect.
BP or SVR>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>
Cardiogenic Shock and Hemodynamic Support: A Realistic Management Approach- Mary Dahling, RN, MSN, CCRN, CNS, Cardiothoracic Surgery, Sentara Norfolk Hospital, Norfolk, VirginiaWhat is cardiogenic shock?
Cath Lab Digest - ISSN: 1073-2667 - Volume 11 - Issue 11 - November 2003 - Pages: 20 - 25
What causes cardiogenic shock? The major cause of cardiogenic shock is ischemic disease, both of the left and right ventricle. Valvular heart disease/dysfunction may also result in cardiogenic shock, a classic example being acute mitral insufficiency or regurgitation. Additional causes include: 1. Trauma from a myocardial contusion; 2. Cardiomyopathies: Hypertrophic, restricted, and dilated; 3. Infectious and inflammatory processes (viral myocarditis, infective endocarditis); 4. Pulmonary hypertension resulting in right ventricular failure; 5. Toxic drugs. The basic concept of cardiogenic shock is pump failure, not a surprise to anyone, but again, impaired forward flow is the key. When cardiac output decreases, the body responds with compensatory mechanisms. Catecholamines (norepinephrine and epinephrine), parasympathetic nervous stimulation, conduction disturbances, and dysrhythmias can all affect heart rate, but typically tachycardia is seen. Systemic vascular resistance (SVR) increases to “tighten” the arterial vascular circuit in an attempt to maintain blood pressure. But these are only temporizing measures. When caring for these patients, it helps to remember that cardiac output = stroke volume x heart rate. So unless immediate intervention is needed for a symptomatic rapid or relatively slow heart rate, efforts are aimed at increasing the stroke volume. Understanding the components of stroke volume helps direct patient management.
Components of stroke volume: Preload, afterload, and contractility Preload is the amount of volume in the ventricle at end-diastolic filling.6 It is measured directly during heart catheterization via the LVEDP or indirectly measured by utilizing the PCWP. Think of preload as the end-diastolic “stretch” of the muscle determined by the volume of blood in the ventricle. Every heart has an optimal preload. Remember Starling’s Law: Increased stretch results in a more forceful contraction and greater stroke volume up to a physiologic limit. In other words, the muscle fiber can be stretched up to a point and result in a good contraction, but if overstretched, the contraction actually weakens and stroke volume decreases. Afterload is resistance to ventricular ejection. Increased afterload translates into increased work for the myocardium. Afterload for either ventricle is affected by several factors, the most important being vascular resistance.6 When the arterial vascular circuit constricts in an attempt to maintain pressure, afterload increases. More oxygen and energy is required for the heart to pump volume out against this increased resistance — contributing to further problems for an ischemic ventricle. Afterload is clinically estimated for the right ventricle by calculating the pulmonary vascular resistance (PVR) and for the left ventricle, the systemic vascular resistance (SVR). Finally, there’s contractility. Contractility is the velocity of myocardial fiber shortening at the cellular level regardless of preload and afterload.6 It’s difficult to measure at the bedside, but one would hope to see evidence of increased contractility when adding an inotropic agent such as dopamine or dobutamine. When thinking about the hemodynamics of cardiogenic shock, keep it simple: The components of cardiac output are: Contractility, Rate, Afterload, and Preload, or “CRAP.” To manage these patients, you’ve got to know CRAP! (This acronym has long been passed down to many a critical care and cath lab staff and is helpful when managing cardiogenic shock). Every therapeutic intervention is aimed towards improving or altering a component of cardiac output — or something in CRAP.
The spiral of cardiogenic shock The underlying pathology of cardiogenic shock is profound depression of contractility resulting in a spiral of reduced CO, hypotension, further coronary insufficiency, and further reduction in contractility. Compensatory mechanisms of tachycardia and increased SVR are typically noted. However, a systemic inflammatory response (fever, elevated white count, low SVR) may also be seen.3
Patient Presentation In addition to tachycardia, patients often present with a narrow pulse pressure (PP). Pulse pressure is the difference between systolic and diastolic blood pressure and reflects stroke volume. Decreased stroke volume causes the pulse pressure to narrow (as is seen in cardiac tamponade). Signs and symptoms of hypotension are present: Weak or absent peripheral pulses; mottled extremities from low flow states; diaphoresis; and pallor. Patients may be restless with changes in level of consciousness. Remember that the kidneys are “seeing” a low flow state when not receiving adequate blood flow — with a response of retaining volume and concentrating urine output.
If left ventricular failure is present, pulmonary edema and dyspnea are hallmarks of cardiogenic shock. An extra heart sound, S-3 or a ventricular gallop, is an early sign of LV failure.5 A murmur may be appreciated as the ventricle dilates from volume overload, resulting in regurgitant flow. Murmurs may also occur with papillary muscle dysfunction from ischemia. Chest pain, which can be typical or atypical, might be present if the cause of failure is ischemic disease. If right ventricular failure is the culprit, the patient will present without pulmonary edema — clear lungs and a normal to slightly raised PCWP. Persistent hypotension, elevated RA (CVP) pressure, and jugular vein distention are often noted as volume “backs up” from the right ventricle and forward flow declines. Suspect a right ventricular infarction in patients exhibiting these symptoms who present with an inferior wall MI. The reduction of preload (hypovolemia, diuretic use, nitroglycerin) intensifies hypotension in these individuals.5 Recording right-sided precordial leads and utilizing echocardiography assists in the diagnosis.
CRAP — Optimizing Preload Does the patient have too much or too little preload? Higher filling pressures may actually be necessary in some patients, but typically those in cardiogenic shock have too much preload in the ventricle. The higher the PCWP (preload) and the lower the cardiac index, the higher the mortality.4 If too much volume is present for the heart to handle, there are the three well-recognized “P”s for dealing with excessive preload: Pee the excess volume, park the excess volume, or pump it on forward! 1. Patients have pulmonary edema and high PCWP? Diurese them — but avoid hypovolemia (may worsen blood pressure—especially with a RV MI). 2. Poor contractility and decreased forward flow? Pump it forward with inotropic support! 3. “Pull” extra volume off the heart (decrease venous return)—i.e., nitroglycerin to dilate venous beds. Park the volume if blood pressure tolerates.
CRAP — Optimizing ContractilityInotropic support with a sympathomimetic agent is indicated. With low blood pressure less than 70 mmHg, norepinepherine 2 to 10 mg /kg/min would be considered.5Norepinepherine is an alpha and beta-1 agonist, meaning it causes vasoconstriction and increases contractility and heart rate. Clinically, the alpha or vasoconstrictive properties (increases SVR) are greater than beta-1 effects, so its use should be limited for temporary stabilization if possible.4
Dopamine is a first-line inotropic agent in cardiogenic shock. It is usually initiated at 3-5 mg/kg/min and titrated up to 10 mcg/kg/min. At higher doses, dopamine provides vasopressor support. Doses greater than 10 mcg/kg/min may have undesirable effects such as tachycardia and increased pulmonary shunting along with the potential to decrease splanchnic perfusion and increase pulmonary arterial wedge pressure.1 Another inotropic agent, dobutamine, is a sympathomimetic amine with stronger beta effects than alpha effect, producing vasodilation (decreasing SVR) and increasing contractility. Dobutamine is initiated usually at 2.5–5mg /kg/min and titrated up to 10 mg/kg/min.4 As it decreases SVR, it may also decrease blood pressure making it difficult to use in those with systolic pressures below 90 mmHg.5
Working via a different mechanism than dopamine and dobutamine are the phosphodiesterase inhibitors milrinone and inamrinone (formerly amrinone). These drugs have both inotropic and vasodilating effects, thus increasing stroke volume with both their contractile and afterload–reducing properties. These vasodilator effects may cause hypotensive episodes to develop and careful titration is needed. A loading dose may be given for both inamrinone and milrinone. The loading dose for inamrinone (Inocor®) is 0.75 mg/kg followed by an infusion of 5 to 10 mg/kg/min with total doses not to exceed 10 mg/kg/day.1Milrinone (Primacor®) is approximately 15–20 times more potent than inamrinone. In addition, clinical studies have reported significantly less thrombocytopenia with milrinone as compared to inamrinone. Loading dose for milrinone is 50 mg/kg followed by a maintenance dose of 0.375-0.750 mg /kg/min.6 Careful dosing consideration of these drugs is required with hepatic and renal dysfunction. By increasing contractility, all inotropic agents increase myocardial workload and in addition, may cause tachyarrhythmias, exacerbating myocardial ischemia.
CRAP — Optimizing Heart Rate With cardiogenic shock, bradycardia is usually not the problem, but if present, a pacing wire may be necessary to sustain an adequate rate and output. Tachycardia is typically present and is related to sympathetic stimulation, a compensatory mechanism or may result from inotropic drug support. Increased heart rates not only decrease diastolic filling time, but also decrease coronary artery perfusion time. In addition myocardial workload is increased. Clearly, if the patient is in a lethal tachycardia or rapid supraventricular tachycardia (SVT), the rhythm will need termination. It is important to try to maintain the atrial contribution to stroke volume. Asynchrony between the atria and ventricles or the absence of atrial contraction (development of atrial fibrillation) may significantly reduce cardiac output.
CRAP — Optimizing Afterload It’s important to facilitate stroke volume ejection and forward flow by reducing the SVR if blood pressure permits. Some inotropic agents reduce SVR. Vasodilators such as nitroglycerin and sodium nitroprusside may also help. Intravenous nitroglycerin is a coronary vasodilator, but also tends to be at normal doses, a venodilator predominately dilating the venous bed. Nitroglycerin helps “park” volume. Nitroprusside, on the other hand, is a more balanced venous arterial vasodilator.6
It is often a challenge to add these drugs because of low blood pressure. As a result, these agents must be used cautiously, if at all, for besides hypotension, a reflex tachycardia may occur and coronary perfusion pressure can drop significantly. Vasodilator therapy should not be attempted in patients with systolic pressure below 90 mmHg.6 So use caution when reducing afterload in the presence of ischemic disease. Afterload reduction is also the mainstay of stabilization for acute mitral regurgitation (MR). In acute MR, blood flow is diverted back through the mitral valve. There is less resistance to flow into the lower pressure left atrium, verses forward flow out the aortic valve against arterial resistance (SVR). Forward flow out the “front door” (aortic valve) needs to be “encouraged”; therefore, therapies are targeted to reducing the SVR. The optimal mechanical afterload reducer is the intraaortic balloon pump, where a balloon is placed in the aorta distal to the subclavian artery and counterpulsates the heart.
With the normal arterial waveform, the dicrotic notch signifies closure of the aortic valve closure and the beginning of diastole. Inflation of the balloon at this time augments diastolic pressure. This in turn increases coronary perfusion pressure. When the balloon deflates, aortic end-diastolic pressure decreases, making it easier for the next stroke volume to be ejected by the left ventricle. The IABP is effective for the initial stabilization of patients with cardiogenic shock. However, an IABP is not definitive therapy; definitive diagnostic and therapeutic interventions (surgical repair of the valve or revascularization) need to be performed.
Fifteen studies from the medical and nursing literature were reviewed from 1964 to 2003. Three studies 2-
The majority of studies on the effects of Trendelenburg position do not lend support that this intervention
* Hypotensive and mentally obtunded patients may first become transiently more alert and then subsequently
A. The evidence supporting the hemodynamic effects of Trendelenburg in treating shock is small and
12. Wong D, Tremper K, Zaccari J, Hajduczek J, Konchiegeri J, & Hufstedler S. (1988). Acute
Class IIIMay be harmful; no benefit documentedNot acceptable, not useful, may beharmful.Class III refers to interventions with noevidence of any benefit; often someevidence of harm