hypertensive emergencies SHOCK/DKA

HTN Condition Specific Therapies

Cocaine toxicity/Methamphetamines & Pheochromocytoma Benzodiazepines (Ativan, Versed) Phentolamine Nitroglycerin Nitroprusside Preeclampsia/Eclampsia Hydralazine Labetalol Nifedipine Magnesium sulfate

DKA

DKA: hyperglycemic state associated with metabolic acidosis and a buildup of ketones in the serum Serum glucose > 250 mg/dl and may exceed 800 mg/dl Metabolic acidosis Anion Gap > 16 (DEFINES) Presence of serum ketones

Hypertension

Defined as a blood pressure measurement of Systolic > 140 mmHg or Diastolic > 90 mmHg As many as 45% of adult patients have at least one incident of increased blood pressure during their stay in the emergency department. It is important to identify which ones need treatment and which ones do not. The fundamental principle is in identifying the presence or absence of end organ dysfunction.

HTN History and Physical

Focus on evidence of end organ dysfunction. Consider circumstances surrounding the hypertension. Attempt to identify an etiology Most common clinical presentations of hypertensive emergencies: Cerebral infarction 24.5% pulmonary edema 22.5% hypertensive encephalopathy 16.3% congestive heart failure 12%

Treatment

Fully dependent on the underlying cause Failure to address shock state in an expedient fashion can result in rapid decline and increase in mortality Do not wait for labs before initiating therapy Initiate empiric treatments as soon as possible

DKA S/S

General weakness Nausea +/- Vomiting Abdominal Pain Increased thirst (polydipsia) Increased urination (polyuria) Tachypnea - in late stages may develop Kussmaul respirations Muscle cramps Altered mental status - lethargy, stupor or coma Odor of ketones on breath May be precipitated by lack of insulin or from infection in patient with IDDM

HHS S/S

Gradual progression of illness Severe dehydration often with history of several days with decreased PO fluid intake More common in disabled or infirm elderly individuals Often precipitated by infection (UTI, Pneumonia) Markedly depressed mental status (lethargy to coma) Decreased urinary output due to hypovolemic state May occur in individuals with NIDDM

HHS

HHS: severe hyperglycemia not associated with metabolic acidosis or ketosis. Serum Glucose often > 1000 mg/dl Little or no serum ketones Severely elevated serum osmolality Often associated with neurologic abnormalities (i.e. coma) Previously referred to as Hyperosmolar Hyperglycemic Non-Ketotic Coma (HHNK)

HTN Symptoms of concern

Headache neurologic deficit (weakness, loss of sensation) confusion/disorientation neck stiffness chest pain shortness of breath back pain cough (may see aortic dissection) abdominal pain flank pain hematuria extremity pain/pallor/change in temperature

Hypertensive Emergency (Accelerated hypertension, Hypertensive crisis, Malignant Hypertension)

Hypertensive emergencies encompass a spectrum of clinical presentations in which uncontrolled blood pressures (BPs) lead to progressive or impending end-organ dysfunction It is the involvement of end-organ dysfunction that defines the emergency! There is no single numeric value that offers a definition. Any organ system can be effected. Hypertensive emergencies now account for approximately 1% of patients with hypertension. Prior to 1950 the one year survival rate associated with this condition was 20%. Currently, the survival rate is 90% when appropriate treatment is administered. The incidence of hypertensive emergency visits to the emergency department has increased by more than two-fold between 2006 and 2013.

Neurologic Manifestation of htn emergency

Hypertensive encephalopathy cerebrovascular accident cerebrovascular infarct subarachnoid hemorrhage intracranial hemorrhage

complications of DKA/HHS TX

Hypokalemia and Hypoglycemia are the most common complications of treatment for DKA and HHS Monitor glucose and electrolytes regularly during the active phase of treatment Cerebral edema is a complication most commonly seen in children with severe DKA treated over-aggressively with fluids and insulin. Mortality rate is 20-40%. Non-Cardiogenic Pulmonary Edema (ARDS) may occur in patients with DKA. If hypoxemia develops, consider this entity.

In Every Patient with Shock

IV Access x 2 Cardiac Monitoring Continuous Pulse Oximetry IV Fluids (even cardiogenic shock) How Much fluid? Depends

Septic Shock TX

IV Fluid Boluses - 30 ml/kg initial Antibiotics IV Start broad spectrum. Can be adjusted based on culture results. Source of infection determines best choices. Pressor Support Norepinephrine Intubation if respiratory failure or refractory hypoxia May require blood transfusion No benefit shown for steroids unless history for adrenal insufficiency Admit to ICU

Neurogenic Shock TX

IV Fluid boluses Pressor Support Norepinephrine Dopamine Steroid Protocol for Spinal Cord Injury Consult with neurosurgery Admit to Neuro ICU at Trauma Center

Anaphylactic Shock TX

IV Fluid boluses Targeted Medications Epinephrine SC Terbutaline Benadryl IV Steroids IV (Dexamethasone, Methylprednisolone) H2 Antagonist IV (Zantac, Pepcid) Intubation if potential for airway compromise Pressor Support Dopamine Norepinephrine Admit to ICU

Hypovolemic Shock TX

IV Fluids IV Fluids IV Fluids Pressors provide little value in hypovolemic states and should not be initiated early. Address underlying reasons for hypovolemia. Admit May require ICU May be admitted to step down unit if improved with fluid resuscitation. Underlying cause is greater determining factor (i.e. DKA)

Cardiogenic Shock Tx

IV Fluids to increase intravascular volume Pressor Support Dobutamine Dopamine Intubation for respiratory failure or refractory hypoxia Cardiac Catheterization if Acute MI (STEMI) Intra-Aortic Balloon Pump Pericardiocentesis or Pericardial Window if Tamponade Cardiac Surgery if acute valvular insufficiency or aortic root dissection Thrombolysis is massive pulmonary embolus Admit to CCU

Hemorrhagic Shock TX:

Identify the source of Bleeding Control the Bleeding Direct Pressure (compression) if possible Get patient to the OR if compression not possible IV Fluid boluses (NS or LR) - 2 Liters If persistent hypotension then initiate blood transfusion Target SBP is > 90 mmHg - Do not attempt to over-compensate for the blood pressure. May result in worsening hemorrhage. Treat coagulopathy if indicated Pressors do not provide much value Admit to ICU. May need transfer to Trauma Center.

In hypertensive encephalopathy the MAP should be:

In hypertensive encephalopathy the MAP should be reduced 25% over eight hours.

In ischemic stroke,

In ischemic stroke, antihypertensive therapy should be withheld unless the SBP is > 220 or DBP is > 120 mmHg! Caveat: if patient is a candidate for thrombolysis then more aggressive therapy is required.

Treatment of DKA & HHS

There are common threads in treatment of both conditions Both need aggressive IV fluid resuscitation, administered as boluses Cardiac monitoring Electrolyte Replacement - if needed Monitor glucose levels hourly by Accucheck Neurologic checks Admission to ICU May benefit from central line insertion

Other Manifestation of htn emergency

Acute renal failure/insufficiency retinopathy eclampsia microangiopathic hemolytic anemia

DKA TX

Administer 1 to 2 Liters of crystalloid over 1 hour, then continue fluids as infusion Treat hypotension with additional IV fluid boluses, not with pressors Initiate IV Insulin Infusion at 0.14 units/kg/hr - Only reason to delay is if K is < 3.3 meq/l Initiate antibiotics if source of infection identified Do not treat with sodium bicarbonate to address metabolic acidosis (reserved for patients with pH < 6.9) Electrolyte replacement - Potassium (K before insulin) If < 3.3 will need immediate KCL replacement added to IV fluid boluses at 20-40 meq/hr If between 3.3 and 5.3 then 20 meq KCL is added to each liter of fluid and continued until potassium is normalized at > 4.0 Do not treat hyperkalemia - this is due to metabolic acidosis and will correct itself with treatment for DKA - If severe hyperkalemia then bolus of sodium bicarbonate should be considered. Treatment of DKA is successful only once Anion Gap normalizes - Insulin drip should be continued until this occurs. Normalization of serum glucose is not a marker of success. Once glucose level < 200 -250 mg/dl, start a D5 1/2NS infusion to maintain serum glucose levels above 150 mg/dl - KCL may need to be added to this fluid for potassium replacement

Pharmaceuticals for Hypertensive Emergencies

All therapy for hypertensive emergencies should be via intravenous route. These are administered as intravenous infusions and should not be given as a bolus dose. Available and Recommended agents: Cardene (nicardipine) DOC Labetalol Sodium Nitroprusside Nitroglycerin

ABG normal values

Arterial Blood Gas pH - 7.35-7.45 paO2 paCO2 35 - 45 mmHg O2 Saturation > 92% HCO3 21 - 27 meq/L Base Deficit

DKA & HHS

Both are life threatening conditions Both require aggressive management Bother are severely dehydrated and hypovolemic Both develop severe electrolyte abnormalities

In subarachnoid hemorrhage the target is to:

In subarachnoid hemorrhage the target is to maintain the SBP < 160 mmHg until the aneurysm is treated or cerebral vasospasm occurs.

In intracerebral hemorrhage treatment is determined based on clinical and radiographic evidence of increased intracranial pressure.

Increased ICP: Target is to maintain MAP just below 130 mmHg or SBP < 180 mmHg for the first 24 hours after symptom onset. No increased ICP: target is to maintain the MAP < 100 mmHg or SBP < 160 mmHg for the first 24 hours after symptom onset.

HTN Diagnostic assessment

LABS -CBC (platelet ct,) Chemistries LFTs urinalysis coagulation profile toxicology screen pregnancy test EKG- Identify signs of ischemia or acute injury. ST segment depressions and elevations. Peaked T waves. Cardiac arrhythmias IMAGING-Determined by clinical presentation Neurologic, then CT Head without contrast MRI Brain (admit cerebral edema) CTA Carotid Arteries (unilateral headache) or Carotid Doppler Ultrasound Cardiovascular s/s then: Chest X-Ray CTA Chest (pericardial effusion, dissection) CTA Abdomen & Pelvis (AAA) Renal: CT Abdomen & Pelvis, Renal Ultrasound

Anaphylactic Shock

Labs: Baseline labs CBC, CMP Not helpful in diagnosis nor treatment EKG: Identify ischemia Imaging: None

Cardiogenic Shock

Labs: CBC BMP PT/PTT Troponin BNP EKG: Identify ACS and need for emergent catheterization Imaging: Chest X-Ray Echocardiogram CT Chest w/ Contrast

Septic Shock (Distributive Shock)

Labs: CBC CMP UA + Culture Blood Cultures x 2 Lactic Acid Imaging: Depends on clinical presentation and suspicion Chest X-Ray (everyone) US Gallbladder (upper abdominal tenderness or abnormal LFT's) CT Abdomen & Pelvis (abdominal tenderness)

DKA Dx

Labs: CBC CMP - Calculate Anion Gap, Identify Electrolyte abnormalities Serum Magnesium, Serum Phosphate UA Arterial Blood Gas or Venous Blood Gas Serum Ketones Blood Cultures, Urine Culture Lactic Acid Imaging: CXR CT Head CT Abdomen & Pelvis Ultrasound RUQ EKG: Assess for cardiac ischemia & dysrhythmias

Hemorrhagic Shock

Labs: CBC (for baseline) CMP (underlying liver dz) PT/PTT Type & Cross Match (to get blood ready) Imaging: Depends on mechanism Femur Fracture = XR Femur Blunt Trauma = CT Chest, Abdomen and Pelvis or FAST Exam Intracranial hemorrhage will never be source of hemorrhagic shock!

Neurogenic Shock

Labs: Not helpful Obtain baseline values Imaging: MRI Cervical Spine CT Head without Contrast CT Cervical Spine

HTN Examination

Measurement of blood pressure in supine and seated positions as well as measurement in both arms. A significant difference in blood pressure between upper extremities may suggest aortic dissection. Retinal examination (hemorrhages, exudates, papilledema). JVD Lung examination (crackles, rales, wheezing) Peripheral edema (right sided heart failure) Level of consciousness (ask about baseline) Visual fields Neurologic exam for focal findings Abdominal exam (pulsatile mass, bruit)

Cardiac Manifestation of htn emergency

Myocardial ischemia myocardial infarction acute left ventricular dysfunction acute pulmonary edema aortic dissection

Situational Hypertension

Panic, pain (autonomic physiologic response

Clinical Assessment of history

Recent illnesses Recent trauma Symptoms preceding arrival to the ED Current or Recent Medications Allergies (medical, food, environmental) Treatment prior to arrival in the ED (home or EMS)

SHOCK

Shock: A state of hypotension that results in hypo-perfusion of end organs with ischemic manifestations. It is important to recognize shock It is important to identify the cause of shock It is important to aggressively treat shock

Management of Hypertension in the Emergency Department

The asymptomatic patient with a systolic blood pressure > 200 mmHg or diastolic blood pressure > 120 mmHg should have initiation of medical therapy in the emergency department and close outpatient follow-up. Initiation of therapy may include an initial dose of IV medication or simply initiation of an oral antihypertensive agent. There is no reason to keep the patient in the emergency department to monitor and document a decrease in their blood pressure. The goal of therapy for hypertensive urgency is to reduce the blood pressure gradually over the course of 24 hours. Overly aggressive management of asymptomatic hypertension may result in more complications and development of symptoms (i.e. syncope, CVA, neurologic deficit) that may necessitate further evaluation, hospitalization, and intervention. If blood pressure elevation is considered to be due to an alternate and modifiable cause then this condition should be treated appropriately and specific antihypertensive therapy may not be required. These conditions often include: Anxiety Acute pain (i.e. traumatic injury, kidney stone) It is completely appropriate to treat these conditions and reassess the blood pressure. If the blood pressure remains elevated after addressing these other conditions then initiation of antihypertensive therapy may be necessary.

hypertensive emergencies:

The duration and severity of pre-existing hypertension, including degree of blood pressure control, should be evaluated. It is the absolute change/rise in blood pressure that impacts end organ function more so than the actual numerical value. Inquire about prior and current treatment. Inquire about use of over-the-counter preparations, such as cold medications and decongestants. Inquire about illicit drug use such as cocaine and amphetamines. Inquire about medical conditions such as previous CVA, thyroid disease, Cushing's disease, autoimmune disease (systemic lupus). In female patients, always inquire about pregnancy status and perform a pregnancy test in all women of reproductive age.

HHS TX

Treat with Fluids, Fluids and more Fluids Pressor therapy should only be considered after sufficient fluid resuscitation, if hypotension persists, with concerns for possible septic shock Insulin therapy should not be started early Precipitous drop in serum glucose can occur in HHS when insulin is administered. Can result in severe complications. After several liters of fluids may administer bolus injections of insulin to gradually bring glucose level down HHS is often precipitated by infection and source should be aggressively sought - initiate empiric antibiotic therapy Address electrolyte abnormalities Patients with severely depressed mental status may need intubation for airway protection

Most important questions to ask in the ER

What do you see when you walk in the room? What are the vital signs?

subarachnoid hemorrage

lowering mortality

brainstem herniation

no chance of survival

Hypertensive Urgency

no symptoms. The significant elevation of blood pressure without evidence of and organ dysfunction. 200/120

Respiratory Alkalosis

pH = High pCO2 = Low

Metabolic Alkalosis

pH = High pCO2 = Normal HCO = High

Respiratory Acidosis

pH = Low pCO2 = High

Metabolic Acidosis

pH = Low pCO2 = Low HCO = Low

Depends on the etiology

sepsis: fever, rashes, productive cough, dysuria hemorrhage:apparent blood loss (trauma, varicose vein). occult blood loss (ruptured AAA, visceral trauma) volume depletion: severe dehydration, diabetic (DKA), water restriction cardiac: shortness of breath, JVD, HJR (hepatojugular reflex), peripheral edema, chest pain anaphylactic: urticaria, shortness of breath, mucosal edema, history of exposure