CPR for 2 Min *Treat Reversible Causes No Yes Shockable? Shockable? No Yes CPR for 2 Min Epinephrine *Amiodarone *Treat Reversible Causes CPR for 2 Min Epinephrine *Amiodarone *Treat Reversible Causes If pulse present begin post resuscitation *If pulse absent continue to arrow or end the cod e Avoid interruption in CPR, except to defibrillate. Push hard (>2 in [5 cm]) and fast (100/m in). Avoid excessive ventilation. Rotate compres- sions every 2 min. Consider capnography ( if PetCo 2 is <10 mm Hg, then improve CPR quality). Consider intra-arterial line (if diasto lic blood pres- sure [BP] is <20 mm Hg, then improve CPR quality). Return of pulse associat ed with sudden increase in PetCo 2 to >40 mm Hg and arterial waveform. (Consider the revers ible causes: 5H \200\231s; 5T \200\231s: Hypovolemia, Hypoxia, Hydrogen ion (acidosis), Hyp o-/Hyperkalemia, Hypothermia; Tension pneumothorax, Tamponade (Cardiac), Toxins, Thrombosis (car- diac, pulmonary). May replace first or second dose of epi with vasopres- sin 40 U IV /IO. From 2010 American Heart Association Guidelines for CPR and ECC. Circulation . 2010;122 (su ppl):729 \200\223767. 738 Headache Life-threatening considerations \212 \212 \212 Organ-threatening causes \212 N arrow angle glaucoma Temporal arteritis (elevated erythrocyte sedimentation rate [ESR], jaw \212 claudication, platelet count >400) Severe anemia e n i c i d e m y c n e g r e m E Meningitis Encephalopathy Intracranial bleed \212 Other potential causes \212 \212 \212 \212 \212 \212 Signs of meningismus? \212 \212 Decreased conscious level or localizing signs? \212 \212 \212 \212 \212 \212 Papilledema? \212 \212 \212 \212 Tension headache Migraine Cluster headache Post-traumatic Drugs (nitrates, calcium-channel blocker) Carbon monoxide poisoning or anoxia Meningitis (may not have fever or rash) Subarachnoid hemorrhage Encephalitis/meningitis Stroke Cerebral abscess Subarachnoid hemorrhage Tumor Subdural hema toma Tumor Severe hypertension Benign intracranial hypertension Any central nervous system (CNS) infection, if prolonged (e.g., >2 wks); e.g., tuberculosis (TB) meningitis Others \212 \212 \212 \212 Worrying headache features or \200\234red flags \200\235 \212 \212 \212 \212 \212 \212 \212 \212 \212 Two other vital questions: \212 \212 Paget \200\231s disease (elevated alk phos) Sinusitis Altitude sickness Cervical spondylosi s First headache or worst headache; Thunderclap headache; Unilateral headache and eye pain; U nilateral headache and ipsilateral symptoms; Cough-initiated headache; raised ICP/venous th rombosis Persisting headache scalp tenderness in those >50; Headache with fever or neck stiffness; Change in the pattern of \200\234usual headaches \200\235 Decreased level of co nsciousness consider subarachnoid hemorrhage consider subarachnoid hemorrhage cluster headache migraine, tumor, vascular temporal arteritis meningitis 739 Where have you been? (Malaria) Might you be pregnant? (Eclampsia; especially if proteinuria and elevated BP) Shortness of breath Wheezing? \212 Asthma \212 COPD \212 Heart failure \212 Anaphylaxis Stridor? (Upper airway obstruction) \212 \212 \212 \212 \212 Crackles? \212 \212 \212 \212 Chest clear? \212 \212 \212 \212 \212 \212 \212 Others \212 \212 Foreign body or tumor Acute epiglottitis Anaphylaxis Trauma (e.g., laryngeal fracture) Angi oedema Heart failure Pneumonia Bronchiectasis Fibrosis Pulmonary embolism (PE) Hyperventilation Metabolic acidosis (e.g., diabetic ketoacidosis [D KA]) Anemia Drugs (e.g., salicylates) Shock (may cause air hunger) Central causes Pneumothorax; pain, increased resonance Pleural effusion Chest pain: Differential diagnosis First exclude any potentially life-threatening causes by virtue of history, brief examination, and limited investigations. Then consider other pote ntial causes. Immediately life-threatening \212 \212 \212 \212 \212 \212 Others \212 \212 \212 Acute MI Angina/acute coronary syndrome Aortic dissection Tension pneumothorax Pulmonary em bolism Esophageal rupture Pneumonia Empyema Chest wall pain: \212 \212 \212 \212 Pleurisy Gastroesophageal reflux Pericarditis Esophageal spasm Muscular Rib fractures Bony metastases Costochondritis \212 \212 \212 \212 740 \212 \212 \212 Herpes zoster Cervical spondylosis Intra-abdominal: \212 Cholecystitis \212 Peptic ulcera tion Pancreatitis \212 Sickle-cell crisis e n i c i d e m y c n e g r e m E \212 Although cardiac pain is usually described as a dull pressure or a substernal pressur e that radiates to jaw, neck, or arm, and is usually associated with exertion, not all card iac chest pain presents classically. It is worthwhile to consider obtaining CXR, ECG, CBC, comprehensive metabolic panel (CMP), and cardiac enzymes (including troponin) on all patien ts who are at risk. Cardiac chest pain can, and does at times, present atypically, so pleas e consider options such as short-stay units or observation units for low-risk patients. Car diac monitoring in appropriate inpatient units is indicated for higher risk patients. Discu ss options with the patient. Remember, just because the patient \200\231s chest wall is ten der to palpation doesn \200\231t mean the cause of the chest pain is musculoskeletal. Make sure you have excluded all potential life-threatening causes. Coma Definition Unarousable unresponsiveness. Causes Drugs, poisoning (e.g., carbon monoxide, alcohol, tricyclics) Hypoglycemia, hyperglycemia ( ketoacidotic, or hyper- Metabolic: osmolar coma) Hypoxia, CO2 narcosis (COPD) Sepsis Hypothermia Myxedema, Addisonian crisis Hepatic/uremic encephalopathy Trauma Infection meningitis; encephalitis, e.g., herpes Neurological: simplex \200\224give IV acyclovir if the slightest suspicion; tropical: Malaria (do thick f ilms), typhoid, rabies, trypanosomiasis Tumor: Cerebral/meningeal tumor Vascular, subdural/subarachnoid hemorrhage, stroke, hypertensive encephalopathy Epilepsy: Nonconvulsive status or postictal state Immediate management See Table 20.2. \212 Assess airway, breathing, and circulation. Consider intubation if GCS <8. Support the circu lation if required (i.e., IV fluids). Give O 2 and treat any seizures. Protect the cervical spine. \212Check blood glucose in all patients. Give 50 mL 50% dextrose IV (or 1 mg of glucagon i ntramuscularly if no IV) immediately if presumed hypoglycemia. IV thiamine if any suggestio n of Wernicke \200\231s encephalopathy (consider giv- ing glucose first). 741 \212 \212 IV naloxone for opiate intoxication (may also be given IM or via endo- tracheal [ET] tube); IV flumazenil for may be considered benzodiazepine intoxication if airway compromised and patient is not known to be chronically dependent on benzodiazepines. Caution must be exerci sed when administering flumazenil to a patient who has benzodiazepine dependency as it may precipitate seizures. Examination (see Table 20.3) \212 \212 Obtain full set, including rectal temperature. Vital signs are vital: Hematoma, laceration, bruising, cerebrospinal fluid (CSF)/ Signs of trauma: blood in nose or ears, fracture \200\234step \200\235 deformity of skull, subcutan eous emphysema, \200\234raccoon eyes \200\235 Stigmata of other illnesses: \212 \212Skin for needle marks, cyanosis, pallor, rashes, poor turgor \212 \212 \212 \212 Liver disease, alcoholism, diabetes, myxedema (alcohol, hepatic fetor, ketosis, uremia) Smell the breath Meningismus Heart/lung exam Abdomen/rectal exam melena Are there any foci of infection? Any features of meningitis?: but do not move neck unless cervical spine is cleared for murmurs, rubs, wheeze, consolidation, collapse for organomegaly, ascites, bruising, peritoneal signs, \212 \212 \212Note the absence of signs: E.g., no pin-point pupils in a known heroin add ict Abscesses, bites, middle ear infection Neck stiffness, rash, focal neurology or a diabetic patient whose breath does not smell of acetone. Quick history from family, ambulance staff, bystanders: Abrupt or gradual onset? Suicide no te present? Was there any seizure activity? Be highly suspicious of cervical spinal injury and consider spinal immobilization if there is uncertainty. Recent complaints \200\224heada che, fever, vertigo, depression? Recent medical history \200\224sinusitis, otitis, neurosur gery, ENT procedure? Past medical history \200\224diabetes, asthma, \206\221 BP, cancer, e pilepsy, psychiatric illness? Drug or toxin exposure (especially alcohol or other recreatio nal drugs)? Any recent travel? Critical considerations: In all undiagnosed coma patients or in those with focal neurological signs, a computed tomography (CT) scan is very helpful. A lumbar puncture (LP) may be needed for meningitis or subarachnoid hemorrhage. 742 e n i c i d e m y c n e g r e m E Table 20.2 Management of coma a ABC of life support \206\223 O 2 , IV access \206\223 Stabilize cervical spine \206\223 Blood glucose \206\223 Control seizures \206\223 Consider IV glucose, thiamine, naloxone, or flumazenil \206\223 Brief examination, obtain history \206\223 Investigations Arteria l blood gasses (ABG), CBC, CMP, liver function tests (LFTs),ESR, c-reactive protein (CRP),t otal CK Ethanol, toxic screen, drug levels Blood cultures, urine culture, CXR \206\223 Rea ssess the situation and plan further investigations. a Check pupils every few minutes during the early stages , particularly if trauma is the li kely cause. Doing so is the quickest way to find a localizing sign ( very helpful in diagno sis, but remember that false localizing signs do occur), and observing changes in pupil beh avior (e.g., becoming fixed and dilated) is the quickest way to find out just how bad thing s are. The Glasgow Coma Scale The GCS was first developed to assess consciousness in trauma patien ts. This scale is now often used in a variety of situations to quantify in a reli- able, ob jective way the conscious state of a person. It can be used by medi- cal and nursing staff for initial and continuing assessment. Three areas are examined when obtaining a GCS score: motor response, verbal response, and eye response. Best motor response This has six grades : 6 Follows command: The patient obeys a command to complete a simple task on your request. 5 Localizing response to pain: The patient responds to pain by reaching toward the painful stimuli. 4 Withdraws to pain: The patient retreats from the painful stimuli in some fashio n, without attempting to localize the response. 3 Flexor response to pain: The patient resp onds to painful stimuli by abnor- mally flexing the upper limbs. 2 Extensor posturing to pa in: The painful stimulus causes limb extension (ad- duction, internal rotation of shoulder, pronation of forearm); decerebrate posture. 1 No response to pain. Note that it is the bes t response of any limb that should be recorded. 743 Best verbal response This has five grades: 5 Oriented: The patient knows who he is, where h e is, and why he is where he is, the year, season, and month. 4 Confused conversation: The patient responds to questions in a conversa- tional manner but there is some disorientation and confusion. 3 Inappropriate speech: Random or exclamatory articulated speech but no con versational exchange. 2 Incomprehensible speech: Moaning but no words. 1 None. Record level of best speech. Eye opening This has four grades: 4 Spontaneous eye opening. 3 Eye opening in response to speech: Any speech or shout, not necessarily request to open eyes. 2 Eye op ening in response to pain: Painful stimuli results in eye opening. 1 No eye opening. An ove rall score is made by adding the individual scores from the three areas assessed. For examp le: A person who is dead has no response to pain + no verbalization + no eye opening and wo uld have a GCS = 3. A severely ill patient would have a GCS of \211 8; a moderate injury, GCS 9 \200\22312; minor injury, 13. In general, \200\234less than or equal to 8, intubate . \200\235 NB: An abbreviated coma scale, the AVPU, is sometimes used in the initial assess ment (primary survey) of the critically ill: \212 \212 \212 \212 alert A = V = responds to P = responds to U = vocal stimuli pain unresponsive Table 20.3 The neurological examination in coma A patient who appears to have an altered level of consciousness has a problem in one of two areas (1) a diffuse, bilateral, cortical dysfunction (usually producing loss of awareness with normal arousal) or (2) damage to the ascending reticular activating system (ARAS) loca ted throughout the brainstem from the medulla to the thalami (usually producing loss of aro usal with unassessable awareness). The brainstem can be affected directly (e.g., pontine he morrhage) or indirectly (e.g., compression from trans-tentorial or cerebellar herniation se condary to a mass or edema). The following are areas to be examined in these patients. Leve l of consciousness : Describe using objective words such as unarousable, responds to questi ons, or responds to pain . \212Respiratory pattern : Cheyne \200\223Stokes, hyperventilati on (acidosis, hypoxia, or, rarely, neurogenic), ataxic or apneustic (breath-holding) breath ing (brainstem damage with grave prognosis). \212Eyes: Almost all patients with ARAS pathology will have eye findings. Visual fields Te st fields with visual threat. No blink in one field suggests hemianopsia and contralateral hemisphere lesion. Pupils Normal, direct, and consensual = intact midbrain. Midposition (3 \200\2235 mm) nonreactive irregular = midbrain lesion. Unilateral dilated and unreactive ( \200\234fixed \200\235) = third-nerve compression. Small, reactive = pontine lesion ( \200\234pinpoint pontine pupils \200\235) or drugs. Horner \200\231s syndrome = ipsilateral lateral medulla or hypothalamus lesion; may precede uncal herniation. 744 (Continued) e n i c i d e m y c n e g r e m E Table 20.3 (Continued) Be aware of patients with false eyes or who use eye drops for glaucoma. Extraocular movemen ts (EOMs) Observe resting position and spontaneous movement, then test the vestibulo-ocular reflex (VOR) with either the Doll \200\231s-head maneuver (normal if the eyes keep looking at the same point in space when the head is quickly moved laterally or vertically) or ice water calorics (normal if eyes deviate toward the cold ear with nystagmus to the other side ). If present, the VOR exonerates most of the brainstem from the CN VII nerve nucleus (medu lla) to the CN III (midbrain). Don \200\231t move the head unless the cervical spine is cle ared. Fundi Papilledema, subhyaloid hemorrhage, hypertensive retinopathy, other disease (di abetic retinopathy) \212 Examine for CNS asymmetry (tone, spontaneous movements, reflexes). Shock Definition Circulatory insufficiency resulting in inadequate tissue perfusion. Shock can be classified into four categories (1) hypovolemic (caused by inadequate circulating vo lume), (2) cardiogenic (caused by inadequate cardiac pump function), (3) distributive (caus ed by peripheral vasodilatation and maldistribution of blood flow (i.e., sepsis), and (4) o bstructive (caused by extracardiac obstruction to blood flow). Shock is often manifested by SBP <90 mm Hg; a weak pulse; evidence of end-organ dysfunction, such as cool or mottled sk in; oliguria; hepatic insufficiency; or altered mental status. However, the signs of shock can be subtle depending on the cause . \212Hypovolemia: Bleeding: Trauma, ruptured aortic aneurysm, ruptured ectopic pregnancy. Fluid loss: Vomiting (e.g., GI obstruction), diarrhea (e.g., cholera), burns, pools of sequestered (unavailable) fluids (third spacing; e.g., in pancreatitis). Heat exhaustion may cause hypovolemic shock (also hyperpyrexia, oliguria, r habdomyolysis, unconsciousness, hyperventila- tion, hallucination, incontinence, collapse, coma, pin-point pupils, LFTs \206\221 , and disseminated intravascular coagulation [DIC, p . 626]). Heart dysfunction that includes dysrhythmias, tachyarrhyth- Cardiogenic: mias, or bradyarrhythmias. Overt pump failure is another cause of cardio- genic shock and can result from acute coronary syndromes, myocarditis, or cardiomyopathy, as well as from acute valvu lar dysfunction (especially regurgitant lesions) or rupture of ventricular septum or ventri cular wall. Pathology that prevents blood from flowing from the Obstructive shock: heart; i ncludes pericardial disease (tamponade), tension pneumothorax, pulmonary emboli, pulmonary hypertension, or other cardiac tumor, as well as obstructive valvular disease (aortic or mi tral stenosis). Blood is maldistributed throughout the body; includes Distributive shock: s eptic shock, anaphylactic shock, and neurogenic shock, as well as effects from vasodilator drugs and acute adrenal insufficiency. Gram \200\223ve (or +ve) septic shock from endotoxi n-induced vasodi- Sepsis: latation may be sudden and severe, with shock and coma but no sig ns of infection (fever, white blood cells [WBCs] \206\221 ). Neurogenic: Endocrine failure : Iatrogenic: \212 \212 \212 \212 745 \212 \212 \212 E.g.,post spinal surgery Addison \200\231s disease or hypothyroidism Drugs (e.g., anesthetics, antihypertensives) Assessment ABC . \212ECG: Rate, rhythm, ischemia? \212General: Cold and clammy: Cardiogen ic shock or fluid loss. Look for signs of anemia or dehydration: Skin turgor, postural hypo tension? Warm and well-perfused with bounding pulse: Septic shock. Any features suggestive of anaphylaxis \200\224history, urticaria, angioedema, wheeze? \212Cardiovascular system (CVS): Usually tachycardic (unless on \222 -blocker or in spina l shock) and hypotensive. But in the young and fit or pregnant women, the systolic BP may r emain normal, although the pulse pressure will narrow, with up to 30% blood volume depletio n. Difference between arms: Aortic dissection \212JVP or central venous pressure: If raised, cardiogenic shock is likely. \212Check abd omen: Any signs of trauma or aneurysm? Any evidence of GI bleeding? Check for melena. Management If BP is unrecordable, call the cardiac arrest team. See Table 20.4 for general management. Specific measures: \212Anaphylaxis (covered in own section) \212 \212 Cardiogenic shock (covered in own section) If no clue to source: Piperacillin-tazobactam 3. 375 \200\2234.5 g IV Septic shock: q6h + vancomycin 15 mg/kg q12h gentamicin. Give collo id or crystal- loid by IV. Consider transfer to ICU if possible for monitoring inotropes (norepinephrine). Goal-directed therapy now includes measurement of lactic acid, central v enous pressure (CVP), inferior venous cava (IVC) measurement, urine output, and hematocrit. See Table 20.5. Hypovolemic shock: Fluid replacement: 20 mg/kg bolus of saline or lactated Ringer \200\231s solution initially; if bleeding use blood; assess risks and benefits. Tit rate against blood pressure, CVP, and urine output. Treat the underlying cause. If severe h emorrhage, exsanguinating, or >1 L of fluid required to maintain blood pressure, consider u sing group-specific blood, or O Rh negative blood. Correct electrolyte abnormalities. Acido sis often responds to fluid replacement. Sponge bath + fanning; avoid ice and Heat exposure (heat exhaustion): immersion. Resuscitate with high-sodium IV fluids, such as 0.9% saline hydrocortisone 100 mg IV. Dantrolene seems ineffective. Chlorpromazine 25 mg IM may be u sed to stop shivering. Stop cooling when core tem- perature <39 C. \212 \212 746 e n i c i d e m y c n e g r e m E Table 20.4 Management of shock If BP is unrecordable, call the cardiac arrest team \206\223 ABC(including high-flow O 2 ) \206\223 Raise foot of the bed \206\223 IV access: Two (wide-bore; get help if this take s >2 min) \206\223 Identify and treat underlying cause \206\223 Infuse crystalloid fast t o raise BP (unless cardiogenic shock) \206\223 Seek expert help early \206\223 Investigat ions CBC, CMP, ABG, glucose, CRP Cross-match and check clotting Blood cultures, urine cultu re, ECG, CXR Others: Lactate, echo, abdominal CT, US \206\223 Consider arterial line, cent ral venous line, and bladder catheter (aim for a urine flow >30 mL/h) 0.5 \200\2231 cc/kg/h r \206\223 Further management: Treat underlying cause if possible Fluid replacement as dic tated by BP, CVP, Ultrasound IVC measurement, urine output Don \200\231t overload with flui ds if cardiogenic shock If persistently hypotensive, consider inotropes NB: Remember that h igher flow rates can be achieved better through peripheral lines than through standard -gau ge central lines. If cause is unclear: Treat as hypovolemia \200\224most common cause and r eversible. Ruptured abdominal aortic aneurysm: Aim for a systolic BP of 90 mm Hg. Table 20.5 SIRS, sepsis, and related syndromes The pathogenesis of sepsis and septic shock is becoming increasingly understood. The system ic inflammatory response syndrome (SIRS) is the early phase of septic shock and is thought to involve cytokine cascades, free radical production, and the release of vasoactive mediat ors. SIRS is defined as the presence of \211 2 of the following features: \212 \212 \212 \212 Related syndromes include: Sepsis : SIRS occurring in the presence of infection. If SIRS continues, then severe sepsis can result. Severe sepsis : Sepsis with evidence of organ hypoperfusion (e.g., hypox- emia, oliguria, lactic acidosis, or altered cerebral func tion) Temperature >38 C or <36 C Tachycardia >90 bpm Respiratory rate >20 breaths/min WBC >12 10 9 /L or <4 10 9 /L, or >10% immature (band) forms 747 (Continued) Table 20.5 (Continued) Septic shock : Severe sepsis with hypotension (systolic BP <90 mm Hg) despite adequate flui d resuscitation or the requirement for vasopressors/ inotropes to maintain BP. If sepsis pr ogresses, the patient may end up with multiorgan dysfunction syndrome. Septicemia was used to denote the presence of multiplying bacteria in the circulation, but the term has been re placed with the definitions above. Anaphylactic shock Type I IgE-mediated hypersensitivity reaction. Release of histamine and other agents causes capillary leak, wheeze, cyanosis, edema (larynx, lids, tongue, lips), u rticaria. More common in atopic individuals. An anaphy- lactoid reaction results from direc t release of mediators from inflamma- tory cells without involving antibodies, usually in r esponse to a drug (e.g., N -acetylcysteine). Common precipitants \212 \212 \212 Signs an d symptoms \212 \212 \212 Drugs (e.g., penicillin), contrast media in radiology Latex Stings, eggs, fish, peanuts, st rawberries Itching, erythema, urticaria, edema Wheeze, laryngeal obstruction, cyanosis Tachycardia, hy potension Management of anaphylaxis Secure the airway; give 100% O 2 Intubate if respiratory obstruct ion imminent \206\223 Remove the cause; raising the feet may help restore the circulation \206\223 Give epinephrine IM 0.3 mg (i.e., 0.3 mL of 1:1000) Repeat every 5 min if needed, as guided by BP, pulse, and respiratory func- tion, until better \206\223 Secure large-bo re IV access \206\223 Diphenhydramine 25 \200\22350 mg IV and methylprednisolone 125 mg IV \206\223 IV (0.9% saline bolus 20 mg/kg; may repeat once) Titrate against BP \206\223 If wheezing, treat for asthma May require ventilatory support \206\223 If still hypotensive, admission to ICU and an epinephrine (adrenaline) drip may be needed nebulized albuterol . Get expert help. 748 Further management \212 \212 H \212 2 blocker, such as cimetidine 300 mg or ranitidine 1 00 mg (orally, e n i c i d e m y c n e g r e m E Admit to ward; monitor ECG. Continue Benadryl 25 \200\22350 mg/4 \200\2236 h PO/IV if itchi ng. IV, IM) Suggest a \200\234Medic-alert \200\235 bracelet naming the culprit allergen. Teach about self-injected epinephrine (e.g., 0.3 mg, EpiPen ) to prevent a fatal attack. Skin-p rick tests showing specific IgE help identify which allergens to avoid. Consider glucagon 1 \200\2232 mg every 5 min IM/IV if on a \222 -blocker ( \222 -blockers blunt tachycardic response and worsen low BPs in this type of shock). Beware of causing nausea with glucagon in the obtunded patient without a definitive airway. \212 \212 \212 \212 Note: Epinephrine IV should be reserved for life threatening situations or when the patient is hypotensive. The IV dose is different: ( 1:10,000 solution) 0.1 mg slowly over 5 min . Stop as soon as a response has been obtained. Acute myocardial infarction A common medical emergency; prompt, appropriate treatment saves lives and myocardium. If in doubt, seek immediate help. Prehospital management Arrange an emergency ambulance. Aspirin 325 mg PO (unless clear con- traindication). Analgesia, e.g., morphine 5 \200\22310 mg IV (avoid IM injections, as risk of bleeding increases if thrombol ysis ultimately given). Sublingual nitroglycerin unless hypotensive. Management See Table 2 0.6 for acute measures. Percutaneous coronary angioplasty (PCA) is preferred to thrombolysi s. If PCA is not available within 1 h, then thrombolysis is also effective in reducing mort ality if given early. Greatest benefit is seen if given <12 h after the onset of chest pain , but some benefit is possible up to 24 h. The door-to-needle/ balloon time for thrombolysi s and PCA should be <90 min. Indications for thrombolysis: Presentation within 12 h of ches t pain with: \211 2 chest leads or \212 ST elevation >2 mm in \212 ST elevation >1 mm i n \211 2 limb leads or \212 Posterior infarction (dominant R waves and ST depression in V \212 New-onset left bundle branch block Presentation within 12 \200\22324 h if continuin g chest pain and/or ST elevation. Thrombolysis contraindications (CI): Consider urgent angi oplasty instead . 1 \200\223V 3 ) \212 \212 \212 \212 \212 \212 \212 \212 \212 Internal bleeding \212 Prolonged or traumatic CPR \212 Heavy vaginal bleeding \212 Acute pancreatitis \212 Active lung disease with cavitation \212 Recent trauma or surger y (<2 wks) Cerebral neoplasm \212 Severe hypertension (>200/120 mm Hg) Suspected aortic dissection Previous allergic reaction Pregnancy or <18 wks postnatal Sever e liver disease Esophageal varices Recent head trauma Recent hemorrhagic stroke. 749 Relative CI: History of severe hypertension, peptic ulcer, history of CVA, bleeding diathes is, anticoagulants. Streptokinase (SK) is the usual thrombolytic agent. Dose : 1.5 million units in 100 mL 0.9% saline IV over 1 h. side effects: Nausea, vomiting, hem- orrhage, stroke (1%), dysrhythmias. Any hypotension usually responds to slowing down or sto pping the infusion. Also watch for allergic reactions and anaphylaxis (rare). Do not repeat unless it is within 4 d of the first administration. Alteplase (rt-PA) may be indicated if the patient has previously received SK (>4 d) or reacted to SK. Dose : 15 mg IV bolus, the n 0.75 mg/kg (max 50 mg) over 30 min, then 0.5 mg/kg (max 35 mg) over 60 min. Accelerated r t-PA has benefit if given within 6 h, especially in younger patients with anterior MI. Stan dard rt-PA is given to patients presenting at 6 \200\22312 h. Tenecteplase is given by bolu s injection (over 10 sec), which in some cases may be an advantage. Dose : 30 mg IV (max 50 mg) if weight is <60 kg; 35 mg IV (max 50 mg) if weight is 60 \200\22369 kg; 40 mg IV (max 50 mg) if weight is 70 \200\22379 kg; 45 mg IV (max 50 mg) if weight is 80 \200\22389 kg; 50 mg IV (max 50 mg) if weight is >90 kg. Complications \212 Recurrent ischemia or failure to reperfuse (usually detected as persisting pain and ST-segm ent elevation in the immediate aftermath of thromboly- sis): Additional analgesia, nitrogly cerin, \222 -blocker; consider rethromboly- sis or do angioplasty if persistent or new ST- segment elevation. Stroke Pericarditis: Analgesics (try to avoid NSAIDs) Cardiogenic shock and heart failure \212 \212 \212 Right ventricular infarction \212 Confirm by demonstrating ST elevation in RV3, RV4 and/or echo. NB: RV4 means that V 4 is pl aced in the right fifth intercostal space in the midclavicular line. Treat hypotension and oliguria with fluids. Avoid nitrates and diuretics. Intensive monitoring and inotropes may be useful in some patients. \212 \212 \212 750 e n i c i d e m y c n e g r e m E Table 20.6 Management of an acute MI Attach ECG monitor and record a 12-lead ECG \206\223 High-flow O 2 by face mask (caution, if COPD) \206\223 IV access Bloods for CBC, CMP, glucose, lipids, cardiac enzymes \206 \223 Brief assessment History of cardiovascular disease; risk factors for heart disease Con traindications to thrombolysis? Examination: Pulse, BP, JVP, cardiac murmurs, signs of hear t failure, peripheral pulses, scars from previous cardiac surgery \206\223 Aspirin 325 mg if not given previously that day and no contraindications; heparin (follow weight-based nom ogram); clopidogrel 300 mg PO; consider eptifibatide (Integrilin) with cardiology consult b efore going to percutaneous coronary angioplasty (PTCA) \206\223 Nitroglycerin 0.4 mg subl ingually unless hypotensive \206\223 If chest pain persists, consider morphine unless hypo tensive \206\223 \222 -Blocker , e.g., metoprolol 5 mg IV (unless asthma or left ventricu lar failure) \206\223 PTCA or thrombolysis (see chart in text) \206\223 CXR Do not delay thrombolysis while waiting unless aneurysm is suspected \206\223 Consider deep vein thromb osis (DVT) prophylaxis \206\223 Continue medication except calcium-channel antagonists (un less specific indication) If pain is uncontrolled, especially if continuing ST elevation, c on- sider rethrombolysis with rt-PA (no bolus), tenecteplase, or rescue angioplasty. 751 Acute coronary syndrome Acute coronary syndrome (ACS) (without ST-elevation) includes unsta ble angina, evolving MI, and non-Q wave or subendocardial MI. Although the underlying patho logy is similar, management differs, and, therefore, ACS is usually divided into two classe s: \212 ACS with ST segment elevation (see acute MI earlier) or new left bundle branch block (LBBB) \212ACS without ST segment elevation (unstable angina or non-q wave MI) ACS is associated with a greatly increased risk of MI(up to 30% in the first month). Patients should be manag ed medically until symptoms settle. They are then investigated by angiography with a view t o possible angioplasty or surgery (coronary artery bypass graft [CABG]). Assessment Brief h istory: Previous angina, relief with rest/nitrates, history of cardiovas- cular disease, ri sk factors for ischemic heart disease (IHD). Examination: Pulse, BP, JVP, cardiac murmurs, signs of heart failure, periph- eral pulses, scars from previous cardiac surgery. Investiga tions ECG: ST depression flat, inverted t waves, or normal. CBC, CMP, glucose, lipids, card iac enzymes, CXR. Measurement of cardiac troponins helps predict which patients are at risk of a cardiac event, and who can be safely discharged early. Management See Table 20.7 for acute management. The aim of drug therapy is twofold: 1 Anti-ischemic (e.g., \222 -blocker , nitrate, calcium-channel antagonist) 2 Antithrombotics (e.g., aspirin, low-molecular-weig ht heparin, eptifibatide), which interfere with platelet activation and so reduce thrombus formation Further measures: \212 \212 \212 \212 Wean off nitroglycerin (NTG) infusion when stabilized on oral drugs. Stop heparin when pain -free for 24 h, but give at least 3 \200\2235 d therapy. Check serial ECGs and cardiac enzy mes for 9 h. Address modifiable risk factors: Smoking, hypertension, hyperlipidemia, diabet es. Begin gentle mobilization. \212 If symptoms recur, refer to a cardiologist for urgent angiography and angio- plasty o r CABG . Prognosis Overall risk of death 1 \200\2232%, but 15% for refractory angina desp ite medical therapy. Risk stratification can help predict those most at risk and allow inte rvention to be targeted at those individuals. The following are associated with an increase d risk: \212 \212 \212 \212 \212 \212 Indications for consideration of invasive inter vention: \212 \212 \212 \212 Hemodynamic instability: Hypotension, pulmonary edema T-wave inversion or ST segment depres sion on resting ECG Previous MI Prolonged rest pain Older age Diabetes mellitus 752 Poor prognosis (e.g., pulmonary edema) Refractory symptoms Positive exercise tolerance test s (ETT)at low workload Non-Q wave MI. e n i c i d e m y c n e g r e m E Table 20.7 Acute management of ACS without ST-segment elevation Admit to a monitored setting \206\223 High-flow O 2 by face mask \206\223 Nitrates: NTG s pray or sublingual tablets as required \206\223 Analgesia: E.g., morphine mg IV + ondanset ron 4 mg IV \206\223 Aspirin: 160 \200\223325 mg if not given previously that day and no c ontraindi- cations reduces risk of mi and death \206\223 \222 -blocker: E.g., metoprolol 50 \200\223100 mg/8 h orally If \222 -blocker is contraindicated (asthma, COPD, left ventr icular function (LVF), bradycardia, coronary artery spasm), give rate-limiting calcium anta gonist (e.g., diltiazem 60 \200\223120 mg/8 h PO) \206\223 Low-molecular-weight heparin e. g., enoxaparin 1 mg/kg/12 h Alternatively: Unfractionated heparin 5,000 U IV bolus then iv infusion Check aPTT q6h. Alter IV rate to maintain aPTT at 1.5 \200\2232.5 \227 control \206\223 IV nitrate if pain continues titrate to pain, and maintain SBP at >100 mm Hg \206 \223 Record ECG while in pain \206\223 High-risk patients (persistent or recurrent ischemi a, st-depression, diabetes, \206\221 troponin) Infusion of a GPIIb/IIIa antagonist (e.g., tirofiban) and, ideally, urgent angiography. Addition of clopidogrel may also be useful \206\223 Optimize drugs: \222 -blocker; Ca 2+ channel antagonist; angiotensin-converting e nzyme (ACE)-inhibitor; nitrate Intensive statin regimens, starting at top dosages , may dec rease long- and short-term mortality/adverse events, e.g., by stabilizing plaques \206\223 If symptoms fail to improve, refer to a cardiologist for urgent angiography angioplasty or CABG Low-risk patients (no further pain, flat or inverted t-waves, or normal ecg, and n egative troponin) May be discharged if a repeat troponin (3, 6, and 9 h) is negative. Treat medically and arrange further investigation(e.g., stress test, angiogram) 753 Severe pulmonary edema Causes \212 Cardiovascular: Usually left ventricular (LV) failure \200\224post-MI \200\223or isch- emic heart disease. Also mitral stenosis, arrhythmias, and malignant hypertension Acute respira tory distress syndrome (ARDS) (Any cause (e.g., trauma, malaria, drugs); look for predispos ing factors (e.g., trauma, postop, sepsis). Is aspirin overdose or glue-sniffing/drug abuse likely ? Ask friends/relatives. Fluid overload Neurogenic (e.g., head injury) See X-RAY PL ATE 2 \212 \212 \212 \212 Differential diagnosis Asthma/COPD, pneumonia, and pulmonary edema are of ten hard to distinguish, especially in the elderly, in whom these may coexist. Do not hesit ate to treat all three simultaneously (e.g., with albuterol nebulizer, furosemide IV, morph ine, fluoroquinolone). Symptoms Dyspnea, orthopnea (e.g., paroxysmal), pink frothy sputum. NB: Drugs; other illnesses (recent MI/COPD)or pneumonia). Signs Distressed, pale, sweaty, p ulse \206\221 , tachypnea, pink frothy sputum, pulsus alternans, elevated JVP, fine lung c rackles, triple/gallop rhythm, wheeze (cardiac asthma). Usually sitting up and leaning forw ard. Quickly examine for possible causes. Investigations \212 CXR(X-RAY PLATE 2 : Cardiomegaly, signs of pulmonary edema. Look for shadowing (usually bil ateral), small effusions at costophrenic angles, fluid in the lung fissures, and Kerley B l ines (linear opacities). ECG: Signs of MI CMP; cardiac enzymes, arterial blood gasses (ABG) Consider echo \212 \212 \212 Management Begin treatment before investigations . See Table 20.8. Monito ring progress: BP, heart rate, cyanosis, respiratory rate, JVP, urine output, ABG. Once sta ble and improving: \212 \212 \212 Daily weights; BP and pulse q6h. Repeat CXR. Change to oral furosemide or bumetanide. If on large doses of loop diuretic, consider the addition of a thiazide or metolazone 2.5 \200 \2235 mg/d PO. ACE-inhibitor if LV failure; also consider echo. If ACE-inhibitor is con- tr aindicated, consider hydralazine and nitrate. Also consider \222 -blocker and spironolacto ne. Is the patient suitable for cardiac transplantation? Consider digoxin warfarin, espe cially if AF. \212 \212 \212 \212 754 e n i c i d e m y c n e g r e m E Table 20.8 Management of heart failure Sit the patient upright \206\223 Oxygen 100% if no preexisting lung disease \206\223 IV a ccess and monitor ECG Treat any arrhythmias (e.g., atrial fib) \206\223 Investigations whi le continuing treatment \206\223 Furosemide 40 \200\22380 mg IV slowly Larger doses requir ed in renal failure \206\223 Nitroglycerin spray two puffs SL or 2 \227 0.3 mg tablets SL Don \200\231t give if systolic BP <90 mm Hg Necessary investigations, examination, and his tory \206\223 If systolic BP>100 mm Hg, start a nitrate infusion ( e.g., isosorbide dinitr ate 2 \200\22310 mg/h IV) keep systolic BP >90 mm Hg \206\223 If the patient is worsening: Further dose of furosemide 40 \200\22380 mg Consider ventilation (invasive or noninvasive; e.g., CPAP; get help)or increase nitrate infusion \206\223 If systolic BP <100 mm Hg, tre at as cardiogenic shock; i.e., consider a Swan \200\223Ganz catheter and inotropic support \206\223 If systolic BP is >180 mm Hg, consider treating for hypertensive LVF Cardiogenic shock This has a high mortality. Ask a senior physician \200\231s help both in formulating an exact diagnosis and in guiding treatment. Cardiogenic shock is caused primar ily by the failure of the heart to maintain the circulation. It may occur suddenly or after progressively worsening heart failure. Causes \212 \212 \212 \212 \212 \212 \212 \212 Arrhythmias Cardiac tamponade Tension pneumothorax MI Myocarditis; myocardial depression (d rugs, hypoxia, acidosis, sepsis) Valve destruction (endocarditis) Pulmonary embolus Aortic dissection 755 Management If the cause is MI, prompt revascularization (thrombolysis or acute angio- plast y) is vital; see MI section for indications and contraindications. \212 \212 \212 \212 Manage in coronary care unit, if possible. Investigation and treatment may need to be done concurrently. See Table 20.9 for details of management. ECG, CMP, CBC, CK, CK-MB, troponin, ABG, CXR, echo. Investigations: If indicated, CT thorax (aortic dissection) and ventilatio n/profusion scan or pulmonary angiogram for PE. \212Monitor CVP, BP, ABG, ECG, urine output. Do a 12-lead ECG every hour until the diagnos is is made. Consider a Swan \200\223Ganz catheter to assess pulmonary wedge pressure and ca rdiac output and an arterial line to monitor pressure. Catheterize for accurate urine outpu t.