Assessment of Critically Ill Patients Week 1-2

1. Assessment of Critically Ill PatientsWeek 1-2 Michael Haines, MPH, RRT-NPS, AE-C

2. Introduction/Objectives • This will be a difficult class, reading and studying is a expectation NOT a suggestion! • Please try your hardest and give your best effort • Objectives of this class are to gain critical assessment skills of the critical patient • Being able to assess a patient beyond surface data is a critical aspect in becoming a qualified clinician and will help to set you apart from mediocre therapists

4. Week 1 • Neurologic Monitoring • Cardiovascular monitoring • We will be covering this in several lectures, including a review of ECG interpretation • Renal Function • We will review renal failure and labs • Liver Function • Nutritional Assessment

5. Components of a Neurological Assessment • 1. Interviewing the patient • 2. Determining level of consciousness • 3. Pupillary Assessment • 4. Cranial Nerve Testing • 5. Vital Signs • 6. Motor Function • 7. Sensory Function • 8. Tone • 9. Cerebral Function

6. Interviewing your patient • Purpose: gather information, either from the family or patient. It also established a baseline sensorium • READ THE PATIENTS CHART FIRST, KNOW PAST HX • Identify the following when assessing neuro status: • Headache • Difficulty with speech • Inability to read or write • Altered level of consciousness or memory • Confusion or change in thinking • Decrease in sensation, tingling, pain • Motor weakness or decreased strength • Vision problems, diplopia • Difficulty swallowing • Tremors, twitches…

7. Consciousness Reticular Activating System (RAS) • Network of neurons and fibers in the brain stem which receive input from the sensory pathways and project to the entire cerebral cortex • Arousal is dependent on adequate functioning of RAS • Arousal is a function of the brain stem, it does not have anything to do with the thinking parts of the brain (basically it allows for physical reaction) • If a patient opens their eyes when called upon, they have an intact RAS for example but does not tell you if they are cognitive, awake or aware

8. Consciousness Cortex • Modulates incoming information via connections to the RAS • Requires functioning RAS • Awareness means that the cerebral cortex is working and that the patient can interact with and interpret his environment • We evaluate awareness in many ways but tend to focus on four areas of cortical functioning: • Orientation • Attention span • Language • Memory

9. Level of Consciousness • Consciousness is defined as the state of being aware of physical events or mental concepts. Conscious patients are awake and responsive to their surroundings • The level of consciousness has been described as the degree of arousal and awareness. • A manifestation of altered consciousness implies an underlying brain dysfunction. • Its onset may be sudden, for example following an acute head injury, or it may occur more gradually, such as in hypoglycemia.

10. Causes of Altered Level of Consciousness • Profound hypoxemia • Hypercapnia • Cerebral hypoperfusion • Stroke • Convulsions • Hypoglycemia • Recent administration of sedatives or analgesic drugs; drug overdose • Tumors • High Ammonia levels from liver failure • Renal failure • Encephalopathy (hepatic, anoxic, metabolic) • Brain lesions, swelling • subarachnoid hemorrhage • alcohol intoxication • Severe shock • Infection

11. ALOC • The clinician must determine the cause of the ALOC and suggest appropriate exams such as: • CT of the brain (to rule out bleeding, swelling…) • ABG to assess Co2, Pao2 • Blood Glucose levels with an Accucheck • Pupil dilation to assess drugs • Physical exams to determine significance • Electrolytes, liver and renal panels, Infection

12. Assessment of LOC • Observe patients response to verbal or motor stimuli • No response to voice or light touch, then attempt painful stimuli such as: • Sternal rub • Supraorbital pressure • Pinching upper arms Localizing is when a patient does a purposeful gesture, such as picks up tubing, pulls at linen Localizing is purposeful and intentional movement intended to eliminate a noxious stimulus, whereas withdrawal is a smaller movement used to get away from noxious stimulus.

13. Assessment of Awareness • The Glascow Coma Scale (GCS) helps us to decrease the subjectivity of our responses • GCSis a neurological scale that aims to give a reliable, objective way of recording the conscious state of a person for initial as well as subsequent assessment. • A patient is assessed against the criteria of the scale, and the resulting points give a patient score between • 3 (indicating deep unconsciousness) and 15 (most awake/alert)

15. LOC • GCS • Individual elements as well as the sum of the score are important. • Generally, brain injury is classified as: • Severe, with GCS ≤ 8 • Moderate, GCS 9 - 12 • Minor, GCS ≥ 13. • Tracheal intubation and severe facial/eye swelling or damage make it impossible to test the verbal and eye responses. In these circumstances, the score is given as 1 with a modifier attached

16. LOC • The AVPU scale is a quick and easy method to assess level of consciousness. It is ideal in the initial rapid ABCDE assessment: • Alert • Responds to voice • Responds to pain • Unconscious

18. LOC terms • Awake/Alert (responds in a meaningful manner to verbal instructions or gestures) • Confused (disoriented to time, place, or person, memory difficulty is common, difficulty with commands, exhibits alteration in perception of stimuli, may be agitated) • Combative • Stuporous(generally unresponsive except to vigorous stimulation, may make attempt at verbalization to vigorous/repeated stimuli, opens eyes to deep pain) • Lethargic (drowsy, oriented when awake but if left alone will sleep) • Obtunded (decreased interest in their surroundings, slowed responses, and sleepines) • Comatose (unarousable and unresponsive, some localization or movement, does not open eyes to deep pain)

19. States of ALOC • Brain Death • Persistent Vegetative State • Locked-in Syndrome (muscle paralysis, involving voluntary muscles, while there is full cognitive function) • Progression from coma to full consciousness is often a gradual occurrence (especially in the case of head trauma) • Recovery from ALOC dependent on: • Age (under 20 better prognosis) • Type of injury (reversible) • Premorbid health • Longer the coma the worse the prognosis • Absence of gag, pupillary reflexes = poor prognosis • Permanent flexion or flaccidness of extremities = poor prognosis

20. Pupillary Assessment • Pupil dilation/constriction • Certain drugs cause constriction of the pupils, such as alcohol and opioids. Other drugs, such as atropine, LSD, MDMA, mescaline, psilocybin mushrooms, cocaine and amphetamines may cause pupil dilation.

21. Pupillary Assessment

22. Pupillary Assessment • Pinpoint: opiate overdose or pontine hemorrhage • Small: Bright room, Horners syndrome, pontinehemorrage ,ophthalmic drops, metabolic coma • Large: dark room, some drugs, orbital injury • Dilated: Always an abnormal finding, terminal stage of anoxia ischemia or at death, anti-cholinergic drugs can dilate pupils • SHAPE: • Ovoid: intracranial hypertension • Keyhole: postCataract surgery

23. Ovoid shape Keyhole shape

24. Pupillary Assessment • Pupils can also react in the following manner: • sluggish: • found in conditions that compress the third cranial nerve, such as, cerebral edema and herniation • nonreactive or fixed: • seen in conditions that compress the 3rd cranial nerve such as herniation, severe hypoxia and ischemia • hippus phenomenon: • with uniform illumination of the pupil, alternating dilation and contraction of the pupil occurs. This is often associated with early signs of transtentorial herniation or may indicate seizure activity.

25. Intracranial Pressure ICP kept below 20 cmH2O Be mindful of things that can increase ICP such as suctioning, stimulation, excessive PEEP levels, high CO2 levels

26. Vital Sign Changes • Changes in vital signs are not consistent early warning signals. Vitals are more useful in detecting progression to late symptoms. Both respiratory and cardiac centers are located in the brainstem. • Therefore, compression of the brainstem will cause changes in vital signs. This is usually a late sign and impending herniation/death will occur if the problem is not resolved. The respiratory centers in the brainstem control rate, rhythm, inspiration/expiration. • The cardiac centers also play a part in cardiac acceleration/inhibition e.g. controlling heart rate and rhythm as well as hemodynamic stability/instability

27. Respiratory Rate • Biots Breathing • Cheyne Stokes • Apneustic • What can cause changes in respirations from a neurological standpoint? • Increased Intracranial Pressure • Initially with increased ICP you should expect to see a slowing of respirations but as the ICP increases so will the rate of respirations. The rhythm of respirations will also become more irregular Spinal Cord Injury • Cervical spine trauma can cause alteration in respiratory effort. If the injury is at level C4 (phrenic segment) or above, total respiratory arrest can occur.

28. Pulse • 1. Assess rate, rhythm, and quality of pulse • 2. Assess tissue perfusion, cardiac output, activity intolerance • 3. Assess for causes of cardiac instability and intervene appropriately • What can cause changes in pulse from a neurological standpoint? Tachycardia • 1. If a patient has tachycardia related to neurological impairment it can mean that they are reaching a terminal phase in their disease process. • 2. In a patient with multiple trauma, hemorrhage must be ruled out (intra-abdominal). Bradycardia • 1. Bradycardia is seen in the later stages of increased intracranial pressure. As BP rises to overcome the increased ICP, reflex inhibition causes a slowing of the HR. • 2. Bradycardia can also be seen with spinal cord injury and interruption of the descending sympathetic pathways

29. Vitals Cardiac Arrhythmias • Cardiac arrhythmias may occur in several neurological conditions. Subarachnoid hemorrhage patients with blood in the CSF and patients who have undergone posterior fossa surgery tend to have an increased incidence of arrhythmia. Blood Pressure • 1. Assess for hypertension, hypotension, and pulse pressure • 2. Assess tissue perfusion, cardiac output Hypertension • Increases in blood pressure are usually associated with rising ICP. • An increased systolic pressure, widening pulse pressure, bradycardia and apnea are advanced stages of increased ICP and are known as Cushing's response.

30. Vitals Hypotension • 1. Decrease in blood pressure is rarely seen as a result of neurological injury. If it is present it is usually accompanied by tachycardia and is terminal. • 2. Hypotension and bradycardia can be seen with cervical spine injuries as a result of neurogenic shock. Temperature • The hypothalamus is the regulatory center for temperature. Regulation of heat is monitored by blood temperature and is controlled through impulses to sweat glands, dilation of peripheral vessels and shivering of skeletal muscles.

31. Vitals Hyperthermia • Temperature elevation in the neurological patient can be caused by direct damage to the hypothalamus or traction on the hypothalamus as a result of increased ICP, CNS infection, subarachnoid hemorrhage etc. Temperature elevations may become very high, very rapidly. They need to be treated aggressively as fever will cause an increase in cerebral oxygen requirements, increased metabolic rate, and increased carbon dioxide production. Increased carbon dioxide production can lead to cerebral vasodilation. Cerebral vasodilation can increase the ICP, leading to more cerebral ischemia. Hypothermia • Can occur with spinal shock, metabolic or toxic coma, or lesions of the hypothalamus.

32. Arrhythmia Review

33. Electrocardiographic (ECG) Assessment • Indications For Obtaining an ECG • Chest Pain • Dyspnea on Exertion • Palpitations • Pedal Edema • History of Heart Disease/Cardiac Surgery • Unexplained Tachycardia at Rest • Hypotension • Diaphoresis • Jugular Venous Distension • Cool, Cyanotic Extremities

34. Standard Monitoring Leads Lead 1

35. Standard Monitoring Leads Lead 2

36. Standard Monitoring Leads Lead 3

37. Initial Approach—Analysis4 Questions • Rate? • Normal • Bradycardia, Tachycardia • Rhythm? • Regular or Irregular • Are there P waves? • Is each P wave related to a QRS with 1:1 impulse conduction? • QRS normal or wide?

38. Systematic Approach to ECG Interpretation • Identify Rate • Evaluate The Rhythm (Spacing Between QRS Complexes ≤ 0.04 Seconds Normal) • Determine Presence of Waves • Measure The P-R Interval (Normal: 0.12 to 0.20 Seconds) • Measure Width of QRS Complex (Normal: ≤ 0.12 Seconds) • Inspect The ST Segment • Identify The Mean QRS Axis

39. Systematic Approach to ECG Interpretation

40. VF

41. VF • Ventricular fibrillation is an irregular rhythm resulting from a rapid discharge of impulses from one or more foci in the ventricles. The ventricular contractions are erratic and seen on the ECG as bizarre patterns of various sizes and configurations. No P waves are seen. Some causes of VF include myocardial ischemia, hypoxia, hypothermia, electrocution, electrolyte and acid-base imbalance, and drug effects. Due to the absence of any effective cardiac output, life must be sustained by artificial means - i.e. external cardiac massage and defibrillation is "the" treatment.

42. VT

43. Polymorphic VT • TX without pulse: • CPR • DEFIB • EPI/Mg 2g

44. Premature Ventricular Contractions (PVCs) • Causes • Congestive Heart Failure • Myocardial Infarction • Hypoxia • Single PVC is no Threat • Warning Signs of Complications From PVCs • Increase in Frequency (Multiple PVCs in One Minute) • Multifocal PVCs

45. Warning Signs of Complications From PVCs • Couplets – Paired PVCs (If Regular, Bigeminy) • Salvos – Three or More PVCs in a Row • R-on-T Phenomenon – PVC Occurs on T Wave; Can Lead to Ventricular Tachycardia And/or Fibrillation

46.    PVC Morphology—Match the Name  • Unifocal PVCs • Multifocal PVCs • Bigeminy • Ventricular Tachycardia • Torsades

47. Common Dysrhythmias • Ventricular Tachycardia • Series of Broad QRS Complexes • Rates of 140 to 300 Beats/Min • No Identifiable P Wave • Sustained Ventricular Tachycardia – Lasts More Than 30 Seconds • Non-Sustained Ventricular Tachycardia – Terminates Spontaneously After a Short Burst • May Become Hypotensive And Lethargic • If Significant Deterioration of Cardiac Output, Patient Becomes Unresponsive • Without Treatment, May Lead to Ventricular Fibrillation

48. VT • Ventricular tachycardia is a rapid, regular heart rhythm that originates in the lower chambers of the heart. • May be monomorphic or polymorphic (Torsades De Pointes), may or may not produce a pulse; in either case it is typically an emergent situation

49. Ventricular TachycardiaMonomorphic*  *Sustained—requires intervention for >30 seconds • Rate • Rhythm • P waves • P → QRS • Therapy Atrial rate normal Onset tachycardia abrupt Regular Present—obscured Blocked—fusion complexes possible Antiarrhythmic agent, cardioversion, high-energy (defibrillation dose) shock

50. Polymorphic VT* *Torsades de pointes—QT prolonged • Rate • Rhythm • P waves • P → QRS • Therapy Atrial rate normal (obscured) Onset tachycardia abrupt Irregular Present—obscured Blocked—fusion complexes possible Unsynchronized high-energy shock, magnesium (beneficial with baseline QTC prolongation)