Traumatic & Acquired Brain Injuries: Week 7 Notes

Week 7 – traumatic & acquired brain & head injuries Intracranial Pressure (ICP)  3 main components of the skull: o Brain tissue o Blood volume o CSF  ICP regulated through these components under normal conditions o Pressure is regulated by changes...

Week 7 – traumatic & acquired brain & head injuries Intracranial Pressure (ICP)  3 main components of the skull: o Brain tissue o Blood volume o CSF  ICP regulated through these components under normal conditions o Pressure is regulated by changes in these 3 components  Normal ICP = 5-15mmHG  ICP – the pressure exerted from the combined volume of brain, blood and CSF in the skull ICP regulation  Influenced by: o Blood pressure Hypotension – less blood is going to the brain because our  vessels are constricted o Cardiac function o Intraabdominal pressure o Intrathoracic pressure What increases intrathoracic pressure? Coughing, sneezing  – you are increasing the pressure in the lungs o Body position o Temperature o Acid-base balance – control the diameter of our vessels  Modified Monroe-Kellie Doctrine: o If the volume of any 3 components of the skull increases in the cranial vault, and the other components are displaced, the ICP will not change, but if there is no compensation or displacement, the ICP will increase o The compensation of components is necessary as the skull is fixed & rigid  cannot compensate o Does not apply to infants, people with skull fractures or a piece of their skull removed ICP Compensatory Mechanisms   CSF volume o Displacement into spinal subarachnoid space or basal subarachnoid cisterns o Altered CSF production and absorption – lesser degree  Blood volume o Compression of cerebral veins and dural sinuses, regional cerebral Vaso activity, changes in venous outflow  Brain tissue o Dural distension or compression of tissue Cerebral Blood Flow  The amount of blood passing through 100g of brain tissue per minute  Blood flow is essential for neuronal functioning & survival – brain cannot store O2 and glucose  Autoregulation is imperative to blood flow regulation o Regulates blood flow based on metabolic needs o Automatic change in BV diameter to maintain blood flow to brain o Dependent on mean arterial pressure (MAP) – how much blood (oxygen) is getting to the body tissues  For most individuals we need a MAP of 60 or greater  If 50, vessels are maximally constricted  further MAP increase will increase ICP MAP calculation  MAP = SBP+2(DSP) /3  Example: What is the map of: o A) 82/48  MAP = 82+2(48)/3  = 59 – not ischemic but can become ischemic if blood is not delivered to the brain o B) 192/11  MAP = 192+2(11)/3  = 71 – MAP is good, but that BP reading is not Calculating Cerebral Blood Flow  Reflected with the cerebral perfusion pressure   If CPP is inadequate, brain perfusion is improved by increased MAP or decrease ICP  Normal CPP is 70-100mmHg o 50-60mmHG needed for adequate perfusion  CPP = Map – ICP o CPP 50 mmHg is associated with cellular ischemia (and death)  Examples: What is the CPP calculation: o BP: 112/50 with ICP 10  Map = 112+2(50)/3 = 71  CPP = 71-10 = 61  Considered adequate perfusion o BP: 172/100 with ICP 20  MAP = 172+2(100)/3 = 124  CPP = 124 – 20 104  CPP low = increases ICP  CPP high = decreases ICP – decrease bp, look at altering the 3 components Cerebral Blood Flow: CO2  If PaCO2 levels are high (>45mmHg): o Causes smooth muscle relaxation o Vasodilation o Decreased vascular resistance o Increases CBF  If PaCO2 levels are low ( 100   Patient positioning o Side-laying o HOB 30 degrees helps to drain the ICP into the body and increase oxygenation o Prevents knee and hip flexion o Slow movements with turning patients  Be mindful of abdominal pressure/distention o Insert NGT  Nutritional support o Hypermetabolic and hypercatabolic state – will require more glucose  Maintain normal ICP, CPP o Monitor MAP, CPP, and ICP – if an invasive monitor present o Medication therapy – mannitol, hypertonic saline corticosteroids o Consider use of sedation o Monitor and maintain normothermia – cooling blanket o Monitor fluid balance o Maintain a quiet and calm environment  Protect from injury o Confusion, agitation, seizures can cause injury o Consider environmental, chemical, physical restraints if necessary o Pad side rails o Use clam approach  Psychosocial support o Pt and family Head Injury  Trauma to – scalp, skull, brain  Types o Scalp laceration – most minor  Scalp has many vessels with poor constrictive ability o Skull Fracture  Multiple types – linear, depressed, simple, comminuted, compound  Can extend to environment OR into dura mater   Severity and type of dependent on how the injury happened  Manifestations based on location of fracture  Basilar skull fracture – battle sign & raccoon eyes  CSF indicative of fracture extending into dura  Otorrhea or rhinorrhea  Classification o Diffuse – concussion – sudden transient, mechanical head injury  Can include post-concussion syndrome o Focal – brain laceration – often from skull. Fracture  Often associated with hemorrhage and hematoma  Hematoma – often near site of skull fracture  Coup – contrecoup  Complications o Epidural hematoma Between dura and inner surface of skull Arterial bleed – forms rapidly: venous bleed: more slow – forming  Patients often unconscious  brief lucidity  decreased LOC o Subdural hematoma  Blood between dura and arachnoid meninges  From damage to parenchymal vessels  Often venous – slow forming  Can be acute, subacute, chronic o Intraparenchymal hematoma  Blood in parenchyma from bleeding brain tissue  Often, frontal or temporal lobes o Traumatic subarachnoid hemorrhage  Injury to superficial vascular structures in SA space  Can cause cerebral vasospasm and decreased BCF  Management o Assessment – similar to IICP, close neuromonitoring o Diagnosis – many applicable depending on pt state o Planning & goals Maintain cerebral perfusion, remain normothermic, keep pt free from pain and infection, attain maximal cognitive, motor, and sensory function o Implementation   Health promotion is key  Prevent MVAs – promote car and driver safety  Acute interventions o Maintain cerebral oxygenation and perfusion o Monitor neuro status – change can be rapid o Monitor hemodynamics o Explain the need for frequent neuro assessment o Promote normothermia o Threat of nausea & vomiting o Know immediate signs to call MD  Decreased GCS and dilated pupils  CSF visible – otorrhea/rhinorrhea  Ambulatory Care o Pts often to rehab after acute hospital stay o Interdisciplinary support o Post-traumatic seizures in week after injury  Prophylactic anticonvulsants for 7 days after injury o Cognitive and emotional sequelae  Support pts and families Week 8 – Neuro II Major cerebral Vasculature  Internal carotids – anterior circulation – provides anterior circulation and helps to provide blood to frontal, parietal and temporal lobes o Frontal, parietal, temporal lobes o Basal ganglia o Diencephalon – thalamus & hypothalamus o Main branches – middle cerebral artery (MCA) & anterior cerebral artery (ACA)  Vertebral arteries – posterior circulation – basilar artery helps to provide blood to middle and lower lobes o Join to form the basilar artery o Middle & lower temporal lobes, occipital lobes  o Cerebellum, brainstem o Diencephalon o Major branches – posterior cerebral artery (PCA) Circle of Willis  Anterior, basilar, and posterior join together to form circle of Willis  Circle of Willis – can see how vasculature is made o If there is any kind of genetic change to the vascular system, we need to consider the role of autoregulation – it may not be as effective in delivering blood to other parts of the brain, leading to collateral circulation Types of Stroke  Transient Venous Attack – TVA (commonly transient ischemia attack – TIA) o TIA – some consider this a stroke while other do not – sometimes judging from the symptoms area of the brain can be determined o Abrupt interruption in blood flow to an area of the brain o A precursor to a stroke is a transient venous attack – TVA meaning it doesn’t last forever – for a period of time, part of the brain isn’t receiving blood, then blood flow is restored  Cerebral vascular attack – CVA – is another form for stroke o Ischemic stroke Thrombotic stroke – either a complete or partial blockage  of a vessel therefore, restricted blood flow  Embolic stroke o Hemorrhagic stroke  Subarachnoid hemorrhage – bleeding that occurs in the subarachnoid area  Intracerebral hemorrhage – bleeding in the brain area Transient Ischemic Attack  A localized area of the brain experiences ischemia for a limited period of time – less than 1 hour  Not an acute infract, but can precede a stroke o Warning sign o Risk of stroke is high after a TIA o Important to seek medical attention   Same etiology as stroke  If it is more than one hour, its not considered a TIA  It's not killing brain tissue but it is a warning that a stroke can occur  Can think of it as a delay of blood flow to a part of the brain Ischemia Stroke – Atherosclerosis  Hardening and thickening of arteries  Causes development of thrombi and emboli  Briefly…  High lipids  fatty streak development  hardens  Inflammation occurs  platelets/fibrin stick to plaque  vessel narrows  A lot of ischemic strokes are caused by atherosclerosis  Lipids into vessel, fatty streak which then turns into hardened plaque, forming at bifurcating areas (where the vessels split) - blood flow is typically more turbulent in these areas, which may cause the plaque to rupture or fissure, which can cause an inflammatory process  Ischemic strokes often start with atherosclerosis which often turns into clots and plaque which may rupture Atherosclerosis Risk Factors  Modifiable o Hypertension o Afib, MI o Diabetes o Dyslipidemia, hypercholesterolemia o Smoking o Obesity o Alcohol use o Birth control o Pregnancy, hormone therapy  Non-Modifiable o Age o Sex o Indigenous, south Asian, African heritage  o Age – risk increases o Avm Ischemic Stroke – Thrombotic  2/3 of all strokes; often preceded by TIA  From inadequate blood flow to brain – secondary to atherosclerosis  Clots form in disease & narrow vessel  Difficult for blood to pass through a narrowed vessel o Decreased blood and oxygen to brain o Blood stasis can cause more clotting – enlarging it o If clot breaks away from plaque, it is called an embolus  Lack of blood flow, lack of oxygen  Clots can sometimes form in patients who have hyperglycemia as it can damage vessels almost like how atherosclerosis damages vessels Ischemic Stroke – Embolic  2nd most common cause of stroke  Occlusion in a cerebral vessel – clot outside the brain travels to a cerebral vessel and becomes lodged  Rapid symptoms – less warning signs  Symptoms are severe unless clot breaks up and blood flow restored  Often cardiac origin  Offers – air embolus, fat embolus from long bones numbers  Embolis – broken off clot  Prior to the embolis, the area was getting good blood flow. Suddenly a clot appears, blocks it, leading to rapid symptoms Hemorrhagic Stroke – Intracerebral Hemorrhage  10% of all strokes  Bleeding in brain tissue from  Sudden onset of symptoms – progression in minutes, hours  Bleeding in the cranial vault compresses brain tissue o Increased intracranial pressure   Strokes associated with a lot of bleeding  Bleeding can increase the size of brain tissue, can become inflamed – increased brain size and mass which increase intracranial pressure  Symptoms depend on the amount of blood, its location, and the duration of bleeding  Symptoms by region o Thalamic – hemiplegia o Subthalamic – vision/eye movement o Cerebellum – headache, vomiting, dysphagia, dysarthria, altered eye movement o Pons – basic life function (Resp) Hemorrhagic Stroke – Subarachnoid Hemorrhage – bleeding in the subarachnoid space  Intracranial bleeding in ventricles  Causes IICP from blood  vasospasm  Cerebral perfusion decreased, causing ischemia & neurological change o Alterations within vasculature - Cerebral aneurysms – outpouching causes decrease in wall width/strength which can cause it to burst  Often from rupture of cerebral aneurysm o “silent killer” o Other causes: AVM, trauma, cocaine  Risk factors – smoking, htn, connective tissue disorders Vasospasm  Occurs from the metabolites of blood o Metabolites are potent vasoconstrictors  Often occurs during clot lysis; 7-10 fays after initial bleed  When blood goes outside of blood vessels, we get concerned about vasospasms  Metabolites outside blood vessels cause them to tighten Neurological Deficits from Stroke  Can be experienced gradually or suddenly – depends on cause  Severity of the loss of function varies according to the location and extend of the brain involved   Prolonged ischemia results in severe deficits or death  Where stroke has happened and how much ischemia determine deficits Time is brain  If blood flow is interrupted for: o 30 seconds – changes in cerebral metabolism o 2 mins – brain metabolism stops o 5 mins – cellular death o 2-3 hrs – inflammatory response Inflammatory response - cleaning up dead cells  Leukocytes and other inflammatory markers o Penumbra creates barrier around ischemic area – minimizes ischemic area so it can be contained Signs & Symptoms: left hemispheric stroke  The left hemisphere (side) of your brain controls the right side of your body  It also controls your speech and language abilities. You may have any of the following: o Trouble swallowing, walking or remembering o Paralysis or weakness on the right side of your body o Falling toward your right side o Lack of awareness of the right side of your body o Trouble speaking, reading, writing, or understanding language o Changes in mood or the ability to pay attention or learn new info  The side of the brain impacted will correlate with the opposite side of the body Signs & Symptoms: right hemispheric stroke  Difficulty remembering, impulsive behr or mood changes  Paralysis on one side or both sides of the body  Trouble walking or falling toward the left side  Lack of awareness of the left side of the body   Trouble swallowing, speaking, reading, writing or understanding language  Changes in mood or the ability to pay attention or solve problems Assessment  ABCs are priorty  If stable obtain hx  Medication hx – blood thinners  Risk factors  Comprehensive neuro exam – Canadian neurologic scale or HIHSS, and. GCS cognition, motor ability, cranial nerves, sensation, proprioception, cerebellar function, deep tendon reflexes Diagnostic Tests  CT or MRI essential – determines if the stroke is  Need diagnostic to know what kind of stroke – treatment depends on the type of stroke o Ex. Can’t give blood thinners if hemorrhagic as it will worsen the bleed  CT o Quick – should be completed in 25 mins and read in 45 mins from time of ED presentation o Often done serially o CTs often done serially – monitored over time o Based on whether the area of ischemia is increasing or staying the same o If it is increasing, do CTs serially  MRI o Shows extent of brain injury o More specific for site of lesions/blockage o MRIs are difficult to get in some places and also take longer  CBC – hemoglobin and platelet counts  INR/PTT – clotting times before initiating antithrombotic  Other brain studies o CTA  o MRA o Cerebral or carotid angiography o Digital subtraction angio - less contrast dye and less vascular manipulation o Transcranial doppler ultrasonography - measures velocity of blood flow  For cardiac assessment o Electrocardiogram o Chest x ray o Cardiac markers o Echocardiography Interventions: Thrombotic Stroke – Medical management  Fibrinolytic therapy – tPA – tissue plasminogen activator o tPA is a naturally occurring endothelial protein that we already have in our blood – breaks down clots o converts plasminogen to plasmin – enzyme that breaks down clots o can dissolve a clot with –hours o door-to-needle time ---mins o must be screened: many contraindications o risk of “delayed” bleed 7-10 days after admin o no anticoagulants or antiplatelet medications admin  Anticoagulants o Heparin, enoxaparin, aspirin (ASA), Plavix (clopidogrel) o Do not dissolve clots but prevent new ones o Never give to a pt who has hemorrhagic – will cause even more bleeding and possibly death Interventions: Thrombotic Stroke – surgical management – endovascular treatment  No antiplatelet or anticoagulant medication  Once confirmed, treatment is surgical o AVM – surgical resection or radiotherapy  o Aneurysm – clipping or coiling  Clip – cut it off (similar to aaa)  Coil – metal coil into lumen of aneurysm, then thrombus forms in the aneurysm coils and it becomes sealed off from the vessel; an endothelial layer develops to wall off the aneurysm more o If IICP or large bleed – craniotomy to remove pressure  High risk of vasospasm o Calcium channel blockers, IV milrinone (vasodilation)  May go through vessel but can also go through brain tissue, skull (this will relieve pressure) Acute Stroke Interventions  Manage increased ICP o Osmolar diuretics – Mannitol, glucose By increasing the osmolality of blood, fluid may be drawn  from the brain  Excess fluid will be urinated out  Overuse may cause severe electrolyte imbalances and result in seizures o Loop diuretics – Lasix Loop diuretics Inhibit resorption of water and sodium in the  kidneys  Manage serum osmolality o Avoid fluid overload or using hypo-osmolar solutions (D5W)  Can worsen intracranial pressure o 0.45% or 0.9% normal saline preferred o Keeping clients moderately dehydrated can be beneficial to reduce cerebral edema  Monitor vital signs  Monitor urine output  Elevate head of the bed o Maintain elevation 25-30 degrees with a midline position Complications   If symptoms are recognized early and treated appropriately, clients can recover with rehabilitation  Clients may have residual deficits – may be transient or permanent o Monitor deficits resulting from unilateral weakness or paralysis o Dysphagia o Incontinence o Aphasia o Cognitive/ behavioural changes o Sensory perceptual deficits Nursing Diagnosis  Decreased intracranial adaptive capacity  Risk for aspiration  Impaired physical mobility  Impaired verbal communication  Unilateral neglect Nursing Management: Planning  Goals include: o Maintain stable or improved level of consciousness o Attain maximum physical functioning o Maximize self-care abilities and skills o Maintain stable body functions o Maximize communication abilities o Avoid complications of stroke o Maintain effective personal and family coping  Respiratory o Management is priority – secure airway, effective breathing pattern o Risk for complications – pneumonia, atelectasis, obstruction o May require intubation & ventilation  Cardio o Monitor VS and cardiac rhythm o Monitor intake and output; adjust intake on pt needs with care team  o Monitor IV fluids o High risk for dvt  Musculoskeletal o Maintain optimal function – ROM and PROM o Prevent joint contractures  Integumentary o Susceptible to breakdown from loss of sensation, immobility, and decreased circulation  GI/GU o Constipation very common, often prescribed stool softeners +/- (psyllium fiber; physical activity beneficial o Support adequate fluid intake o Poor bladder control in acute phase o Avoid long-term use of indwelling catheters, support bladder retraining  Nutrition o Require early assessment/intervention o May need IV fluids and electrolyte replacement o Nutritional replacement common o Integrate RD & SLP if possible o Swallowing assessment essential  Test swallowing, chewing, gag reflex, and pocketing before beginning oral feeding  Test swallowing with water (thickened, if needed)  Ensure pt is in high-fowlers position  Engage in good oral care after eating  Coping o Emotional, social, and financial coping o Integrate SW if possible o Role changes  Communication o Assess ability to speak and understand  Sensory-perceptual changes o Vision change common – diplopia, ptosis, loss of corneal reflex, homonymous hemianopsia Week 9 – Vascular Disorders Peripheral Artery Disease  atherosclerosis causing thickening, narrowing the arteries  Seen in the bigger vessels – aortoiliac, femoral...  Starts to develop younger but symptoms become more prominent in older age  With diabetes, the lower structures are impacted  Thickening of arterial walls, resulting in a narrowing of arteries o Aortoiliac, femoral, popliteal, tibial, peroneal  Associated with CAD  Etiology & Pathophysiology o Leading cause: atherosclerosis  atherosclerosis  Fatty deposits in vessel walls  Fatty streak  Pro-inflammatory markers (like cytokines)  Start of coagulation cascade – coagulation markers  Fatty streak turns into plaque, clots form on plaque  Starts to develop at a young age. Don't see signs until the vessels are significantly occluded o Thickening of intima & media layers o Inflammation and endothelial injury contribute o Symptoms when artery is --% occluded o Risk factors: Smoking, diabetes, uncontrolled hypertension, hyperlipidemia  Others: age family hx, hyperuricemia, obesity, sedentary, lifestyle, stress, hyperhomocysteinemia o Prevention  Lifestyle – diet (reduce saturated fats, increase fiber, reduce LDL cholesterol and increase HDL), exercise  Diabetes impacts vessel walls with hyperglycemia – development of plaques sticking to the sugary vessels or the lumen of hyperglycemic vessels, causing plaque and clotting   Hyperhomocysteinemia – amino acid used to build up proteins  Clinical manifestations o Dependent on site, extent of obstruction, availability of collateral circulation  Collateral circulation - Obstruction or not enough blood flow from a vessel, requiring creation of new vessels to bypass the obstruction. Feeds the parts not getting enough blood and oxygen  Often seen in lower vessels  Feet at more risk because they are more distal and they have smaller vessels o Intermittent claudication “leg attack” – about 10% of patients  Aortoiliac – glutes/thighs  Femoral & or popliteal – calf o Appearance and integrity of limbs o Paraesthesia – unaware of the extent of lower body injury  Reduced blood flow to nerves for normal sensation – tingling, numbness  Risk for injury (pressure injuries, poor fitting shoes) and infection o Pallor o Pain at rest o Thickened toenails Happen when toes aren't getting enough flow  Thick and yellow  Can be better seen in patients with darker skin tone (not as  easy to see other symptoms) o Sometimes elevating the limb prevents blood flow to the feet Critical lower limb ischemia  Diagnosed with 2+ weeks of chronic ischemia rest pain  PAD often develops slowly – prolonged ischemia of skin & muscle  atrophy  Decreased arterial blood flow can cause delayed wound healing o Arterial ulcers, difficulty healing o Infection, necrosis, gangrene  Blood flow so compromised that the tissue/limb (lower) begins to die (become ischemic)  Ischemia can spread - develop into necrosis and spread proximally  Necrosis --> infection which can then spread easily through the bloodstream  Diagnosis o Doppler US with duplex  Duplex – looks at flow throughout the vessel  Not usually done by nurses, more advanced o Manual Doppler does not replace palpation of a pulse o Segmental BP o Ankle-brachial index o CT angiography  Prevention o DM & atherosclerosis (CAD, PAD) = increased risk of CV event o Risk factors modification  Aggressive management of LDL  Lifestyle modification  Smoking cessation  Optimal BP control  Optimal glycemic control  Reduce Na intake  DASH diet o Pharmacologic interventions o Exercise – slow & progressive  Formal & supervised  At home – walking  Treatment o Conservative  Protect from trauma  Decrease pain  Prevent infection  Promote perfusion  There may be contraindications, comorbidities o Revascularization  Surgical, endovascular  Percutaneous transluminal angioplasty + stent  Atherectomy  Endarterectomy o Peripheral artery bypass graft   Most common  Graft with autogenous or synthetic  Creates a bypass around the lesion  Saphenous vein is often used  Take another vessel (often peronial or poplitial), find area of blockage, create a graft to bypass the place of blockage  Interventions o Assess hx & risk factors  Hx, DM  Tobacco use, exposure second had smoke  Hypertension, hyperlipidemia, hypertriglyceridemia  Hyperuricemia, impaired renal function  Obesity, sedentary lifestyle  Increased CRP, homocysteine  Family hx  Stress o Assess for clinical manifestations - Changes in colour, sensation, warmth o System assessments  Cardio – PP – palp vs doppler, temp/cap refill, bruits  Neuro – decreased O2 delivery to brain  MSK – sensation, movement of limbs  Nursing intervention Post-operative o Monitoring – Q15 min, then q1h o Pain management o Monitor perfusion and bleeding o Avoid knee flexion o Ambulate POD #1 o Avoid sitting with legs down - Blood pooling, edema, poor return to heart o May use graduate compression stockings o Monitor for infection o VS  Just manipulated blood vessels  Risk of bleeding (drop in BP, increased HR, etc.)  Be cautious with positioning - flexion Venous Thrombosis   Thrombus formation – associated with inflammation of vein  Most common vein disorder  Superficial or deep  Venous thromboembolism – VTE: spectrum of DVT or PE  Can reduce blood return to the heart. Blood in the veins decreases and can pool, clot Etiology: Virchow’s Triad  Venous stasis: dysfunction values, inactive muscles o Obesity, CHF, afib, pregnancy, long inactive periods  3 main factors that can cause venous thrombosis  Specifically abdominal obesity can slow movement in the lower extremities  Endothelial damage o Direct – surgery, trauma, intravascular cannulation o Indirect – chemo, vasculitis, diabetes, sepsis, Hyperhomocysteinemia o Stimulates platelet activation & initiates coagulation cascade o Can disrupt vessel's ability to function normally o IV causes vessel disruption o Vesicant drugs – drugs that are hard on vessels (like chemotherapy or vancomycin which has an abnormal pH that can be hard on vessel walls)  Hypercoagulability of blood o Blood more likely to clot o Many disorders and medications predispose hypercoagulation state o Smoking o Some autoimmune diseases, pregnancy, smoking o Recruitment of clotting factors throughout the body, leading to development of clots  Pathophysiology o Localized platelet aggregation & fibrin entrap RBCs, WBCs and platelets  create thrombus  Frequently formed on valves as venous stasis often occurs here  o As the clot increases, more blood cells collect and create a tail that occludes the vein lumen o If a thrombus partially occludes a lumen, it is often covered by endothelium and the thrombotic process is stopped o If the thrombus does not become attached, it will be lysed OR it becomes organized and adherent to vessel wall in 5-7 days  Organized thrombi can detect and cause emboli  Turbulent blood flow is a factor in the detachment – can move through venous circulation to heart and lodge in pulmonary vasculature: PE o Thrombus tail  Flaps around with turbulent blood flow  Can break off easily and become an embolism, travel to other parts of the body o Endothelium can engulf the thrombus. When that doesn't happen, the tail moves with turbulent blood flow, breaks off, embolism o More turbulent blood flow can be caused by plaque build-up, damage to the walls (like an IV catheter), where vessels split (blood becomes more turbulent where it's trying to split), sugar in hyperglycemic patients Superficial Vein Thrombosis  Palpable, firm, cord-life structure vein  Area may be tender, warm and rubor  Possible – mild fever, mild leukocytosis, edema  Common cause: IV cannulation o Small vein, caustic med, IV longer than 48 hr  Risk factors o Increased age, pregnancy, obesity, malignancy, estrogen treatment, recent sclerotherapy, long distance travel, chromic venous insufficiency, hx of VTE, SVT  Interprofessional Care o US to confirm diagnosis – and rule out DVT o If IV – related  Remove IV  If related to IV med/solution – warm compression, elevate, oral NSAIDs  (systemic anticoagulation NOT indicated) o If the lower extremity or in greater saphenous or near saphenofemoral junction – LMWH or unfractionated heparin, then warfarin o Wear compression socks/bandages, mild exercise o Typically patients don't need long-term system anticoagulation (heparin infusions) - may need prophylactic heparin dosing  Clinical manifestations o Unilateral edema o Tenderness with palpation o Dilated superficial veins o Sensation of fullness in leg o Paresthesia o Warm skin o Fever o Homans sign – positive  Flex foot – pain in deep calf: also reproducible with squeeze  Conflicting opinions for its use  thrombus to break off o Not palpable o In arm (brachial vein) caused by PICC line o Leg feels "heavy" - fullness o Squeezing can cause thrombus to break off Thrombosis T – trauma H – hormones, OCPs R – road traffic accidents O – operations M – malignancy B – blood disorders, polycythemia O – orthopedic surgery/old age S – serious illness I – immobilization S – splenectomy DVT Complications  Post thrombotic syndrome – from chronic venous hypertension from vein wall and valve damage (acute inflammation)  vein valve damage, outflow obstruction (blood to the heart) o Symptoms – pain, heaviness, swelling, cramps, pruritic, paresthesia, “bursting” pain with exercise, venous claudication o Signs – persistent edema, hyperpigmentation, eczema, secondary varicosities, lip dermatosclerosis o Advanced stages – venous ulcers Venous ulcers are often darker, larger in size – from lack of  good blood return to the heart, blood starts to pool o Symptoms usually within 2 yr of VTE  PE  Phlegmasia cerulea dolens – rare o When toes get swollen, cool, edematous and become bright blue in colour o Pooling isolated to the toes  Interprofessional care o Prevention and prophylaxis is key – all hospitals in Canada should have thromboprophylaxis policy o Early ambulation Bedrest – turn and reposition; passive and active lower  extremity ROM  If ambulating – up for meals, ambulated 4-6x/day  Educate pt and family o Graduated stockings  Increased blood low velocity, prevent vessel dilation, improve valve function, and stimulate endothelial fibrinolytic activity  No wrinkles  Must be worn properly  Preventative only – do not wear if VTE  o Sequential compression devices  Inflatable, wrapped around legs  Apply external pressure  Must be worn continuously at rest  Can be used with other measures – anticoagulation, stockings  Pharmacologic Care o Goals – prevent clot formation – prophylaxis If clot known, prevent new development, prevent spread, prevent embolization o 3 major drug classes  Vit k antagonists – long term use  Requires INR monitoring, med must be taken at the same time each day  Dietary considerations – minimize foods with vit k  Thrombin inhibitors  Indirect – heparin, LMWH (enoxaparin) o Heparin-induced thrombocytopenia is a risk – requires CBC monitoring o Heparin: IV/SC – frequent aPTT monitoring with IV), LMWH: SC less monitoring needed  Direct – dabigatran, Hirudin Derivatives o Bind directly to thrombin, no plasma protein or platelet interactions o Continuous IV infusion, SC or oral – depending on med o No antidote  Factor Xa inhibitors – rivaroxaban, apixaban  Produced rapid anticoagulation  Used for VTE treatment and prophylaxis  No coagulation monitoring needed  Factor VII as antidote  Intervention: HIT - Heparin-induced thrombocytopenia o Check lab values for target therapeutic levels, inform MD/NP if outside target o Evaluate lower extremity for ecchymosis/hematoma development if intermittent compression is being used o Check platelet for signs of HIT  o Monitor for bleeding (urine, stool), emesis, sputum, epistaxis & bleeding gingivae, excessive menstrual bleeding o Inspect skin frequently especially under splints, etc for signs of bleeding, oozing or visible bleeding from trauma or surgical incision o Fall risk assessment and prevention o Clotting and bleeding cascade simultaneously o The diagnosis of HIT is based on three criteria:  1) The patient is receiving or has had recent exposure to UFH or LMWH.  2) At least one clinical feature of the syndrome is present (significant fall in platelet count, new venous and/or arterial thrombosis).  3) There is laboratory evidence of HIT antibodies Anticoagulation therapy for VTE – prophylaxis  Consider – is the pt bleeding? o How big is their risk of developing VTE  Low – likely not a surgical pt  Med – general, gynaecological, urologic surgery  High – trauma  What other diagnoses does the pt have?  Treatment o Initial treatment  LMWH, unfractioned heparin, or fondaparinux  Overlap with warfarin, for at least 5 days or until the INR is 2.0 or higher for 24 hrs o Pt with one or more comorbidities, complex medical issues or a very large VTE are hospitalized for treatment o They usually receive IV unfractioned heparin o Depending on the extent of the clot, pts can be managed safely an effectively as outpatients  Medication interaction alert o Pts taking anticoagulants should avoid taking ASA, NSAIDs, fish oil supplements, garlic supplements, certain antibiotics and ginko biloba Thrombolytic Treatment for VTE  Given via catheter  Directly dissolves clot with thrombolytic drug  Can reduce symptoms and improve venous flow  May reduce valvular reflux and decrease post thrombotic syndrome  Post-thrombotic syndrome (PTS) is a venous stress disorder that develops from long-term effects from a previous deep venous thrombosis (DVT). The morbidity associated with PTS may be significant and patients can present with edema, chronic pain, swelling, skin changes, and heaviness of the affected limb Surgical therapy for VTE  Mechanical thrombectomy  VC interruption devices – IVC filter o Venous congestion o Used with PE, proximal leg VTE with bleeding  Placed in body through catheter femoral vessels, fed into IVC, catches emboli/travelling clots before they go into the heart  Can become clogged with clots, needs to be replaced Management of VTE  Assess for risk factors – subjective data o Prolonged rest/immobility, medications, surgery, IV cannulation, central venous catheter, pregnancy, heart failure, coagulation disorders  Physical assessment – objective data o General – fever, anxiety pain o Integ – increase size of limb, shiny, warm, erythematous, tender o Cardio – warmth & distention in superficial veins, edema, cyanosis of extremities – neck & back if superior VC involved  Lab results o Leukocytosis, abnormal coagulation, increased hematocrit, increased RBC, d-dimer positive  D-dimer – protein fragment your body makes when clot dissolves  Considerations o Minimize venipuncture o Use small gauge needle for venipuncture and apply manual pressure to venipuncture sites for at least 10 minutes o Avoid IM injections  Increased risk of bleeding o Risk of bleeding is greater Pt on LMWH or unfractionated hep with gastro-duodenal ulcer, prior bleeding hx, thrombocytopenia, hepatic or renal failure o Assess pt for mental status changes  Especially in older pt – cerebral bleeding  Routine care & pt teaching o Avoid straining to have a bm o Apply stocking devices properly and as ordered o Protect the skin – moisture, and use paper tape after venipuncture o Avoid disruption of established clots – do not rub or massage the area o Avoid restraints if possible o Pt should not forcefully blow their nose o Avoid restrictive clothing o Electric razor only o Soft tooth brush or mouth swabs o Reposition and provide care in a gentle manner  Ambulatory & home care o Focus on modification of VTE risk factors  Compression stockings – pt cannot be measured for “everyday” compression stocking until edema has resolved  Wear for 2 years post VTE  Monitoring and following through with lab checks and values  Take meds as prescribed  Encourage smoking cessation, stop using birth control or hormone replacement, avoid stting or standing in motionless, leg dependent position o If pts are planning to travel, LMWH may be recommended before hand Pulmonary Embolism  Blockage of pulmonary artery by thrombus, fat, air, tumor, infective vegetation, amniotic fluid  Thrombus material that travels through the venous circulation to the heart and into the narrowing blood vessels until it blocks alveolar perfusion  Most arise as DVT in legs o Also: R heart (afib), upper extremities – packing wires, central line), pelvic veins (birth or surgery) o Lethal Pes from femoral or lilac vein  30 % morality  Decrease to 6-8% mortality with treatment  Risk factors o Immobility or reduced mobility o Surgery within the past 3 months o Hx of DVT o Malignancy o Obesity o Oral contraceptives & hormone therapy o Cig smoking o Prolonged air travel o Heart failure o Pregnancy o Clotting disorders  Signs and symptoms o “classic” traid – occurs in about 20% of pts  dyspnea  Hemoptysis  Chest pain o Slow or sudden onset o Mild-moderate hypoxemia is common – measured with ABG o Cough, pleuritic chest pain, crackles, fever, louder pulmonic heart sound, altered mental status o May have ECGs changes  Clinical Manifestations – symptoms typically related to size of emboli  o Small emboli – often undetectable unless underlying heart disease – causes severe cardiac compromise o Medium emboli – pleuritic chest pain, dyspnea, slight fever, productive cough, with blood-streaked sputum, pleural friction rub, tachycardia o Large emboli – abrupt hypotension, pallor, fever, dyspnea, hypoxemia, possible chest pain  ECG changes – tachy, RV strain  Morality with symptoms ~10%  Complications o Pulmonary infarction when:  Occlusion of a medium or large vessel (>2cm diameter)  Insufficient collateral blood flow from bronchial circulation  Pre-existing lung disease o Many small emboli cause a decrease in capillary bed and pulmonary hypertension – avoid 50% of pulmonary bed involved  Diagnostics – Spiral CT o Ct scan with contrast o Contrast is required to view the blood vessel s o Pt must have IV asses to give the contrast – dye o If pt cannot have contrast a ventilation – perfusion (VQ) scan is done  VQ – perfusion and ventilation  Two components – most accurate when both are performed  1. Perfusion scanning involves IV injection of a radioisotope. A scanning device images the pulmonary circulation  2. Ventilation scanning involves inhalation of radioactive gas. Scanning then reflects the distribution of gas through the lung o D-dimer o Pulmonary angiography o ABG o CXR o ECG changes  Interprofessional care o Prevent PEs – early ambulation post-op, prophylactic anticoagulant in hospital  o Treat as soon as PE expected  Prevent further growths or multiplication of thrombi  Prevent thrombus from entering pulmonary vasculature  Provide cardiopulmonary support if needed o Turn and reposition, DB&C, spirometry o Oxygen if needed o Intubate if needed o Shock – vasopressors, IV fluids o Treat pain  Pharmacologic therapy o Fibrinolytic drugs Tissue plasminogen activator (tPA) or alteplase (Activase)  Dissolves the PE and the source of the thrombus in the pelvis or deep leg veins  Given when pt with a PE is hemodynamically unstable, and has R ventricular dysfunction  Treatment should begin immediately  Pt should receive properly managed anticoagulant therapy to prevent further emboli o Heparin Prevents future clots but does not dissolve existing clots; need to identify what has caused clots to decide the future plan of care  Pts need to be closely monitored (aPPT levels) o Warfarin  Taken for 3-6months  Surgical treatment – Embolectomy  Required if the pt does not respond to conservative therapy, embolectomy, may be required  Rare procedure – 50% mortality rate  If a pt has this procedure a vena cava filter is also placed PE Nursing considerations  Prevention -same as VTE  Acute interventions o Bed rest, semi flowers o Iv access  o Know ADE of meds o Oxygen as needed o Carefully monitor VS, cardiac dysrhythmias, SPO2, ABGs, and lung sounds o Lab results o Assess to complications of anticoagulation therapy & PE o Assess fall risk o Assess and treat pain and anxiety – can experience a “sense of doom”  Home care o Recognizing any comorbidities – if any exist – and their thrombo- embolic disease o Teaching regarding a long-term anticoagulant therapy & the importance of attending follow up ppts  Emotional support o Pt and family Week 10 – Inflammatory heart conditions and basic ECGs Endocardium -inner lining of the heart Myocardium - middle layer of the heart Pericardium - outer layer of the heart Pericardial cavity - fluid for lubrication to pump and move without friction Infective endocarditis (IE)  Infection of the endocardium and or cardiac valves  4 categories o L side native valve - valves which you are born with o L side prosthetic valve - implanted in your body o R side – VDU, wires o Intrathoracic and IV devices  R sided endocarditis is more common than L side in people who use drugs  Etiology & Pathophysiology o Infective organism enters the bloodstream or enters the heart directly o Blood flow allows for the accumulation of organisms to infect the heart and or valve surface o Previous cardiac conditions  Previous endocarditis  Prosthetic valves - more likely to have organisms build up on them than native valves  Rheumatic heart disease o Non-cardiac conditions  Recreational IV drug use – more likely if skin infection or non-sterile needles  the drug itself does not typically cause the infection to occur but rather the non clean equipment or infection at injection site  Hospital-acquired infections – bacteremia o Procedure-related risks  Pacemaker insertion, implanted defibrillator wires, cardia catheterization  Recent dental, urological, gynecological, surgical procedures  Poor oral hygiene Infective Endocarditis (IE)  Clinical Manifestations o Non-specific, multi-organ  Chills, weakness, malaise, fatigue, arthralgia, back pain, abdominal discomfort  Low grade fever - 90% of pts  Heart murmur – 80% of pts o Joint pain, muscle aches, back pain, abdominal discomfort, weight loss, headache, heart failure o Splinter Hemorrhage – commonly seen, but also common it its with endocarditis o Osler’s nodes – bulging in the fingers from blood vessel osculation o Janeway’s lesions – small flat, painless or hemorrhagic spots o Roths spots – clot or change behind the eye Clinical Manifestations of Emboli  Left side  o Spleen – splenomegaly (big spleen), abdominal rigidity, pain in LUQ o Kidney – flank pain, hematuria, azotemia (build up of N) o Brain – hemiplegia, ataxia, aphasia, vision changes, decreased LOC o Limbs – gangrene  Right sided o Lungs – pulmonary embolism Diagnostics for IE  Through health hx o Recent surgery or delivery o Recent IVDU o Valvular or congenital heart disease o Presence of prosthetic valves o Recent infection – skin, resp, UTI o Recent cardiac catheterization  Blood cultures – essential for diagnosis o At least, two sets, 60 min apart o Keep for 3 weeks if no growth  Blood work – to identify bacterium, 60 mins apart – sometimes it takes a while for the pathogen to grow o Leukocytosis – increased leukocytes o Elevated CPR o Elevated ESR  Imaging o Echocardiogram – especially if blood cultures are negative and there is a high suspicious of IE  Looks at how the heart is able to pump out blood (Valve functioning) and shows if there’s anything on the blood  TEE can visualize vegetations  Two types  Transthoracic – put a probe on your chest  Transesophageal – put a probe down your esophagus to look at the heart o More detailed and is closer to the heart  o Less common o Chest x – ray – cardiomegaly – enlarged heart  ECG – valves lay in proximity to cardiac tissue o Can observe dysrhythmias and cardiac complications – seeing if theres structural changes to the heart Treatment for IE  Prophylactic antibiotics – before dental surgery or surgical procedures if high – risk  Anti-infective treatment – identify organism from blood cultures, treat with appropriate anti-infective  Treatment often long-term (4-6 weeks) o Often hospitalized for IV anti-infectives o Repeat blood cultures to assess effectiveness of treatment o Monitor therapeutic closing, renal function, ototoxicity with some anti-infectives  Valve replacement  Fever – ASA, Tylenol, fluids, rest  Bedrest not indicated unless HF present Nursing Assessment & Diagnosis – IE  focused cardiac assessment – murmus  MSK – arthralgia  GI – oral mucosa  Integ – conjunctive, skin, limbs  Nursing diagnosis o Decreased cardiac output o Activity intolerance Treatment goals of IE 1. Obtain normal or baseline cardiac function 2. Perform Adls without fatigue 3. Gain knowledge of the therapeutic regimen to prevent reoccurrence of endocarditis  Teach pt and family to recognize signs and symptoms of life-threatening complications of IE:  o Cerebral emboli – change in LOC o Pulmonary edema – dyspnea o HF – chest pain, increased SOB Nursing Interventions – IE  Identify individuals who are at higher risk for developing IE & provide health teaching on how to prevent IE – reoccurrence  Monitor VS frequently – fever  If pt uses IV drugs recreationally, support with withdrawal/treatment  Assess heart sounds – murmurs and general system assessment  Monitor lab and diagnostic tests findings  Monitor for complications, treat URTIs quickly, support good nutrition  Collect blood cultures and administer antibiotics  Pt may be candidate for PICC line due to length of antibiotic therapy Acute Pericarditis – outside sac of heart  Pericardium consists of o Visceral pericardium o Parietal pericardium o Between is pericardial space – 20-30mL of fluid  Purpose to o Anchor the heart o Provides lubrication o Prevents excess dilation  Pericarditis – inflammation of the pericardial sac  5% of people in ED with chest pain have pericarditis  Etiology o High – income countries – idiopathic  Unknown why o Low -income countries – TB  Tb is endemic in lower income countries  Less access to healthcare  Poor-living together – more people living closer together o Viral – coxsackievirus B o Post MI – 48-72hrs  o Dressler’s syndrome o Cancer o Trauma o Reaction to medication  Pathophysiology o Inflammatory response o Influx of neutrophils, monocytes, macrophages o Increase in pericardial vascularization – increased blood flow o Pericardium becomes hyperemic o Fibrin deposits on the visceral pericardium – the characteristic pathological finding  Clinical manifestations o Progressive and severe chest pian – sharp and pleuritic o Worsening chest pain when supine & with deep inspiration  Radiate to neck/arms/shoulder  Also to trapezius – unique to pericarditis o Dyspnea o Pericardial friction rub  scratching, grating, high-pitched sound  Caused from friction between pericardial and epicardial surfaces  Heard at lower L sternal border when pt is leaning forward  Sometimes hard to differentiate with pleural friction rub  Complications o Pericardial effusion – accumulation of fluid in pericardial sac  Large – can compress adjoining structures  Lungs – cough, dyspnea, tachypnea  Phrenic nerve – hiccups  Laryngeal nerve – hoarse voice o Tamponade – as effusion grows, increased pressure and compression on heart  Muffled heart sounds, jugular vein distention, decreased cardiac output  Pulses paradoxus – decreased SBP with inspiration  Diagnostic tests o Chest x rays – cardiomegaly o Ecg changes – diffuses st elevation  Key for diagnosis if present   Present if 90% of pts with pericarditis o Echocardiogram o Pericardial biopsy o Pericardiocentesis  Interprofessional care o Determine cause  If bacterial – give antibiotics o Chest pain and inflammation  Given NSAIDs and colchicine  Steroids if not responsive – last resort o Pericardiocentesis to remove fluid if indicated  High risk procedure  Guided by US and ECG  Done in acute tamponade  Stop anticoagulants – if currently taking them  Nursing interventions o Assess and treat pain and anxiety – trapezius sharp, worse with inspiration o Keep HOB at 45-degree angle o Give overbed table for support o Admin NSAIDs with food o Monitor ECG o Monitor signs and symptoms for tamponade Myocarditis  Focal or diffuse inflammation of the myocardium  Caused by virus, bacteria, fungi, parasite, radiation, medications, idiopathic o Coxsackie A&B most common in North America  Often occurs with pericarditis o Myopericarditis o Perimyocarditis  Results in cardiac dysfunction and can lead to dilated cardiomyopathy  It is the muscle - the layer that does the work o Thicker than the rest of the layers  Clinical Manifestations  o Early similar to viral illness – fever, fatigue, myalgia, pharyngitis, dyspnea, lymphadenopathy, nausea & vomiting o Early – cardiac – usually 7-10 days after viral infection  Pericardial friction rub, pericardial effusion, pleuritic chest pain o Late – cardiac – heart failure, S3 heart sound, crackles, jugular venous distention, syncope, angina, edema  Diagnostics o Histology – examining a sample of myocardium via endomyocardial biopsy  High specificity o ECG – appears like pericarditis o Blood work – leukocytosis, lymphocytes, elevated ESR & CRP, increased troponin  Collaborative interprofessional care o If the pt also has heart failure Likely needs inotropic and vasopressor medication – ICU  level care  LVAD device – CV-ICU  Medications – similar to HF – beta blockers, ACEs, diuretics, help to reduce preload and volume overload o Immunosuppressive therapy  To reduce myocardial inflammation and prevent damage o Provide oxygen, bedrest, decrease activity o Have emergency equipment on standby  Nursing Interventions o Assess for HF o Assess and manage anxiety o Discuss interventions with pt and family o Recovery is often spontaneous but, may develop dilated cardiomyopathy o If severe HF occurs, may require heart transplant Cardiac Conduction  The cardiac cells in the heart can initiate an electrical impulse that travels through the heart muscle and stimulates its contraction: automaticity  Excitability allows the heart tissue to be depolarized by a stimulus – allows transmission from one cell to the next   SA node  AV node  Bundle of branches (L & R)  Purkinje Fibers  Most electrical impulses occur in the SA node which travels to the AV node  From the AV node the impulse goes to the bundle of branches (left and right) to the Purkinje fibers Electrophysiology of Dysrhythmias  Main pacemaker is SA node – discharge at 60-100bpm  A pacemaker from another area of the heart may discharge IF: o If the SA node is slower than another pacemaker, the other one will discharge at its intrinsic rate  AV node – 40-60bpm  His-Purkinje – 20-40bpm o The secondary pacemaker may discharge faster than the SA node  Early beats  Ectopic foci – somewhere outside of the normal conduction pathway  Ectopic foci - sometimes the impulse may come from the AV node or other areas of the heart - If the SA node is too slow  Every cell has automaticity - every cell can make an impulse Cardiac Cells – Depolarization  The cardiac cell membrane is semi- permeable and allows the concentration of o Intracellular K to be high o Intracellular Na to be low o This is normal  When the cell is at rest, it is negative  When a cell – or group of cells is stimulated, each cell membrane change its permeability o Rapid influx of Na into the cell  cell becomes positive depolarization Cardiac Cells – Repolarization  The ions move back across the membrane to their “normal” state o Repolarization o Occurs a bit more slowly than depolarization  The depolarization and repolarization can be represented in phases  o 0 – rapid depolarization o 1, 2, 3 – repolarization o 4 – polarized resting state  Antidysrhythmic meds impact various phases Understanding the Cardiac Complex  P wave – atrial depolarization  PR interval - spread of electrical acitivity through the AV node, bundle of His, and Purkinje fibres  QRS complex – ventricular depolarization  ST segment – time between ventricular depolarization and repolarization  T wave – ventricular repolarization  QT internal – total time for depolarization and repolarization of the ventricles ECG Monitoring  Graphical tracing of electrical impulses  Waveforms are produced by movement of charged ions across the membranes of myocardial cells  ECG leads are attached to the chest wall o Electrode pad and conductive gel  Types of monitoring – up to 15 leads o Common 3, 5, 12 o 3 & 5 – allow for interpretation of rhythm o 12 lead looks at L vent from 12 angles o 15 lead looks at L vent anteriorly  Rhythm Assessment o must known how to measure time and voltage on ECG o squares are used to calculate HR and intervals to interpret rhythms o paper has large squares (dark) and small squares (light)  large = 25 small squares 5x5  0.5mV high & 0.2s long; 300 large squares is 1 min  small = 1mV vertically, 0.04s horizontally Sinus Rhythm  Sinus – p waves present, p before QRS  Regular – the same distance between P and QRS  Rate between 60-100 Sinus Bradycardia  Conduction is the same path as SR, but the SA node is firing slower than 60bpm  Rate – less than 60  P-wave before every QRS  What does the p-wave look like? – looks normal  Are there spaces between QRS’s equal Sinus Tachycardia  Discharge rate from SA is higher than 100  Can be normal response  Look at waveforms and intervals – normal o Depends on the pt – stress, activity level, pain  Is there significance to this? Pre-Atrial Contraction – PAC  Impulse originates in R atrium, but NOT SA node  Once it reaches the AV node, it can be: o Stopped – non-conducted o Slowed – longer PR interval o Conducted – moved through vent  HR will vary irregular  Isolated PAC not concerning but frequently PACS may need treatment A-Flutter   Saw-toothed flutter wave coming from the SAME (abnormal) area in atria that is not the SA node  Rarely occurs in a healthy heart  Impulses conducted to ventricles in a ratio  PR cannot be measured, QRS usually normal  Decrease in CO (no atrial kick — atrial filling time decreased) Atrial Fibrillation  Most common dysrhythmia in ED; 1-2% of Canadians have Afib  Many ectopic foci in atria  Cannot see P wave, or calculate PR intervals  Atria fibrillating (shaking)  QRS usually normal Atrial Fibrillation and Stroke  Loss of atrial kick — the contraction of atria that moves blood into ventricles  Without this, CO is decreased as less blood is moving through the heart  Some blood will stay in atria — increased risk of clotting o 3-5x increased risk of stroke  Patients need anticoagulant therapy if >48h in Afib o Must be on anticoagulant for 3-4 weeks prior to cardioversion Synchronized Cardioversion  Used to treat unstable tachycardias  Synchronizes the delivery of the energy ("shock") with the R wave of the QRS complex  Operator must remember to synchronize the machine o Press a button on most machines  Lower energy needed (usually)  Patients are usually awake o Nursing considerations? Ventricular Fibrillation  Severe derangement of cardiac rhythm o Multiple ectopic areas in ventricles  Ventricles quivering/fibrillating  NO ventricular contraction = NO cardiac output  Death imminent without treatment  o treatment is defibrillation Defibrillation  Passage of electric current through heart to depolarize cardiac cells  Repolarization allows for SA node to take over as pacemaker  CPR immediately after  Can be done with: o manual device (in hospitals)  Require a clinician to interpret the rhythm and deliver shock o Automatic device (AEDs in hospital and in community)  Have rhythm identifying capability to support user Asystole  Absence of cardiac activity  Patient will be unresponsive, pulseless, and apneic  Immediate treatment: CPR Pacemakers Electronic device used to stimulate heart when normal pathways are damaged or diseased Can be temporary or implanted Impulse travels from pacemaker, through leads, to myocardium when the impulse is "captured" by the heart, and the heart is stimulated to contract Can pace atria and/or ventricles Most are "demand" pacemakers o Sense the heart's electrical activity and fire when the heart drops below a specified rate. o These pacemakers have:  A sensing device to inhibit the pacemaker from firing if its not needed  A pacing device that will trigger the pacemaker if there is no impulse during a preset timeframe Pacemaker Use  Traditionally for bradycardias  Now used for tachycardias — will pace the atria very quickly to override an atrial tachycardia (AF or Aflutter)  Pacemaker is implanted over the pectoral muscle on the non-dominant side  Temporary pacemakers are used in emergency settings  Power source is outside of the body  o Transvenous — leads threaded to R atria and ventricle, used until permanent PM can be inserted o Epicardial — used in surgery, leads are passed through the chest wall to atria and ventricles o Transcutaneous — non-invasive, impulses across chest wall with defib pads Patient Monitoring – Pacemaker  Check ECG to evaluate electrical status  Two common complications: o Failure to sense: PM is not sensing the spontaneous cardiac activity from the patient and fires when it shouldn't o Failure to capture: electrical charge from the PM is insufficient to produce contraction  Also must check for pulse on patient!  Nursing Interventions o After pacemaker is inserted:  Patients may ambulate once rate and rhythm are stable  Check insertion site for bleeding and signs of infection  Avoid movement of arm/shoulder to prevent dislodgement  Provide patient teaching — activity, body image, improvement in functional ability  Encourage patients to check function of pacemaker regularly at PM clinic or home with telephone transmitter devices (if applicable) Weel 11 – Acute Abdomen Abdominal Pain Can be a result of: Inflammation Peritonitis Obstruction Internal bleeding Appendicitis Pancreatitis Cholelithiasis Cholecystitis Trauma Bowel obstruction Ruptured ovarian cyst Ectopic pregnancy Testicular torsion Abdominal aneurysm Peptic ulcer disease  Pain locations Right Hypochondriac – liver gallbladder, right kidney, small intestine Epigastric region – stomach, liver, spleen, adrenal glands Left hypochondriac – spleen, colon, left kidney, pancreas Right lumbar – gallbladder, liver, right colon Umbilical region – umbilicus (naval), parts of the small intestine, duodenum Left lumbar – descending colon, left kidney Right iliac – appendix, cecum Hypogastric region – urinary bladder, sigmoid colon, female reproductive organs Left iliac – descending colon, sigmoid colon Pain assessment O – onset P - provoking Q - quality R – radiating S – severity T – timing U – understanding Assessment and Health Hx  Inquire about: o Changes in weight o Changes in appetite o Nausea &/or vomiting (and quality/quantity/frequency) o Diarrhea/constipation o Abdominal distension o Jaundice o Indigestion (heartburn, dyspepsia) o Use of medications (NSAIDs, antiacids, antibiotics) o Recent abdominal surgery  Physical examination – order is important o Inspection – shape & contour, skin color, umbilicus, movement, presence of stomas  Auscultation o Listen with:  Diaphragm – bowel sounds  Bell – vascular sounds o Start in RLQ and move through all quadrants o Document your findings   Present/absent, increased/decreased (hyperactive/hypoactive), high-pitched, gurgling, rushing o Listen for 2-5 minutes in each quadrant if not immediately heard  Normal -- high-pitched, gurgling  Bruits should NOT be hear  Percussion o To assess for fluid and/or masses o Done lightly over entire abdomen o Normal sounds (air)  Higher-pitched, tympany o Fluid/mass sounds  Short, high-pitched, minimal dullness  Palpation o Done lightly! o Gently press with pads of fingers, approx. 1cm deep o Palpate all quadrants  Leave painful area until last o Can be very helpful for diagnosis Appendicitis  Appendix: o Small, finger-like projection that goes between the cecum (small intestine) and ascending colon (large intestine) o Located in RLQ o Creates mucous which drains into colon  Appendicitis: o Inflammation of the appendix o Occurs when appendix is obstructed o 8% of population, usually between 10-30y  Pathophysiology o Blockage of appendiceal lumen by fecalith, dried mucous, parasites o Inflammation and mucous build-up and hardening o Venous engorgement and invasion of bacteria o Pus forms, pressure in appendix increases o Blood flow to appendicular artery is compromised o Ischemia results, eventually necrosis and perforation – which can cause peritonitis  Clinical Manifestations o Pain is very common (periumbilical)  Continuous, starts in center of abdomen and moves to RLQ  Various ways to assess this pain   Rosving’s sign:  Posas sign:  Obturator sign:  Dunphy’s sign: pain elicited by coughing  McBurney’s point:  Blumberg’s sign: o Nausea/vomiting o Anorexia o Fever  Diagnosis o History and physical exam are very important! o Blood Tests o o o o Radiography/Imaging: o  Treatment and Management o Surgical removal of the appendix – laparoscopic o Pre-op care: antibiotics and fluids for 6-8h before surgery if perforated  No not compression o Post- op care  Vital signs  Assess abdomen  Assess and treat pain  Assess for bleeding (damage to appendicular or cecal artery)  Hydration  Antiemetics  Ambulate (POD 0 or 1) o Health teaching:  Avoid bending, stretching, heavy lifting  2weeks if laparoscopic  4-6 weeks if open surgery  Splint abdo when getting out of bed & coughing  Resume normal activity in:  2-3 weeks if laparoscopic  4-6 weeks if open surgery  Monitor for signs and symptoms of infection The Gallbladder  Located in the RUQ just below the liver  Temporarily stores bile   Attached to the main duct that carries bile from the liver to the intestine  After eating, the gallbladder contracts and bile moves from the gallbladder through the cystic duct and the common bile duct into the small intestine  Bile is used in the small intestine to help breakdown fat Cholelithiasis Stones in the gallbladder Most common disorder of the biliary system Can (often) be asymptomatic 80-90% of all gallstones are caused from bile that is supersaturated with cholesterol Precipitation of cholesterol Cholesterol precipitant remains in gallbladder mucous and forms stones Stones grow and: stay in gallbladder OR pass through ducts where they can lodge and cause an obstruction If obstruction in cystic duct – bile can still flow If bile cannot flow, stasis can cause inflammation Pain is common Severity depends on movement +/- obstruction from stone Signs and symptoms of obstructed bile flow Bleeding Clay-coloured stool Dark amber urine (foamy) Intolerance of fatty foods No urobilinogen Obstructive jaundice Pruritis Steatorrhea Risk factors Female Age – increasing Genetics Diet Sedentary lifestyle Metabolic syndrome Obesity Medication Cholecystitis  Commonly associated with cholelithiasis Inflammation of the gallbladder Can be acute or chronic Acute: gallbladder becomes edematous and hyperemic, then distended from bile or pus Cystic duct is occluded Wall becomes scarred Decreased gallbladder function if large amounts of tissue become fibrotic Clinical Manifestations Inflammatory No pain to severe pain “indigestion” Biliary colic from stone moving through ducts (or lodged in duct) Acute pain in RUQ which refers (radiates) to R shoulder/scapula Symptoms usually 3-6h after fatty meal Fever Jaundice Restless Nausea and vomiting Diaphoresis Leukocytosis Positive Murphy’s sign Diagnostics History and physical assessment Ultrasound (CT if no result from U/s) ERCP Endoscopic retrograde cholangiopancreatography Visualization of gallbladder, cystic duct, hepatic duct, bile duct Can obtain samples of fluid (bile) and/or remove stones Bloodwork LFTs, CBC (WBC), bilirubin, urinary bilirubin Amylase and lipase Complications Acute cholecystitis From cholelithiasis Cholangitis Acute pancreatitis Sepsis Peritonitis Rupture of gallbladder Treatment – Cholecystectomy  Laparoscopic surgery Over 90% of cholecystectomies Abdo inflated with CO2 to visualize structures 4 small puncture holes Forceps enter via puncture hole, retract and resect gallbladder Contraindicated if cholangitis, gangrene, perforation, portal hypertension, bleeding disorders Open surgery Incision through skin and abdominal wall Bile duct is also explored, stents are often placed Improves patency of duct and supports drainage of bile uncommon Nursing interventions after laparoscopic cholecystectomy Monitor breathing, vitals (standard post-op) Manage pain, nausea, vomiting Referral pain to shoulder may occur Place in sims position Encourage flatus Monitor return of bowel sounds Document voiding Health teaching Abdominal Aortic Aneurysm Most common condition affecting the aorta Permanent, localized outpouching or dilation of the aorta Most common location is just below renal arteries between sternum and umbilicus Classification and Shape A true aneurysm is formed in the artery wall and has at least one wall intact Fusiform: Saccular: Etiology and Pathophysiology Atherosclerotic plaques deposited in intimal layer of aorta wall, these cause degenerative changes to the media wall, which causes the aorta to lose elasticity, weaken, and dilate Dilated aortic wall becomes lined with thrombi that can embolize and cause acute ischemic events in distal structures Clinical Manifestations Thoracic AA Deep, diffuse chest pain to interscapular area May be asymptomatic Ascending aorta & aoretic Arch  Hoarse voice, coughing, & dysphagia Angina TIAs Jugular venous distention Abdominal aorta Often asymptomatic and detected on physical exam Bruit in abdomen Pulsating mass slightly L of umbilicus Symptoms dependent on pressure on nearby structures Back pain Abdo pain ”blue toe syndrome” Complications Most severe: rupture! Bleeding may be contained by nearby structures in abdomen Severe retroperitoneal back pain Flank ecchymosis (Grey-Turner’s sign) Leaking into thoracic or abdominal cavity Present to hospital in hypovolemic shock Hypotension, tachycardiac, low urine output, decreased LOC, decrease SpO2 90% mortality rate if blood in abdominal cavity Risk factors Male – 65+ Caucasian Smoking Atherosclerosis Hypertension Hyperlipidemia Genetics Blunt trauma Diagnostic CXR Abdo XR ECG US CT MRI Angio Interprofessional interventions Stabilize pt Surgical repair Open surgical Removes the dilated section of aneurysm in AAA  Replaces and aneurysm with prosthesis (synthetic; sutured in place) Artery wall will cover graft Allows for the flow of blood Patient to ICU for complex monitoring Endovascular (EVAR) Incision in groin (femoral artery) Specialized catheter with stent-graft attached enters femoral artery Dye is injected to guide the catheter & stent-graft to aneurysm Once in place, the stent-graft is unfolded placed against artery wall Blood flows against graft, not dilated aorta wall Nursing Interventions Thorough assessment and history “hands off” if pulsating mass (no palpation) Provide education and support to patient and family Brief description of AAA, pre-op routines, post-op expectations (location, drain, lines, monitoring) Prepare for surgery as per hospital policy Administration of fluids, blood products as indicated Monitor urine output (especially if aneurysm proximal to renal arteries!) Avoid hypertension Avoid prolonged hypotension Monitor for signs of infection Week 12: reproductive problems Ectopic Pregnancy The implantation of a fertilized ovum anywhere outside of the uterus Approximately 3% of all pregnancies are ectopic 98% of ectopic pregnancies occur in the fallopian tube The remaining 2-3% occur in the ovary, abdomen, or cervix Development of ecoptic pregnancy A blockage in the Fallopian tube Anything that slows peristalsis in the Fallopian tube The zygote implants within the fallopian tube wall Gestational sac grows until it spans the tubal wall Sac grows until it causes tubal rupture Tubal rupture acute peritonitis symptoms Less acute symptoms usually appear before this  6-8 weeks after the LNMP Typically, occurs weeks before a rupture would occur Risk Factors for Ectopic Pregnancy PID Prior ectopic pregnancy Progestin releasing IUD Progestin only birth control failure Prior pelvic/tubal surgery IVF procedures Embryo transfer Ovulation induction Clinical manifestations Abdo pain Missed menses Irregular period/vaginal bleeding Morning sickness Breast tenderness GI disturbance Malaise Syncope Emergent clinical manifestations If the fetus continues to grow in the fallopian tube, the tube will rupture With rupture, heavy bleeding in the abdomen is likely, symptoms often include lightheadedness, hypotension, and signs of hypovolemic shock Treated as an emergency Diagnostic tests A serum pregnancy test done If negative: likely not an ectopic pregnancy If positive: ectopic pregnancy could be possible  further testing If the patient is stable, a vaginal ultrasound and β-HCG If no intrauterine pregnancy: Spontaneous abortion (β-HCG will decrease over time) Ectopic pregnancy CBC if concerned about blood loss &/or patient going for surgery Interprofessional Management Surgery Done immediately Conservative approach Limits damage to reproductive system May not be possible if tube ruptures Laparoscopic preferred Medical management  Methotrexate – if stable and fetus is of small gestational size Blood transfusions and IV fluids Interventions Depends on pt condition Before diagnosis – carefully monitor abdo pain and vaginal bleeding Monitor VS – signs of shock Provide education Prep for abdo surgery Monitor emotional wellbeing and provide support Testicular torsion Twisting of the spermatic cord that supplies blood to the testes and epididymis Interrupts blood supply Most common in males under 20y Pathophysiology Testicle rotated around spermatic cord Blocks blood flow to testicle Can lead to necrosis Symptoms Sudden severe pain in scrotum and lower abdo on affected side Swelling and redness Causes Most common – testicle not strongly attached to scrotum at birth Minor trauma around scrotum Less common - Vigorous physical activity or during sleep Treatment Immediate surgical detorsion – ideally within 6hr of symtpoms Outcomes If blood supply is not restored within 6 hr – ischemia Ischemia can cause necrosis of the teste, requiring surgical removal and decrease the ability to have children To preserve testicular function – time to treatment is essential Viability is strong if corrected within 6-8h (Schick & Sternard, 2023) Salvage of the testicle is 24h (Hazeltine et al., 2017) Spermatogenesis impacted after 2h, likely destroyed after 4-6h (Hazeltine et al., 2017) Clinical manifestations  Severe scrotal pain Edema of affected testis and or scrotum Scrotal tenderness N& V Absence of Urinary symptoms Fever WBC or bacteria urine Prehn Sign Diagnostic test to evaluate for testicular torsion Lifting scrotum on the affected side and assess for changes in pain Positive Prehne’s sign: pain goes away Negative Prehne’s sign: possible testicular torsion TWIST Criteria  Testicular swelling – 2 points  Hard testis – 2 points  Absent cremasteric reflex - 1 point  N& V – 1 point  High riding tes tis – 1 point  Score 0-2: Low risk o 100% negative predictive value for torsion o Generally, no ultrasound or urological consultation required  Score 3-4: Intermediate risk o ultrasound warranted  score 5 or above: High risk o 100% positive predictive value for torsion o ultrasound not required, urgent urological consultation and surgery required to salvage testis Other Testicular Torsion Diagnostic Loss of cremasteric reflex Not reliable under 1y Absent on side of edema Doppler ultrasound Collaborative care Surgery ASAP unless torsion resolves spontaneously Must be done to restore blood flow Teste is often surgically attached to scrotum to prevent future torsion Manual Detorsion  The right testicle shows the characteristic medial torsion with elevation and horizontal lie of the testis.  After appropriate sedation and analgesia has been administered, manual detorsion is performed by grasping the testicle and rotating it within the scrotum outward (medial to lateral) one to two full 360 degree turns. prompt relief of pain, lower position of the testis in the scrotum, and return of arterial flow on Doppler ultrasound suggests detorsion. If there is no improvement, try rotating the testicle in the opposite direction (lateral to medial) because approximately one-third of torsed testicles may have lateral rotation.