Week 2 M/S

what is CPR

achieves adequate cerebral and coronary perfusion, compromising a patient’s chances for neurologically intact survival

roles in a code blue

• lead (dr or nurse)

• recording/documentation

• airway

• medications

• compressions/cpr

• energy

• crash cart

• runner

CAB

circulation, airway, breathing

neurological re-check

• LOC

• orientation

• motor function

• pupillary response

abnormal neuro check

• lethargic: drowsy, appropriate but thinking is slow, inattentive

• obtunded: difficult to arouse, confused with aroused

• stupor or semi-coma: only responds to physical stimulation, responds to pain

• coma: completely unconscious, no response to pain

• light coma: some reflex activity

• deep coma: no motor response

glasgow coma scale

• 15 = fully alert and oriented

• 8 or less: endotracheal intubation to protect airway

potential causes of unresponsiveness

• neuro: stroke, seizure, trauma

• resp: pulmonary embolism, resp arrest

• cardio: MI, cardiac arrhythmia, cardiac arrest

• endo: hypoglycaemia

what to do if pt is not responding

establish unresponsiveness

• shout

• trapezius squeeze or pinch

• press on supraorbital nerve (medial aspect of supraorbital ridge)

• angle of the jaw

• *these have a higher yield than the traditional sternal rub & nail bed squeeze

definite pulse and normal breathing

• vital signs

• assess responsiveness

• glasgow coma scale

• bloodwork/imaging test

definite pulse and no breathing

• check pulse

• open airway, bag valve mask

• 1 breath every 5 sec

• pulse check every 2 min

definite pulse + no breathing

• Obstruction

• Inadequate respiratory effort

• Medications

what is SBAR

• non critical: communication related to identified problems

• critical: communication of changes in pt condition

coronary artery disease

progressive atherosclerotic disorder of the coronary arteries that results in narrowing or complete occlusion of 1+ arteries

• affects medium-sized arteries that perfuse the heart and major organs

• progressive buildup of plaque in arteries

types of coronary artery disease

• asymptomatic

• stable angina: at rest there is enough oxygen in blood; when exercise: not enough oxygen in blood → chest pain

• acute coronary syndrome:

  • unstable angina: unable to get enough O2

  • myocardial infarction: begins having damage to heart

  • sudden coronary death

what causes decreased O2 supply

• anemia

• CAD

• hypoxia

• COPD, asthma, pneumonia

• arrhythmias

• CHF

• coronary spasm

• thrombosis

• valve disorders

increased O2 demand/consumption

• anxiety

• cocaine use

• hyperthermia

• hyperthyroidism

• physical exertion

• aortic stenosis

• arrhythmias

• cardiomyopathy

• hypertension

stages of development in atherosclerosis

• fatty streak

• fibrous plaque

• complicated lesion

what does the endothelium regulate

• dilation and constriction of vessels

• thrombosis - formation of blood clots

• transport of substances to and from the vascular space

• growth and apoptosis of vascular wall

endothelial dysfunction

• inadequate vasodilation

• prothrombotic

• altered permeability

• increased secretions growth factors

• increased oxidation of LDL

collateral circulation

ways to bypass clot and get to other side → still able to perfuse

• can happen when fatty plaque happens over time

• woman in menopause can have plaque build up quickly → this doesn’t happen

women and heart disease

• #1 killer of Canadian women

• 10 times more than breast cancer

• manifest 10-20 years later in life than men

why does CAD affect more women than men

estrogen helps counterbalance plaque buildup in arteries

• menopause = less estrogen 

• less likely to build-up collateral circulation

gender differences in symptoms CAD

challenges of care for woman dealing with CAD

• failure to recognize and difficulty interpreting symptoms

• failure of HCP to recognize prodromal symptoms 

• ECG and stress test less sensitive 

• plaque tend to be distributed diffusely 

• less likely to be evaluated for risk factors or treated aggressively 

atypical presentation in the elderly of CAD

• symptoms: SOB, fatigue and weakness, abdominal or epigastric discomfort 

• often have preexisting conditions making this an already vulnerable population: hyperension, CHF, previous AMI 

• likely to delay seeking treatment 

atypical presentation in the pt with diabetes

atypical presentation due to autonomic dysfunction

• neuropathy could cause lack of feeling in chest = lack of chest pain

• common symptoms: generalized weakness, generalized feeling of not being well, syncope, lightheadedness, change in mental status

non-modifiable risk factors CAD

• age

• male > female until 65

• genetics

• ethnicity 

modifiable risk factors major for CAD

• tabacco use 

• abdominal obesity 

• hypertension >140/90 mmHg

• hyperlipidemia 

• physical inactivity 

contributing factors for CAD

• phychological risk factors

• elevated homocysteine levels

• diabetes mellitus

• metabolic syndrome 

who is at low-risk among non-smokers without diabetes 

• total cholesterol 4.7 mmol/L

• untreated blood pressure <120/<80

should be assessed every 3-5 years 

who is at moderate-risk among non-smokers without diabetes 

• total cholesterol 4.8-5.1 mmol/L

• untreated systolic pressure 120-139 mmHg or diastolic pressure 80-89mmHg

ho is at high-risk among non-smokers without diabetes 

• total cholesterol 5.2 to 6.1 mmol/L

• untreated systolic blood pressure 140 - 159 mmHg or diastolic blood pressure 90-99 mmHg

should be assessed every year

major risk factors of CAD

• treated hyperlipidemia or total cholesterol 6.2 mmol/L

• treated hypertension or untreated systolic pressure >160 or diastolic pressure >100 mmHg

• current smoker 

• diabetes 

who should screen for CAD

Men ≥ 40 years of age; women ≥ 50 years of age or post-menopausal)

■ Anyone with the following conditions regardless of age

• Smoker

• Hypertension

• Elevated cholesterol

• Diabetic

• Family history

• Erectile dysfunction

• Obesity

• Inflammatory disease

• COPD

• HIV

initial assessment for CAD

want to do it before medications

• baseline VS and 12 lead ECG → within 10 min 

• assessment of chest pain 

• associated symptoms 

• physical assessment  

• medications

secondary assessment for CAD

• personal and family history

• environment factors 

• psychosocial history 

• pt’s attitudes and beliefs about health and illness 

ECG findings 

goal: complete within 10 min of presentation to ER

• primary diagnostic tool 

• changes in QRS complex, ST segment, T wave → leave ECG leads on to continue to see changes and get worse/better

• dynamic process and evolves over time 

• repeat ever 15-30 min to 2-4 hr 

ECG interpretation

anterior site of the heart

• indicitive: V1, V2, V3, V4

• affected coronary: L anterior descending 

lateral site of heart

• indicative: 1, aVL, V5-6

• affected coronary: circumflex or LAD

inferior site of heart

• indicative: II, III, AVF

• affected coronary: R posterior descending

posterior site of heart

• indicative: reciprocal changes leads V1, V2, V3 

• affected coronary: R posterior descending &/or circumflex 

ST depression

when the ST does not come back to baseline 

• heart is not getting enough oxygen 

• damage is not permanent and there are things that can be done 

ST elevation

caused by more significant lack of oxygen

• can cause an MI 

• if not quickly fixed, can cause permainte cell death 

additional patient complaints or presentations

• difficulty breathing 

• excessive sweating 

• unexplained nausea or vomiting 

• generalized weakness 

• dizziness

• syncope or near-syncope

• palpitations

• isolated arm/jaw pain

• fatigue

• dysrhythmias

assessment of CAD

• 12 lead EKG (within 10 min and repeat q15-30 min)

• cardiac monitor 

• chest x-ray 

• coronary angiography: imaging that see’s blood through coronary artery 

• exercise stress test: increase O2 demand = see changes in rhythm 

• echocardiogram: tells dr motion of heart + how well it is contracting 

• laboratory studies

cardiac angiography

used to assess:

• coronary arteries

• pressures in cardiac chambers

• valve function 

• ventricular function 

stress test 

• ischemia, ST segment changes, Arrhythmia 

• tests functional capacity

• efficacy of medical or surgical intervention

• can also be used as a follow up measure to see improvement

echocardiography

used to assess:

• myocardial structures

• ventricular function: ejection fraction and heart motion abnormalities 

• effusions

• thrombus 

• ischemia 

what lab studies to complete CAD assessment 

• serum cardiac markers: troponin (gold standard + specific to heart), Serum creatinine kinase, and myoglobin 

• c-reactive protein: not specific to heart 

• lipid profile: elevated cholesterol = higher chance CAD

• electrolytes: important part of how depolarization happens 

• kidney function: can impact other organs, decreased perfusion to kidneys = decreased perfusion to heart 

serum cardiac markers

• Serum creatinine kinase

  • fractionated into bands - CK-MB 

  • rises 3-12hr, peaks in 24h

  • returns to normal 2-3 days 

• troponin: 

  • 2 subsets cTnT and Ctn1

  • greater specificity than CK-MB

  • levels rise within 3-12 hr, peak 24-48, return to normal 5-14 days 

assessment for chronic stable angina

• pain lasts 3-5 min → responds well to nitroglycerin

  • chest pain that occurs intermittently over long period with same pattern of onset, duration, and intensity of symptoms 

• subsides when precipitating factor is relieved (physical exertion, temp, smoking, strong emotions, sex)

• pain at rest is unusual

• ECG shows ST segment depression 

• can be controlled with meds + can be timed to provide peak effects during time of day when angina is likely to occur 

variants of stable angina

• silent ischemia: asymptomatic, associated with diabetes

• nocturnal angina: occurs only at night

• angina decubitus: chest pain only occurs while lying down

• prinzmetal’s angina: occurs at rest in response to a spasm of a major coronery artery 

  • seen in ppl with migraine headaches and Raynaud’s phenomenon 

  • may be relieved by moderate exercise 

assessment of unstable angina

• chest pain that is new in onset, occurs at rest or has worsening pain

• chronic: increases in frequency, duration or severity

• unpredictable and not received by rest → refractory to nitroglycerin

• associated with deterioration of once stable atherosclerotic plaque

• unstable lesion can progress to MI or return to stable lesion

myocardial infarction

servere prolonged low O2 supply (ischemia) resulting in necrosis

• 90% associated with acute coronary thrombosis

• presence of Q wave - area of necrosis, permanent

• transmural verus subendocardial

Inferior MI

anterior MI

lateral MI

ST: Stemi

full muscle is deprived of oxygen, no blood flow

• full thickness

non ST: non stemi

partial amount of muscle is deprived of oxygen 

• partial thickness 

symptoms of a MI

severe, immobilizing chest pain not relieved by rest, position change, or nitrate admin (diabetic pt may not experience pain)

• epigastric pain → indigestion 

• SOB, diaphoresis, N&V

• SNS stimulation: increase glucose, vasoconstriction, increase BP and HR

• CO falls: lower BP, crackles, JVD, peripheral edema, hepatic engorgment 

• pulmonary edema 

• dizziness 

• extra heart sounds 

• fever

diagnosis of an MI

2/3 criteria required

• chest pain >30 min

• ECG - Q waves / ST segment elevation / T wave inversion 

• serum cardiac markers: Troponin T, Creatine Kinase (CK)

the overall goals for a pt with ACS include

• relief of ischemic pain

• ‘prevention of myocardium → decrease O2 demand or increase O2 supply

• immediate and appropriate treatment of ischemia → drug therapy + interventions 

• effective coping with illness-associated anxiety 

• participation in rehab plan 

• reduction of risk factors

collaborative care + acute interventions

• prompt recognition of S&S → assessment of ABC, hemodynamic stability, preliminary history 

• 12 lead and continuous ECG monitoring 

• bloodwork

• oxygenation 

• IV access

• initial meds 

• immediate repercussion therapy 

initial medications for those with coronary artery disease

• ASA (160-325 mg)/Plavix (600mg) → prevent additional platelet activation and interferes with platelet adhesion 

• oxygen 

• Nitro → S/L (x3)  followed by IV for persistent pain, hypertension or heart failure 

• morphine: if nitro is ineffective → decrease myocardial O2 consumption, decrease BP/HR, decrease contractility 

additional medications for those with coronary artery disease

• B-adrenergic blockers: initiated within 24 h/no contraindications

• LMWH or IV heparin: minimally 48 hr after MI → to prevent re-thrombosis or acute stent thrombosis

• ACE inhibitors

• P2Y12 inhibitors

• antidysrhthmic medications 

• cholesterol lowering meds 

• stool softeners 

repercussion therapy

• mechanical repercussion: primary percutaneous coronary intervention

• pharmacologic reperfusion: fibrinolytic therapy

  • streptokinase, alteplase, reteplase, tenecteplase

  • STEMI only  

percutaneous coronary intervention

indications for angioplasty

• electively for chronic stable angina 

• urgently for unstable angina 

• emergently for myocardial infarction

• 1-2 vessel disease 

• should be performed within 120 min of first medical contact → ideally 90 min

medications accepted for PCI: delayed >120 min

ASA 160mg po chew STAT

■ Fibrinolytic IV (STEMI only) – in consultation with cardiologist

■ Plavix 300mg po STAT

■ Unfractionated Heparin bolus 60 units/kg (maximum 5000 units) is given intravenously, followed by a continuous heparin drip at 12 units/kg/hr (maximum 1000 units/hr)

medications accepted for PCI: immediate ASA 160mg po chew STAT

ASA 160mg po chew STAT

■ Plavix 300mg po STAT

■ Unfractionated Heparin bolus 70units/kk (maximum 4000 units)

■ Standing by for transfer to Cath Lab

nursing management for PCI

• angina: may be caused by transient coronary vasospasm

• vascular site care: assessing for bleeding and swelling at sheath site

• peripheral ischemia: secondary to cannulation of vessel, assess for adequate circulation

• renal protection: hydration, fluids, D/C of some meds 

pharmacological reperfusion: fibrinolytic therapy

target is within first 30 min

• ideally within 1st hour after onset of symptoms → less than 6 hr has improved result 

• dysrhythmias are self-limited → no treatment 

• major complication is bleeding: surface bleeding to major bleed (stop infusion) 

eligibility criteria for fibrinolytic therapy

• Patients with recent onset (less than 12 hours) of chest pain and persistent ST elevation

• Patients who present with bundle branch blocks (BBBs) that may obscure

ST segment analysis and a history suggesting an acute MI

• Chest pain unresponsive to sublingual nitroglycerin

• No conditions that might cause a predisposition to hemorrhage

absolute contradictions to fibrinolytic therapy

• Active internal bleeding or bleeding diathesis (except for menstruation)

• Known history of cerebral aneurysm or arteriovenous malformation

• Known intracranial neoplasm (primary or metastatic)

• Previous cerebral hemorrhage

• Ischemic stroke within past 3 mo

• Significant closed head or facial trauma within past 3 mo

• Suspected aortic dissection

relative contradictions to fibrinolytic therapy

• Active peptic ulcer disease

• Current use of anticoagulants

• Pregnancy

• Prior ischemic stroke not within past 3 mo; dementia; or known intracranial disease not covered under absolute contraindications

• Surgery (including laser eye surgery) or puncture of noncompressible vessel within past 3 wk

• Internal bleeding within past 2–4 wk

• Serious systemic disease (e.g., advanced or terminal cancer, severe liver or kidney disease)

• Severe uncontrolled hypertension (BP >180/110 mm Hg)

• Traumatic or prolonged (>10 min) cardiopulmonary resuscitation

coronary artery bypass graft (CABG)

goal: resestablish blood flow distal to blockage 

• isnt an emergent procedure 

who is considered for a CABG

• left main disease 

• multivessel disease 

• satisfactory improvement is not reached with medical management 

• pt is not a candidate for PCI

• lifestyle limting angina unresponsive to medical therapy or PCI

post MI ongoing assessment and care

• pain: if cardiac muscle is still not getting enough O2, causes more pain

• bleeding/surgical site care, chest tubes, pacer wire care

• catherter site, assessment of extremties

• monitoring: cardiac, resp, VS, O2

• rest/sleep, activity is gradually increasing

• anxiety → due to lack of understanding

• effectiveness of interventions

• emtotional and behaioural reactions

• evaluation of left ventricular function

• driving → after 1 week post-op

• pt education