Week 3 - Cardiac Flashcards
what are a few key terms for ischemic chest pain
Occur in both exertion or at rest. does not alter due to change in position or posture Not exacerbated by movement or deep inspiration. Described as Tightness Pressure Heaviness Indigestion Ache
what are topical locations of angina
Chest - central or left sided, may involve epigadtrium
arms - left arm may be both
throat
what are the 3 radiation areas of a typical angina
jaw
back
shoulders
key points of typical angina
radiation to arms or neck increases the likelihood that the pain is myocardial ischemia. not all patients presents typical
symptoms, especially women
what are the features of myocardial ischaemia
shortness of breath sweating nausea vomiting palpitations dizziness weakness
what is “Chronic” Stable Angina
- Usually due chronic narrowing of the coronary artery.
- Blood flow may be adequate to supply the myocardium during periods of rest and low activity resulting in no pain
- Inadequate blood supply during conditions of increased myocardial oxygen demand (exercise, stress) pain
what is stable angina
Onset/pattern of pain is often predictable Occurs in response to activities that increase HR and BP (myocardial workload) - exercise - sexual activity - emotional stress Often worse - early in the morning - after a heavy meal in cold weather Usually resolves within 2-10 minutes - rest - GTN
how should chronic stable angina be managed
Pharmacotherapy
- Nitrates
>Short and long acting
- Antiplatelet therapies
> Aspirin
> Clopidogrel
- Calcium Channel Blockers
- Beta Blockers
- Perhexiline
Revascularization
- Percutaneous Coronary Angioplasty (PTCA) +/- intracoronary stent
- Coronary Artery Bypass Surgery (CABG)what are the signs and key points of Stable angina turning into unstable angina
Signs that stable angina may becoming unstable:
more frequent
more severe
lasting longer
not responding to rest/GTN
occurring with less exertion
occurring at rest
waking the patient from sleep.
Key Points
Stable angina can progress to unstable angina.
Unstable angina is associated with greater risk of death than stable angina
symptoms of Acute Myocardial Infarction (AMI)
Pain is usually prolonged and severe Often associated with fear, anxiety, distress May occur with no prior warning May be preceded by unstable angina May occur at rest May be associated with a precipitating factor, such as vigorous physical exercise emotional stress medical/surgical illness
what are the major presenting symptoms of Atypical AMI
Some patients with AMI do not experience angina pain Known as silent ischaemia The major presenting symptoms in these patients include dyspnoea diaphoresis nausea/vomiting pre-syncope/syncope sudden loss of consciousness confusion profound weakness
key points of Acute Myocardial Infarction
Estimated that 50% of all AMI deaths occur before the person reaches hospital
Pre-hospital goals:
- Reduce mortality
>basic life support
>advanced life support
>early defibrillation
Minimise delay from symptom onset to reperfusion therapy
how is Acute coronary syndrome diagnosed
Diagnosed on the basis of ECG/cardiac enzymes
Unstable Angina
Not total occlusion of epicardial coronary artery
No ST elevation on the ECG
Cardiac enzymes (troponin/CK) normal
Non-ST elevation myocardial infarction (NSTEMI)
Not usually total occlusion of epicardial coronary artery
No ST elevation on the ECG
Elevated cardiac enzymes (troponin/CK)
ST elevation myocardial infarction (STEMI)
associated with occluded epicardial coronary artery
ST elevation on the ECG
Elevated cardiac enzymes (troponin/CK)
what key notes are to be asked about patient history in regards to cardiac diseases
Chest pain assessment (watch the video on learnonline) Past illnesses Allergic reactions Medication history Alcohol, drug and tobacco habits Social history Cardiovascular risk factors
what are the non-modifiable risk factors
Age
CVD predominantly affects middle aged and older Australians – but is becoming more common in younger Australians (male and female)
Gender
more common in men than women, as women are thought to be protected by oestrogen prior to menopause
women have equal risk to men by age 65.
Family history of CVD
The risk of CVD is increased if a first degree relative <60 years of age is diagnosed with heart or blood vessel disease.
what are the modifiable risks
Smoking Hypertension Diabetes Physical inactivity Poor nutrition Alcohol consumption Psychosocial factors
what are the psycosocial risk factors
Psychosocial factors associated with risk for CVD include: depression social isolation lack of quality social support poor personal economic resources lower levels of education poor living and working conditions stress limited access to health care and social services
what can be monitored by a 12-lead ECG
Rate Rhythm Ischaemic changes ST segment elevation ST segment depression T-wave abnormalities Q-waves Conduction abnormalities Bundle branch block Axis deviation Left ventricular hypertrophy Incremental Leads Posterior leads (v7,v8,v9) Right ventricular leads (v4R)
what are the initial blood test that are taken when
Blood tests Serum troponin I or T levels CK-MB if troponin not available Creatine kinase (CK) Full blood count Serum creatinine eGFR Electrolytes serum lipid levels within 24 hours blood glucose level
Cardiac Imaging
Chest x-ray heart lungs should not delay reperfusion treatment Radionuclide Studies thallium-201 technetium-99m sestamibi positron emission tomography echocardiography
Angina: Treatment Goals
Relieve angina symptoms increase myocardial O2 supply decrease myocardial O2 demand Decrease the risk of myocardial infarction Prolong survival Reduce disease progression
Unstable angina pectoris Management
Oxygen therapy if required (O2 sat below 93%) Cardiac Monitoring Arrhythmias ST-segment and T-wave changes Rest Reversal of precipitating factors hypertension anaemia stress Pharmacotherapy Nitrates Anticoagulant Antiplatelet Calcium Channel Blockers Beta Blockers Perhexiline Revascularisation Percutaneous Coronary Angioplasty (PTCA) +/- intracoronary stent Coronary Artery Bypass Surgery (CABG)
Acute Myocardial Infarction maagement
Pathogenesis is the same as that of UAP and so the treatment is similar BUT:
Time is muscle!!!
Urgent revascularisation (opening the artery) is required
PTCA
Fibrinolytic therapy
STEMI: Primary therapeutic strategies
Initial treatment I.V. access IV nitrates antiplatelet therapy anticoagulation O2 therapy aspirin morphine
STEMI: Reperfusion strategies
Percutaneous transluminal coronary angioplasty (PTCA) \+ Clopidogrel \+/- GPIIb/IIIa agents (abciximab) treatment of choice if provided promptly by a qualified interventional cardiologist In an appropriate facility
Fibrinolysis (thrombolytic therapy)
should be considered early if PCI is not readily available
particularly in rural and remote areas.
not routinely recommended in patients who present more then 12 hours after symptom onset and are asymptomatic and haemodynamically stable.
Coronary artery bypass graft (CABG) surgery
suitable anatomy and are not candidates for fibrinolysis or percutaneous coronary intervention (PCI)
cardiogenic shock
in association with mechanical repair.
