week 2 term 1 Flashcards
- what is the Vascular supply to the heart and anatomy of the coronary arteries? And what are the associated areas which are served by what vessels
Vascular supply to the heart (coronary arteries)
- The heart is supplied by the right and left coronary arterie s which arise from the ascending aorta
- The right coronary artery mainly supplies the right atrium and ventricle. It’s branches are:
oRight conus artery
oAnterior ventricular branches
(inc. marginal branch)
oPosterior ventricular branches
oPosterior descending artery
oAtrial branches
- The left coronary artery is larger & supplies most of the heart
and left atrium / ventricle. It has two main branches are:
o Anterior descending branch
o Circumflex artery
What is cardiac pain, what are the mechanisms?
- Cardiac pain can be due to ischaemic cardiac disease or non-ischaemic cardiac disease.
- Examples of ischaemic causes for cardiac pain are stable angina, unstable angina and myocardial infarction.
- Examples of non-ischaemic cause m ms for cardiac pain include myocarditis, pericarditis or aortic dissection.
- In ischaemic cardiac disease, cardiac pain is felt due to the build-up of lactic acid (hence drop in pH) of the myocardium. (PICTURE 1) .
what are different mechansims of pain? (eg somatic vs visceral)
Pain is due to stimulation of specific nerve fibres to the brain by actual or potential tissue damage
There are three main types:
Visceral pain:- Is caused by organs & transmitted by the autonomic nervous system. Is poorly localised, dull/vague tenderness, may be colicy & patient tends to move around.
Parietal pain:- Sharp pain associated with inflammation of the parietal pleura. Is well localised, sharp and the patient tends to lie still.
Referred pain:- Pain felt at one location due to pathology at a different location. Is due to structures that develop from the same embryonic segment or dermatome.
WHAT is referred pain? (cardiac specific)
Referred pain: (PICTURE 2)
- Refers to pain which is usually at a distance from its original source.
- Referred pain typically occurs because tissue in different parts of the body develop form the same embryonic dermatome.
● An example of referred pain is that myocardial pain may be referred to the abdomen as hypogastric pain left jaw and arm
explanation detailed:
The cardiac general visceral sensory pain fibers follow the sympathetics back to the spinal cord and have their cell bodies located in thoracic dorsal root ganglia (. As a general rule, in the thorax and abdomen, general visceral afferent (GVA) pain fibers follow sympathetic fibers back to the same spinal cord segments that gave rise to the preganglionic sympathetic fibers. The central nervous system (CNS) perceives pain from the heart as coming from the somatic portion of the body supplied by the thoracic spinal cord segments 1-4. Classically the pain associated with a myocardial infarction is located in the mid or left side of the chest where the heart is actually located. The pain can radiate to the left side of the jaw and into the left arm
Explain the Haemodynamic effects of cardiac dysfunction, and the pathogenesis of oedema/ raised JVP?
If there is left ventricular dysfunction resulting in backpressure through the left atrium into the pulmonary system. Consequently, leading to right ventricular dysfunction and right atrial back pressure. The result of this will elevate the JVP and peripheral oedema (due to increased pressure and fluid in the systemic veins). Alternatively, there could be right ventricular dysfunction resulting in the same consequences
Haemodynamic Effects of Cardiac Dysfunction (heart failure):
Pathogenesis of Oedema: Oedema is excess of fluid in intercellular components of a tissue ® swelling
In left-heart failure:
o Left ventricle ineffective at pumping blood to body \ blood pools in pulmonary system ® increased fluid in pulmonary system ® pulmonary oedema
o As fluid fills the alveoli, this reduces the effective lung volume available for respiration and patient becomes short of breath (dyspnoea
In right-heart failure:
o Right ventricle ineffective at pumping blood to lungs \ blood pools in systemic veins ® increased intravenous pressure (hydrostatic pressure) ® increased fluid in legs ® swelling
NB: Oedema in the legs can also be due to venous obstruction by a thrombus
Raised JVP
- Is a sign of right heart failure and gives an indication of right atrial pressure
- Elevated systemic venous pressure causes distention of superior jugular vein
Explain the gnereral ECG changes in Myorcardial infaction?
Myocardial infarction can result in either a NSTEMI or STEMI episode.
- NSTEMI account for about 30% and STEMI for the other 70% of all MI
- NSTEMI occurs by developing a complete occlusion of a minor coronary artery or a partial occlusion of a major coronary artery previously affected by atherosclerosis - this causes partial thickness damage of the heart muscle
- STEMI occurs by developing complete occlusion of a major coronary artery - causing full thickness damage of the heart muscle
The usual ECG findings of a NSTEMI are ST depression or T wave inversion - there is NO ST elevation and later does not progress to a Q wave
- ST elevation & T wave invesion indicates proximal occlusion of major coronary artery (STEMI)
Acute anterior (septal) infarct
ST elevation in leads V2 to V6
Acute inferior infarct
ST elevation in leads II, VIII, AVF
Acute lateral infarct
ST elevation in leads I, II, AVL, V5, V6
NB: Pericarditis (not MI)
ST elevation and PR depression
what features would be seen on an Anterior MI ECG?
Anterior Myocardial Infarction
- results from occlusion of the LAD
- carries the worst prognosis of all infarct locations, mostly due to larger infarct size
- In Anterior STEMI
- ST segment elevation and Q wave formation in the precordial leads (V1-V6) + high lateral leads (I and aVL)
- Reciprocal ST depression in the inferior leads (mainly III and aVF)
- Septal area illustrated by V1-V2
- Anterior portion by V2-V5
- Anteroseptal = V1-V4
- V5 and 6 will be involved in an extensive Anterior STEMI and
what ECG changes would be seen in an inferior STEMI
Inferior STEMI
- more favourable prognosis than anterior myocardial infarction
- block to the RAD most commonly (80%), less commonly left circumflex, occasionally all three
- up to 20% of patients with inferior STEMI will develop significant bradycardia due to second or third degree heart block
- On an ECG inferior STEMI
- ST elevation in II, III, aVF
- Progressive development of Q waves in II, III, aVF
- Reciprocal ST depression in aVL
what ECG changes would be seen in an lateral MI?
Lateral STEMI
- the lateral wall of the LV is supplied by branches off the LAD and the left circumflex
- Lateral STEMI on an ECG
- ST elevation in the lateral leads (I, aVL, V5-V6)
- Reciprocal depression in the inferior leads (III, aVF)
What causes troponin and enzyme levels to change?
- Cardiac biomarkers should be measured in all patients who present with chest discomfort consistent with ACS. Elevations of cardiac enzyme levels should be interpreted in the context of clinical and ECG findings.
- Cardiac troponins T and I are the preferred markers for myocardial injury as they have the highest sensitivities and specifities for the diagnosis of acute MI.
- Troponin is a protein released from myocytes when irreversible myocardial damage occurs. It is highly specific to cardiac tissue and accurately diagnoses MI with a history of ischaemic chest pain or ECG changes reflecting ischaemia.
- Cardiac troponin level is dependent on infarct size, thus providing an indicator for the prognosis following an infarction.
- Serum levels increase within 3-12 hours from the onset of chest pain, peak at 24-48 hours and return to baseline over 5-14 days.
- Troponin levels should be measured at presentation and again 10-12 hours after the onset of symptoms.
- May not be detectable for 6 hours after the onset of myocardial cell injury. The most sensitive early marker for MI is myoglobin. Myoglobin is found in cardiac and skeletal muscle. It is released more rapidly from infarcted myocardium than troponin and CK-MB and may be detected as early as 2 hours after an acute MI. High sensitivity but poor specifity.
- Myocardial muscle creatine kinase (CK-MB) is found mainly in the heart. Levels increase within 3-12 hours of onset of chest pain, reach peak values within 24 hours and return to baseline after 48-72 hours. Sensitivity and specificity are not as high as for troponin levels.
- Troponin levels may also be elevated in patients with myocarditis, aortic dissection, congestive heart failure, sepsis, acute PE and CKD.
What is pericarditiis and the ECG changes seen with it?
Pericarditis
- Inflammation of the pericardium produces characteristic chest pain (retrosternal, pleuritic, worse on lying flat, relieved by sitting forward), tachycardia and dyspnoea
- there may be an associated pericardial friction rub or evidence of a pericardial effusion
- Wide ST segment changes occur due to involvement of the underlying epicardium
ECG findings
- Widespread concave ST elevation and PR depression through most of the limb leads (I, II, III, aVL, aVF) and precordial leads (V2-V6)
- reciprocal ST depression and PR elevation in lead aVR
- sinus tachycardia is also common in acute pericarditis due to pain and or pericardial effusion
Stages of Pericarditis
- Stage 1 - widespread STE and PR depression with reciprocal changes in aVR
- Stage 2- normalisation of ST changes, generalised T wave flattening (1 to 3 weeks)
- Stage 3- flattened T waves become inverted ( 3 to several weeks)
- Stage 4- ECG returns to normal
what questions would you ask someone with acute chest pain? (history)
Should cover basic history (presenting complaint, history of presenting complaint, etc. etc.)
- Questions for taking a pain history include: NILDOCARF
- Nature of the pain (tight, crushing, etc.)
- Intensity of the pain (on scale of 1 to 10)
- Location of the pain (get patient to point)
- Duration of the pain
- Onset (what was the patient doing when it started)
- Concomitant factors (any other symptoms)
- Aggrevating factors (what makes it worse)
- Relieving factors (what makes it better)
- Frequency
- Note: atypical chest pain presentations –
- Some patients will only present with breathlessness
- Men are more likely to rate pain on a lower scale than women
- Women are more likely (compared to men) not to feel chest pain during a heart attack but rather higher rates of ‘atypical presentations’ (inc. vomiting, fatigue, back pain) and have increased psychological causes (eg. panic attack)
Extened history (full history)
- Do you identify as an Aboriginal or Torres Strait Islander?
- HPC
- What were you doing when it started? (exertional/ non-exertional)
- Describe the pain (character)?
- Is it sharp/ dull/ burning/ heavy or tight?
- Does the pain radiate anywhere?
- Neck, arm or back?
- How painful is it from a scale of 1/10
- How long did it last for?
- Did you have any sweating, palpitations, SOB, dizziness, fainting, nausea or vomiting?
- Have you have this before? Have you had MI/ angina before?
- pMHx
- Have you had angina/ heart attack before?
- HTN/ diabetes/ dyslipidaemia/ peripheral vascular disease
- Other relevant past medical history.
- Allergies: do you have any allergies?
- Medications
- Do you take any regular medications?
- Immunisations:
- Are you up to date with your immunisations?
- Family history
- Any family history of cardiac/ respiratory problems?
- Other family history
- Social history
- Do you smoke/ drink / exercise?
- What is your diet like? Does it contain lots of fat or is it generally healthy?
- What do you do for a living?
- What do you do in your free time?
- Who do you live with?
- Do you have any children?
- Have you travelled anywhere recently?
- System’s review
- CVS
- Are you SOB on exertion?
- Have you ever woken up at night short of breath?
- Can you lie flat w/o feeling breathless?
- Have you had swelling of your ankles?
- Have you had palpitations?
- Do you have pain in your legs on exercise?
- Do you ever get cold/blue hands/ feet?
- Have you ever had ARF, heart attack or high BP?
- Do you have any breathing difficulties? cough
- Respiratory
- SOB? cough? sputum? blood? wheezing? fevers? night sweats?
- Have you ever had pneumonia or Tb?
- GIT
- Do you have indigestion? heartburn? difficulty swallowing?
- Any nausea/ vomitting? or vomitted blood?
- Any pain or discomfort in your tummy?
- MSK
- Do you have painful/ stiff joints?
- Any inujries to the chest recetly?
- Neurological and mental state
- Have you had any fainting episodes, dizziness?
- Have you ever had a stroke?
- Do you feel anxious?
- Have you had weakness in you arms or legs?
- CVS
List the clinical features fo ACS:
3 conditions make up the term ACS; Unstable angina, MI & Sudden Cardiac Death.
The signs and symptoms of acute coronary syndrome, which usually begin abruptly, include the following:
- · Chest pain (angina) or discomfort, often described as aching, pressure, tightness or burning
- Pain radiating from the chest to the shoulders, arms, upper abdomen, back, neck or jaw
- ·Nausea or vomiting
- Indigestion
- Shortness of breath (dyspnoea)
- Sudden, heavy sweating (diaphoresis)
- · Light-headedness, dizziness or fainting (LOC)
- Unusual or unexplained fatigue
- Feeling restless or apprehensive
How do you make a diagnosis of ACS? what would be initial and confirmatory investigations?
laboratory
FBC
- UEC/ glucose (especially K)
- Cardiac troponin I
- Normal levels are considered vary according to the exact assay that is being used
- In general terms a normal level is considered to be < 99th percentile for the assay
- may persist for 5-14 days post infarction
- Reinfarction can also be assessed via troponin levels (CK/CKMB is now obsolete and not required)
- Rising versus falling levels
- For the vast majority of patients being investigated for possible MI, a rising pattern is suggestive of the diagnosis of MI
- In patients who present late following MI, troponin elevations may have already peaked and in this context, a falling troponin pattern is significant
- Note that all troponin assays, regardless of their detection sensitivity do not rule out unstable angina or stable coronary ischemia
Clinical management decisions should not be based solely on troponin levels, but on thorough investigation and risk assessment that includes detailed clinical assessment, observation, repeated ECG tests, and where available functional testing
An initial troponin level should be done on all cases of suspected ACS with a second level done at 6 hours (sensitive assay) or 3 hours (highly sensitive assay) from the onset of the chest pain.
Note that some patients that fit specific low risk stratification criteria may be suitable for validated accelerated diagnostic pathways.
ECG
- All patients who present with a suspected ACS must have an ECG within 10 minutes of first acute clinical contact
- A clinician with ECG expertise should review the ECG
- The immediate decision pathway then involves the ECG stratification of STEMI, from NSTEACS
- STEMI minimum criteria:STEMI is defined as presentation with clinical symptoms consistent with ACS (generally of ≥ 20 minutes duration) with persistent (> 20 minutes) ECG features in ≥ 2 contiguous leads of:
- ≥ 2.5 mm (i.e ≥ 2.5 small squares) ST elevation in leads V2-3 in men under 40 years, or ≥ 2.0 mm (i.e ≥ 2 small squares) ST elevation in leads V2-3 in men over 40 years
- ≥ 1.5 mm ST elevation in V2-3 in women
- ≥ 1 mm ST elevation in other leads
- New LBBB (LBBB should be considered new unless there is evidence otherwise)
- Findings in ACS
- may be normal
- classic changes in acute myocardial infarction
- peaked T waves with ST elevation
- gradual loss of R wave
- development of pathological Q wave and TWI
- anatomical localisation of ST elevation
- Anteroseptal = LAD
- Anterolateral = Cx
- Inferior = RCA
- Posterior = Cx or PDA (off RCA)
- Minimal S-T changes can be difficult to interpret, especially in those with pre-existing CAD or other significant CVS disease. In such cases:
- Comparison with old ECGs will be useful
- Modified Sgarbossa criteria can help if LBBB or paced:
- concordant ST elevation of > 1mm
- concordant ST depression of > 1mm in V1, V2 or V3
- discordant ST elevation of > 5mm
- In cases of LBBB urgent echocardiography may be useful, if readily available, to detect wall motion abnormalities (suggesting myocardial ischaemia) and hence assist in decision making
- CXR
This should not be allowed to delay any treatment measures, especially reperfusion therapies.
If an x-ray is done this should be in the Resus bay, except for stable low risk patients who may be suitable to leave the department for their x-ray, this will need to be judged on a case by case basis.
Look for cardiomegaly, cardiac failure and differentials of chest pain (e.g. PE, pneumonia, pneumothorax, esophageal rupture, aortic dissection)
Echocardiography (not a routine test in ACS, but may be considered on an urgent basis in selected cases)
Confirmation of wall motion abnormalities when the diagnosis of ACS is unclear (pericarditis or myocarditis is being considered for example or in cases of LBBB)
Cardiogenic shock
Inferior infarction where evidence of right ventricular infarction is being sort
If secondary complications are suspected, such as cardiac tamponade or valvular disruption
Coronary Angiography
This is the definitive investigation for any patient with a STEMI who is to undergo a PCI
Patients with high or very high risk NSTEACS should be referred to cardiology urgently for consideration of a urgent coronary angiogram.
Explain the basic management principles of a patient with an acute ACS?
STEMI MANAGEMENT:
Initial management
- All patients must be triaged to a monitored resuscitation bay (ABC)
- IV access, and blood tests taken
- Oxygen therapy if hypoxic
- Analgesia- opioids; morphine, fentanyl
- Anti-emetic as required
- Aspirin as soon as you are concerned
Further management
- GTN if pain not controlled by opioids
- Anti-Platelet therapy as required
- Heparin
- Reperfusion if patients present whiten 12 hours of symptom onset
- Surgical interventions according to local hospital practice
- Thrombolysis
NSTEACS MANAGMNET:
Non-ST elevation acute coronary syndrome, and includes non-STEMI and unstable angina
Initial management
- All patients must be triaged to a monitored resuscitation bay
- IV access, and blood tests taken
- Oxygen therapy if indicated
- Analgesia: Nitrates, Opiates
- Anti-emetic as required
Depending on the risk stratification level of patient also consider
- Anti-platelet therapy
- anticoagulation
- Repercussion therapy
How is ACS best managed in a rural setting? What facilities would exist locally e.g. Ravenshoe, Hughendon or Emerald?
Fibrinolytic Therapy Fibrinolytic therapy is more widely available and is beneficial in a wider range of patients who may not have access to PPCI38-40. Fibrinolytic therapy can be safely given by a trained paramedic, nurse or physician using established protocols41-45. (LOE I) The efficacy is greatest given the first three hours of the onset of symptoms. Without timely access to primary PPCI, patients with symptoms of ACS and ECG evidence of ST elevation infarction or true new bundle branch block or true posterior infarction should be treated with fibrinolytic therapy as soon as possible. In patients presenting early after the onset of chest pain (<1-2 hours) and in certain clinical subsets (<65 years-of-age, anterior STEMI), prehospital fibrinolysis may offer similar outcomes compared to PPCI20,46,47. (LOE II) There are a number of contraindications to fibrinolysis that health care practitioners need to be well aware of (see Table 1)1,48. In addition, the older patients are a difficult patient group. They have a high absolute risk of death from their STEMI, have an increased absolute benefit from fibrinolytic therapy but the risk of intracranial bleeding from fibrinolysis is also higher. This is increased in the presence of systolic hypertension of over 180 mmHg. The benefits of fibrinolytic therapy are less impressive in areas of infarction other than an anterior STEMI location.
