GEP (Life support) Week 4 Flashcards
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Identify the hidden anatomical areas
- The heart is oriented like a pyramid on it’ side: it has an anterior surface, a diaphragmatic surface, a base and pulmonary surfaces
- The anterior surface is made up mostly of the right ventricle, and the atria sit behind the ventricles in the anatomical position.
- The internal divisions of the heart create external grooves called sulci:
- Coronary Sulcus: separates the atria from the ventricles
- Anterior/Posterior Interventricular Sulci: separate the two ventricles of the heart and are continuous inferiorly.
Identify the hidden anatomical positions and information
Identify the hidden anatomical position
Identify the hidden anatomical position
What are the 2 main nodes in the heart essential for cardiac conduction
-Sino atrial and atrioventricular nodes.
-Made of autonomous pacemaker cells- generate action potential.
-Depolarisations happens fast in specialised pacemaker cells, and slower in ordinary myocytes.
Brief description of the cardiac conduction from SA node
-Impulse starts at the sino-atrial node
-Signal spreads across the atria, causing the muscle to contract
-Signal reaches the AV node, where it is delayed for a short time
-Continues into the bundle of HIS
-Splits into right and left bundle branch
-Eventually becomes continuous with Purkinje fibres that depolarise the ventricles, causing ventricular contraction.
Describe the cardiac cycle
Describe the formation of Atherosclerosis
**Inflammatory process of the formation of lipid rich streaks in arteries. **
1. Damage to the endothelial cells that make up the intima of the artery (inner layer).
2. Cholesterol (LDL) circulating in the bloodstream accumulates at site of damage.
3. Cholesterol becomes oxidised, triggering an immune response and migration of macrophages to the injured site.
4. Macrophages engulf the cholesterol and form FOAM CELLS. These then die.
5. Accumulation of foam cells beneath the endothelium creates fatty streaks.
6. Smooth muscles migrate and proliferate, forming a fibrous cap over the fatty streak/plaque.
7. Artery narrows, creating partial occlusion of the artery and ischaemia. In some cases plaque rupute occurs, creating embolism and total occlusion.
8. Process accelerated by risk factors- eg smoking, familial hypercholesterolaemia.
Most commonly affected arteries: coronary, abdominal aorta, carotid, popliteal. Plaque forms more easily at bifurcations.
What are modifiable factors and non-modifiable factors of CV risk factor
Modifiable means it can be modifies and changes
Non-Modifiable are factors that cannot be altered.
Modifiable
-Smoking.
-Low blood level of high-density lipoprotein (HDL) cholesterol.
-High blood level of non-HDL cholesterol.
-Sedentary lifestyle/lack of physical activity.
-Unhealthy diet.
-Alcohol intake above recommended levels.
-Overweight and obesity.
Non-modifiable
-Age — CVD is strongly age-dependent, primarily affecting people aged over 50 years. The older a person is, the greater the risk of developing CVD.
-Gender — at all ages men have a higher risk of CVD than women, and on average develop CVD about 10 years earlier.
-Family history of CVD — this may reflect a shared environment, genetic factors, or both. A positive family history of premature CVD death is associated with an increased risk of early and lifetime CVD.
-Ethnic background — for example, people of South Asian or sub-Saharan African origin have an increased risk of CVD, while people of South American or Chinese origin have a lower risk compared with people of European origin.
Name other co-morbidities and social factors that increase the risk of the CVS
Co-morbidities
-Hypertension.
-Diabetes mellitus (and pre-diabetes/metabolic syndrome).
-Chronic kidney disease.
-Dyslipidaemia (familial and non-familial).
-Note: some drugs can also cause dyslipidaemia such as some antipsychotics, immunosuppressants, and corticosteroids.
-Atrial fibrillation.
-Rheumatoid arthritis, systemic lupus erythematosus, and other systemic inflammatory disorders.
-Influenza.
-Serious mental health problems (schizophrenia, post-traumatic stress disorder) — anxiety is an independent risk factor for coronary artery disease (CAD).
-Periodontitis.
Social factors
-Socioeconomic status — death from CVDis three times higher among people who live in the most deprived communities compared to those that live in the most affluent.
-Lack of social support —people who are isolated or disconnected from others are at increased risk of developing and dying prematurely from coronary artery disease (CAD). Alack of social support increases CAD risk and worsens the prognosis of CAD.
Risk factor management:
Education and awareness.
Lifestyle modification- diet, exercise, quit smoking.
Timely and correct management of co-morbidities.
Social support for those that need it.
Early detection and management.
Please Define:** Ischaemia, Infarction, Acute coronary syndrome, Angina, Myocardial infarction**
Ischaemia: reduced perfusion leading to reversible tissue dysfunction.
Infarction: severely reduced perfusion leading to irreversible tissue death (necrosis).
Acute Coronary Syndrome: spectrum of conditions resulting from sudden and severe hypoperfusion of myocardium.
Angina: myocardial hypoperfusion → ischaemia → hypoxia + tissue dysfunction + pain.
Myocardial Infarction: ↑↑myocardial hypoperfusion → ischaemia → hypoxia + tissue death + pain.
Ishaemia: blood flow decreased leading to hypoxia
Infarction: blood flow cutoff leading to necrosis
What are the clinical presentation of stable angina
-Central, constricting chest pain/discomfort
-+ radiation to jaw, neck, shoulders or arms
-Only on exertion!
-Resolves with <20 mins rest!
Stable angina:
NOT an acute coronary syndrome.
Symptoms relived by resting for ∼20mins, and by Glyceryl Trinitrate (GTN) spray.
What are the clinical presentation of unstable angina
-Central, constricting chest pain/discomfort
-+ radiation to jaw, neck, shoulders or arms
-Occurs at rest!
-Not resolved by >20mins rest!
Unstable angina:
An acute coronary syndrome.
Not sufficiently relieved by GTN spray.
Clinical features of Myocardial infarction
-Central, constricting chest pain/discomfort
-+ radiation to jaw, neck, shoulders or arms
-+ nausea, vomiting, palpitations, sweating, clamminess, SOB, sense of impending doom
What are the difference of STEMI and NSTEMI Myocardial infarction
Looking at a cross-section of myocardium, necrosis first occurs furthest away from occluded artery (subendocardial zone).
Necrosis may then progress outwards, towards occluded artery.
-Infarction that involves less than the full thickness of myocardium = a subendocardial infarction, seen as a NSTEMI.
-Infarction that involves the entire thickness of myocardium = a transmural infarct, seen as a STEMI.
What is the healing process for Myocardial Infarction
0-24 hours: Necrosis leading to immune neutrophils infiltration (lysis of dead cells).
1-3 days: Continued immune response (breaking down dead cells).
3-14 days: Macrophage infiltration (phagocytosis of cellular debris); Granulation tissue formation (myocardium is fragile).
14 days – >1 month: Scar tissue formation (akinetic myocardium).
What are the complications of Myocardial Infarction
Arrhythmia (in short term)
Myocardial necrosis → loss of cardiac pacemaker cells → dysfunctional electrical conduction.
May manifest as ventricular tachycardia, ventricular fibrillation, bradycardia or heart block.
Heart failure (in long term)
Myocardial necrosis → dysfunctional contraction → inadequate cardiac output → compensation → failure.
ACS algorithm
UAP = unstable angina (pectoris)
What are the ST elevation location on ECG relating to where the MI is occruing
What are cardiac biomarkers
-Cardiac biomarkers: proteins that leak out of injured cells due to damage+ ischaemia.
-Troponins (T+I), creatine kinase (CK-MB), myoglobin, lactate dehydrogenase.
-Troponins have highest sensitivity and specificity.
Summary of ACS
