Cardiac Flashcards
Outline 2 key studies advocating the benefits of exercise for health
Paffenbarger- Harvard Alumni - 27% lower mortality if expending >2000 calories a day
Blair - fitness lowers mortality
Quantify the benefit of increased MVPA
Extra 10 mins approximately - 10% reduction in mortality
150 MVPA a week - 30-40% less
750 - 50% less
What conditions has strong evidence for the benefit of exercise?
CHD, stroke, HTN, hyperlipidaemia, type 2 diabetes Mellitus, metabolic syndrome, colon cancer, breast cancer, depression
What conditions have moderate evidence for physical activity?
Hip fracture, lung cancer, endometrial cancer
How much exercise should children do a day?
60 minutes minimum
Define preload and afterload
Blood in ventricles before contraction - EDV
Blood in ventricles after contraction - ESV
How do you calculate stroke volume, ejection fraction and shortening fraction?
Preload - afterload
((EDV - ESV) / EDV) * 100
((EDD - ESD / EDD) * 100
What 3 factors affect HR
SNS
PNS
Adrenaline
What 2 factors affect afterload?
Contractility
Systemic vascular resistance
What 2 factors affect contractility?
Myocardial mass
Length-tension relationship of myocardial fibres
What 4 factors affect preload?
Ventricular size
Venous size
Ventricular plasticity
Length-tension relationship of myocardial fibres
What 2 factors affect venous return?
Blood volume
Pumps- muscular/respiratory/ventricular
How much blood does the average adult have? Where is most of it?
5L
2/3 in veins
What organs use the most blood at rest and during exercise?
27% liver and 22% kidneys
84% muscles
What is the main blood vessel that determines vascular resistance? Outline the process of it’s vasodilation
Arterioles
Endothelium releases NO due to autonomic stimulation, which penetrates the smooth muscle and causes dilation
What stimulates vasodilation?
Increased: NO, bradykinin, prostaglandins, K+, CO2, lactate
Decreased: pO2
What stimulates vasoconstriction?
Increased SNS activity, releasing noradrenaline causing the alpha receptors to constrict
How does exercise increase venous return?
Muscles contract
Increased SNS
Constriction of venous smooth muscle
What is the effect of respiration on venous return
Expiration - increase thoracic pressure - push blood to heart
Inspiration - decrease thoracic pressure - pull blood to heart
What affects afterload?
Volume of blood in arteries Pressure in aorta Compliance of aorta Size of aorta/pulmonary arteries Inertia of blood Total peripheral resistance
What is the effect of increased afterload?
Decreased stroke volume - increased preload
Decreased velocity of contraction and ejection
Increased O2 consumption
What triggers the cardiovascular response to exercise? Where are they? How do they work?
Mechanoreceptors - muscle spindles - detect stretch and increase SNS
Metaboreceptors - muscle spindles - detect raised lactate/prostaglandin/phosphate/acidity and increases SNS
Baroreceptors - carotid sinus and aortic arch - increased arterial stretch and so lowers SNS, raises PNS thus lowering BP
Chemoreceptors - carotid sinus and aortic arch - raised CO2 cause raised SNS
Bainbridge reflex - more RA filling causes stretch causing increased SNS
What are the branches of the left and right coronary artery?
Left anterior descending, left marginal artery, left circumflex
Right marginal artery and posterior interventricular arter
What are the limits to coronary perfusion?
Tachycardia
Low diastolic pressure
Ischaemic heart disease
Outline the process of atherosclerosis
Endothelial injury - fatty streak - macrophages invade and become foam cells -
either: necrosis - calcium infiltrate - hardening of artery
Or: growth factor - smooth muscle cover - stable/unstable plaque - occlusion
What coronary artery is responsible for: anterior, septal, lateral, inferior, posterior, atrial MI?
LAD LAD LCx RCA RCx RCA
What factors can lead to endothelial injury?
Normal wear and tear Fibrinogen Free radicals HTN a Turbulent flow Viral Carbon monoxide
How does an unstable plaque lead to an MI?
Plaque ruptures - platelet aggregation - thrombus - occlusion - distal ischaemia
Where would the MI be if the LAD, Right coronary/marginal or LCx was occluded?
Anterioseptal
Inferior and right hand side
Lateral
How does an unstable angina differ from a stable angina?
Pain at rest/with less provocation and is more painful
May have a thrombus
May have biological markers
What are the ECG changes associated with ischaemia, injury and infarction?
T wave inversion +/- ST depression
T wave inversion and ST elevation
Pathological Q waves
Explain the mechanism behind ECG changes in ischaemia and injury
Slow to repolarise and remains more positively charged
Delayed depolarisation and tall T waves due to potassium leakage from dead cells
Outline the stages of change in an ECG after an MI
Normal - Tall T waves - ST elevation - Pathological Q waves and T wave inversion, less ST elevation - Pathological Q waves and upright T waves
What is the 1 year mortality for an MI in: proximal LAD, middle LAD, distal LAD, Left circumflex, small inferior
25 12 10 8 7
When do cells start dying and when are 80% and 100% of cells dead?
30 minutes
3 hours
6 hours
Why do enzymes leak and what determines when they leak?
Cell dies so holes appear in the cell membrane
Size and solubility
Name 3 enzymes that are looked for after an MI, the reference range, when they initially appear, when they peak and how long they remain elevated for
Troponin - <0.004ng - 4-6 hours - 12-24 hours - 6-8 days
CK - 14-179IU - 4-6 - 12-36 - 3-4
CK-MB - <10.4ng - 4-6 - 12-24 - 2-3
LDH - 105-333IU - 8-12 - 48-72 - 7-10
Initial treatment of MI
Morphine, oxygen (sometimes), GTN spray, aspirin
List some medication to be taken after an MI
Heparin, beta blockers, ace inhibitors, calcium channel blockers, statins
What is the WHO’s definition of health?
A state of complete physical, mental and social well-being and not merely the absence of disease or infirmity
