WK1 - Cardiovascular System Flashcards
1
Q
Provide some cool facts about the heart.
A
- approx. 300g
- broad base located superiorly
- apex located inferiorly/points anteriorly and approx 45deg to left
- elcosed in fibrous protective sac (pericardium)
- 3 layers (epicardium (ext layer), myocardiom and endocardium (inner layer - epethelial cells)
2
Q
What is the flow of deoxygenated blood?
A
- SUP/INF vena cava
- R atrium
- through tricuspid valve
- R ventricle
- through pulmonary valve
- pulmonary artery
- lungs
3
Q
What is the flow of oxygenated blood?
A
- lungs
- pulmonary veins
- L atrium
- through mitral valve
- L ventricle
- aortic valve
- aorta
- to rest of body
4
Q
What do the interior chambers of the heart do?
A
Atria: thin walled and receive blood
R - receives from systemic circulation through SUP/INF vena cava
L - receives from lungs via 4 pulmonary veins
Ventricles: thicker and stronger walls to deliver blood
R - (pulmonary pump) Sends deoxygenated blood through pulmonary artery to
pulmonary circulation to be oxygenated
L - Sends oxygenated blood through the aorta to systemic circulatio
5
Q
What are the atroiventricular valves?
A
Tricuspid valve (RA –> RV)
Mitral valve (aka bicuspid) (LA –> LV)
6
Q
What are the semilunar valves?
A
Pulmonary valve (RV–> pulmonary artery)
Aortic valve (LV –> aorta)
7
Q
What are the acute marginal coronary arteries?
A
R coronary artery
POS descending artery
R marginal artery (descends of R coronary artery)
8
Q
What are the left “main” arteries?
A
L coronary artery
L circumflex artery (descends off L coronary artery)
L marginal artery (descend off L circumflex artery)
9
Q
What are the obtuse marginal artieries?
A
L ANT descending ( or interventricular) artery ( descended from L coronary artery)
Diagonal Branch
10
Q
When does filling occur?
A
during diastole with closure of the aortic valve
11
Q
What does the L coronary artery do?
A
L main - arises from aorta, splits into LAD and LCx to supply L side of heart
LAD supplies: LV, interventricular septum, RV and iNF areas of apex (in most people)
LCx supplies: INF walls of LV, LA and SA Nodes (45% persons)
12
Q
What does the R coronary artery supply?
A
- RA
- RV
- INF wall of LV ( in most persons)
- AV node and nudle of His (in most)
- SA node (55% persons)
13
Q
What is the location and origination of PDA?
A
Runs down POS interventricular sulcus to apex where it meets LAD
Originates:
* typically as a branch of RCA (70%, known as R dominance)
* Or be branched from LCx (10%, known as L dominance)
* or as anastomosis of RCA and LCx (20%, known as Co-dominance)
14
Q
What is happens during circulation to the heart?
A
coronary arteries control amount of O2 delivered to heart muscle
* blood forced into coronary arteries during systole
* blood enters cardiac muscle fibres during diastole (when relaxed)
15
Q
Explain the source of energy of the heart’s metabolism.
A
Highly resistant to fatigue - large number of mitochondria =
increased ATP production
* Almost exclusively aerobic metabolism, therefore the heart requires constant supply of O2
* Principle source is free fatty acid oxidation (60%) –
followed by CHO (35%
16
Q
Explain more about the hearts metabolism.
A
High extraction of O2 at rest, ~70-80% delivered = limited reserve for increased myocardial work
* Increased demand is met via Increased blood flow (rate and force), with a reduction in resistance (via dilation of coronary arteries)
Implications for:
* Vascular stiffening with aging
* Reduced cardiac output under various conditions/diseased states
17
Q
Which nerve innervates the heart?
A
- at rest, heart is predominantly under vagal control
- innervated by vagus nerve ( X cranial), originating in the medullar oblongata (brainstem) cardioinhibitory centre
18
Q
What is released when PNS activated?
A
Stimulation releases acetylcholine (cholinergic agonist to decrease…
* intrinsic rate (chronotropy)
* conduction velocity (dromotropy)
* contractility (inotropy) or atria
* rate of myocardial relaxation (lusitropy) of atria
19
Q
What happens to heart during SNS?
A
- during stress, heart is predominantly under sympathetic control
- heart is innervated by sympathetic nerves, originating in medulla oblongata (brainstem)
20
Q
What is released during stimulation of the SNS?
A
Releases norepinephrine and acts on 2 types of adrenergic receptors within heart.
- Alpha receptors - excitatory) = vasoconstriction of arteries/veins
- beta receptors - excitatory/inhibitory = increase intrinsic rate (chronotropy, contractility (inotropy), conduction velocity (dromotropy), rate of myocardial relaxation (lusitropy) AND increase smooth muscle relaxation (for vasodilation)
21
Q
Define EDV and ESV
A
EDV = volume of blood in LV at end of diastole just before systole
ESV = volume of blood in LV at end of systole
22
Q
Define stroke volume
A
volume of blood pumped out of LV during systolic contraction.
SV (mL) = EDV - ESV
23
Q
Define ejection fraction (%)
A
fraction of blood pumped out of heart during systolic contraction
% = [(EDV-ESV)/EDV]*100
24
Q
Define CO.
A
(Q) = volume of blood pumped by heart (i.e. stroke volume per minute)
Q (L/min) = HR*SV
25
What are normal values for EDV and ESV?
EDV
males 107 +/- 27mL
females 84 +/- 22mL
ESV
males 40 +/- 12mL
females 30 +/- 10mL
26
What are the normal values for ejection fraction and stroke volume?
EF
males 63 +/- 6%
females 64 +/- 6%
Normal targets 50-70%
SV
males 74.3 +/- 17.2
females 62.5 +/- 14.3
27
What are the normal values of HR and CO?
males HR 66 +/- 10bpm
females 69 +/- 11bpm
normal HR targets 60-100bpm
CO
males 4.8 +/- 1.2L/min
females 4.3 +/- 1.0L/min
28
What is stroke volume and what affects it?
SV = EDV-ESV
1. Preload = EDV stretch. Influences contractility through Frank-Starling Mechanisms (increase stretch of ventricles = increase force of contraction)
2. afterload = load against which muscle exerts its contractile force. Influences ability to eject blood, affected by systemic vascular resistance/aortic compliance
3. inotropy = ventricular contractility. influenced by neural control/pathology
29
What is Systemic vascular resistance (SVR)?
Based on Poiseulle's Law - resistance to blood flow is influenced by...
1. viscosity (no. of RBC's, concentration of plasa proteins)
2. diameters of arterioles/capillaries (vasoconstriction and vasodilation) - BP, O2/CO2 content, pH, Hormones (adrenaline), histamines, lactic acid
3. vessel length - increases during growth and obesity
Resistance = (8nl)/(pi*r^4)
30
What is peripheral circulation? Explain the mechanisms and factors that affect it.
Blood flows from areas of higher pressure to areas of lower pressure (e.g. highest systolic pressure out of heart, to lower systolic pressure throughout arterial tree)
* based on BP
Factors:
* age, emotional state, exercise
31
What is BP? Define the different types and how to calculate it.
BP = pressure exerted by blood against vessel walls
SBP = pressure during ventricular contraction
DBP = pressure during ventricular relaxation
Pulse pressure = SBP-DBP
BP=CO*SVR
32
What are the leading causes of death in Aus males in 2020?
1. CHD 10,040 males
2. dementia inc. alzheimer
3. lung cancer
4. cerebrovascular disease
5. prostate cancer
33
What are the leading causes of death in Aus females in 2020?
1. dementia inc alzheimers
2. CHD 6547 females
3. cerebrovascular disease
4. lung cancer
5. BCa
34
List some common CVDs.
Heart disease
- CHD
- heart failure (inc. cardiomyopathy)
- inflammatory
Cerebrovascular disease/stroke
Peripheral vascular disease
35
What is atherosclerosis?
Disease affecting arterial blood vessels (chronic inflammatory response)
Atherosclerotic plaques develops from accumulation/swelling in artery wall (intimal layer) - from macrophages, cell debris, lipids (chol/fats), Ca2+ and fibrous tissue
* fatty streak, fibrous/complicated plaque
In coronary arteries, this can lead to...
* heart attack (MI)
* angina (ischaemic chest pain)
* aneurysm (weakening of vessel wall)
36
Explain the development of athersclerotic plaques.
1. normal
2. fatty streak creating foam cells
3. lipid-rich plaque creating a lipid core
4. fibrous cap causing thrombus
37
How does atherosclerosis affect arterial structure and functional capacity?
Arterial structure
- decrease coronary artery blodo flow
- O2 distribution to myocardium
Functional capacity
- altered vascular tone affecting endogenous vasoilation
- stiffening
Leading to ischaemic/infarction
38
What is the difference between ischaemia and infarction?
Ischaemia = insufficient blood supply (transient impairment/obstruction)
* O2 demand > O2 supply - affected by increase metabolic demand, vascular resistance, HR
* 2ndary to atherosclerosis
* can lead to collateral artery formation (arteriosclerosis)
Infarction = lack of blood supply (permanent complete obstruction)
- can be caused by erosion or rupture of atherosclerotic plaque (any size)
- can be due to other causes (clot, dissection, conduction)
myocardial ischaemia/infarction used when obstructed blood supply is to myocardium (heart) - Type 1 = spontaneous, type 2 = 2ndary to CAD
39
What does O2 supply to myocardium depend on?
* integrity of pulmonary system
* haemoglobin content
* structural and functional integrity or coronary arteries
* HR
* BP
* coronary artery resistance
40
What are the causes and severity of an infarction?
Cause
* type 1 = spontaneous
* type 2 = 2ndary to CAD
Severity
* impacted artery (L main, LAD, LCx, RCA)
* location along artery (prox/distal)
* time w/o blood supply (amount of necrosis)
Myocardial cells can withstand ischaemia for ~20mins before necrosis, HOWEVER, hypoxia causes electrical conduction changes in cells within 1min
41
Describe Troponin
Released during MI from cystolic pool of myocytes.
Subsequent release prolonged with degradation of actin/myosin filaments.
Differential diagnosis of troponin elevation inc. acute infarction, severe pulmonary embolism causing acute R heart overload, failure and myocarditis.
42
What is angina pectoris?
1st manifestation (Sx) of CAD
feeling = strangling, tightness and heaviness of chest
Sx of ischaemia - reversible (increase blood flow GTN, Re vasc procdure and decrease metabolic demand)
4 basc categories
43
What are the 4 categories of angina pectoris?
1. stable - predictable - occurs at same workload
2. unstable - unpredictable
3. variant/prinzmental's angina - coronary artery spasm, occur at rest, unaffected by exertion, cardiac arrhythmias may occur
4. silent- no pain/chest discomfort - may be as many 70% of episodes - diabetics (neuropathy) - ECG changes
44
What is a stroke?
* rapidly developing loss of brain function due to disturbance in blood vessels supplying blood to brain
- ischaemia (via thrombosis)/ischaemic stroke (embolism)
- haemorrhagic stroke
45
What is the difference between thrombosis and embolism?
Thrombosis happens when a blood clot, aka thrombus, grows in blood vessels = reduce blood flow.
Embolus = foreign material that travels within body. If it becomes stuck and severely blocks the flow of blood, the issue is called an embolism.
46
What is peripheral arterial disease?
Inc. all diseases caused by obstruction of large arteries in arms/legs
Can be acute/chronic and result from: atherosclerosis/thrombus/embolism
Other terms:
- peripheral vascular disease (PVD)
- peripheral artery occlusive disease (PAOD)
47
What is heart failure and what are the causes?
* Condition resulting from structural/functional cardiac disorder that impairs ability of heart to fill/pump sufficient amount of blood throughout body.
Causes
* idiopathic, ischaemic, arrhythmic, diabetes/ HIV congenital, valve disease, substance abuse, disease of heart muscle
47
What is cardiomyopathy and list some potential causes?
Heart muscle disease
"myo" = heart, "pathy" = disease
Deterioration of myocardium function//risk of arrhythmia/sudden death
Causes:
* virus/infection
* valve
* alcohol/substance abuse
* iodopathic, chemi, pregnancy, familial/genetics, arrhythmic, hypertensive, metabolic (thyroid)
48
Define inflammatory and the types.
Inflammation of heart muscle/ surrounding tissue
Types:
* endocarditis (endocardium= inner layer, valves)
* myocarditis (myocardium=muscle)
*pericarditis (pericardium=fibrous outer sac)
*inflammatory cardiomegaly
48
What is the difference between stable and unstable angina?
Stable angina (more common) – attacks have a trigger (such as stress or exercise) and stop within a few minutes of resting.
Unstable angina (more serious) – attacks are more unpredictable (they may not have a trigger) and can continue despite resting.
49
Is CVD preventable?
According to the 2017-18 National Health Survey:
* 9 in 10 Australians had at least one risk factor
* 1 in 4 Australians (25%) have 3 or more risk factors
* 1 in 5 Australians (20%) have high blood pressure
Presence of multiple risk factors accelerates development of atherosclerosis
50
What are risk factors?
Range of health related behaviours, conditions/other factors that increase risk of health disorder or other unwanted condition or event
Modifiable vs non-modifiable -- influenced by socioeconomic, environmental, societal factors
51
Provide examples of non-modifiable risk factors.
AGE
* strongest risk factor for CHD
* people in 7th decade of life have 10x greater risk than those in 3rd decade
BIOLOGICAL SEX
* males>women until 7th decade of life
* protective effect of oestrogen during middle age
FAMILY HX
* 2 fold greater risk fi 1st degree relative had CHD (malves <55y; female <65y)
* even further risk fi multiple 1st degree relatives or they were aged <45y
52
What is the INTER-heart Study?
International case-control study of acute MI undertaken in 52 countries
* 30k subjects
* 90% causes of AMI could be attributed to 9 measurable modifiable risk factors
Risk Factors:
* smoking, abnormal lipids, hypertension, idiabetes, abdominal obesity, psychosocial factors, alcohol consumption, lack of regular PA, insufficient fruit/vege consumption
53
What is the risk of smoking relative to CVD?
Leading reversible risk factor for CVD
* ~ 12% of the burden (death and illness)
Smoking cessation:
* ↓ risk of recurrent MI by 50% in 1 year
* ↓ risk to that of a non smoker within 2 years
Smoking rates are declining (AIHW, 2021):
* In 2019, 11% of 14y+ smoked daily
* In 1991, 24% of 14y+ smoked daily
54
What is the risk of hypertension relative to CVD?
* risk factor for stroke and CAD
- systolic BP stronger risk factor than diastolic BP
- according to ABS, 30% Aus aged >25y had high BP
55
What is optimal, normal and high normal BP?
<120 / <80
120-129 / 80-84
130-139 / 85-59
56
What is the BP range for Grade 1 (mild), Grade 2 (moderate), Grade 3 (severe) and Isolated systolic hypertension?
140-159 / 90-99
160-179 / 100-109
>180 / >110
>140 / <90
57
What is the Tx for hypertension?
Lifestyle:
* increase PA
*reduced weight/waist
* dietary changes
* smoking cessation
* alcohol reduction
Pharmacological Tx
* diuretics
* beta-blockers
* Ca2+ antagonists
* Angiotensive-converting enzyme inhibitors (ACE)
* angiotensi II receptor blockers (ARBs)
58
What is dyslipidaemia?
Cholesterol = fat-like substance (lipid) produced by liver, found in cell membranes
◦ Linear relationship with CVD risk and increasing blood cholesterol levels
◦ total blood cholesterol of 5.5 mmol/L = high and 6.5 mmol/L or greater is very high risk
◦ Desired level < 4.0 mmol/L
59
What is the diff between LDL and HDL? What is triglyceride?
LDL= bad, causes plaque build-up by carrying cholesterol from liver to tissues
◦ High levels – independent predictor of CVD risk: Desired level <2.0 mmol/L
HDL = good - protective effect to reduce plaque build-up, carries cholesterol back to liver
◦ Low levels – independent predictor of CVD risk: Desired level > 1.0 mmol/L
TG - another type of fat - affected by dietary fat/alcohol intake - excess levels can cause plaque
Desired level <2.0mmol/L
60
What are the lipid targets?
Total-cholesterol <4.0 mmol/L
* HDL-cholesterol ≥1.0 mmol/L
* LDL-cholesterol <2.0 mmol/L
* Triglycerides <2.0 mmol/L
* Non HDL-cholesterol <2.5 mmol/L
61
What is the Tx of lipids?
LIFESTYLE
* healthy weight
* alcohol reduction
* increase PA
* dietary changes (fat modification, increase fibre/fruit/vege, plant stanols or sterols)
PHARMA Tx
* statins
* fibrates (lower Trig and increase HDL)
62
What are the Sx of diabetes mellitus?
Polyuria - excessive urination
Polydipsia - excessive thirst
Weight loss
increase susceptibility to infections
63
How is diabetes mellitus Dx?
Fasting Plasma glucose >6.9mmol/L - easier/faster/less expensive/ - 8hrs fasting
OGTT (>11mmol/L)
- person consumes glucose drink (75g glucose), with blood samples taken afterwards to determine rate of glucose cleared from blood
- 8hrs fasting, more sensitive to diagnose pre-diabetes
HbA1c
* glycated haemoglobin >6.5%
* reveals glucose levels over longer period (3M)
* Aus new diagnostic criteria for diabetes
Impaired fasting glucose = >6.1mmol/L but <6.9mmol/L
OGTT (>7.8mmol/L but <11mmol/L)
64
What % of adults are physically inactive?
According to the National Health Survey (2017-2018):
* 54% of Australian adults are not sufficiently active
* 34% of Australian adults are not doing any physical activity
* 40% of Indigenous adults are not doing any physical activity
Recommendationsshould align with the National Physical Activity
Guidelines for Australians
◦ 150-300mins moderate intensity physical activity + 2 resistance
sessions per week
65
What is the prevalence of obesity?
Overweight/obesity = abnormal/excessive fat accumulation that may
impair health (WHO).
* 54% of Aus adults overweight/obese
* Increased from 38% of adults 15 years ago
66
What is metabolic syndrome?
AKA Syndrome X
Central obesity: waist circumference men ≥ 94 and women ≥ 80
* PLUS ANY 2:
1. Raised TG level: (mmol/L) ≥ 1.7, or specific Tx for this lipid abnormality
2. Reduced HDL cholesterol: (mmol/L) < 1.03 males and < 1.29 females
3. Raised BP: (mm Hg) ≥ 130/85, or Tx of previously Dx hypertension
4. Raised fasting plasma glucose: (mmol/L) ≥ 5.6, or previously Dx T2DM
67
What are the metabolic/vascular benefits of 10% weight loss?
BP - falls ~10mmHg
Diabetes - decreases up to 50% in fasting glucose for newly Dx
People at risk e.g.
impaired glucose tolerance:
◦ >30% fall in fasting or 2hr-insulins
◦ >30% increase in insulin sensitivity
◦ 40-60% fall in incidence of diabetes
Lipids:
◦ Fall of 10% in total cholesterol
◦ Fall of 15% in LDL-C
◦ Fall of 30% in triglycerides
◦ Rise in 8% in HDL-C
Mortality
◦ >20% fall in all cause mortality
◦ >30% fall in deaths related to diabetes
◦ >40% fall in deaths related to obesity
68
Provide guidance on alcohol consumption?
No more than 10 standard drinks per week
No more than 4 standard drinks in one day
69
How do psychosocial factors affect risk of CVD?
Link between depression and CHD
* depression 3x more common in patientsa after MI than general community
* depression doubles risk of another cardiac event 1-2yrs after MI
Patients screened using Patient Helath Questionnaire
Social isolation / chronic life stress can progress CHD
70
Provide some statistics on health literacy.
Health literacy = knowledge/skills required to access, understand and use info relating ot health issues
- impacts persons health/cost to broader community
- according to ABD< 59% of 15-74y had below adequate health ltieracy
- people living rural / poorer self-assessed health status were more likely to have lower health literacy
- places greater risk of adverse health outcomes
