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EXMD4742 > WK1 - Cardiovascular System > Flashcards

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)
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2
Q

What is the flow of deoxygenated blood?

A
  1. SUP/INF vena cava
  2. R atrium
  3. through tricuspid valve
  4. R ventricle
  5. through pulmonary valve
  6. pulmonary artery
  7. lungs
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3
Q

What is the flow of oxygenated blood?

A
  1. lungs
  2. pulmonary veins
  3. L atrium
  4. through mitral valve
  5. L ventricle
  6. aortic valve
  7. aorta
  8. to rest of body
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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

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5
Q

What are the atroiventricular valves?

A

Tricuspid valve (RA –> RV)
Mitral valve (aka bicuspid) (LA –> LV)

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6
Q

What are the semilunar valves?

A

Pulmonary valve (RV–> pulmonary artery)

Aortic valve (LV –> aorta)

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7
Q

What are the acute marginal coronary arteries?

A

R coronary artery
POS descending artery
R marginal artery (descends of R coronary artery)

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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)

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9
Q

What are the obtuse marginal artieries?

A

L ANT descending ( or interventricular) artery ( descended from L coronary artery)

Diagonal Branch

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10
Q

When does filling occur?

A

during diastole with closure of the aortic valve

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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)

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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)
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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)

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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)

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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%

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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

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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
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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

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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)
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20
Q

What is released during stimulation of the SNS?

A

Releases norepinephrine and acts on 2 types of adrenergic receptors within heart.

  1. Alpha receptors - excitatory) = vasoconstriction of arteries/veins
  2. 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)
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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

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22
Q

Define stroke volume

A

volume of blood pumped out of LV during systolic contraction.

SV (mL) = EDV - ESV

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23
Q

Define ejection fraction (%)

A

fraction of blood pumped out of heart during systolic contraction

% = [(EDV-ESV)/EDV]*100

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24
Q

Define CO.

A

(Q) = volume of blood pumped by heart (i.e. stroke volume per minute)

Q (L/min) = HR*SV

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25
Q

What are normal values for EDV and ESV?

A

EDV
males 107 +/- 27mL
females 84 +/- 22mL

ESV
males 40 +/- 12mL
females 30 +/- 10mL

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26
Q

What are the normal values for ejection fraction and stroke volume?

A

EF
males 63 +/- 6%
females 64 +/- 6%
Normal targets 50-70%

SV
males 74.3 +/- 17.2
females 62.5 +/- 14.3

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27
Q

What are the normal values of HR and CO?

A

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

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28
Q

What is stroke volume and what affects it?

A

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
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29
Q

What is Systemic vascular resistance (SVR)?

A

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
Q

What is peripheral circulation? Explain the mechanisms and factors that affect it.

A

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
Q

What is BP? Define the different types and how to calculate it.

A

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
Q

What are the leading causes of death in Aus males in 2020?

A
  1. CHD 10,040 males
  2. dementia inc. alzheimer
  3. lung cancer
  4. cerebrovascular disease
  5. prostate cancer
33
Q

What are the leading causes of death in Aus females in 2020?

A
  1. dementia inc alzheimers
  2. CHD 6547 females
  3. cerebrovascular disease
  4. lung cancer
  5. BCa
34
Q

List some common CVDs.

A

Heart disease
- CHD
- heart failure (inc. cardiomyopathy)
- inflammatory
Cerebrovascular disease/stroke
Peripheral vascular disease

35
Q

What is atherosclerosis?

A

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
Q

Explain the development of athersclerotic plaques.

A
  1. normal
  2. fatty streak creating foam cells
  3. lipid-rich plaque creating a lipid core
  4. fibrous cap causing thrombus
37
Q

How does atherosclerosis affect arterial structure and functional capacity?

A

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
Q

What is the difference between ischaemia and infarction?

A

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
Q

What does O2 supply to myocardium depend on?

A
  • integrity of pulmonary system
  • haemoglobin content
  • structural and functional integrity or coronary arteries
  • HR
  • BP
  • coronary artery resistance
40
Q

What are the causes and severity of an infarction?

A

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
Q

Describe Troponin

A

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
Q

What is angina pectoris?

A

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
Q

What are the 4 categories of angina pectoris?

A
  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
Q

What is a stroke?

A
  • 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
Q

What is the difference between thrombosis and embolism?

A

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
Q

What is peripheral arterial disease?

A

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
Q

What is heart failure and what are the causes?

A
  • 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
Q

What is cardiomyopathy and list some potential causes?

A

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
Q

Define inflammatory and the types.

A

Inflammation of heart muscle/ surrounding tissue

Types:
* endocarditis (endocardium= inner layer, valves)
* myocarditis (myocardium=muscle)
*pericarditis (pericardium=fibrous outer sac)
*inflammatory cardiomegaly

48
Q

What is the difference between stable and unstable angina?

A

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
Q

Is CVD preventable?

A

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
Q

What are risk factors?

A

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
Q

Provide examples of non-modifiable risk factors.

A

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
Q

What is the INTER-heart Study?

A

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
Q

What is the risk of smoking relative to CVD?

A

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
Q

What is the risk of hypertension relative to CVD?

A
  • 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
Q

What is optimal, normal and high normal BP?

A

<120 / <80

120-129 / 80-84

130-139 / 85-59

56
Q

What is the BP range for Grade 1 (mild), Grade 2 (moderate), Grade 3 (severe) and Isolated systolic hypertension?

A

140-159 / 90-99

160-179 / 100-109

> 180 / >110

> 140 / <90

57
Q

What is the Tx for hypertension?

A

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
Q

What is dyslipidaemia?

A

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
Q

What is the diff between LDL and HDL? What is triglyceride?

A

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
Q

What are the lipid targets?

A

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
Q

What is the Tx of lipids?

A

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
Q

What are the Sx of diabetes mellitus?

A

Polyuria - excessive urination
Polydipsia - excessive thirst
Weight loss
increase susceptibility to infections

63
Q

How is diabetes mellitus Dx?

A

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
Q

What % of adults are physically inactive?

A

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
Q

What is the prevalence of obesity?

A

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
Q

What is metabolic syndrome?

A

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
Q

What are the metabolic/vascular benefits of 10% weight loss?

A

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
Q

Provide guidance on alcohol consumption?

A

No more than 10 standard drinks per week

No more than 4 standard drinks in one day

69
Q

How do psychosocial factors affect risk of CVD?

A

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
Q

Provide some statistics on health literacy.

A

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

EXMD4742 (9 decks)

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