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Cardiovascular System > Physio > Flashcards

Physio Flashcards

1
Q

What is the order of electrical flow within the conducting system of the heart?

A

1) SA node
2) Internodal tracts
3) AV node
4) Main branch
5) L/R Bundle
6) Purkinje Fibre

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2
Q

How frequently does the SA node usually depolarise?

A

~80 times/min

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3
Q

True or false: Every part of the heart’s conducting system is capable of discharging electrical signals autonomously.

A

True

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4
Q

When does the SA node NOT set the pace of the heart? What happens then?

A

When the SA node is compromised, slower components (eg. AV node) will take over and set the pace of the heart.

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5
Q

How does the conducting system help the atria function as a priming pump?

A

There is a SA-AV delay (0.13s) in depolarisation, allowing time for the atrium to fully fill the ventricles before they pump.

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6
Q

Describe the blood supply of the conductive system of the heart.

A

Right Coronary Artery supplies everything

Left Anterior Descending Artery supplies (i) Right bundle (ii) Left bundle

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7
Q

Which part of the brain controls the regulation of heart rate via the autonomic nervous system?

A

Vasomotor centre

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8
Q

What are 4 receptors/inputs that communicate information to the vasomotor center to regulate heart rate?

A

1) Afferent pain fibres (pain → ↑HR)
2) Chemoreceptors (↓pH/↑CO2 → ↑HR)
3) Respiratory centre (Inspiration → ↑HR)
4) Baroreceptors (↓BP → ↑HR)
5) H+ ions

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9
Q

Describe how the ANS system can regulate heart rate.

A

Sympathetic:
NE → ß1 of SAN → ↑Na+/Ca+ influx → depolarise → ↑HR

Parasympathetic:
ACh → Muscarinic of SAN → ↑K+ influx → polarise → ↓HR

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10
Q

Describe the heart rate can be regulated directly (w/o ANS).

A

1) Temperature (↑temp → ↑HR)
2) Thyroxin (thyroid hormone → ↑HR)
3) Catecholamines (stress hormone → ↑HR)

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11
Q

How does sympathetic and parasympathetic activation affect the membrane potential and action potential?

A

Sympathetic: more +ve resting, shorter pre-potential

Parasympathetic: more -ve resting, longer pre-potential

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12
Q

What are the 5 phases of ventricular muscle contraction?

A

0) Fast voltage-gated Na+ channel → Na+ influx → depolarisation

1) Outward-rectifying K+ channel → K+ efflux → slight repolarisation

2) Voltage-gated Ca2+ channel → Ca2+ influx → continued but slow repolarisation (depolarisation masked by K+ repolarising)

3) more outward-rectifying K+ channel → ↑K+ efflux → repolarisation back to resting potential

4) inward-rectifying K+ channel → maintain resting potential (~-85mV)

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13
Q

Which part of the cardiac cycle corresponds to the P wave of an ECG?

A

Atrial depolarisation

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14
Q

Which part of the cardiac cycle corresponds to the QRS complex of an ECG?

A

Ventricular depolarisation

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15
Q

Which part of the cardiac cycle corresponds to the T wave of an ECG?

A

Ventricular repolarisation

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16
Q

Which part of the ECG corresponds to AV nodal delay?

A

PR interval

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17
Q

Which part of the ECG corresponds to electrical conduction in the ventricles?

A

QT interval

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18
Q

Which part of the ECG corresponds to when the ventricles are isoelectric?

A

ST interval

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19
Q

What does a tall QRS complex indicate in a px?

A

Hypertrophy

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20
Q

What does a tall T wave indicate in a px?

A

Hyperkalaemia

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21
Q

What does an elevated ST-segment indicate in a px?

A

Myocardial Infarction

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22
Q

What does a depressed ST-segment indicate in a px?

A

Myocardial Ischaemia

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23
Q

What does a RSR- indicate in a px?

A

Ventricular block

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24
Q

What does a tall p wave indicate in a px?

A

Atrial hypertrophy

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25
Q

Which leads face the septal region of the heart?

A

V1, V2

Reciprocal: None

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26
Q

Which leads face the anterior region of the heart?

A

V3, V4

Reciprocal: None

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27
Q

Which leads face the lateral region of the heart?

A

I, aVL, V5, V6

Reciprocal: II, III, aVF

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28
Q

Which leads face the inferior region of the heart?

A

II, III, aVF

Reciprocal: I, aVL (Lateral)

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29
Q

Which leads face the posterior region of the heart?

A

None

Reciprocal: I, II, III, IV (Anteroseptal)

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30
Q

Which coronary vessels could be affected/occluded in a px with ST-elevation in leads V1-4 and no reciprocal?

A

Left Anterior Descending

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31
Q

Which coronary vessels could be affected/occluded in a px with ST-elevation in leads I, aVL, V3-6 and reciprocal in II, III, aVF?

A

Left Circumflex Artery

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32
Q

Which coronary vessels could be affected/occluded in a px with ST-elevation in leads II, III, aVF and reciprocal in I, aVF?

A

Right Coronary Artery

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33
Q

Which coronary vessels could be affected/occluded in a px with no ST-elevations but inverted in V1-4?

A

Right Coronary Artery (posterior descending branch)

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34
Q

Where are the electrodes placed for a 12 lead ECG reading?

A

Limb leads:
LA: L wrist
RA: R wrist
LL: L ankle (medial side)
N: R ankle (medial side)

Chest leads:
V1: 4th ICS R of sternum
V2: 4th ICS L of sternum
V3: btwn V2&4
V4: 5th ICS Mid-clavicular
V5: 5th ICS Anterior axillary
V6: 5th ICS Mid-axillary

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34
Q

Which of the ECG electrodes are standard limb leads (bipolar)?

A

I, II, III

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34
Q

Which of the ECG electrodes are augmented vector limb leads (unipolar)?

A

aVL, aVF, aVR

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34
Q

How do you determine if the mean QRS axis is normal?

A

I and aVF are +ve

or I +ve, aVF -ve but II +ve

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35
Q

What is the mean QRS axis deviation if I+, aVF-, II-?

A

Left axis deviation

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36
Q

What is the mean QRS axis deviation if I-, aVF-?

A

Extreme axis deviation

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37
Q

What is the mean QRS axis deviation if I-, aVF+?

A

Right axis deviation

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38
Q

Right ventricular hypertrophy would lead to ________ QRS axis deviation.

A

Right

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39
Q

Left ventricular hypertrophy would lead to ________ QRS axis deviation.

A

Left

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40
Q

Myocardial contraction occurs when calcium binds to ______.

A

Troponin C

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41
Q

Calcium enters myocardial cells through _____________.

A

Voltage-gated Ca2+ channels.

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42
Q

Calcium is removed from the myocardial cytoplasm by the _______________.

A

Na/Ca exchanger

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43
Q

Ventricular muscle relaxation is a (passive/active) process.

A

Active

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44
Q

What is the Frank Starling Mechanism?

A

The intrinsic ability of the heart to adjust pumping capacity to handle changing volumes presented to it.
↑VEDL → ↑SV (until it plateaus)

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45
Q

What is the definition of contractility?

A

The change in work performed by the heart, not brought about by a change in initial fiber length

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46
Q

Contractility of the heart is regulated by the _______________.

A

Sympathetic nervous system

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47
Q

What is the difference between contractility and starling’s mechanism?

A

Stroke volume increase in both, but:
Starlings: ↑EDV → ↑SV
Contractility: same EDV but ↑SNS → ↑SV

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48
Q

How is contractility of the heart measured?

A

Ejection fraction= (SV/EDV) x 100%

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49
Q

What is the normal range of ejection fraction?

A

55-75%

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50
Q

In the cardiac cycle, filling occurs at (high/low) pressures whilst blood is ejected at (high/low) pressures.

A

Filling: low pressure
Ejection: high pressure

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51
Q

How does the heart alternate between phases of high and low ventricular pressures between systole and diastole?

A

Rapid ↑P: Isovolumetric contraction (Both AV and SL closed before aortic open)
Rapid ↓P: Isovolumetric relaxation (Both AV and SL closed before AV open)

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52
Q

When does the mitral valve open and close?

A

opens at end of isovolumetric relaxation when P ventricle<P atria

closes at start of isovolumetric contraction/start of systole

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53
Q

When do the AV valve open and close?

A

opens at end of isovolumetric contraction when P ventricle>P aorta (start of ejection phase of systole)

closes at end of ejection phase (end of systole)

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54
Q

What produces the S1 heart sound?

A

Closure of Mitral valve at start of isovolumetric contraction

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55
Q

What produces the S2 heart sound?

A

Closure of AV valves at end of ejection/systole

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56
Q

What produces the S3 heart sound?

A

After opening of MV by rapid ventricular filling

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57
Q

In what type of px is S3 heard?

A

S3 can be a normal finding in children, pregnant females and well-trained athletes
Abnormal in normal adults (don’t usually have very compliant ventricles)

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58
Q

What produces the S4 heart sound?

A

During atrial systole, late in ventricular diastole
Produced by contraction of the atria pushing blood into a stiff or hypertrophic ventricle

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59
Q

In what type of px is S4 heard?

A

px with LVH (usually secondary to diastolic heart failure or active ischemia)

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60
Q

Which wave of an ECG/heart sound corresponds to the start of ventricular systole/isovolumetric contraction?

A

R wave, S1

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61
Q

Which wave of an ECG/heart sounds corresponds to the start of ventricular diastole?

A

End of T wave, S2

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62
Q

Which vein is observed for Jugular Venous Pulse?

A

Internal jugular vein

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63
Q

Why is the internal jugular vein used for examination of a px jugular venous pulse?

A

Internal jugular vein (IJV) connects to the right atrium without any intervening valves, resulting in a continuous column of blood. The presence of this continuous column of blood means that changes in right atrial pressure are reflected in the IJV (e.g. raised right atrial pressure results in distension of the IJV).

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64
Q

How can a jugular venous pulse be accentuated?

A

Use Hepatojugular reflex

65
Q

When is JVP raised?

A

When RA pressure>0-5mmHg
eg. tricuspid/pulmonary stenosis/regurg, ASD, RHF

66
Q

When does ventricular systole occur in a ECG?

A

Between R wave and end of T wave

67
Q

What are the 5 components of the jugular venous pulsation?

A

A wave: atrial contraction
C wave: carotid transmission
X descent: ↓P following A
V wave: passive filling of atria from I/SVC
Y descent: ↓P during atrial + ventricular diastole

68
Q

What causes the apex beat to be palpable?

A

The tapping of the LV against the chest wall during contraction

69
Q

Where is the apex beat located normally?

A

5th ICS, mid clavicular line

70
Q

True or false. The apex beat is caused by ventricular systole, pushing the apex of the heart against the chest wall.

A

False. The apex beat is the point farthest outwards (laterally) and downwards (inferiorly) from the sternum at which the cardiac impulse can be felt.

71
Q

When does splitting of S2 occur?

A

During inspiration when pulmonary valves close later than aortic valve (RV handles more blood during inspiration)

72
Q

Which heart defect is associated with a ejection systolic mumur, heard on the 2nd R ICS, and L sternal edge?

A

Aortic stenosis

Can cause carotid bruit (radiation of murmur to R carotid artery)

73
Q

Which heart defect is associated with a pansystolic mumur, heard over the apex?

A

Mitral regurgitation

74
Q

Which heart defect is associated with a mid-diastolic mumur, heard over the apex?

A

Mitral stenosis

75
Q

Which heart defect is associated with a early diastolic mumur, heard over the left sternal edge, 4th ICS?

A

Aortic regurgitation

76
Q

What type of left ventricular hypertrophy is caused by aortic regurgitation?

A

Eccentric

77
Q

How is BP affected by aortic regurg?

A

↑Systolic, ↓ Diastolic pressure

78
Q

What type of left ventricular hypertrophy is caused by aortic stenosis?

A

Concentric

79
Q

Why is most of the blood volume in the venous system?

A

High compliance of veins

80
Q

What are the 2 ways to calculate cardiac output?

A

SV x HR
or
Arterial pressure / Total Peripheral resistance

81
Q

What is the main site of resistance in the circulatory system?

A

Arterioles

82
Q

What is the main factor in determining the resistance in arterioles?

A

Much smaller radius than arteries

83
Q

Ohm’s law governs _______ in circulation by relating flow, pressure and resistance.

A

Rate of blood flow

84
Q

Poiseuille Hagen formula governs _________, particularly in arterioles.

A

Resistance

85
Q

When total peripheral resistance ↑, pressure in circulation (↑/↓) for any rate of flow.

A

TPR↑ → P↑

86
Q

What is tissue perfusion?

A

Rate of blood flow into capillary network

87
Q

What are 5 factors affecting tissue perfusion?

A

Blood flow in arteries: (Systemic factors)
1) Arterial BP
2) Cardiac output

Arteriolar vasomotor tone: (Local factors)
1) Local factors (↓flow → ↑metabolic products → ↑ local NO → arteriolar vasodilation)
2) Autoregulation (reflex vasoconstriction to ↑BP)
3) Circulating hormones (Epinephrine, Norepinephrine, ADH)
4) SNS

88
Q

How is tissue perfusion clinically assessed?

A

Capillary refill time

The performing examiner applies manual pressure to the ventral surface of the distal phalanx of fingers or toes until the nailbed is blanched. This pressure is maintained for ten seconds and then released. The amount of time, in seconds, that transpires before reperfusion occurs and normal color returns to the digit is the CRT.

89
Q

What are 4 starling’s forces at the capillary determining capillary exchange?

A

1) Capillary pressure (hydrostatic by blood)
2) Colloid osmotic pressure (inward pull by proteins eg. albumin)
3) Interstitial fluid pressure (-ve, maintained by lymphatics)
4) Interstitial colloid pressure (+ve from proteins)

90
Q

What is the net starling’s force at the capillary (inward/outward) and how is it removed?

A

Net outward ~0.3mmHg
Excess extravasated fluid (3L/day) removed by lymphatic system

91
Q

How does heart failure cause edema?

A

↑Venous pressure → ↑outward capillary pressure → ↑ fluid extravasation

92
Q

How does Nephrotic syndrome cause edema?

A

Plasma protein (eg. albumin) loss → ↓oncotic pressure → ↑ fluid extravasation

93
Q

How does filariasis cause edema?

A

Obstruct lymphatic flow → extravasated fluid not cleared, accumulates locally

94
Q

How does acute inflammation cause edema?

A

↑ Capillary permeability → ↑ fluid extravasation

95
Q

What is the definition of cardiac output?

A

Volume of blood pumped by left ventricle into the aorta per min

96
Q

What are 3 cardiac factors affecting cardiac output?

A

1) Preload (volume)
2) Heart (contractility, HR)
3) Afterload (TPR)

97
Q

What are 2 definitions of heart failure?

A

1) Failure of heart to pump at sufficient rate to meet metabolic requirements of tissues

2) Only able to meet metabolic Dd at elevated filling pressures (after compensation)

98
Q

How does Hemorrhage affect CO?

A

↓ Preload and afterload → ↓CO
↑contractility and HR (compensatory)

99
Q

How does MI or bradycardia affect CO?

A

↓ contractility and HR respectively → ↓CO

100
Q

How does hypertension affect CO?

A

↑Afterload → ↓CO

101
Q

What are the typical presentation for px with acute heart failure that manifest as a result of acute compensation?

A

↑SNS, ↓PNS:
↑HR
↑Sweating
↑contractility (heart palpitations)
pallor

102
Q

What are the typical presentation for px with chronic heart failure that manifest as a result of chronic compensation?

A

RAAS activation:
Oliguria
Oedema
SOB (orthopnea, NPD)
Low BP
Fatigue
Raised JVP

103
Q

How is RAAS activated in heart failure?

A

↓BP → detected by macula densa → JG secrete renin
Renin → AT1 → AT2 → ↑BP
AT2 → Aldosterone → Salt and water retention → ↑BP

104
Q

Why is activation of RAAS maladaptive?

A

Chronically elevated levels of AT2
→ remodels heart (inflammation, fibrosis, hypertrophy) → ↓effective as a pump
→ decreases NO (impt vasodilator) → ↑TPR → ↑workload/afterload

105
Q

What is the criteria for HFrEF?

A

EF<40%

106
Q

What is the criteria for HFpEF?

A

EF>50%

107
Q

What is the criteria for borderline HFpEF/HFmrEF?

A

40%<EF<50%

108
Q

How do you differentiate left and right heart failure?

A

RHF: Backpressure on systemic venous circulation
1) Raised JVP
2) Hepatosplenomegaly
3) Peripheral Oedema

LHF: Back pressure on pulmonary circulation
1) Engorged pulmonary veins
2) SOB (exertional dyspnea, Orthopneam NPD)
3) Raised JVP
4) Coarse crepitations in lungs
5) 3rd heart sound

109
Q

What are 6 Ix for a px with suspected HF?

A

1) CXR (venous distention, pulmonary edema)
2) ECG (STEMI)
3) BNP
4) EF
5) Troponin 1
6) Echo (E/A ratio)

E/A >2 → Restrictive filling
E/A <1 → LV diastolic dysfunction

110
Q

What counteracts the effects of AT2?

A

AT1-7 produced by ACE 2 enzyme

111
Q

Why is the endothelial layer of the coronary arteries most vulnerable to ischaemia?

A

1) Coronary arteries branch into myocardium (<Ss than epicardium, > impact when flow ↓)
2) Coronary vessels in myocardium are compressed in systole
3) Tension > in myocardium

112
Q

A full thickness infraction results in a STEMI/NSTEMI?

A

STEMI

113
Q

An NSTEMI is caused by what degree of myocardial infarction?

A

Non-full thickness (between endo/myocardium)

114
Q

What is the normal coronary blood pressure/flow?

A

60-160mmhg

115
Q

How is coronary blood flow kept relatively constant between mean arterial pressures of 60 to 140 mmHg?

A

Autoregulation by:
1) NO → vasodilation
- produced by endothelium under shear stress and local metabolites
- ↓Ca release by myocardium → inhibit vasoconstrictor endothelin-1
- inhibiting the release of norepinephrine from sympathetic nerve terminals

2) Myogenic response
- “stretch-sensitive” receptors/channels on myocytes
- ↑P → depolarisation and Ca release → vasoconstriction.
- ↓P → muscle relaxes, maintaining blood flow

116
Q

Why does angina pectoris occur?

A

Metabolic Dd > Coronary supply

117
Q

What are 3 factors that ↑ the workload of the left ventricle, possibly leading to angina?

A

1) ↑Arterial pressure & Stroke volume (eg. HTN)
2) ↑HR (eg. stress, exercise)
3) ↑ventricle radius (eg. eccentric hypertrophy)

118
Q

What are 2 factors that ↓ coronary supply, possibly leading to angina?

A

1) Occlusion (eg. atherosclerosis)
2) Diastolic duration (eg. Afib, tachycardia)
3) Diastolic pressure (eg. aortic regurg)

119
Q

Blood flow in the left coronary artery is higher during (diastole/systole).

A

Blood supply to the LV occurs predominantly during diastole. The tension in the ventricular walls during systole impedes blood flow in the coronary arteries.

120
Q

The (left/right) ventricle is more susceptible to changes in diastolic time and pressure.

A

Left
Blood flow to the right ventricle is about equal in both phases of the cardiac cycle. The tension in the walls of the right ventricle during systole is lower compared to the left ventricle.

121
Q

What are 2 forms of acute CAD?

A

1) MI
2) Unstable angina

122
Q

What are the medical interventions for acute CAD (4)?

A

1) Ix
2) Percutaneous coronary interventions
3) CBAG
4) Drugs + lifestyle modifications

123
Q

What are 3 forms of chronic CAD?

A

1) Stable angina (#1)
2) Vasospastic angina
3) Microvascular angina

124
Q

What are the medical interventions for chronic CAD (3)?

A

Address Dd<Ss
1) Nitrates
2) ß-blockers
3) Ca channel blockers
4) Ivabradine

125
Q

What are the differences between stable angina and unstable angina?

A

Unstable angina typically have pain even at rest

Stable: fixed obstruction (degree relatively stable/time)
Unstable: Dynamic obstruction (clots may break down and reform, can ↑ size rapidly)

126
Q

Why are cardiac reserved diminished in the aged?

A

1) ↓organ performance
2) Pre-existing compensatory mechanisms already used

127
Q

What are 5 reasons why maximal CO is reduced in the elderly?

A

1) Heart is stiffer
a) ↓Ca reuptake to SER → slower relaxation
b) Interstitial fibrosis of myocardium (by AG2)
c) ↑ TPR by (i) progressive replacement of elastic by cross-linked collagen (ii) endothelial dysfunction by oxidative stress/inflammation (iii) artherosclerosis

2) ↓early diastolic filling → ↑late filling by atrial systole
3) ↓ diastolic time (↑AP duration → longer systole)
4) ↓SV (↓ filling)
5) < responsive to SNS stimulation

128
Q

A stiffer aorta leads to (higher/lower) systolic and (higher/lower) diastolic pressures.

A

Higher systolic
Lower diastolic
(widened pulse pressure)

129
Q

Why are the elderly more predisposed to having postural hypotension?

A

Degeneration of baroreceptor reflexes

130
Q

What are 3 factors that lead to the degeneration of baroreceptor reflexes in the aged?

A

1) ↓responsiveness of baroreceptors to stretch
2) ↓ elasticity of aorta and carotid arteries
3) change in ANS
4) ↓ responsiveness of heart to ANS

131
Q

Why is exercise capacity reduced in older adults?

A

1) Max HR↓
2) Heart is less responsive to SNS → max contractility ↓

132
Q

Why are older adults more prone to develop systolic hypertension?

A

Aortic stiffness:
→ ↓ buffering capacity of the aorta during systole
→ ↑ pulse pressure wave velocity → reflected pulse pressure wave to return to the aorta more quickly and in phase with systole of the next cycle → ↑ systolic BP

133
Q

Why is diastolic BP lower in older adults?

A

Stiff aorta (↓elasticity)
(Diastolic BP is dependent on the elastic recoil of the aorta)

134
Q

Why are older adults more prone to develop HF with atrial fibrillation (AF)?

A

↓ early diastolic filling (stiffer ventricles)
→ more dependent on atrial “kick” (contraction) for ventricular filling
- Atrial “kick” is absent in AF, no coordinated contraction of the atrial muscle → ↓ ventricular filling more significantly in older adults compared to younger patients

135
Q

What are 5 reasons why are older adults more prone to develop ischemic heart disease?

A

1) ↑ Atherosclerotic plaques
2) ↓ Elasticity of coronary arteries (↓ compensatory dilation)
3) ↓ Diastolic pressures by aortic stiffness → ↓myocardial perfusion
4) ↑ Afterload due to aortic stiffness and peripheral resistance
5) ↑ Afterload → LVH → ↑Dd

136
Q

What are 3 ways to calculate mean arterial pressure calculated?

A

1) CO x TPR
2) 2/3 diastolic + 1/3 systolic
3) Diastolic + 1/3 pulse pressure

137
Q

What is systemic pressure?

A

Pressure in the arterial system during systole

138
Q

What is diastolic pressure?

A

Pressure during diastole due to elastic recoil by the arteries (aortic, pulmonary, large)

139
Q

When can the pulse be auscultated with a sphygmomanometer?

A

When diastolic<Pressure<systolic

140
Q

What is pulse pressure?

A

Difference between systolic and diastolic pressures

141
Q

What is the normal pulse pressure?

A

40mmHg

142
Q

When is blood pressure at its physiological lowest?

A

During sleep 2200-0400hrs (diurnal variation)

143
Q

How is blood pressure generated?

A

Ventricular contraction

144
Q

How is high blood pressure from ventricular contraction maintained?

A

1) Valves in heart ensure directional flow
2) Thick walls → low R in arteries
3) Arterioles at end of arteries → high R

145
Q

What is postural hypotension?

A

Sitting to standing
→ ↓venous return (veins very compliant)
→ ↓SV (↓ preload)
→ ↓ MAP

146
Q

Under what blood pressures do baroreceptors have the greatest sensitivity to pressure changes?

A

Around their normal operating pressure of 100mmHg

147
Q

What happens to baroreceptors in px with chronic HTN?

A

Their response curve shifts right (↑ mean operating point and ↑ range of greatest sensitivity)
(↑ “normal” BP)

148
Q

How is arterial blood pressure autonomically regulated in the short term?

A

↑SNS
- Arteriolar vasoconstriction → ↑peripheral resistance
- Venous vasoconstriction → ↑ venous return
- ↑ ventricular contractility→ ↑CO

↓PNS
- ↑HR → ↑CO

149
Q

How is arterial blood pressure autonomically regulated in the longterm?

A

RAAS

150
Q

How is ↓BP detected in the kidneys?

A

1) JG cells: sense tension (BP) in arterioles
2) Macula densa: sense transport of Cl- (cotransported with Na and thus water)

151
Q

What is the main etiology of primary/essential hypertension?

A

No known cause

152
Q

How does smoking predispose a px to HTN?

A

Dysregulation of vascular smooth muscle tone → ↑ R of arteries and arterioles

153
Q

How does obesity predispose a person to HTN?

A

1) Angiotensinogen released from adipocytes
2) ↑ blood volume/preload
3) Increased blood viscosity (dysregulation of clotting)

154
Q

How does hypertension lead to increased risk of heart failure?

A

↑BP → ↑ afterload → myocardial hypertrophies → ↑Dd → HF

155
Q

How does hypertension lead to increased risk of atherosclerosis, thrombosis, aneurysms, etc.?

A

Damage to blood vessels

156
Q

What are 6 lifestyle changes to manage HTN?

A

1) Maintain BMI of 18.5 to 22.9kg/m^2
2) Exercise (150min moderate exercise/week; 10k steps/day)
3) 7-8 hours of sleep/day
4) Healthy diet (5-6g of sodium/day; higher potassium; more fruits, veg, fish, poultry, nuts; less dairy, red meats, sweets)
5) Quit smoking
6) Reduce caffeine and alcohol
7) Reduce stress

157
Q

What is the definition of hypertension?

A

When arterial BP above a level that increases risk for developing complications

158
Q

What is the definition of circulatory shock?

A

When arterial pressure is insufficient to maintain perfusion
Systolic < 80mmHg
Mean BP < 60mmHg

159
Q

What are 4 types of shock?

A

1) Hypovolemic (loss of vol.)
2) Cardiogenic (inadequate CO/pumping)
3) Obstructive (Obstruction to blood flow)
4) Distributive (distributive vasodilation)

160
Q

What are 2 examples of hypovolemic shock?

A

1) Haemorrhage
2) Severe diarrhoea, vomitting

161
Q

What are 3 causes of cardiogenic shock?

A

1) MI
2) Arrhythmias
3) Severe valvular defects

162
Q

What are 3 examples of obstructive shock?

A

1) Pulmonary embolism
2) Tension pneumothorax
3) Pericardial tamponade

163
Q

What are 3 examples of distributive shock?

A

1) Sepsis
2) Anaphylactic
3) Neurogenic

Cardiovascular System (12 decks)

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