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Medicine - Year 2 > Block 13 - Cardiorespiratory systems (cardio) > Flashcards

Block 13 - Cardiorespiratory systems (cardio) Flashcards

1
Q

What is the progression of heart disease? (5)

A

Asymptomatic > Stable angina > Acute coronary syndrome (unstable angina > AMI) > Heart failure > Death

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2
Q

Explain the timeline of atherosclerosis (4)

A
  • Fatty streak augmented by smooth muscle and platelets > inflammation
  • Fibrous cap forms on top > vessel enlargement
  • Core becomes necrotic which increases inflammation
  • Cap thins and ruptures > thrombus formation
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3
Q

What does an ECG look like in a patient who has just exercised and has stable angina?

A

ST depression

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4
Q

What is acute coronary syndrome?

A

Progression from unstable angina to acute myocardial infarction

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5
Q

What is the pain like in angina?

A

‘central tight chest pain’

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6
Q

What does an ECG look like in a patient with unstable angina?

A
  • Normal
  • ST elevation
  • No ST elevation
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7
Q

What is the difference between an ‘interval’ and a ‘segment’ on an ECG?

A

Intervals are bigger and overlap peaks

Segments are smaller and are between peaks

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8
Q

What happens to the ECG when you block a coronary artery (5 stages)

A
  1. peaked T wave (min)
  2. ST elevation (min>hr)
  3. loss of R wave and Q wave formation (hr>day)
  4. T wave inversion
  5. T wave normalisation but persisting Q wave (month)
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9
Q

What happens if you block the LAD or RCA?

Which has the worse prognosis?

A

LAD: reduced supply to the L ventricle (worse prognosis)
RCA: reduced supply to the inferior wall of L ventricle and R ventricle
(right coronary artery)

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10
Q

What ECG change can an NSTEMI have which is worse?

A

ST depression

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11
Q

What protein is measured in the blood to diagnose a heart attack?

A

Troponin

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12
Q

6 other causes of increased troponin

A 
PE
AF
Sepsis
Hypertension
Aortic or brain haemorrhage
Renal dysfunction
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13
Q

How do you die from an MI?

A

Arrhythmia

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14
Q

Explain the pathophysiology behind a myocardial rupture

A

A hinge forms at the edge of the infarct zone

Breakage of this causes bleeding into the pericardial sac

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15
Q

What is a false aneurysm?

A

When the rupture is incomplete and heals itself

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16
Q

How are ruptures diagnosed?

A

ECHO

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17
Q

What is the mitral valve made from?
What is the blood supply to the 2 muscles?
Which muscle has less chance of rupturing?

A

Mitral valve made from 2 leaflets controlled by papillary muscles
Posteromedial muscle supplied by PDA from RCA
Anterolateral muscle supplied by LAD and LC (dual)

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18
Q

How do patients present with a papillary muscle rupture?

A

Hypotension, Shock, Pulmonary oedema

Mid-late systolic murmur

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19
Q

How do patients present with an interventricular septum rupture?

A

Haemodynamic compromise

Harsh, loud and holosystolic murmur as blood shunted from L to R

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20
Q

What is left ventricular dysfunction?

4 symptoms

A

Large infarct causes lasting damage

SOB, peripheral oedema, orthopnoea, PND

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21
Q

How is left ventricular dysfucntion diagnosed?

A

NTProBNP

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22
Q

What does the New York Heart Classification classify?

Explain the 4 classes

A

Classifies how bad the left ventricular dysfunction is

  1. No symptoms on normal activity (normal exercise)
  2. Symptoms on normal activity (slight limitation)
  3. Symptoms on less than normal activity (exercise limitation)
  4. Symptoms at rest (no activity without discomfort)
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23
Q

What is sudden cardiac death?

A

Death due to ventricular fibrillation (VF)

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24
Q

What is the difference between myocytes and pacemaker cells?

A

Myocytes = atria and ventricles
Depolarise after stimulation
Intrinsic ability to send impulses

Pacemaker = SAN, AVN and conducting tissue

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25
Q

What are the 4 stages of the cardiac action potential?

A

Phase 0: Inflow of Na > rapid depolarisation
Phase 1: Na channel closure > rapid repolarisation then Cl in and K out
Phase 2: Plataeu, delay repolarisation due to slow inward Ca and K out
Phase 3: 2nd repolarisation by K out and Ca in
Phase 4: Resting membrane potential

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26
Q

Draw the cardiac action potential

A

See image in revision folder

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27
Q

How is resting membrane potential in the heart maintained?

A

Increased intracellular K so it diffuses out
Negative intracellular ions cannot penetrate membrane > slight negative charge at rest
K out of Na/K ATPase (active)
Na/Cl exchange (passive)

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28
Q

What are the stages of the nodal action potential?

A

Phase 0: Depolarisation (Ca comes in)
Phase 3: Repolarisation (slow increase in K out and inactivation of Ca in)
Phase 4: Spontaneous depolarisation (slow Na in)

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29
Q

Draw the nodal action potential

A

See image in revision folder

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30
Q

What 2 stimuli do the SAN AND AVN respond to?

A

Neural and hormonal

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31
Q

Where is the AVN and what is its protective role?

A

Base of inter-atrial septum, only connection across the annulus fibres
Prevents high atrial rates > ventricles

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32
Q

What are the annunuls fibres?

A

Provide insulation between the atria and ventricles

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33
Q

What are the conduction velocities of the:

  • His and purkinje
  • Ventricular and atrial muscles
  • AVN
A
  • His and purkinje: fastest (2-5ms)
  • Ventricular and atrial muscles: (1ms)
  • AVN: slowest (0.05ms) - time for atrial to fill
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34
Q

What is the intrinsic rate of the:

  • SAN
  • Bundle of His
  • Purkinje cells
A
  • SAN: 105bpm
  • Bundle of His: 40bpm
  • Purkinje cells: 15bpm
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35
Q

What happens to the heart rate at rest?

A

Vagal inhibition predominates to slow the heart down from 105bpm

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36
Q

What is the heart rate in complete heart block?

Why?

A

Annulus fibre conduction is blocked so bundle of his predominates and the heart rate is 40bpm

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37
Q

What is the absolute refractory period?

A

Phase 0-3

No way to stimulate heart

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38
Q

What is the relative refractory period?

What is the clinical significance?

A

Phase 3-4

At the T wave - this is when you shock the heart

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39
Q

How long should the P-R interval be?

What happens?

A

0.12-0.20 seconds
3-5 small boxes

(AVN > Atrial conduction)

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40
Q

How long should the QRS interval be?

What happens?

A

0.08-0.12 seconds
2-3 small boxes

(ventricular conduction and contraction)

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41
Q

How long should the QT interval be?

What happens?

A

0.30-0.46 seconds
12 small boxes

(repolarisation of ventricles)

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42
Q

Which interval is dependent on heart rate?

How do you calculate corrected heart rate?

A

QT interval

QTc = QT/√RR

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43
Q

When does QT = QTc?

A

60 bpm

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44
Q

How many milliseconds is:

  • a small square
  • a large square
  • 1 minute
A
  • a small square: 40ms
  • a large square: 200ms
  • 1 minute: 300 x 200 = 60,000ms
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45
Q

How do you calculate heart rate on an ECG?

A

300/number of squares

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46
Q

Define bradycardia and tachycardia

What is normal heart rate for an adult and child?

A

Bradycardia is less than 60bpm
Tachycardia is more than 100bpm
Normal is between 60 and 100 (children = 100-120)

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47
Q

What drugs increase/decrease sympathetic and parasympathetic activity?
(and thus increase or decrease heart rate)

A 
Decrease PNS (increase heart rate): Atropine
Increase SNS (increase heart rate): Adrenaline, Salbutamol
Decrease SNS (decrease heart rate): Beta blockers
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48
Q

What does the ECG look like in sinus bradycardia?

A

Regular QRS
P wave in front of every QRS
Normal AV delay

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49
Q

What happens to the ECG in asystole? (2 stages)

A

No QRS = ventricular standstill

No waves = total asystole

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50
Q

3 treatments for asystole

A

CPR and Adrenaline

Pacemaker

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51
Q

First degree heart block:

  • ECG
  • Symptoms
A

Regular QRS
P wave but prolonged PR
Asymptomatic and normal pulse
Symptoms (dizzy and faint) = BAD

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52
Q

What are the 2 types of second degree heart block?

A

Mobitz type 1 (wenkebach)

Mobitz type 2

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53
Q

Mobitz type 1 (wenkebach)

  • ECG
  • Treatment
A

Regular QRS
Progressive PR prolongation until the P wave fails
No treatment unless symptomatic

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54
Q

Mobitz type 2

  • ECG
  • Progression
A

Regular QRS
Not all P waves followed by QRS
Monitored as easily progresses to type 3

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55
Q

Third degree heart block:

  • Another name
  • ECG
  • Management
A

Complete heart block
Wider QRS (generated from ventricles so 30-35bpm)
No P waves or relationship between P and QRS
ICU

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56
Q

Another name for tachy-brady syndrome

A

Sinus sick syndrome

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57
Q

What causes sinus arrest?

Does it always need treating? (e.g.)

A

SAN failure
No atrial depolarisation > ventricular asystole + sinus arrest
Common when sleeping

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58
Q

What causes left bundle branch block?

What does the ECG look like?

A 
Poor left ventricle function 
WiLLiaM 
 - V1 looks like a V (W)
 - V2 looks like an M
 - L = left
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59
Q

What happens in right bundle branch block?

What does the ECG look like?

A 
R ventricle strain (lung disease/congenital)
MaRRoW
  - V1 looks like an M
 - V2 looks like a W
 - R = right
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60
Q

3 ways to treat sinus bradycardia?

A

Fitness
Remove drugs
Treat cause

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61
Q

4 examples of drugs which cause sinus bradycardia

A

Beta blocker, Digoxin, Amiodarone, Diltiazem

62
Q

4 examples of physiological causes of sinus bradycardia

A

Hypothyroidism, Hyperkalemia, Hypothermia, Vasovagal

63
Q

What is a common cause of heart block?

A

Recent MI which has blocked the right coronary artery (blood supply to the AVN)

64
Q

What does the ECG look like generally in a bundle branch block?

A

Wide, double peaked QRS

T wave inverted

65
Q

What does the ECG look like in supraventricular (atrial) tachycardia?

A

Regular QRS

Less than 120msec apart

66
Q

What does the ECG look like in ventricular tachycardia

A

Regular QRS

More than 120msec apart

67
Q

What does the ECG look like in atrial fibrillation

A

Irregular QRS

Less then 120msec apart

68
Q

What is the diagnosis if the QRS complexes are irregular and more than 120msec apart?

A

Atrial fibrillation

But ventricular fibrillation if in short bursts and the patient ill

69
Q

What are the 3 mechanisms of tachycardia?

A

Atria send impulses quickly
Accessory circuit from the purkinje fibres to the AVN
Short circuit within the AVN

70
Q

How does adenosine aid with the diagnosis?

A

Blocks the AVN so slows the rate if supraventricular but has no affect if it is ventricular

71
Q

6 symptoms of a 2nd / 3rd degree heart block

A

Faint, Dizzy, Lightheaded, Fatigue, SOB, Chest pain

72
Q

What happens in atrial flutter with variable block?
How fast do the atria and ventricles beat?
What does the ECG look like?

A

Regular atrial activity and ventricle beat after every few p waves
Atria rate = 300bpm
Ventricle rate = less than 300bpm

ECG = saw tooth apperance

73
Q

What happens in atrial flutter with 2:1 AV conduction?
How fast do the atria and ventricles beat?
What is the heart rate?

A

2 flutter waves for every QRS complex
Atria rate = 280bpm
Ventricle rate = 140bpm

HEART RATE = 150bpm

74
Q

What is the heart rate in atrial flutter with 4:1 AV conduction

A

75bpm

75
Q

How do you treat atrial flutter?

A

Often reverts on its own but likely to recur > AF

Shock into sinus rhythm and anticoagulate

76
Q

What is the ECG like in atrial fibrillation?

A

No P waves

Irregularly irregular QRS (narrow complex)

77
Q

How do you treat atrial fibrillation?

A

Rhythm control via cardioversion (electrical or IV flecinide if a stable left ventricle and structurally normal heart)

Ensure you give anticoagulants before shocking if they’ve been in AF for a while

78
Q

Ventricular tachycardia:

  • Another name
  • Heart rate
  • ECG
  • Associated with ___ (2)
A

Broad complex tachycardia
Fast heart rate
QRS more than 120ms
Associated with sudden death or ventricular fibrillation

79
Q

Ventricular fibrillation:

  • Heart rate
  • ECG
  • Treatment
A

Heart rate = 300-600bpm (irregular)
No P waves
Shock

80
Q

Torsades de pointes:

  • Another name
  • ECG
  • Treatment
A

Polymorphic ventricular tachycardia
Wide QRS, unstable R-R, axis shift at isoelectric line
Reverses itself

81
Q

6 causes of torsades de pointes

A 
Heart block
Bradycardia
Na/Mg
Long QT (congenital)
Class 1 anti-arrhythmic drugs
Antidepressant overdose
82
Q

5 things that can cause sinus tachycardia

How is it treated?

A

Hyperthyroidism, Anxiety, Heart failure, Hypovolemia, Sepsis

Investigate and remove the cause

83
Q

How do you treat stable ventricular tachycardia? (3)

A

IV Na and Mg
IV Amiodarome
Cardioversion

84
Q

How do you treat stable supra-ventricular tachycardia?

A

If it doesn’t self revert:
IV Adenosine
Vagotonic manoevures

85
Q

Give 4 examples of vagotonic manoevures

A

Valsalva manoeuvre
Child in cold shower
Right carotid massage (stimulates the AVN)
Ocular pressure

86
Q

6 methods of managing arrhythmia

A 
Treatable cause
Vagotonic manoeuvres
DC cardioversion
Pacemaker
Surgery 
Drugs
87
Q

What changes in the ECG when there are atrial ectopic beats?

Is it concerning?

A

P wave is earlier

No concern

88
Q

What happens in a junctional ectopic beat?

What does it cause

A

Conduction from AVN

Causes bradycardia

89
Q

What changes in the ECG when there are ventricular
ectopic beats?
What causes them normally

A

Broad wave
No bundle branch block
Coffee

90
Q

DC shock (4) vs Drugs (3)

A

Shock is immediate but doesn’t always work, needs a GA and drugs after to stop reversal
Drugs can take a while to act and have side effects but are needed to prevent reversal

91
Q

What is Pouiseuille’s law?

A

Explains the relationship between the flow rate, pressure, resistance and fluid viscosity

92
Q

Define pressure

What needs to change to increase the pressure?

A

Pressure = CO x resistance

SO either CO or resistance increases

93
Q

What happens in the early phase of primary hypertension?

A

Increased CO and blood volume increase

unknown why

94
Q

What happens in the chronic phase of primary hypertension?

A

Normal CO and blood volume
Blood pressure is increased due to increased systemic vascular resistance due to abnormal vasculature
(smaller lumen and thickened walls)

95
Q

What happens to vascular tone in primary hypertension?

5 reasons why

A

Vascular tone increases

  • Increased Na and H2O
  • Increased sympathetic activity
  • Increased ANG2
  • Alcohol
  • Selection pressures
96
Q

What exactly activates RAAS?

A

Increased pressure in the afferent arteriole

97
Q

2 changes to the endothelium in diabetics with primary hypertension

A

Oxygen free radical damage

NO impaired in the endothelium

98
Q

4 changes to the vessels in secondary hypertension

A

Increased CO
Increased systemic vascular resistance
Increased blood volume
Increased neurohormonal activation

99
Q

Causes of secondary hypertension

A

Renal artery stenosis, Chronic renal disease, Conn’s syndrome, Pneochromocytoma, Coarctation of the aorta

Cushing’s, Pregnancy, Alcohol, Thyroid, Sleep apnoea, SAME (syndrome of apparant mineralocorticoid excess)

100
Q

What chronic renal disease do many diabetics suffer from?

A

Diabetic neuropathy

101
Q

How do you diagnose Conn’s syndrome?

Another name for it?

A

Increased bp, Decreased K
Decreased renin : Increased aldosterone

Primary hyperaldosteronism

102
Q

What is pheochromocytoma
What are the 2 different effects?
Is it curable?

A

An curable adrenal medullary tumour which secretes catecholamines

  • alpha-mediated effect: vasoconstriction
  • beta-mediated effect: increased CO
103
Q

How do you diagnose coarctation of the aorta?

A

Feel the radial and popliteal arteries at the same time

104
Q

5 changes to the heart caused by secondary hypertension

A 
Accelerated coronary atheroma
Concentric LV hypertrophy
Fibrosis
Increased peripheral resistance
Reduced flow in vessels (thicker vessels > epicardial 'small vessel' disease > reduced blood flow to heart)
105
Q

Which artery does accelerated coronary artheroma not occur in?
Why?

A

Not in the pulmonary artery (unless pulmonary arteriole hypertension)

106
Q

Define concentric and eccentric

A 
Concentric = IN
Eccentric = OUT
107
Q

Explain what happens in a dissecting aortic aneurysm

A

The aorta wall tears causing the intima to be stripped from the media
This forms a ‘false lumen’
Eventually the false lumen (media) is completely stripped away = life treatening

108
Q

What can hypertension cause to happen in the brain?

A

Thrombotic stroke

Haemorrhagic stroke

109
Q

What are the 2 stages of hypertensive retinopathy?

What is it a sign of?

A

Early - Artery Vein nipping
Late - exudates, haemorrhages, pappiloedema

Poorly controlled hypertension

110
Q

What is the eye the only place you can see?

A

Only place you can visibly see small vessels

111
Q

What does hypertension do to the kidney?

A

Accelerates glomerular loss (reduces kidney function)

112
Q

Define accelerated (malignant) hypertension

A

Recent elevation of blood pressure associated with organ damage and cerebral changes

113
Q

What happens in accelerated (malignant) hypertension

A

Normal auto-regulation of blood through the brain is lost as cerebral arteries dilate so pressure exceeds homeostatic control

114
Q

4 impacts of accelerated (malignant) hypertension

A

Papilloedema (increased ICP)
Necrosis of small arteries
Damage to RBC as vessels obstructed by fibrin
Loose capacity to think

115
Q

3 risk factors of accelerated (malignant) hypertension

A

Men, Smokers, Secondary hypertension

116
Q

Define pre-load

A

Pressure in the VENTRICLE just before the heart starts to contract

117
Q

Define after-load

What is it altered by?

A

Pressure once the AORTIC VALVE has opened AGAINST WHICH the heart has to eject blood
(altered by the blood vessels)

118
Q

4 changes to the heart muscle in heart failure

A

Heart is the same size in systole and diastole
Heart dilated so can’t pump hard
Heart doesn’t contract simultaneously
Heart pulled around by contractions

119
Q

What does heart failure increase the risk of? (2)

A

Sudden death due to rhythm disturbance

More MI’s

120
Q

Define acute heart failure

A

Accumulation of fluid in the wrong place, secondary to the heart malfunctioning

121
Q

Define carcinogenic shock

A

Acute heart failure caused by a large heart attack wiping out a large proportion of heart muscle

122
Q

What does starling’s law state?

A

The increased load on the heart, the harder it works

123
Q

What happens when you exercise? (in relation to starling’s law)

A

Increased venous return > heart pumps more blood

124
Q

What happens to the starling curve during heart failure?

A

The curve moves down and to the right

The heart needs a higher pre-load to maintain the same level of ventricular work

125
Q

What is starling’s relation?

A

The forces that govern whether fluid remains or leaves a vessel

126
Q

What can the alveolar capillary membrane do to reduce oedema?

A

Thicken

127
Q

Why does blood pressure increase in heart failure?

A

The heart views it as a haemorrhage situation so preserves blood flow to organs by increasing pressure

128
Q

What does the sympathetic system do?

When is this activated (2)

A

Increases heart rate and blood pressure
Sweaty, cold and clammy

Heart attack or pulmonary oedema

129
Q

8 things which may cause pulmonary oedema

A 
Acute ischaemia or infarction (e.g. coronary artery)
Arrhythmia
Environment (stress, drugs, salt)
Hypertension
Infection
Lack of compliance
Papillary muscles detach from valve (mitral regurg)
Pulmonary embolism
130
Q

6 symptoms of anasacra

A 
Ascites
Gradual weight gain
Pitting oedema
Pleural effusion 
Raised JVP
Reduced muscle mass
131
Q

What has to happen to the CO for oedema to form?

Explain

A

CO decreases

Decreased renal perfusion > RAAS

132
Q

3 characteristic of chronic heart failure

A

Symptoms
Evidence of cardiac dysfunction at rest (imaging)
Treatment response

133
Q

What is VE/VCO2?

How does this differ from normal in heart failure?

A

Minimum ventilation/CO2 production

In heart failure you need to breathe more to get rid of the same amount of CO2

134
Q

What are the 4 mechanisms of chronic heart failure?

A
  1. Haemodynamic
  2. Neurohormonal
  3. Peripheral
  4. Metabolic
135
Q

What is the law of laplace?

A

Tension = (Pressure in chamber X Radius of chamber)

/ thickness of wall

136
Q

Define tension

What changes in heart failure

A

Amount of work the heart does before it contracts

In heart failure, the heart is dilated (increased radius) so has to contract more to overcome tension

137
Q

What happens to stroke volume and ejection fraction in heart failure

A

The heart pumps the same amount of blood per beat (same stroke volume) but has a reduced ejection fraction so pumps less blood out

138
Q

Give 5 examples of neurohormonal systems which are activated in chronic heart failure

A

ADH, Adrenergic, Endothelin, RAAS, Natriuretic peptides

139
Q

What does aldosterone produce which is bad in heart failure?

A

Fibrosis

140
Q

What are the 2 types of Natriuretic peptides?

What do they do?

A

A and B

Inhibit RAS, reduce aldosterone, reduce endothelin, reduce catechols

141
Q

How are neurohormonal systems activated in chronic heart failure?

A

Neuroendocrine activation > Fluid retention, Vasoconstriction, Apoptosis and LVH > Heart failure > Neurohormonal activation

142
Q

What are the 2 types of skeletal muscle?

A

Type 1: Aerobic and slow

Type 2: Anaerobic and fast

143
Q

Explain the ergoreflex and how it is affected in heart failure

A

Ventilation increases with exercise and decreases without
Trapping exercise metabolites inside the body causes ventilation to remain high (but a slight decline)
In heart failure, you breathe more for a given amount of exercise (VE/VCO2) so there is no slight decline and ventilation remains higher

144
Q

Define catabolic and anabolic hormones

A

Catabolic break down

Anabolic build up

145
Q

What happens to catabolic and anabolic hormones in heart failure?

A

Increased catabolic

Resistance to anabolic

146
Q

2 types of ventilation support

A

CPAP: Continuous Positive Airways Pressure
IPPV: Invasive Positive Pressure Ventilation

147
Q

4 treatments for anasacra?

A 
Bed rest (Heparin to reduce clots)
Fluid restriction
Diuretics
Mechanical support e.g. dialysis if patients struggling
148
Q

What happens when you recover from pulmonary oedema or anasacra?

A

You are treated for chronic heart failure

149
Q

What are the 5 classes of adrenergic receptors?

A 
A1: postsynaptic > vasoconstriction
A2: presynaptic > -ve feedback
B1: cardiac > inotropy
B2: peripheral > vasodilation
B3: metabolic
150
Q

What is the aim of chronic heart failure treatment?

A

Reduced heart rate > reduced death

Medicine - Year 2 (19 decks)

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