Case 15 Flashcards
(273 cards)
1
Q
Diastasis
A
Middle phase of diastole when initial phase of passive filling has slowed down.
Absent during exercise.
2
Q
Mitral annulus
A
Fibrous ring attached to mitral valve leaflets
3
Q
Arrangement of cardiac muscle fibres
A
Subepicardial = left handed helix (clockwise) Subendocardial = right handed helix (anticlockwise)
4
Q
Factors which increase systolic pressure:
A
Anything which increases afterload.
Aortic stenosis, hypertension, ventricular dilatation
5
Q
Factors which increase diastolic pressure:
A
Anything which increases preload +/- increased diastolic pressure
Hypervolaemia, increased atrial contractility, decreased HR, increased ventricular compliance
6
Q
End diastolic pressure volume relationship
A
Passive filling curve for the ventricle
7
Q
Steep end diastolic pressure volume relationship suggests
A
A less compliant ventricle
Pressure increasing more with every unit increase in volume
8
Q
Steep end systolic pressure volume relationship
A
Increased contractility
9
Q
Causes of systolic heart failure
A
Dilated cardiomyopathy
Coronary artery disease (reduced blood supply to heart)
Valve disease - regurgitation/stenosis
Arrhythmias
10
Q
Mechanism for systolic heart failure
A
Underlying disease causing death of cardiomyocytes.
Walls become thin, ventricles are large.
Weakened heart muscle has decreased inotropy.
Stroke volume reduced.
Reduced ejection fraction
11
Q
Mechanism for diastolic heart failure
A
Hypertrophy and stiffening of cardiac muscle due to underlying disease.
More space taken up by muscle - less space for filling.
Large muscle requires greater O2 supply which cannot be reached - fibrotic scar tissue
Increased stiffness of muscle - reduced ejection.
Preserved ejection fraction
12
Q
Causes of diastolic heart failure
A
Chronic hypertension
Aortic stenosis
Hypertrophic cardiomyopathy
Restrictive cardiomyopathy
13
Q
Left Ventricular Dysfunction
A
Decreased longitudinal function.
Increased radial function.
(Heart becomes more spherical)
14
Q
How do we increase rate of ventricular filling during exercise?
A
Increased untwisting of left ventricle causes pressure in left ventricle to fall.
Pressure gradient across mitral valve between LA and LV
Suction of blood from LA into LV
15
Q
Why does reduced relaxation affect cardiac output?
A
Less untwisting of ventricle - Reduced suction from LA into LV during ventricular filling = Reduced stroke volume
Tension causes compression of coronary arteries - ischaemia of cardiac myocytes.
16
Q
First-pass Gadolinium MRI
A
Used to assess myoardial perfusion
17
Q
Symptoms of right sided heart failure
A
Fatigue Palpitations Peripheral oedema Weight gain Raised JVP Frequent urination at night
18
Q
Symptoms of left sided heart failure
A
Fatigue Palpitations Decreased urination Dyspnoea and coughing (worse when lying down) Weight gain
19
Q
Heart Failure Functional Class I
A
Breathless only on marked exercise
20
Q
Heart Failure Functional Class II
A
Breathless on moderate exercise
21
Q
Heart Failure Functional Class III
A
Breathless on mild exercise
22
Q
Heart Failure Functional Class IV
A
Breathless on minimal exercise
23
Q
Heart Failure Functional Class V
A
Breathless at rest
24
Q
How useful is breathlessness as a symptoms in diagnosis of heart failure?
A
87% sensitive i.e. seen in a lot of patients with heart failure
51% specific i.e. seen in a lot of other conditions as well
(Orthopnoea is less sensitive but more specific)
25
First line imaging technique for suspected heart failure
Echocardiogram
26
Kerley lines
Seen when interlobular septa in the pulmonary interstitium become prominent
A sign of pulmonary oedema
27
BNP is released in response to...
End diastolic wall stress (excessive stretching of ventricular wall)
28
Effects of BNP
Decreases Na+ reabsorption, therefore decreasing H2O reabsorption.
Overall, decrease in total blood volume.
29
How useful is BNP in diagnosis of heart failure?
90% sensitive
| 65% specific
30
Clinical measurement of BNP
N-terminal pro-BNP
31
Most common cause of restrictive cardiomyopathy in older people
Amyloid
32
Biplane Simpson Technique
Assesses volumes i.e. determines ejection fraction
33
L wave in mitral doppler velocity graph
Seen in impaired relaxation, between E and A waves.
Represents continued pulmonary vein mid diastolic flow through LA into LV after EARLY (passive) filling.
(i.e. Blood travelling from pulmonary vein to LV directly since mitral valve is open)
34
Mitral Doppler Velocity : E/A < 1
Impaired relaxation
35
Normal mitral valve inflow pattern
Rapid early (passive) phase of filling, slower late phase of filling generated by atrial contraction
36
Late ventricular filling may be faster than early filling due to...
Impaired relaxation.
Early filling is slow due to reduced gradient between LA and LV.
Late filling higher since it is generated by atrial contraction
37
Mitral Doppler Velocity :
Features of impaired relaxation
Late filling greater than early filling since it is generated by contraction.
Prolonged isovolumetric relaxation time
Decreased blood velocity out of heart
Change in heart shape longitudinally
Pronounced L wave (continued mid diastolic flow between E and A)
38
Mitral Doppler Velocity :
How does a pseudonormal diastolic heart failure occur?
Early and late filling have increased in velocity due to higher LA and LV pressures.
Ratio of E:A appears normal
39
Mitral Doppler Velocity :
Features of restrictive diastolic heart failure?
Decreased mitral inflow (due to reduced press. gradient)
Short duration of ventricular filling (due to high press. in LV)
End diastolic mitral regurgitation (due to high pressure at end of diastole)
Retrograde flow from atria into pulmonary vein (not all blood can enter less compliant ventricle)
40
Secondary mitral regurgitation
Mitral valve is intact
| Change in geometry and dysfunction of LV is causing regurgitation.
41
S2 Heart sound
Closure of aortic valve
42
Heaves
Parasternal impulse
| Due to hypertrophy of right ventricle
43
Signs of tricuspid regurgitation
Pan systolic murmur
Raised JVP
Enlarged pulsatile liver
44
Systolic murmur
Starts at S1 and ends at S2
45
Causes of midsystolic murmur
Aortic or pulmonary valve stenosis
46
What does a midsystolic murmur sound like?
From S1 to S2
| Starts softly, increases in intensity then decreases in intensity.
47
Causes of pansystolic murmur
Mitral/tricuspid regurgitation
| Ventricular septal defect
48
What does a pansystolic murmur sound like?
From S1 to S2
| Intensity is high throughout
49
Causes of diastolic murmurs
Aortic/Pulmonary valve regurgitation
| Mitral/tricuspid valve stenosis
50
What does a diastolic murmur caused by Aortic/Pulmonary valve regurgitation sound like?
Begins immediately after S2 and quickly reaches maximal intensity.
Intensity then diminishes throughout diastole.
51
What does a diastolic murmur caused by Mitral/Tricuspid valve stenosis sound like?
Delayed beyond S2 (i.e. until AV valves open)
More intense early during diastole then decreases in intensity
Atrial contraction near the end of diastole can cause a brief increase in intensity just before S1
52
Normal Blood pressure
120/80
53
Blood pressure in premenopausal women
5-10mmHg lower than normal
54
Blood pressure at which antihypertensive treatment should be initiated
160/100mmHg
55
Blood pressure 140-150/90-99
Take into account other factors (heart and kidney problems, diabetes) prior to starting antihypertensive treatment
56
Conn's Syndrome
Hyperaldosterone state
57
How does hypertension cause left ventricular hypertrophy?
HTN causes increased afterload.
| Hypertrophy of myocytes since they must work harder during systole.
58
How does hypertension affect atherosclerosis?
Accelerates atherosclerosis due to wall stress
59
How does hypertension affect vascular walls?
Increases thickness of tunica media in muscular arteries
Hyperplasia of muscle and collagen deposition (increased stiffness).
60
How does hypertension cause renal failure?
Proliferation of small blood vessels in kidney.
Hypertrophic and hyaline changes in arterioles.
Sclerosis of glomeruli causes nephron to become ischaemic - undergo atrophy and fibrosis.
Eventually, kidney contracts with a finely scarred surface (Nephrosclerosis)
61
How does hypertension cause intracerebral haemorrhage?
Pathological changes in intracerebral vessels:
Microaneurysms of perforating arteries
Accelerated atherosclerosis
Hyaline arteriosclerosis
Hyperplastic arteriosclerosis
62
Pathological consequences of hypertension
```
LV hypertrophy
Athersclerosis
Changes in vascular walls
Renal failure
Intracerebral haemorrhage
Subarachnoid haemorrhage
Dissecting aneurysm of aorta
```
63
Renal Factors which increase cardiac output
Decrease GFR
Increase Na+ reabsorption
Activation of RAAS
Sympathetic drive
64
Renal Factors which decrease cardiac output
Renal production of prostaglandins (enhance GFR)
65
Renal factors which increase total peripheral resistance (vasoconstriction)
Sympathetic drive
Activation of RAAS
Endothelin
66
Renal factors which decrease total peripheral resistance (vasodilation)
Renal PGs
Renal kinins
NO
Platelet activating factor
67
How do natriuretic peptides lead to hypertension?
Inhibit Na+/K+ ATPase in smooth muscle cells of blood vessel walls.
Increased Na+
Inhibits Na+/Ca2+ exchanger
Increased Ca2+ in smooth muscle cell = VASOCONSTRICTION
68
Liddle's Syndrome
Overexpression of Na+ channel in apical membrane of CD
Elevated Na+ reabsorption in nephron
Therefore, elevated blood pressure early in life
69
How does metabolic syndrome increase risk of hypertension?
Increased Na+/H+ exchanged in PCT.
(H+ excreted, Na+ reabsorbed)
i.e. abnormally high Na+ reabsorption
70
How does obesity cause hypertension?
High insulin, activates Na+/K+ ATPase
| Increased Na+ reabsorption in PCT
71
Medications which increase risk of hypertension
NSAIDs
Oestrogen
Corticosteroids
72
Stage 1 Hypertension
Clinic BP > 140/90
| Daytime BP > 135/85
73
Stage 2 Hypertension
Clinic BP > 160/100
| Daytime BP > 150/95
74
Stage 3 Hypertension
Clinic BP
Systolic > 180
Diastolic > 110
75
Investigations using urinalysis in hypertension
Protein
Albumin:Creatinine ratio
Haematuria
76
Blood tests used in investigation of hypertension
```
Glucose
Electrolytes
Creatinine
estimated GFR
Total and HDL cholesterol
```
77
Grade 1 Hypertensive retinopathy
Tortuosity of retinal veins (silver wiring)
78
Grade 2 Hypertensive retinopathy
```
Tortuosity of retinal veins (silver wiring)
Arteriovenous nipping (thickened arteries passing over veins)
```
79
Grade 3 Hypertensive retinopathy
Tortuosity of retinal veins (silver wiring)
Arteriovenous nipping (thickened arteries passing over veins)
Flame haemorrhages
Cotton wool exudates
80
Grade 4 Hypertensive retinopathy
Tortuosity of retinal veins (silver wiring)
Arteriovenous nipping (thickened arteries passing over veins)
Flame haemorrhages
Cotton wool exudates
Papilloedema
81
Why is a 12 lead ECG performed in investigation of hypertension?
To detect LV hypertrophy
82
Conn's Syndrome
Primary Hyperaldosteronism
| XS K+ secretion and Na+ reabsorption
83
How would you distinguish between primary and secondary hyperaldosteronism?
Primary - renin is low
| Secondary - renin is high
84
Causes of secondary hyperaldosteronism
Coronary heart failure
Renal artery stenosis
Cirrhosis
Nephrotic syndrome
85
Adrenal causes of secondary hypertension
Conn's Syndrome
Secondary Hyperaldosteronism - coronary heart failure, RAS, cirrhosis and nephrotic syndrome
Phaeochromocytoma
86
Phaeochromocytoma
Adrenal medullary tumor secreting catecholamines
87
Labile hypertension
Spasms of vasoconstriction and organ ischaemia.
| Associated with phaeochromocytoma (XS catecholamines)
88
Renal causes of secondary hypertension
```
Renal ischaemia (Renal vascular disease)
Renal parenchymal disease
```
89
When do we suspect renal artery stenosis?
Sudden appearance of HTN in an older person.
Resistant to usual HTN medication
Abrupt deterioration in BP control (previously stable)
Deterioration of renal function.
90
How does renal parenchymal disease cause hypertension?
Loss of renal vasodilator substances
| Reduced GFR = salt and water retention = increased ECF volume and cardiac output
91
Macula Densa Cells release...
Adenosine
92
Macula densa cells are activated by...
Increased [Na+] in distal tubule
93
Effect of adenosine
Vasodilator
94
Most common cause of secondary hypertension
Renal parenchymal disease
95
Compensated Heart Failure
Stroke volume can be maintained as a result of increased preload
96
Decompensated Heart Failure
Volume expansion and increased preload does not bring stroke volume back up to normal
97
Why does left sided heart failure cause pulmonary hypertension ?
Right ventricle pumps blood into the pulmonary circulation until left ventricular preload is increased sufficiently.
98
Organ responsible for EPO production
Kidney
99
EPO and renal dysfunction
Less EPO produced by dysfunctional kidney.
| Exacerbates free radical production and poor O2 supply
100
Direct effect of Angiotensin II on the heart
Positive inotrope
101
Most common cause of cardiomyopathy
Ischaemic heart disease
102
Definition of hypertrophic cardiomyopathy
A condition causing increased wall thickness that is not explained solely by loading conditions.
103
Epidemiology of Hypertrophic cardiomyopathy
Prevalence ~ 0.1%
Males affected more than females
Seen in athletes
Leading cause of death in young adults
104
Features of hypertrophic cardiomyopathy
```
Wall thickness >15mm (normally <12mm)
Myocardial fibrosis
Disarray (loss of uniform architecture)
Abnormal mitral valve apparatus
Abnormal microcirculation
Abnormal ECG
```
105
Most common cause of hypertrophic cardiomyopathy
40-60% are caused by sarcomeric protein gene mutations
106
Most sarcomeric protein mutations causing hypertrophic cardiomyopathy
Myosin Heavy Chain 7 (MYH7)
Myosin binding protein C3 (MYBPC3)
107
Pathophysiology of hypertrophic cardiomyopathy
Disarray
Myocyte hypertrophy
Abnormal coronary arteries (hypertrophy decreases luminal area) - ischaemic episodes leading to fibrosis
108
How does hypertrophic cardiomyopathy cause mitral regurgitation?
Septal hypertrophy causes narrowing of outflow tract.
Narrow outflow tract has a suction effect (Venturi Effect).
Pulls mitral valve leaflet towards septum - opening of mitral valve
109
How does hypertrophic cardiomyopathy cause atrial fibrillation?
Results in mitral regurgitation.
Increased pressure in right atrium.
Dilatation of atrium - a cause of AF
110
Why does hypertrophic cardiomyopathy cause angina?
Hypertrophic myocardium has a higher O2 demand.
Hypertrophy also compresses coronary vessels - microvascular diease
O2 supply:demand mismatch
111
Symptoms of hypertrophic cardiomyopathy
```
Angina
Syncope
Dyspnoea
Sudden death
(May be asymptomatic prior to sudden death)
```
112
Examination findings in hypertrophic cardiomyopathy
Pulse has a rapid upstroke/downstroke
Ejection systolic murmur (between S1 and S2)
113
Sokolov-Lyon equation
(S wave in V2) + (R wave in V5) > 35mm
More than 35mm in left ventricular hypertrophy
114
ECG changes in hypertrophic cardiomyopathy
LV Hypertrophy - deep S wave in V2 and tall R wave in V5
May show atrial fibrillation
ST segment changes
T wave inversion
115
Cardiac MRI in hypertrophic cardiomyopathy would show:
Fibrotic changes - patchy, midwall
Ventricular hypertrophy
Abnormal papillary muscle insertion
Elongated anterior mitral valve leaflet (due to venturi effect)
116
Ideal echocardiogram view for viewing hypertrophic cardiomyopathy
Parasternal short axis
117
When is LV myomectomy indicated?
HCM
Outflow gradient > 50mmHg
NYHA III/IV
Syncope despite optimal medical therapy
118
What is LV mymectomy?
Removal of left ventricular wall
Used in treatment of HCM
119
Complications of myomectomy
AV block
Aortic regurgitation
Mortality (3-4% with mitral valve surgery)
120
Advantage of myomectomy over Alcohol septal ablation
Lower risk of AV block
Septal ablation is dependent on septal branch anatomy.
Can treat mitral valve pathology at the same time
121
Advantages of alcohol septal ablation over myomectomy
Less invasive (percutaneous)
Better recovery - better for elderly px with many comorbidities
No risk of aortic regurgitation
122
When is alcohol septal ablation indicated?
HCM
Outflow gradient > 50mmHg
NYHA III/IV
Syncope despite optimal medical therapy
123
Procedure for Alcohol Septal Ablation
Percutaneous route.
Small amount of pure alcohol infused into septal artery to produce a small heart attack
124
Alcohol septal ablation is not recommended in cases with...
Concurrent mitral valve/apparatus pathology
125
First line surgery for asymmetrical septal hypertrophy
Left ventricular myomectomy
126
Second line surgery for asymmetrical septal hypertrophy
Pacing of RV apex - to maintain AV synchrony
127
Risk Factors for Sudden Cardiac Death:
```
Family History of SCD
Syncope
Non sustained ventricular tachycardia
Blood pressure response to exercise
Septum > 30mm
```
128
High risk of Sudden Cardiac Death:
> 2/5 of the following:
```
Family History of SCD
Syncope
Non sustained ventricular tachycardia
Blood pressure response to exercise
Septum > 30mm
```
129
Management of individuals at high risk of sudden cardiac death
ICD - terminates life threatening ventricular tachycardias in HCM
130
Definition of Dilated Cardiomyopathy
A condition characterised by cardiac enlargement with reduced systolic function, absence of primary valve disease, and non significant coronary artery disease.
131
Epidemiology of Dilated cardiomyopathy
Prevalence ~ 0.5%
Males > females
Blacks > whites (2:1)
Accounts for 1/3 of all heart failure and a majority of heart transplantation
132
Myotonic Dystrophy is a cause of which cardiomyopathy?
Dilated cardiomyopathy
133
Infective causes of dilated cardiomyopathy
HIV
| Lyme disease
134
Medical treatment of dilated cardiomyopathy
Diuretics
B-blockers (reduce HR)
ACE-I/ARB (reduce afterload)
Aldosterone antagonists (reduce ECF volume)
135
Protein affected in Duchenne Muscular dystrophy
Dystrophin
136
Prevention of Cardiomyopathy in Duchenne Muscular Dystrophy
ACE-I (perindopril)
137
Anthracyclines are used in...
Cancers (>50% of cancers use this treatment)
138
Common long term cardiac effects of Anthracyclines
Left ventricular systolic dysfunction occurs in 40% of patients more than a year after treatment
139
How does anthracycline induce cardiomyopathy?
Produces potent reactive oxygen species
140
Cancer drugs associated with cardiomyopathy
Anthracycline
| Trastuzumab
141
Cardiac effect of Trastuzumab
Reduced LV ejection fraction
142
Trastuzumab (cancer treatment) must be stopped if...
Ejection fraction falls by more than 10% and EF is less than 50%
143
Arrhythmogenic RV Cardiomyopathy
A condition mainly affecting the right ventricle (15% involve LV) characterised by fibro fatty infiltration, ventricular dilatation and hypertrabeculation.
144
ECG for Arrhythmogenic RV Cardiomyopathy
```
T wave inversion in V1-V3
Epsilon wave (small positive deflection buried in the end of the QRS complex)
```
145
Ventricular trabeculation
Two layered myocardium, with a non compacted inner layer and a compacted outer layer
Deep recesses in communication with ventricular chamber.
146
Echocardiogram for Arrhythmogenic RV Cardiomyopathy
RV dilatation and aneurysm
| RV hypertrabeculation
147
Definition of restrictive cardiomyopathy
Normal cardiac size
Reduced systolic function
Biatrial dilatation
Usually resulting from myocardial infiltration
148
Most common cause of restrictive cardiomyopathy
Amyloid
149
Causes of restrictive cardiomyopathy
```
Amyloid
Haemachromatosis
Sarcoidosis
Radiation fibrosis
Endomyocardial fibrosis
```
150
ECG changes in restrictive cardiomyopathy
```
ECG may show:
Low voltage QRS
Bundle branch block
AV block
Pathological Q waves
Atrial and ventricular dysrhythmias
```
151
How does increased Ca2+ in cardiomyocytes cause contraction?
Binds to troponin, allowing tropomyosin to move away from myosin binding sites on actin.
Myosin and actin can bind - cross bridge formation
152
MLCK is found in..
Smooth muscle cells
153
How does Angiotensin II cause vasoconstriction?
Binds to AT1R (GPCR)
Activation of PLC which converts PIP2 to IP3 and DAG.
IP3 binds to its receptor on SR.
SR releases Ca2+
Ca2+ binds to calmodulin forming a complex which activates MLCK.
MLCK phosphorylates myosin, allowing actin and myosin to interact.
154
Effects of Angiotensin II
```
Dipsogenic (increased thirst)
Vasoconstriction
Cardiac hypertrophy
Aldosterone secretion (Na+ reabsorption)
ADH secretion
```
155
MOA of ramipril
ACE-I
156
Indication for ramipril
```
Hypertension
Cardiac failure (with LV dysfunction)
```
157
Common ADRs of Ramipril
```
Cough and dyspnoea
Hyperkalaemia
Headache/drowsiness
Weakness/fatigue
Chest pain
Sun sensitivity
```
158
Serious ADRs of ramipril
```
Renal Failure
Liver dysfunction
Allergic reaction
Increased WBCs
Angioedema
Pancreatitis
```
159
Contraindications for ramipril
Renal Artery Stenosis
Afro-Caribbean Px (may respond less well)
Previous angioedema associated with ACE-I
160
Indication for Candesartan/Losartan
Hypertension
Cardiac Failure
In patients intolerant to ACE-I e.g. Afro-Caribbean background
161
Common ADRs of Losartan/Candesartan
```
Cough and dyspnoea
Hyperkalaemia
Headache/drowsiness
Weakness/fatigue
Indigestion
Upper respiratory tract infection
Abnormal taste
```
162
Serious ADRs of Candesartan/Losartan
```
Kidney/Liver failure
Allergic reaction
Angioedema
Arthralgia and myalgia (joint and muscle pain)
Hyponatraemia
```
163
Contraindications of Candesartan/Losartan
```
Pregnancy
Renal Artery Stenosis
Mitral/Aortic valve stenosis
Elderly
HCM
Hx of angioedema
Primary aldosteronism
```
164
Why is bisoprolol used in heart failure?
Reduces work load of the heart.
Decreased sympathetic activity.
Reduced slope of phase 4 of pacemaker action potential - negative chronotrope
Reduced Ca2+ to myocytes - negative inotrope
165
Indications for bisoprolol
Cardiac failure
Hypertension
SVT
166
Common ADRs of Bisoprolol
```
Bronchospasm
Cold extremities
Loss of libido
Sleep disturbance
Dizziness
Dyspnoea
GI disturbance
```
167
Serious ADRs of bisprolol
Raynaud's
Bronchospasm
Serious allergic reaction
(Skin conditions: Toxic epidermal necrosis, Stevens Johnsons Syndrome, Lupus erythema, Erythema multiforme)
168
Contraindications of bisprolol
```
Asthma/COPD
Cardiogenic shock
Bradycardia
Heart block
Phaeochromocytoma
Sick sinus syndrome
```
169
MOA of Digoxin
Na+/K+-ATPase inhibitor
| Increased Na+ in cells inhibits Na+/Ca2+ exchange, Increased Ca2+ in cells = positive inotropy
170
How does digoxin act as an antiarrhythmic agent?
Inhibits Na+/K+-ATPase in brainstem cardiac centre. Increased vagal stimulation of AVN. Therefore, decreased chronotropy.
171
Indication for Digoxin
Systolic heart failure
Atrial Fibrillation
Atrial Flutter
172
Age group more likely to be given digoxin for heart failure
Elderly
173
Common ADRs of Digoxin
```
Arrhythmias
Blurred/Yellow vision
Nausea/Vomiting/Diarrhoea
Dizziness
Hyperkalaemia
```
174
Serious ADRs of Digoxin
```
Confusion
Depression + Psychosis
Anorexia
Gynaecomastia
Thrombocytopenia
```
175
Contraindications of digoxin
Constrictive pericarditis
HCM
Heart Block
Arrhythmias (SVT w/ accessory pathway e.g. WPW OR VT)
176
MOA of furosemide/bumetanide
Inhibits Na+/K+/2Cl- symporter in thick ascending limb.
| High concentration of ions in urine, reduces reabsorption of H2O
177
Why is furosemide the strongest diuretic?
Acts in the ascending limb of the loop of Henle (Loop diuretic)
Acts earlier in the tubule than others, therefore more time to prevent reabsorption of water.
178
Indication for furosemide
Oedema
| Cardiac failure
179
ADRs of furosemide
HYPOKALAEMIA
```
Acute urinary retention
Blood disorders
Metabolic alkalosis
GI disturbance
Pancreatitis
Postural hypotension
Increased serum cholesterol
```
180
Contraindications of Furosemide (loop diuretics)
```
Anuria
Comatosed/Precomatosed
Liver cirrhosis
Renal failure
Severely hypokalaemic or hyponatraemic
```
181
Why is bendroflumethiazide a weaker diuretic than furosemide?
Furosemide acts in ascending limb, bendroflumethiazide acts in DCT.
Thiazide diuretics act later in the tubule, therefore have less time to inhibit H2O reabsorption.
182
Indication for bendroflumethiazdie
Hypertension
Oedema
Cardiac failure
183
Common ADRs of bendroflumethiazide
```
Hypokalaemia
Altered plasma lipid concentration
Gout
Electrolyte disturbance
GI disturbance
```
184
Serious ADRs of bendroflumethiazide
Blood disorders:
Agranulocytosis and leucopenia (causes low WBCs)
Thrombocytopenia
Pancreatitis
Severe skin reactions
Visual disturbance
185
Contraindications of Bendroflumethiazide
```
Pregnancy
Addison's - hypocortisolism (Causes dehydration and electrolyte imbalance)
Hypercalcaemia
Hyponatraemia
Refractory hypokalaemia
Symptomatic hyperuricaemia
```
186
MOA of spironolactone
Competitive inhibitor of aldosterone receptor. Prevents Na+ reabsorption and K+ secretion.
Therefore, K+ sparing diuretic.
187
Indications for spironolactone
Hypertension
| Cardiac failure
188
Common ADRs of spironolactone
Hyperkalaemia
189
Serious ADRs of Spironolactone
```
Acute renal failure
Hepatotoxicity
Hyperkalaemia
Stevens Johnson Syndrome
Thrombocytopenia
```
190
Contraindications of Spironolactone
Addison's
Anuria
Hyperkalaemia
191
ECG changes in hyperkalaemia
Peaked T waves
Prolonged QRS (and abnormal morphology)
Eventual loss of P waves
Bradycardia (and even eventual asystole)
192
ECG changes in hypokalaemia
```
Large P waves
prolonged PR interval
ST depression
T wave flattening/inversion
U waves
```
193
Pathogenesis of Anaemia of Chronic Disease
Reduced RBC survival
Reduced EPO production
Reduced response to EPO due to apoptosis of RBC precursors
Hepcidin-induced Altered iron metabolism - reduced plasma iron levels
194
Why is EPO production reduced in chronic disease?
Cytokines released in chronic disease
195
Why do many patients with heart failure have anaemia/iron deficiency?
Absolute iron deficiency i.e. malnourished or malabsorption
Anaemia of chronic disease (low RBCs, low EPO, altered iron metabolism)
ACE-I and ARBs result in reduced EPO synthesis.
196
Obstructive sleep apnoea
Collapse of pharyngeal airway
| Sleep test shows complete cessation of airflow for >10s, thoracoabdominal movements present
197
Central Sleep Apnoea
Unstable feedback of respiratory control system
Sleep test shows complete cessation of airflow for >10s, thoracoabdominal movements absent (brain not stimulating respiratory muscles)
198
Apnoea/Hypopnoea Index
Total number of apnoea/hypopnoea events per hour of sleep
199
Mild Sleep Apnoea
5-15 apnoea/hypopnoea events per hour of sleep
200
Moderate sleep apnoea
16-30 apnoea/hypopnoea events per hour of sleep
201
Severe sleep apnoea
>30 apnoea/hypopnoea events per hour of sleep
202
Why are external jugular veins not used to measure JVP?
They become small and barely visible in hypertension.
| They are superficial and prone to kinking.
203
Why are left jugular veins not used to measure JVP?
They are not in a straight line - transmission of haemodynamic changes in right atrium is disrupted.
204
Features of Jugular Venous Pulses
Non palpable
Obliterated by pressure on clavicle
Decreased by inspiration, increased by expiration
Usually 2 pulsations/systole
Prominent descents
More prominent with increased abdo pressure
205
Measuring and calculating JVP
Measure vertical distance from sternal angle to vertical ruler at the level of JVP.
Add 5cm
1.3cm = 1mmHg
206
How far does the right atrium lie below the sternal angle?
5cm
207
Normal vertical distance from sternal angle to JVP
<4cm
208
Normal vertical distance from centre of right atrium to JVP
<9cm
209
Normal jugular venous pressure
<7mmHg
210
JVP Waveform: A wave
Active atrial contraction
| Ascent
211
JVP Waveform: X
Atrial relaxation
| Descent
212
JVP Waveform: C
Bulging of tricuspid valve with ventricular contraction
| Ascent
213
JVP Waveform: X'
Downward movement of tricuspid valve with ventricular contraction
(Descent)
214
JVP Waveform: V
Passive atrial filling
| Ascent
215
JVP Waveform: Y
Atrial emptying with opening of tricuspid valve
216
JVP Waveform: H
Relatively slow ventricular filling - diastasis
Between bottom of y descent and beginning of A ascent.
217
JVP waveform which corresponds with S1
A (Ascent)
218
JVP waveform which comes after S1
X (descent)
219
JVP waveform which corresponds with S2
V (ascent)
220
JVP waveform which comes after S2
Y (descent)
221
Cause of prominent a waves in JVP waveform
Tricuspid stenosis
Aortic stenosis
RV hypertrophy
Tricuspid regurgitation
222
Causes of Cannon Waves in JVP waveform
i.e. Very prominent a waves
Caused by atrial contraction against a closed tricuspid valve due to dissociated between atrial and ventricular contraction
223
Causes of absent a waves in JVP waveform
Atrial fibrillation Hyperkalaemia
224
Cause of single wave wavepattern in JVP waveform
HR > 120/min
| Tricuspid regurgitation
225
Absent X wave in JVP waveform
Atrial fibrillation
Tricuspid regurgitation
Constrictive pericarditis
(Prevention of relaxation of RA)
226
Prominent X wave in JVP waveform
Cardiac tamponade
227
Prominent V wave in JVP waveform
RV failure
Tricuspid regurgitation
Atrial septal defect
(Increased passive atrial filling)
228
Diminished V wave in JVP waveform
Hypovolaemia
Venodilators
(Decreased passive atrial filling)
229
Rapid Y descent in JVP waveform
Constrictive pericarditis
230
Slow Y descent in JVP waveform
Tricuspid stenosis
Pericardial tamponade
Tension pneumothorax
(Prevention of atrial emptying)
231
Kussmaul's sign
Paradoxical rise in JVP during inspiration
Caused by constrictive pericarditis, cardiac tamponade, restrictive cardiomyopathy
WHY?
Increased venous return on inspiration
232
Positive test for hepatojugular reflux.
What does this indicate?
Pressure applied to liver for 30s. Rise in JVP for >10s
Early cardiac failure
233
Cause of false positive Hepatojugular reflux test
Valsalva - abdominal guarding
| Fluid overload
234
Cause of false negative Hepatojugular reflux
Budd Chiari
| Compression of SVC/IVC
235
Frailty
Reduced homeostatic reserve. Small stressors have a massive impact.
236
Sarcopenia
Loss of muscle mass with loss of muscle strength and function
237
Delirium
Acute disorder of mental processes accompanying organic brain disease.
May be manifested by hallucination, delusions, disorientation.
Can be caused by intoxication, infection, deficiency and metabolic disorders.
238
Barthel Score
```
Activities of daily living including:
Continence
Grooming
Feeding
Transfer
Dressing
Mobility
Stairs
```
Out of 16
(Only useful in hospital)
239
Cranial nerves which carry information on blood pressure to the brain
Vagus (X)
| Glossopharyngeal (IX)
240
Information on blood pressure from baroceptors in aortic arch are carried to the brain via...
Vagus nerve (X)
241
Information on blood pressure from baroreceptors in carotid sinus are carried to the brain via...
Glossopharyngeal nerve (IX)
242
NTS is located in...
The medulla
243
Bainbridge Reflex
Stretch receptors in vana cava and right atrium detect an increase in blood volume.
Generate an increase in heart rate to prevent congestion of venous system
244
Central chemoreceptors detect...
Changes in pCO2 ([H+] in CSF)
245
Central chemorecpetors are located in...
Ventrolateral surface of medulla
246
Central chemoreceptors respons (quickly/slowly)
Slowly
247
Peripheral chemorecepetors detect...
low O2, high CO2 and high H+
248
Peripheral chemoreceptors are located in
Carotid and aortic bodies
249
Peripheral chemoreceptors respond (quickly/slowly)
Quickly
250
Myogenic Mechanism in regulation of GFR
Constriction of preglomerular (afferent) resistance vessels.
Rapid - responds in 3-10s
251
Tubuloglomerular feedback mechanism in regulation of GFR
Macula densa cells detect an increased [Na+] in DCT when GFR is increased.
Macula densa cells then release adenosine which causes vasoconstriction of afferent arteriole.
Therefore, GFR decreases.
252
Why does adenosine not cause vasoconstriction of efferent arteriole?
Efferent arteriole does not have voltage gated Ca2+ channels
253
Effect of SNS on GFR
Reduces GFR to normal level (when it has increased during exercise/haemorrhage)
Causes vasoconstriction of renal arterioles (afferent > efferent)
254
Effect on GFR of Vasoconstriction of afferent arteriole
Decreased GFR
255
Effect on GFR of Vasoconstriction of efferent arteriole
Increased GFR
256
Effect of ANP/BNP on GFR
Increased due to relaxation of interglomerular mesangial cells
+ Afferent dilatation
257
Effect of angiotensin II on GFR
Low dose = increased GFR (Efferent constriction)
| High dose = decreased GFR (afferent constriction
258
Aldosterone is released from
Zona glomerulosa of adrenal cortex
259
Effect of aldosterone on sodium reabsorption
Increased sodium reabsorption by activation of Na+/K+-ATPase
260
Effect of prostaglandins on the kidney
Afferent arteriole dilatation therefore GFR is increased.
Decreased Na+ reabsorption
261
Effect of aldosterone on ion levels in blood
Increased Na+
| Decreased K+ and H+
262
S3 sound is generated by
Sudden deceleration of blood into LV from LA
| Due to thin walled, dilated left ventricle with generalised decreased contraction.
263
When in the cardiac cycle is S3 heard?
Early in diastole
264
S4 sound is generated by
Contraction of atria against a stiffened vessel wall
265
When in the cardiac cycle is S4 heard?
Late diastole
266
Pathological causes of S4 additional heart sound
Hypertrophy due to: Hypertension, Aortic stenosis etc
| Scar tissue formation due to coronary heart disease.
267
Causes of raised JVP
```
RV failure
Pericardial compression
Tricuspid stenosis
SVC obtruction
Circulatory overload
Renal failure
Atrial septal defect with mitral valve disease
```
268
Causes of displacement of apex beat
Obesity - deviation of heart axis
| Change in shape of heart e.g. more spherical in HF
269
Cardiothoracic ratio should normally be:
50% (i.e. heart should take up 50% of the width of the thoracic cavity)
270
Causes of poor pulses in lower limb
Hypertension - damage to vessel walls due to stress
Diabetes - wall damage due to hyperglycaemia
271
Renal bruit is due to..
Turbulent flow in a renal artery
272
Renal bruits are ausculated for at...
the periumbilical region
273
Protein ++ in urine suggests
Kidney damage
