1
Q
What are the core values of a doctor?
A
Advocacy Caring Commitment Compassion Competence (most important) Integrity Spirit of enquiry
2
Q
What sympathy and empathy are, and appreciate their value and limits
A
SYMPATHY = The quality or state of being affected by the condition of another with a feeling similar or corresponding to that of the other; the fact or capacity of entering into or sharing the feelings of another or others; fellow-feeling EMPATHY = ability to understand & appreciate another person's feelings, experience, etc
3
Q
What are the 4 key attributes of care which must be maintained, whatever one’s values, as defined by GMC?
A
- Must act in accordance with relevant legislation
- Must not treat pts unfairly
- Must not deny pts access to appropriate services or care
- Must not cause patients distress
4
Q
What are 4 arguments against the practice of conscientious objection & abortion?
A
- Inefficiency & inequity
- Inconsistency
- Commitments of a Dr
- Discrimination
5
Q
What are the broad strategies upon which drug therapy is based?
A
- To increase cardiac contractility
- To decrease preload and/or afterload to decrease cardiac work demand by relaxing vascular smooth muscle & reducing blood volume
- Inhibit the RAAS
- Prevent inappropriate rise in HR
6
Q
What are the problems associated with each of the compensatory mechanisms?
A
- Frank-starling:
- increase in vascular volume leads to increased EDV
=> increased muscle stretch & oxygen consumption - Sympathetic activity
Initially it’s helpful but long term it is not:
- tachycardia, vasoconstriction, decreased perfusion of tissues, cardiac arrhythmias, renin release
- decreases the workload of the heart => ischaemia, damage to myocytes, decreased contractility
- desensitisation of beta (but not alpha) receptors - Renin-angiotensin
- decrease in renal blood flow increases renin release
=> increased angiotensin II formation (it’s a vasoconstrictor plus stimulates aldosterone release)
=> sodium & water reabsorption is increased both directly & indirectly
- angiotensin II & aldosterone are involved in inflamm responses leading to deposition of fibroblasts & collagen in the ventricles => increases stiffness & decreases contractility of the heart, leading to myocardial remodelling & progressing dysfunction.
7
Q
What are the 3 areas in which BMA support conscientious objection, and know which of these are legally protected?
A
Abortion
Fertility treatment
Withdrawal of life-sustaining treatment
8
Q
Describe the NYHA (New York Heart Association Classification of Heart Failure)
A
I = No limitation of physical activity. Ordinary physical activity does not cause undue fatigue, palpitation, dyspnea (shortness of breath).
II = Slight limitation of physical activity. Comfortable at rest. Ordinary physical activity results in fatigue, palpitation, dyspnea (shortness of
breath).
III = Marked limitation of physical activity. Comfortable at rest. Less than ordinary activity causes fatigue, palpitation, or dyspnea.
IV = Unable to carry on any physical activity without discomfort. Symptoms of heart failure at rest. If any physical activity is
undertaken, discomfort increases.
9
Q
What is the classification of systolic vs diastolic dysfunction based on?
A
Ejection fraction (%)
10
Q
Describe (i) Systolic Ventricular dysfunction (ii) Diastolic ventricular dysfunction.
A
slide 6
11
Q
Systolic dysfunction commonly results from conditions that affect what? (HINT: there’s 3 things)
A
- Contractility
- e.g. IHD, cardiomyopathy - Volume overload
- Pressure overload
- valvular stenosis, hypertension
12
Q
What are the 4 causes of diastolic dysfunction?
A
- Impedance of ventricular expansion
- Increased wall thickness
- Delayed diastolic relaxation
- Increased HR
13
Q
What are the causes of right ventricular dysfunction?
A
- Conditions impeding flow into the lungs
- pulmonary hypertension
- valve damage/stenosis/incompetence - Pumping ability of RV
- cardiomyopathy
- infarction - LV failure
- Congenital heart defects
14
Q
What are the causes of left ventricular dysfunction?
A
- Hypertension (increase in TPR)
- Acute MI
- Aortic/mitral valve stenosis/regurgitation
- Increase in pulmonary pressure can lead to RV failure
15
Q
What is the dominant cause of mortality in diabetic pts? Why do they think this is the case?
A
Cardiovascular complications
- due to elevated oxidative stress
16
Q
Give examples of diabetes-associated metabolic disorders?
A
hyperglycemia hypertriglyceridemia hypercholesterolemia hypoalphalipoproteinemia increased levels of advanced glycation end products, glycated & oxidised lipoproteins
17
Q
Give examples of systemic diseases that affects the CVS? (HINT: there’s 10)
A
Diabetes mellitus Hypertension COPD Amyloidosis Rheumatoid Arthritis Vasculitides & SLE Thyroid Disease Sarcoidosis Nutrition Drugs
18
Q
What are the 4 examples of drugs that can affect the CVS?
A
anti-cancer
immunosuppressive
diabetogenic
anti-inflammatory
19
Q
What is amyloidosis?
A
A group of rare but serious conditions caused by deposits of abnormal protein, called amyloid, in tissues and organs throughout the body
Amyloid is a description of proteins which have folded abnormally and then collected together. In this form they do not break down as easily as normal proteins and can build up in tissues and organs.
If this build-up causes the tissues or organs to stop working properly, the resulting conditions are called amyloidosis.
20
Q
Define (i) stenosis (ii) incompetence.
A
(i) Narrowing of the valve outlet caused by thickening of valve cusps, or increased rigidity or scarring
(ii) (also known as insufficiency or regurgitation) caused by an incomplete seal when the valves close, allowing blood to flow backwards
21
Q
What are the common causes of cardiac valve stenosis and incompetence? (HINT: there’s 3 categories)
A
- Congenital Heart Disease - bicuspid valve, atresia
- Cardiomyopathy (hypertrophic, dilated)
- Acquired - rheumatic fever, MI, age related (idiopathic aortic calcific stenosis), endocarditis
22
Q
Define the term infective endocarditis.
A
The infection of a valve with the formation of thrombotic vegetations. The virulence of organisms determines the damage & severity
= is classified into acute & sub-acute
- bacteraemia is common
23
Q
What are the the risk factors for infective endocarditis? (HINT: there’s 3)
A
- Valve damage - as before, especially rheumatic fever
- Bacteraemia - dental, catheterisation, 10% are unknown
- Immunosuppression
24
Q
What is a vegetation.
A
A growth or excrescence of any sort. Specifically, a clot, composed largely of fused blood platelets, fibrin, and sometimes microorganisms, adherent to a diseased heart orifice or valve, and often initiated by infection of the structures involved
25
What are the local and systemic complications of infective endocarditis?
1. cerebral & retinal emboli
2. Bronchopneumonia, Pulmonary infarct
3. Myocarditis
4. Splenomegaly
5. Anaemia
6. Renal infarcts, glomerulonephritis
7. Haematuria
LOCAL = clubbing & splinter haemorrhages
26
What are the principles of diagnosis, treatment and prevention of infective endocarditis?
Treat strep infection with antibiotics
Prophylactic cover for invasive procedures e.g. dental work
Replace damaged valves
Blood Cultures & IV antibiotics
27
What are the names of some organisms that cause infective endocarditis?
Group D streptococcus, gut commensald, skin strep (i.e. coxiella, fungi, candida)
28
What are the causes of ischaemic heart disease?
1. Chronic coronary insufficiency
2. Angina
3. Unstable coronary disease
- MI, sudden ischaemic coronary
4. Heart Failure
5. Arrhythmia
29
What are the macroscopic features of a coronary artery atheroma?
Fatty streak
Fibro-fatty plaque
Plaque disruption - plaque rupture, plaque erosion
30
What are the clinical features of acute myocardial infarction?
1. Chest Pain
- severe, crushing radiating to jaw & arm
2. Associated "autonomic' symptoms - nausea, sweating, terror
3. Breathlessness
31
What are the pathological features of acute myocardial infarction?
1. Plaque rupture (70-75%)
2. Plaque Erosion (25-30%)
3. Coronary embolism
4. Coronary artery spasm/drugs
5. Coronary anomaly
6. Spontaneous coronary dissection
32
What are the complications associated of acute myocardial infarction?
?
33
What are the clinico-pathological features of chronic ischaemic heart disease?
?
34
What are dysrhythmias? Why may they arise?
Dysrhythmia describes conditions where the co-ordinated sequence of electrical activity in the heart is disrupted, Due to: changes in the heart cells, changes in the conduction of the impulse through the heart or a combo of the 2.
35
How are dysrhythmias classified?
Broadly classified as
- atrial (supraventricular)
- junctional (associated with AV node)
- ventricular
- tachycardias or brachycardias
36
What are the 2 commonest types of tachyarrhythmia?
```
Atrial fibrillation
Supraventricular tachycardia (SVT)
```
37
What 4 broad categories of events do dysrhythmias arise from?
1. Heart block
2. Ectopic pacemaker activity
3. Delayed after-depolarisations
4. Circus Re-entry
38
How does heart block arise?
It results from damage (usually ischaemia) to a part of the conducting system. It often affects the AV node - the only path for conduction between atria & ventricles
Impulses can either be slowed, partially blocked or completely blocked
39
How is Heart Block classified?
1st Degree HB - AV node is slightly affected & conduction slowed. Have an abnormally long P-R interval, otherwise every atrial depol (P wave) is passed to the ventricles (QRS)
2nd Degree - more serious damage to AVN => partial block where only some of the atrial depol lead to ventricular depol (QRS)
3rd Degree - AVN completely blocked, no conduction progresses to ventricles. Atria depol (&beat) at inherent rate & the ventricles depol (&beat) at a pace set by Purkinje fibres
40
What are the subtypes of second degree heart block? (HINT: there's 3 subtypes)
MOBITZ (type2) - most beats conducted with a constant P-R, but occasional an atrial depol without a ventricular depol
2:1 or 3:1 - describes ratio of P waves to QRS complexes
WENCKEBACH - Progressive lengthening of P-R interval until a P wave fails to produce a QRS complex. The P-R interval then shortens & normal conduction occurs before the P-R interval starts to lengthen again
41
The spontaneous electrical discharge of the SAN is from the combined effect of what 3 things?
1. Decrease in K+ outflow
2. Funny Na+ current
3. Slow inward Ca2+ current
42
What are the ways/reasons that other areas of the heart can develop pacemaker activity? (HINT: there's 4 ways)
1. If damaged (ischaemia, CHD, rheumatic heart disease, hypertension etc)
2. increased sympathetic activity (stress, exercise etc)
3. Increased sensitivity to catecholamines (GA, caffeine, hyperthyroidism etc)
4. Cardiac glycoside toxicity
43
What is early after-depolarisation?
Occurs towards the end of phase 2 (plateau due to inwards Ca2+). Results in a prolonged QT
It is triggered by fluctuating increases in Ca2+ permeability
Can set off self-sustaining depolarisations
44
What are delayed after-depolarisations?
Following every AP, some of the Ca entering in phase 2 has to be removed back to ECF (done via ca/3Na exchange). Normally a net influx of + & insignificant depolarisation.
If Ca intracellularly rises, the after-depol can get increasingly larger & become self-perpetuating (triggering AP)
Delayed repol increases Ca intracellularly which leads to increased after-depol & can lead to dangerous ventricular dysrhythmias
45
What is circus re-entry movements?
When an electrical impulse can re-stimulate (re-enter) a region of the heart AFTER its refractory period has passed
Comes from an unusual direction & before the tissue would have been re-stimulated by the next normal impulse from the SAN
- either a unidirectional block or a transient block can generate these circus re-entries
46
the differences in the electrical activity of the different parts of the heart and between normal and abnormal pacemaker cells which allow antidysrhythmic drug treatment
?
47
the importance of correct identification of location and nature of the dysrhythmia for proper choice of antidysrhythmic drug
?
48
genetic basis of VT and ionchannelopathies
?
49
the management of atrial fibrillation
?
50
What are the 12 steps (in order) for ECG interpretation?
1. Identity, standardisation
2. Rate
3. Rhythm
4. P wave
5. P-R interval
6. QRS complex
7. QT interval
8. ST segment
9. T wave
10. Axis
11. Other abnormal components
12. Formulate an interpretation
51
How is the rate calculated on an ECG?
300 divided by the number of big squares per R-R interval
52
How many seconds does a (i) small square (ii) large square represent?
(i) 0.04s
| (ii) 0.2s
53
What are the four questions to ask yourself when assessing the rhythm of an ECG?
1. Are normal P waves present? (<0.25mV & upright in II, III & aVF)
2. Are the QRS complexes narrow-normal <120ms (0.12s - 3 boxes) or wide >120ms?
3. Is there always one P wave followed by one QRS complex?
4. Is the rhythm regular or irregular (arrhythmia)?
- mark the position of 3 successive R waves & slide mark forward to check intervals are equal
54
What is normal rhythm called? What are the 4 types of arrhythmias? Describe how they would appear on an ECG.
Sinus rhythm = normal
1. Atrial Fibrillation = no discernable P waves & irregular QRS complexes
2. Atrial Flutter = P waves usually 4 per one QRS, ventricular activation is perfectly regular at 75 per min
3. Junctional (nodal) tachycardia = normal QRS but no P waves
4. Ventricular tachycardia = rate increases to 150 per min after 2 sinus beats. QRS become broad & T waves difficult to identify. Final beat shows return to sinus rhythm
55
What 2 things can an absent P wave result in?
Atrial fibrillation
| Nodal (junctional) rhythm
56
What are the 2 types of abnormal P waves? What do they look like on an ECG & what do they cause?
1. P-mitrale: Bifid wave = Left atrial hypertrophy
| 2. P-pulmonale: peaked wave = Right atrial hypertrophy
57
From where is a P-R interval measured? What is the normal range? What does a prolonged P-R interval imply?
From the beginning of P to the beginning of Q wave
Normal range = 0.12-0.2s (120-200ms)
Implies delayed AV conduction
58
From what points on an ECG is the QRS complex measured? What is the normal duration of said complex? What is the dimensions of a normal Q wave?
Beginning of Q to end of S
Normal duration <120ms (0.12s = 3boxes)
Normal Q wave <40ms (0.04s = 1 box) & <2mm depth
59
If the QRS complex duration is >120ms what does this suggest? If the voltage is low (<5mm) what 5 potential diseases could this be illustrating?
Ventricular conduction defects - bundle branch block (Left & right)
1. hyperthyroidism
2. COAD
3. Myocarditis
4. Pericarditis
5. Pericardial effusion
60
What are the factors evident on an ECG to suggest (i) Left ventricular hypertrophy (ii) Right ventricular hypertrophy?
(i) V5 R wave >25mm OR the sum of V1 S wave + V5&6 S waves >35mm
(ii) Dominant R wave in V1
T wave inversion in V1-3 or V4
Deep S wave in V6
61
If a Q wave is >40ms & has a depth >2mm what 2 things could this suggest?
This would be present a couple of hours/days after acute MI
| But if present in lead III then consider pulmonary embolism
62
Where is the QT interval measured from? How is the corrected QTc interval calculated? What is the normal range for a QT interval
From start of QRS to the end of T - but it varies with rate
QTc = QT/ square root of the R-R interval
normal value = 380-420ms
63
What 8 things can cause a prolonged QT interval to show up on an ECG?
1. acute myocardial ischaemia
2. myocarditis
3. bradycardia
4. head injury
5. hypothermia
6. U&E imbalance (decreased K+, Ca2+, Mg2+)
7. Congenital
8. Drugs (quinidine, antihistamines, macrolides, amiodarone, phenothiazines)
64
Where is the ST segment measured? What is it like normally? What does depression of an ST segment suggest?
From end of ventricular depol to staart of ventricular repol
normally isoelectric
depression = ischaemia
65
What are the 2 things that make a ST segment abnormal? What disease/condition causes this?
Elevation >2mm in 2 adjacent chest leads OR elevation > 1mm in 2 adjacent limb leads
INFARCTION - which can be confused with easy take off (common in fit young individuals)
66
What does a normal T wave look like? What does an abnormal T wave look like? What condition causes this abnormality?
Inverted in aVR & V1 & V2 in young
Abnormal = inverted in I, II & V4-6
- ischaemia/infarction
67
What effects does digoxin have on an ECG? (HINT: there's 2 effects)
T wave inversion
| ST segment sloping depression
68
What is the normal axis range? What is the axis? What does a normal axis look like on an ECG?
Between -30 and +90
Is the sum of all ventricular forces during ventricular depolarisation
Shows upwards deflections in leads I, II & III
69
What are the boundaries of (i) right axis deviation (ii) left axis deviation? What do both look like on an ECG & what conditions cause them?
(i) +90 to +180
(ii) -30 to -90
RIGHT = negative QRS in lead I. RV hypertrophy, PE, MI.
LEFT = negative QRS in leads II & III. LV hypertrophy & MI
70
During an Acute MI, the ECG evolves through 3 stages, what are these 3 stages?
1. T wave peaking followed by T wave inversion
2. ST segment elevation
3. Appearance of new Q waves
71
What will the ECG look like for an (i) anterior infarct (ii) anterolateral infarct (iii) inferior infarct?
```
(i) sinus rhythm
Q waves in V2-4
inverted T waves in V4-6
(ii) sinus rhythm
Q waves in I, II, aVL, V3-5
raised ST segments in V2-6
(iii) sinus rhythm
Q waves in leads III & aVF
depressed ST segments in aVL & V6
```
72
What does pulmonary embolism look like on an ECG?
large S wave in lead I
deep Q wave in lead III
Inverted T wave in lead III
73
What does (i) hyperkalaemia (ii) hypokalaemia (iii) hypercalcaemia (iv) hypocalcaemia look like on an ECG?
(i) Tall, tented T wave, widened QRS
(ii) small T waves, prominent U waves
(iii) short QT interval
(iv) long QT interval, small T waves
74
How is hypertension treated?
```
A(B)CD
ACE inhibitor/angiotensin blocker
(Beta blocker)
Calcium Antagonists
Diuretic esp Thiazise diuretic
```
Also alpha blocker (doxazosin), spironolactone
75
What is the difference in hypertension treatment order sequence for those (i) under 55 years old (ii) greater than 55 years old?
(i) Start A
then add C if needed, followed by D
Then either B, alpha blocker of spironolactone
(ii) Start C
then add A if needed, followed by D
Then either B, alpha blocker or spironolactone
76
How is chronic heart failure treated?
1. Give DAB to all (unless contraindicated)
(diuretic)
ACE inhibitor
Beta blocker
2. Give spironolactone/eplerenone to nearly all
3. Selected treatments - cardiac resynchronisation therapy to those with long QRS on ECG
implantable cardiac defibs to severe pts
77
How is chronic stable angina pectoris treated?
1. To prolong SURVIVAL, all get SAAB
- aspirin
- statin
- ACE inhibitor
- Beta blocker
2. To RELIEVE SYMPTOMS, sequentially use:
- beta blocker
- calcium antag or nitrates
- coronary angioplasty
- new antianginals (ivabradine, ranolazine)
- coronary artery surgery
78
How is a STEMI treated?
in EMERGENCY:
- aspirin
- angioplasty (if near hospital)
- thrombolysis (if far away)
also: aspirin & clopidogrel (or ticagrelor)
Low MW heparin or Fondaparinux (inhibits factor X)
Statin
ACE inhibitor
Beta blocker i.e. SAAB
79
How is an NSTEMI treated?
Aspirin & clopidogrel (or ticagrelor)
Fondaparinux
Angioplasty (not as emergency)
Statin
ACE inhib
Beta blocker i.e. SAAB
80
What is done to treat Atrial Fibrillation? What are these drugs targeting?
1. PREVENT EMBOLI
- warfarin/rivaroxaban
2. CONTROL RATE (crucial)
- beta blocker
- digoxin
3. CONTROL RHYTHM (seldom done)
- DC cardioversion
- amiodarone if heart failure
- sotalol possible
- Flecainide only if heart structure/function normal
81
What are the 3 causes of a stroke?
cerebral thrombosis
cerebral embolus
cerebral haemorrhage
82
Why is a CT scan neccessary before choosing treatment for stroke? What treatment can be used?
```
To differentiate haemorrhage form clot
- if NO haemorrhage then aspirin (acutely for 2 weeks) & thereafter clopidogrel
ALSO,
- statin
- ACE inhibitor
- Indapamide
```
83
What are the common side effects of (i) ACE inhibitors (ii) Beta blockers (iii) calcium antagonists (iv) diuretics (v) angiotensin blockers?
(i) cough, renal dysfunction, angioneurotic oedema, never in pregnancy
(ii) brachycardia/heart block, tired, asthma
(iii) ankle oedema for amlodipine, heart block for diltiazem & verapamil
(iv) hypokalaemia, diabetes, gout
(v) renal dysfunction, never in pregnancy
84
What are the strategies for the treatment of heart failure?
1. Increase cardiac contractility
2. Decrease preload and/or afterload to decrease cardiac work demand by relaxing vascular smooth muscle or by reducing blood volume
3. Inhibit the RAAS
4. Prevent an inappropriate rise in HR
85
What are the various signs & symptoms of heart failure? (NOTE: there's 8, list as many as poss)
- shortness of breath
- swelling of feet & legs
- chronic lack of energy
- difficulty sleeping due to breathing problems
- swollen or tender abdomen with loss of appetite
- cough with frothy sputum
- increased urination at night
- confusion and/or impaired memory
86
What 6 conditions increase your chances of developing heart failure?
1. Hypertension
2. Coronary heart disease (CHD) - atherosclerosis of coronary arteries
3. Cardiomyopathy - causes often unclear but it may be genetic, due to infections, alcohol misuse, medications
4. Atrial fibrillation
5. Anaemia
6. Overactive thyroid gland
87
What are the 5 main types of drugs used in chronic heart failure? Give examples for each type.
1. Loop diuretics - e.g. furosemide
2. ACE inhibitors - e.g. ramipril, lisinopril
3. Angiotensin II receptor blockers - e.g. candesartan
4. Beta blockers - bisoprolol, carvedilol
5. Aldosterone receptor antagonists - e.g. spironolactone
88
Why are beta blockers used in the treatment of heart failure?
They may slow the HR, which could decrease cardiac output
- BUT it allows ventricles to fill more completely during diastole
- some may cause vasodilation & therefore decrease the afterload
89
What are the common side effects of (i) angiotensin converting enzyme inhibitors (ii) angiotensin AT1 receptor antagonists (ARBs) (iii) Aldosterone receptor antagonists (iv) loop diuretics?
(i) persistent dry cough, dizziness, tiredness, headaches
(ii) dizziness, headaches, back/leg pain
(iii) hyperkalaemia, hyponataemia, nausea, hypotension
(iv) acute gout is common with high doses
90
What drug can be used to treat atrial fibrillation? Describe its MoA.
DIGOXIN
- is a cardiac glycoside derived from the foxglove plant (digitalis purpurea).
- it increases vagal efferent activity to the heart => decreasing SAN firing rate (decreasing HR) & decreasing conduction velocity in the AVN
- it also increases contractility by indirectly increasing intracellular calcium levels & subsequent storage in SR
91
What drugs are used to treat chronic heart failure coexisting angina?
oral nitrates
| amlodipine
92
What are the 2 things that need to be done to treat acute heart failure?
1. Normalise ventricular filling pressures
| 2. Restore adequate tissue perfusion
93
What are the initial drug treatments used for acute heart failure?
1. IV loop diuretics
- cause venodilation & diuresis
2. IV opiates/opioids
- reduce anxiety & preload
3. IV, buccal or sublingual nitrates
- reduce preload & afterload
94
What are the second line of drug treatments used to treat acute heart failure?
1. Inotropes, beta-agonists (e.g. dobutamine)
- increase myocardial contractility
2. Dopamine
- increases renal perfusion, increases BP
3. Inotropes, adrenaline
- increase myocardial contractility
95
What does an increase in contractility result in?
An increase in SV, which increases CO
| => increasing the clearance of pooled blood in the ventricles
96
What do baroreceptors do as the CO increases?
They sense change in MABP & decrease sympathetic drive & so decrease HR & decrease TPR (allowing parasympathetic tone to dominate)
97
What is cardiac failure?
The failure of the heart to pump sufficient blood to satisfy metabolic demands
Results in under-perfusion which causes fluid retention & increased blood volume
98
Define (i) acute heart failure (ii) chronic heart failure (iii) acute-on-chronic heart failure.
(i) rapid onset of symptoms often with a definable cause (e.g. MI)
(ii) slow onset of symptoms, associated with, for example, ischaemic or valvular heart disease
(iii) when chronic failure becomes decompensated by an acute event
99
What is systolic cardiac failure? What are the causes? What are the effects? What treatment is given?
Failure of the pump to move blood in systole resulting in reduced ejection fraction & reduced ventricular contraction
CAUSES = Myocardial ischaemia, infarction & scarring, myocarditis, drugs (alcohol, cocaine, anti-cancer cytotoxics), muscular disorders (DMD)
Effects = reduced CO, feedback to atria & rt. side of heart, pulmonary oedema followed by peripheral oedema
TREATMENT = support
100
What is diastolic cardiac failure? What are the causes? What are the effects? What treatment is given?
Failure of the ventricular wall to relax. The ventricle is stiff & restrictive. The reduced ventricular filling leads to reduced blood for systole. Elevated end diastolic pressure.
CAUSES: scarring plus most causes of systolic
EFFECTS: none, pulmonary & peripheral oedema. Response to exercise = tachycardia & pulmonary acute oedema
TREATMENT: Reduce AV conduction
101
What does (i) right ventricular failure (ii) left ventricular failure primarily effect?
(i) Systemic circulation
| (ii) Pulmonary circulation
102
What are the 9 causes of left & right ventricular failure?
1. Coronary heart disease
2. Hypertension
3. Cardiomyopathies
4. Drugs - beta blockers, calcium antags, antiarrhythmics, cytotoxic agents
5. Toxins - alcohol, medication, cocaine, trace elements
6. Endocrine - diabetes mellitus, cushing syndrome, hypo/hyperthyroidism etc
7. Nutritional - deficiency of thiamine, selenium. Obesity
8. Infiltrative - sarcoidosis, amyloidosis, haemochromatosis
9. Others = chagas' disease, HIV infection, peripartum cardiomyopathy, end-stage renal failure.
103
What are the clinical effects of (i) right ventricular failure (ii) left ventricular failure?
(i) pitting oedema in peripheries, dilation of liver veins => congested liver & may be large & tender (if severe can affect kidney function)
(ii) causes pulmonary oedema, with associated symptoms
leads to pulmonary hypertension & eventually, Rt ventricular failure
104
What is the common name used to describe right AND left ventricular failure?
Congestive cardiac failure
105
Define (i) "forward" failure (ii) "backward" failure.
(i) reduced perfusion of tissues. Tends to be more associated with advanced failure
(ii) due to increased venous pressures. Is dominated by fluid retention & tissue congestion
106
Define (i) pulmonary hypertension (ii) systemic hypertension.
(i) high blood pressure that affects the arteries in your lungs and the right side of your heart
(ii) high blood pressure in the systemic arteries . High systemic BP is usually caused by the constriction of the small arteries. BP of above 140/90 mmHg
107
What 3 things is hypertension a major risk factor for?
1. CVD
2. Ischaemic heart disease
3. Accelerated atherosclerosis
108
What are the causes of secondary hypertension?
1. Renal disease
2. Endocrine disease
3. Others - coarctation, pre-eclampsia & hypertension in pregnancy
4. Drugs & toxins: alcohol, cocaine, erythropoietin, adrenergic medications, herbal remedies, liquorice
109
What are the end organ effects of systemic hypertension?
```
HEART:
- LV hypertrophy (fibrosis, arrhythmias)
- Coronary artery atheroma (ischaemic heart disease)
- cardiac failure
KIDNEY:
- nephrosclerosis (proteinuria, haematuria)
- chronic renal failure
- acute renal failure associated with malignant
BRAIN:
- atherosclerosis
- ischaemia & TIA
- infarct
- haemorrhage
EYES:
- hypertensive retinopathy
```
110
What are the causes of pulmonary hypertension?
1. Increased pulmonary vascular resistance
2. Diffuse lung disease, e.g. COPD
3. Elevated left atrial pressure e.g. LV failure, mitral valve stenosis
4. Recurrent pulmonary emboli
5. Primary pulmonary hypertension
6. Left-right shunts e.g. ASD, VSD
111
What are the end-organ effects of pulmonary hypertension?
Pulmonary arteries
| Heart
112
What are the barriers to exercise that some cardiac patients may have?
- bad weather
- too tired
- not in the mood
- don't know how to
- can't afford it
- fear
- don't have time
113
Why are motivational interview techniques useful with this patient group?
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Setting goals that are smart
Specific
Measurable
Achievable
Realistic
Time based
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114
What are the physiological benefits of exercise specific to cardiac disease? (HINT: there's 5)
1. Improvement in functional capacity
2. Improved CV efficiency
3. Reduction in atherogenic & thrombotic risk factors
4. Improvement in coronary blood flow, reduced myocardial ischaemia & severity of atherosclerosis
5. Reduction in risk of CV disease mortality
115
What are the psychological benefits of exercise specific to cardiac disease? (HINT: there's 9)
1. Reduced anxiety & depression
2. Enhanced mood
3. Enhanced self-efficacy
4. Restoration of self-confidence
5. Decreased illness behaviour
6. Increased social interaction
7. Resumption of chores/hobbies
8. Resumption of sexual activity
9. Return to work/vocation
