Week 4 Flashcards
What are the core values of doctors as they relate to the doctor/patient relationship? 9 (5 c’s)
Compassion Commitment Caring Competence Confidentiality Spirit of enquiry Responsibility Integrity Advocacy
Explain what sympathy and empathy are, and appreciate their value and limits
Sympathy: Being affect by the condition of another with a feeling similar to that of the other
Empathy: The ability to understand and appreciate another person’s feelings/experiences
Limits
- Sympathy can be received as**
- Empathy is limited by medical education and practice
Name the 4 key attributes of care which must be maintained, whatever one’s values, as defined by GMC
Doctors may practice medicine in accordance with their beliefs but they:
- Must act in accordance with relavent legislation
- Must not treat patients unfairly
- Must not deny patients access to appropriate services or care
- Must not cause patients distress
Name the areas in which BMA support conscientious objection, and know which of these are legally protected
- Emphasise the balancing act between doctors’
freedom & the rights of the patient to receive
appropriate care - A treating doctor’s primary obligation is to their
patient - They support CO in 3 cases: abortion), fertility treatment & withdrawal of life-sustaining treatment
- For other case may request but not a right
State 4 reasons why some argue that conscientious objection should not be allowed in medical practice.
- Inefficiency and inequity
- Inconsistency
- Commitments of a doctor
- Discrimination
Ie Doctors values should not determine medical care
Explain the value of a patient’s narrative (4)
Value of narrative:
- To decrease diagnostic and therapeutic error
- Increase personal connections from shared experiences
- Increases empathic opportunities
- Patients feel understood/cared for
Limits of conscientious objection as described by the GMC
You are allowed to refuse participation in a particular procedure. But cannot refuse to treat a patient/group of patients.
What are the two main components that influence afterload?
Vascular resistance
Ventricular wall tension
Increased contractility increases CO ______ of preload and afterload
Increased contractility increases CO INDEPENDENT of preload and afterload
What are the 4 classes of heart failure in the NYHA (New York Heart Association)?
Class I
-No limitation of physical activity. Ordinary physical activity does not undue fatigue, dyspnea
Class II
-Slight limitation of physical activity. Comfortable at rest. Ordinary physical activity results in fatigue, palpitations, dyspnea
Class III
-Marked limitation of physical activity. Comfortable at rest. Less than ordinary activity causes fatigue, palpitation or dyspnea.
Class IV
-Unable to carry on any physical activity without discomfort. Symptoms of heart failure at rest. If any physical activity is undertaken, discomfort increases
Difference in ejection fraction between systolic and diastolic ventricular dysfunction?
Systolic ventricular dysfunction: Impaired cardiac contractility therefore decrease ejection fraction
Diastolic ventricular dysfunction: Normal ejection fraction but impaired diastolic ventricular relaxation and decreased filling therefore decrease in SV and CO
Systolic dysfunction:
Results from conditions that affect…. (4)
Consequences on CVS?
Systolic dysfunction results from conditions that affect:
- Contractility e.g. IHD, cardiomyopathy, MI
- Chronic volume overload
- Pressure overload e.g. Valvular stenosis, hypertension
- Advanved aortic stenosis
Consequences to CVS:
- Increased EDV (preload)
- Ventricular dilation
- Increased ventricular wall tension
Diastolic dysfunction:
Causes? 5
Causes:
- Impedance of ventricular expansion e.g. constrictive pericarditis etc
- Increased wall thickness
- Delayed diastolic relaxation
- Increase HR
- Transient myocardial ischemia
What are the tissue consequences of:
- Right heart failure?
- Left heart failure?
Right heart failure:
- Congestion of peripheral tissues
1. Oedema and ascites
2. Liver congestion –> Impaired liver function
3. GI tract congestion –> Anorexia, GI distress, weight loss
Left heart failure:
- Right heart failure
- Decrease cardiac output
- Activity intolerance
- Signs of tissue perfusion
- Cyanosis and signs of hypoxia - Pulmonary congestion
- Cough with frothy sputum
- Orthopnea
- Paroxysmal nocturnal dyspnea
Causes of right ventricular dysfunction (4)
1. Conditions impeding flow into the lungs – Pulmonary hypertension – Valve damage / stenosis / incompetence 2. Pumping ability of right ventricle – Cardiomyopathy – Infarction 3. Left ventricular failure 4. Congenital heart defects
Cause of left ventricular dysfunction (4)
- Hypertension (↑TPR)
- Acute myocardial infarction
- Aortic or mitral valve stenosis or regurgitation
- Increase in pulmonary pressure can lead to
right ventricular failure
In the early stages of heart failure, what is the aim of the compensatory mechanisms?
To maintain CO
Although long term they worsen the condition
What are the 4 main compensatory mechanisms directly acting on the heart?
- Frank-starling mechanism
- Increase HR
- Increase contractility
- Increase in vascular resistance
All a result of decrease in CO
Explain the following problems with the compensatory mechanisms for cardiac faulure:
- Frank-starling
- Sympathetic activity
- Renin-Angiotensin
- Frank-starling mechanism
- Increase in vascular tone leads to increase in EDV
- Increase in muscle strength and O2 consumption - Sympathetic activity: Initially helpful but long term…
- Tachycardia, vasoconstriction, decrease perfusion of tssues, cardiac arrhythmias, renin release
- Increase workload of the heart
- Desensitization of beta but not alpha receptors (TPR remains high but HR eventually decreases) - Renin-angiotensin
- Decrease in renal blood flow stimulates release of renin
- Increase renin release therefore increase angiotensin II formation: Vasoconstrictor, stimulates aldosterone release
- ->Na and H2O reabsorption is increased directly (decreased flow to kidneys_ and indirectly (via aldosterone)
- Angiotensin II and aldosterone: Involved in inflammatory responses leading to deposition of fibroblast and collagen in the ventricles
- -> Stiffness and decreased contractility of the heart hence progressing dysfunction
Strategies for treatment of heart failure (4)
- Increase cardiac contractility
- Decrease preload and/or afterload to decrease cardiac work demand
- By relaxing vascular smooth muscle
- By reducing blood volume - Inhibit the RAAS
- Prevent inappropriate increase in HR
Name 8 systemic diseases that affect the CVS
- Diabetes mellitus
- Hypertension
- COPD
- Amyloidosis
- Vasculitides and SLE
- Rheumatoid arthritis
- Thyroid disease
- Sarcoidosis
Comment briefly on the CVS effects of Diabetes mellitus
Diabetes Mellitus causes microvascular disease due to basement membrane thickening. This impairs O2 diffusion into respiring tissues (particularly the retina)
BM thickening due to glycation.
Diabetes leads to accelerated vascular damage
Comment briefly on the CVS effects of hypertension
Left ventricular hypertrophy leads to hypertension
Hypertension causes vascular damage. E.g:
1. Promotes atherosclerosis
2. Increase TPR
3. Coronary ischemia
4. Aneurysm
Comment briefly on the CVS effects of Chronic obstructive pulmonary disease
In COPD there is emphasyma present. These are areas of lung tissue involved in gas exchange that are destroyed/ imparied. This limits the vascular bed available for gas exchange.
Comment briefly on the CVS effects of Amyloidosis
What is amyloid?
Amyloid deposition in vascular vessels inhibits normal vessel function such as vasoconstriction
Diseases caused:
- Heart failure
- Nephrotic syndrome
Caused by: Plasma cell neoplasm (e.g. Myeloma), chronic inflammatory disorder
Amyload:
Extracellular beta-pleated sheet material. Composed of immunoglobin light chains, serium amyloid protein A, peptide hormones, prealbumin
Comment briefly on the CVS effects of Rheumatoid arthritis
CVS caused: Pericarditis, cardiomyopathy, rheumatoid nodules, vasculitis, arrhythmia, atherosclerosis
Comment briefly on the CVS effects of Thyroid disease
Patients with overt and subclinical thyroid dysfunction are at increased risk of heart failure
Thyroxidine drug puts a big stress on the CVS in hypothyroxic patients
What is sarcoidosis?
Comment briefly on the CVS effects of Sarcoidosis
Sarcoidosis: Sarcoidosis is a rare condition that causes small patches of red and swollen tissue, called granulomas, to develop in the organs of the body. It usually affects the lungs and skin.
Comment briefly on the CVS effects of Nutrition
Stronger famine exposure is associated with a higher CHD risk, especially if it’s during postnatal periods of development e.g. adolescence
Comment briefly on the CVS effects of drugs
The following drugs have CVS effects:
- Anticancer
- Immunisuppressive
- Diabetogenic
- Anti-inflammatory
What are the 4 strategies for treating cardiac failure`
- Increase cardiac contractility
- Decrease preload and/or afterload to decrease cardiac work demand
- By relaxing vascular smooth muscle
- By reducing blood volume - Inhibit the RAAS
- Prevent inappropriate increase in increase in heart rate
Signs and symptoms for heart failure (8)
- Shortness of breath
- Swelling of feet and legs
- Chronic lack of energy
- Difficulty sleeping due to breathing problems
- Swollen or tender abdomen with loss of appetite
6, Cough with frothy sputum - Increased urination at night
- Confusion and/or impaired memory
Conditions that increase your chances of developing heart failure
- Hypertension
- Coronary heart disease (CHD): Atherosclerosis of coronary arteries
- Cardiomyopathy: Causes often unclear but may be genetic, due to infections, alcohol misuse, medications
- Atrial fibrillation
- Anaemia
- Overactive thyroid gland
Body unable to distinguish between heart failure and ____
Hypovolemia
The body responds the same to both, but the response will not correct the underlying issue in heart failure although it alleviates immediate symptoms
What are the 5 main drugs used to treat chronic heart failure
- Loop diuretics e.g. Furosemide
- ACE inhibitors e.g. Ramipril, Lisinopril
- Angiotensin II receptor blockers (ARBs) e.g. candesartan
- Beta-blockers e.g. Bisoprolol, carvedilol
- Aldosterone receptors antagonists e.g. spironolactone
Which drug groups are classed as:
- Kidney function modifiers in CHF
- RAAS inhibitors
- Kidney function modifiers in CHF: Loop diuretics, Aldosterone antagonists
- RAAS inhibitors: ACE inhibitors, ARBs
Why use a beta-blocker to treat heart failure?
- Slows HR
- Decrease CO
- Allows ventricles to fill more completely during diastole
- Vasodilation which decreases afterload
Side effects of:
- ACE inhibitors
- ARBs
- Aldosterone receptor antagonists
- Loop diuretics
- ACE inhibitors = Persistent dry cough, dizziness, tiredness, headaches
- ARBs = Dizziness, headaches, back/leg pain
- Aldosterone receptor antagonists = Hyperkalaemia, hyponatraemia, nausea, hypotension
- Loop diuretics = Acute gout is common with high doses
3 additional treatments for chronic heart failure for co-existing problems
- Atrial fibrillation: Digoxin
- Persistent sodium/water retention: Additional diuretics (e.g. thiazides)
- Co-existing angina: Oral nitrates, amlodipine
2 actions of digoxin
Increase vagal efferent (from brain to heart) activity to the heart.
- Decreases SAN firing rate
- Decreases conduction velocity in the AV node
Increases contractility by increase Ca levels indirectly
What are the two aims of treatment of acute heart failure
- Normalise ventricular filling pressure
2. Restore adequate tissue perfusions
Treatment of Acute Heart Failure:
- Initial drug treatments
- Secondary drug treatments
- Initial drug treatments
- IV loop diuretics: Cause venodilation and diuresis
- IV opiates/opiods: Reduce anxiety and preload
- IV, buccal or sublingual nitrates: Reduce preload and afterload - Secondary drug
- Inotropes, beta-agonists: Increase myocardial contractility
- Dopamine: Increases renal perfection, increases BP
- Inotropes, adrenaline: Increase myocardial contractility
Increasing contractility with treating cardiac failure:
- Effect on stroke volume?
- Response of baroreceptors?
Increase contractility will increase stroke volume, which increases CO. Leads to increase clearance of pooled blood in the ventricles
As CO increase, barareceptors sense change change in MABP and decrease sympathetic drive. This the decreases HR, and TPR decreases.
What makes up a heart valve?
- Valve ring
- Cusp
- Chordae tendineae
- Papillary muscles (mitral and tricuspid only)
4 functional failures in valves?
- Mitral stenosis
- Mitral incompetence
- Aortic stenosis
- Aortic incompetence
Tricuspid and pulmonary valve as above but less common and less severe
Stenosis:
Define?
Affect of aortic stenosis on bp?
Stenosis: Narrowing of the valve outlet caused by thickening of valve cusps or increase rigidity or scarring
Aortic stenosis= No increase in bp as flow cannot get out, but LV has to pump harder
Incompetence:
Define?
Affect of aortic incompetence on bp
Incompetence: Incomplete seal when valve closes, allowing blood to flow backwards
Also called: Insufficiency /regurgitation
Aortic incompetence effect on bp: Higher systolic and lower diastolic.
What valves are responsible for the systolic and diastolic heart sounds?
Systole: Mitral and tricuspid closure
Diastole: Aorta and pulmonary closure
What are 3 common cause of cardiac valve stenosis and incompetence
- Congenital heart disease Bicuspid valve, atresia
- Cardiomyopathy
- Acquired: Rheumatic fever, MI, age, endocarditis
Aortic stenosis: Cause? 3 Risks? 3 Consequences? 3 Symptoms?
Causes:
- Calcification of congenital bicuspid valve
- Senile calcific degeneration
- Rheumatic fever
Risks:
- Right ventricular hypertrophy (as it have to compete with backwash into pulmonary circulation)
- Syncope
- Sudden cardiac death
Consequences:
- Increase the work of the heart
- Ventricular hypertrophy
- Causes cardiac failure late in the clinical course
Symptoms:
- Dyspnoea
- Angina
- Syncope
Aortic incompetence:
Cause? 3
Consequences? 5
Causes:
- Marfan’s syndrome
- Rheumatic fever
- Infective endocarditis
Consequences:
- Increases the volume of blood to be pumped significantly
- Increases the work of the heart
- Cardiac hypertrophy
- Cardiac failure
- Can occur in the presence of aortic stenosis
Mitral incompetence:
Cause?
Risks?
Caused by problems with:
- Cusp
- Rheumatic disease= scarring, contraction
- Floppy valve and marfan’s syndrome = Stretch
- Infective endocarditis = perforation - Chordae: As above
- Valve ring: As above, age
- Papillary muscle e.g. post MI
Risks:
- Pulmonary hypertension
- Right ventricular hypertrophy
To list the barriers to exercise that some cardiac patients may have
- Bad weather
- Too tired
- Not in the mood
- Fear
- Money
- Time constraint
To explain why motivational interview techniques are useful with this patient group
Motivational interviewing is a client-centered, directive counseling approach aimed at promoting motivation in clients to change certain behaviors. Its effect is to reduce defensiveness and promote disclosure, engagement, and participation, thereby motivating the client to make behavioral changes.
To list the benefits of exercise specific to cardiac disease:
Physiological? 4
Psychological? 9
Physiological benefits:
- Improved cardiovascular efficiency
- Reduction in atherogenic and thrombotic risk factors
- Improvement in coronary blood flow, reduced myocardial ischaemia and severity of atherosclerosis
- Reduction in risk of cardiovascular disease mortality
Psychological benefits:
- Reduced anxiety and depression
- Enhanced mood
- Enhanced self-efficacy
- Restoration of self-confidence
- Decreased illness behaviour
- Increased social interaction
- Resumption of chores/hobbies
- Resumption of sexual activity
- Return to work/vocation
Goals for cardiac rehab should be SMART. What does that stand for?
- Specific
- Measurable
- Achievable
- Realistic
- Time based
What are the different phases of a workout?
Warm up -15 mins
Conditioning phase -20 mins
Cool down- 10 mins
What is the scale used to monitor intensity of exercise?
SING: Ideal for warm up
TALK: Moderate exercise
GASP: You are working too hard
What is rheumatic fever?
A non-contagious acute fever marked by inflammation and pain in the joints. It chiefly affects young people and is caused by a streptococcal infection.
Is an acute multi-system disease- heart (myocarditis, valvulitis, pericarditis), joints, connective tissue
Mitral stenosis:
Causes?
Consequences?
Causes:
- Congenital (rare)
- Post rheumatic fever
Consequences:
- Restricts blood flow to left ventricle
- Atrial fibrillation
- Back pressure results in pulmonary hypertension
- End result = right heart failure
Define infective endocarditis.
What is the prime investigation for it?
Infection of valve with formation of thrombotic vegetations.
As the heart is a protected, contained environment. It is a prime location for bugs to settle and grow.
Defined as acute and sub-acute.
Prime investigation = blood culture
Risk factors for infective endocarditis? 3
- Valve damage
- Bacteremia (i.e. anything that exposes the circulation to bacteraemia)
- Dental
- Catheterisation - Immunosuppresion
What is the pattern of occurrence for rheumatic fever?
Occurs in children: 4-16 years
May occur in recurrent episodes
Describe the composition of a vegetation
Composed of:
- Platelets
- Fibrin
- Microcolonies of microorganisms
- Scant inflammatory cells
In the subacute form of infective endocarditis, the vegetation may also include a center of granulomatous tissue, which may fibrose or calcify.
Describe the local and systemic complication of infective endocarditis
Local complications:
-Myocarditis
Systemic complications:
- Cerebral and retinal emboli
- Splenomegaly + infarcts
- Anaemia
- Haematuria
- Renal infarcts
- Clubbing
- Splinter haemorrhages
Describe the principles of diagnosis, treatment and prevention of infective endocarditis
Treatment:
•Treat Strep infection with antibiotics
•Prophylactic cover for invasive procedures eg dental work
•Replace damaged valves
Prevention: •Clinical suspicion •Clinical signs •Imaging •Blood culture •Intravenous antibiotics
Atherosclerotic coronary diseases lead to… (4)
- Chronic coronary insufficiency e.g. Angina
- Unstable coronary disease
e. g. MI - Heart failure
- Arrhythmia e.g. Acute ischaemia
Describe the macroscopic features of coronary artery atheroma
Pathology:
- Fatty streak
- Fibro-fatty plaque
- Lipid rich core with fibrous cap
Describe the clinical and pathological features of acute myocardial infarction
Pathological features: Fibro-fatty plaque disruption, either: rupture or erosion
Clinical features:
- Chest pain (severe, crushing, radiating to jaw and arm)
- Associated “autonomic” symptoms (e.g. nausea, sweating, terror)
- Breathlessness
- Raised cardiomyocyte markers in blood (Troponin T or I)
- Abnormal ECG
Describe the complications of acute myocardial infarction (STEMI):
Immediate?
Early?
Late?
Immediate:
- Ventricular arrhythmia and death
- Acute left heart failure
Early:
- Myocardial rupture
- Mitral valve insufficiency
- Ventricular septal defect
- Mural thrombus and embolization
Late:
- LV dilatation and heart failure
- Arrhythmia
- Recurrent MI
Describe the causes of ischaemic heart disease
- Age
- Hypertension
- Hypercholestrolaemia
- Smoking
- Diabetes
- Obesity
- Physical inactivity
Angina: Symptoms? Cause? Presentation on ECG? Approaches to treatment? Classes of drugs used for treatment? (4)
Symptoms:
- Gripping central chest pain
- Radiation to arm and jaw
- Clear and precise relationship to exercise
- Alleviated by rest
- Worsened by food and the cold
- No autonomic features
Cause: Sub endocardial ischaemia.
-Due to mismatch of supply and demand.
ECG: ST depression
Treatment:
- Drugs to reduce myocardial oxygen consumption
- Improve coronary flow reserve (e.g. Percutaneous coronary intervention, CABG)
Drugs:
- B-blockers
- Nitrates (GTN)
- Calcium channel blockers
- Ikf channel inhibitors
What two regulatory systems control coronary circulation?
- Autoregulation
2. Metabolic regulation
How are MIs classified?
- By site of infarction (pathology)
- Full thickness, transmural
- Subendocardial - By ECG (clinical)
- ST elevation myocardial infarction (STEMI)
- Non-ST elevation myocardial infarction (NSTEMI)
What are two approaches to managing a STEMI?
Adjunctive therapy?
- Anti-platelet agents
- Aspirin
- Clopidogrel - Immediate revascularization
- Primary PCI
- Thrombolysis
Adjunctive therapy (after anti-platelets and revascularization):
- B-blockers
- Statin
- ACE inhibitors
Treatment of a NSTEMI?
- Antiplatelet therapy
- Aspirin
- Clopidogrel - Anti-ischemaeics (b-blockers, nitrates)
- Statins
- ACE inhibitors
- Coronary angiography and revascularization (given early if troponin raised or symptoms continue)
Right bundle branch block:
-Presentation on ECG?
- QRS prolongation
2. “M” shape of right ventricle leads (V1,V2)
AV block:
Different classifications?
How does it arise?
Classifications:
- 1st degree: Lengthening of the PR interval
- 2nd degree: Mobitz Type 1 (progressive lengthening of PR interval until P wave blocked and the PR short again), Mobitz Type 2 (block after 2/3 conducted beats in regular pattern)
- 3rd degree: Complete AV disssociation
How does circus movement result in tachycardia?
Continuous repetitive propagation of an excitatory wave traveling in a circular path, returning to its site of origin to reactivate that site.
The one event crucial to the development of a reentrant tachycardia is the failure of a group of fibers to activate during a depolarization wave.
Understand genetic basis of VT and ionchannelopathies
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Atrial fibrillation:
- ECG presentation?
- Symptoms?
- Management?
- Main risks?
ECG presentation: Irregular narrow complex tachycardia with no P waves
Symptoms:
- Fast ventricular response rate- SOB, hypotension
- Slow conduction - dizziness, syncope
- Embolism of left atrial thrombus
Management: control rate or rhythm?
Control rate unless:
-Symptomatic with high ventricular response rates refractory to treatment
-Acute presentation with clear precipitating
Control rate via: Drugs to slow AV conduction, AV node ablation, permanent pacemaker
Control rhythm via: Cardioversion, maintenance of sinus rhythm
Risks: Thrombo-embolism (esp CVA)
Left bundle branch block:
-Presentation on ECG?
- Widening of QRS complex
- Left ventricle leads (V5, V6, AVL) are positive with notch
- V1 is negative
What are the full names of the following bifascicular block conditions:
- RBBB with LAD?
- RBBB with RAD?
- Right bundle branch block with Left Axis Deviation (anterior hemiblock)
- Right bundle branch block with Right Axis deviation (posterior hemiblock)
What does bifascicular block mean?
Bifascicular block most commonly refers to conduction disturbances below the atrioventricular (AV) node in which the right bundle branch and one of the two fascicles (anterior or posterior) of the left bundle branch are involved.
Two types of tachycardia?
- Narrow complex/supraventricular tachycardia (incl Atrial flutter, atrial fibrillation, AVNRT, AVRT)
- Broad complex tachycardia ( incl VT, SVT)
3 basic mechanisms of tachycardias?
- Ectopic focus i.e. tissue with rapid pacemaker function
- Re-entry/ circus movement
- Fibrillation
Two types of tachycardia?
- Narrow complex/supraventricular tachycardia (incl Atrial flutter, atrial fibrillation, AVNRT, AVRT)
- Broad complex tachycardia ( incl VT, SVT with aberration, SVT with pre-existing BBB morphology on ECG)
What is the basis for the adenosine test in narrow complex/supraventricular tachycardias?
Adenosine will stop any tachycardia with re-entry over the AV node i.e. AVNRT and AVRT
What is the basis for the adenosine test in narrow complex/supraventricular tachycardias?
What are the 3 responses to the test?
Adenosine will stop any tachycardia with re-entry over the AV node i.e. AVNRT and AVRT
Responses:
- No effect= Wrong diagnosis
- Transient slowing with/without revealed P waves
- Restoration of sinus rhythm AVNRT or AVRT
Ventricular tachycardia (VT):
- ECG presentation?
- VT or SVT with aberration?
- Mechanisms?
ECG presentation: Broad complex, no p waves associated with QRS complex
VT characteristics:
- Wide QRS >140msec
- Absence of LBBB or RBBB morphology
- P and QRS waves at different rates
- Fusion beats (when sinus and ventricular beat coincides)
- Cannon waves in JVP
Mechanisms:
- Acute LV damage
- Chronic LV damage
- Abnormalities of Na and K channels= Long QT interval syndrome
Ventricular fibrillation:
Characteristics?
Treatment?
Characteristics:
- ECG chaotic
- No detectable cardiac output
- Often preceded by VT
Treatment:
- Blow to chest
- DC cardioversion
- IV adrenaline
- ICD implantation
How do you calculate QTc?
GTc= (QT)/root of RR
What is Torsade de Pointes?
Torsade de pointes is a distinctive form of polymorphic ventricular tachycardia (VT)
Characterized by a gradual change in the amplitude and twisting of the QRS complexes around the isoelectric line.
Torsade de pointes is associated with a prolonged QT interval, which may be congenital or acquired.
Result of inhibition of K channel
What is brugada syndrome?
Genetic disorder that results in a reduced flow of sodium ions into the heart cells, which alters the way the heart beats.
Treated by insertion of an ICD
What is Wolff-Parkinson-white syndrome?
In WPW syndrome, there’s an extra electrical connection in the heart, whichallows electrical signals to bypass the usual route and form a short circuit. This means the signals travelround and round in a loop, causing episodes where the heart beats very fast.
“Anatomical AV bypass tract with non-decremental conducting properties”
Result: Short PR interval
Treatment of hypertension:
First choice?
Second choice for resistant hypertension?
First choice: A(B)CD
- ACE inhibitors
- (Beta-blocker)
- Calcium antagonists
- Diuretic
Second choice for resistant hypertension:
- Alpha blocker: Doxazosin
- Spironolactone
How does treatment for hypertension differ with the age of a patient?
Below 55yrs: -Start A -Add C -Add D Then either B, alpha blocker or spironolactone
Above 55yrs -Start C -Add A -Add D Then either B, alpha blocker or spironolactone
Treatment for chronic heart failure
- Give DAB to all
- Give spironolactone/ eplerenone
- Selected treatments:
-Cardiac Resynchronisation Therapy
(= Biventricular Pacing)
to those with long QRS on ECG
-Implantable Cardiac Defibrillators to severe patients
In severe heart failure, ARB or ACEI replaced by sacubitril-valsartan.
Treatment for chronic angina:
- To prolong survival
- To relieve symptoms
- To prolong survival: SAAB
- Aspirin
- Statin
- ACEI
- Beta blocker - To relieve symptoms
- Beta blockers
- Calcium antagonist or Nitrates
- Coronary Angioplasty
- Antianginals (Ivabradine, ranolazine)
- Coronary artery surgery
What is the relevance of troponin in the bloodstream?
Indicates an MI as troponin is released when cardiac cells died.
Either: STEMI or NSTEMI dependent on ECG
What are the 4 entities for actute chest pain?
- STEMI (troponin positive)
- NSTEMI ((troponin positive)
- Troponin negative ACS
- Non cardiac chest pain
STEMI treatment?
Emergency
- Aspirin
- Angioplasty
- Thrombolysis (if far away from hospital)
Additional
- Clopidogrel/ticagrelor (targets platelets)
- LMW Heparin (inactivates thrombin)
- Fondaparinux (targets clotting factors)
+SAAB
NSTEMI treatment?
- Aspirin and Clopidogrel OR Ticagrelor (for platelets)
- Fondaparinux (for clotting factors)
Angioplasty (not as emergency)
+ SAAB
Troponin negative ACS treatment
SAAB + selective use of angioplasty
What does SAAB represent?
The combination of drugs commonly used to prolong survival in patients with angina.
(Statins, ACEI,, Aspirin, Beta-blockers)
If patients with angina have been given all the appropriate treatment, yet have persisting chest pain, what drug can be given?
Glycoprotein IIb/IIIa inhibitor e.g. Tirofiban
Other antiplatlets e.g. ticagrelor, prasugrel
Treatment for atrial fibrillation:
- Prevent emboli
- Control rate
- Control rhythm
- Prevent emboli
- Warfarin/ Rivaroxaban - Control Rate (crucial)
- Beta Blocker
- Digoxin - Control Rhythm (seldom done)
- DC Cardioversion
- Amiodarone if heart failure
- Sotalol (II/III) possible
- Flecainide (Ic) only if heart structure/function normal
Stroke (CVA);
Causes?
Treatment if no haemorrhage visible on CT scan?
Causes:
- Cerebral thrombosis
- Cerebral embolus
- Cerebral haemorrhage
Treatment: -Thrombolysis (in emergency) -Aspirin (acutely and for 2 weeks) -Clopidogrel (onwards of 2 weeks) \+ Statin, ACEI, indapamide
Common side effects of the following:
- ACEI
- B-blockers
- Calcium antagonists
- Diuretics
- ARB
- ACE Inhibitors
- Cough
- Renal dysfunction *(worsen or improve)
- Angioneurotic oedema
- Never in pregnancy - Beta Blockers
- Bradycardia /Heart Block
- Tired
- Asthma (Not in asthmatics) - Calcium Antagonists
- Ankle oedema for Amlodipine
- Heart Block for Diltiazem & - Verapamil - Diuretics
- Hypokalaemia
- Diabetes
- Gout - Angiotensin Blockers
- Renal dysfunction * (worsen or improve)
- Never in pregnancy
How do you calculate rate on an ECG?
300/number of big squares between R-R interval
How are normal p waves detected?
- Less than 0.25mV (two small squares)
- Uptight in II, III and AVF
What is the normal width of QRS complex?
120ms
What is the ECG presentation of the following conditions:
- Atrial fibrillation
- Atrial flutter
- Junctional (nodal) tachycardia
- Ventricular tachycardia
- Left atrial hypertrophy
- Right atrial hypertrophy
- Left ventricular hypertrophy
- Right ventricular hypertrophy
- AF = No discernible P waves, irregular QRS complexes
- Atrial flutter = P waves at high rate, giving a sawtoothed appearance. 4 waves per QRS complex
- Junctional (nodal) tachycardia = Normal QRS complexes but absent p waves
- VT= After 2 sinus beats, the rate increases to 150bpm. QRS complex is broad, t waves absent. Final beat shows a return to sinus rhythm.
- Left atrial hypertrophy= Bifid p wave
- Right atrial hypertrophy = Peaked p wave
- Left ventricular hypertrophy = R wave in V5 > 25mm (5 big boxes)
- Right ventricular hypertrophy = Dominant R waves in V1, T waves inversion in V1-V4, deep S wave in V6
What is the normal range of a P-R interval?
Prolonged interval implies??
0.12-0.2s (i.e. 3-5 small boxes)
Prolonged interval = Delayed AV conduction
Normal duration of the QRS complex (ventricular depolarization)?
Duration and depth of Q wave?
QRS duration: Less than 0.12s (3 small boxes)
Duration of Q wave = <0.04s
Depth of Q wave= less than 2mm/0.2mV
Two indications of an abnormal QRS complex?
- If duration is over 0.12s
- Due to ventricular conduction defect (e.g. RBBB, LBBB) - Low voltage <5mm (0.5mV)
- Due to hypothyroidism, COAD, myocarditis, pericarditis
Conditions which result in a prolonged QT interval? 8
- Acute myocardial ischaemia
- Myocarditis
- Bradycardia
- Head injury
- Hypothermia
- U&E imbalance
- Congenital
- Drugs
When interpreting an ECG, what does isoelectric mean?
The line which the wave returns to is at the same potential before and after the QRS complex
What does the ST segment demonstrate?
The time from the end of ventricular depolarization to the start of ventricular repolarisation
What abnormalities of the ST segment would be highlight:
- Infarction?
- Ischaemia?
- Infarction: Elevation >2mm in 2 adjacent chest leads or elevation >1mm in two adjacent limb leads
- Ischaemia: Depression
During ventricular repolarisaition (i.e. T wave) which leads are normally inverted?
Inverted: V1 and aVR (V2 in young)
Not inverted normally: I, II, V4-6
Effect of digoxin on t wave
- T wave inversion
2. ST segment sloping depression
What is the ECG presentation of the following conditions:
- Left axis deviation
- Right axis deviation
LAD= negative WRS deflections in II and III RAD= Negative deflections in I
What are the MI ECG changes?
ECG evolution 4 stages:
- T wave peaking
- T was inversion
- ST elevation
- Appearance of new Q waves
ECG changes in a PE
- Large S wave in lead I
- Deep Q waves in lead III
- Inverted T wave in lead III
What 5 structures are supplied by the phrenic nerve?
Pericardium Mediastinal parietal pleura Diaphragm Diaphragmatic pleura Diaphragmatic peritoneum
Where do the phrenic and vagus nerves lie in relation t the root of the lung?
Vagus: Posterior to lung root
Phrenic: Anterior to lung root
What structures to the left and right recurrent laryngeal nerves loop around?
Left recurrent laryngeal nerve: Passes posterior to ligamentum arteriosum
Right recurrent laryngeal nerve: Loops around and passes posterior to the right subclavian artery
Define cardiac failure
Failure of the heart to pump sufficient blood to satisfy metabolic demands.
Results in underperfusion which causes fluid retention and increased blood volume
Appreciate the difference between acute and chronic cardiac failure
Acute heart failure: Rapid onset of symptoms, often with definable cause e.g. MI
Chronic heart failure: Slow onset of symptoms, associated with ischaemic or valvular heart disease
Acute-on-chronic: Chronic failure becomes decompensated by an acute event
Appreciate the difference between systolic and diastolic cardiac failure
Systolic heart failure:
- Failure of the pump to move blood in systole
- Reduced ejection fraction
- Reduced ventricular contraction
Diastolic heart failure:
- Failure of ventricular wall to relax
- Restrictive, stiff ventricle
- Reduced ventricular filling leads to reduced blood for systole
- Elevated end diastolic pressure
Appreciate the difference between right and ventricular failure
Right: Effects systemic circulation
Left: Effects pulmonary circulation
Describe the 8 causes of left and right ventricular failure
Hint: D TECHNIC
- Coronary heart disease: Most common is atherosclerosis
- Hypertension
- Cardiomyopathies-Familial/genetic
- Drugs- Beta-Blockers, calcium antagonists, antiarrhythmics, cytotoxic agents
- Toxins Alcohol, medication, cocaine, trace elements (mercury, cobalt, arsenic)
- Endocrine Diabetes mellitus, hypo/hyperthyroidism, Cushing syndrome, adrenal insufficiency, excessive growth hormone, phaeochromocytoma
- Nutritional Deficiency of thiamine, selenium, carnitine. Obesity, cachexia
- Infiltrative Sarcoidosis, amyloidosis, haemochromatosis, connective tissue disease
Describe the clinical effects of left and right ventricular failure
Left:
- Pulmonary oedema: X-ray presents fluffy shadows on the lungs. This is fluid. Microscopically oedema is seen filling the air spaces
- Pulmonary hypertension
- Eventually right ventricular failure
- Reduced perfusion of tissues
Right:
- Pitting oedema in systemic circulation
- Cirrhosis (Congestive hepatopathy)
- Increased venous pressures
Both present clinically with breathlessness, fatigue
Name the causes of (secondary) systemic hypertension
- Renal disease
- Endocrine disease e.g cushings
- Others: Coarctation
- Drugs and toxins
End organ effects of systemic hypertension:
- What are the end organs?
- What is the difference in effects between idiopathic and secondary hypertension?
- What are the changes specific to the heart?
- Changes to the kidney?
- Changes to vessels?
- Changes to brain?
End organs: Brain, heart, kidneys, arteries, eyes
In idiopathic hypertension: Slow changes in vessels and heart with chronic end-organ dysfunction
In secondary/malignant hypertension: Rapid change sin vessels with acute end-organ dysfunction.
Heart: Left ventricular hypertrophy, coronary artery atheroma, cardiac failure
Kidney: Nephrosclerosis, chronic renal failure, acute renal failure
Vessels: Accelerated atherosclerosis, proliferation and hyalinization of arteries/arterioles, fibrinoid necrosis
Brain: Atherosclerosis, Ischaemia, Haemorrhage, TIA infarct
Describe the causes of pulmonary hypertension (6)
- Increased pulmonary vascular resistance
- Diffuse lung disease for example COPD
- Elevated left atrial pressure
- Recurrent pulmonary emboli
- Primary pulmonary hypertension
- Left-right shunts e.g. ASD, VSD
Describe the end-organ effects of pulmonary hypertension
Pulmonary arteries and heart effected.
Name for combined left and right ventricular failure
Congestive cardiac failure
Causes of right ventricular failure
- Secondary to left ventricular failure
- Related to ischaemic lung disease
- ‘Cor pulmonale’ due to pulmonary hypertension
- Primary pulmonary hypertension
Key features of the clinical examination in patients with heart failure
Appearance: Alert? Weight? Nutritional status?
Pulse rate: Rhythm? Character?
Blood pressure: Systolic? Diastolic? Pulse pressure?
Fluid overload: JVP
Peripheral oedema: Ankles and sacrum
Lungs: Respiratory rate, crackles, effusion
Heart: Apex displacement, gallop rhythm, third heart sound, flow murmurs suggesting valvular dysfunction
What is the cause of the white reaction in a cutaneous vascular response?
Pre-capillary sphincter contraction due to mechanical stimuli. Only lasts 15s as the build up of local factors signals for increased blood supply
Not arteriolar contraction as the reaction would be bigger
Note capillary contraction as capillaries have no smooth muscle
What are the stages of the triple response in local injury?
- A red reaction (flush) occurs within 30s which is limited to the area of contact. Due to opening of pre-capillary sphincters.
- Irregular, diffuse flare which affects the surrounding area. Due to axon reflex, adjacent arterioles dilate.
- A swelling/wheal develops.
What is the cause of the “wheal” stage of the triple response?
Local oedema due to:
- Capillary permeability increasing
- Vasodilation of arterioles due to axon reflex + vasoconstriction of venules
What is the difference between orthodromic and antidromic conduction?
Antidromic: Action potentials are relayed to the arterioles in the opposite direction of normal impulses
Orthodromic: Action potentials are being conducted int their usual direction
What is a Valsalva manoeuvre?
How is it performed?
A Valsalva manoeuvre is a forced expiration against a closed glottis
Method:
With the patient lying supine ask them to blow into a 20ml syringe with enough force to push the plunger back.
