Cardio Part 2 Flashcards
1
Q
What is hypertrophic cardiomyopathy (HCM) caused by?
A
sarcomeric protein gene mutations
2
Q
Hypertrophied cardiomyopathy affects how many people?
A
HCM affects 1 in 500 people
3
Q
What does HCM refer to? (Hypertrophied Cardiomyopathy)
A
- Cardiomyopathy refers to primary heart muscle disease – often genetic
- HCM refers to otherwise unexplained primary cardiac hypertrophy
- angina, dyspnoea, palpitations, dizzy spells or syncope
- LVOT (Left ventricular outflow tract) obstruction may be a feature
- HCM - septum or any part of the heart can be affected, it is primary hypertrophy, white area in myocardium - fibrosis scarring in the heart, big thick and stiff heart, diastolic heart failure as the heart cant fill properly, “histology”: myocytes in the heart has branching - wave get eveyrwhere for single contraction at the same time, in HCM, myocytes all over the place, myofibrillar structure is chaotic, myofibrillar disarray, fibrosis is electrical insulator, sometime reaches to muscle that has already repolarised - arrhythmic heart
4
Q
What is Dilated cardiomyopathy (DCM) often caused by?
A
cytoskeletal gene mutations
5
Q
Talk about DCM (dilated cardiomyopathy).
A
- DCM usually presents with heart failure symptoms
- DCM - LV/RV or 4 chamber dilatation and dysfunction
- DCM - present heart failure, heart is dilated, normal thin wall, terrible left ventricular function, the heart can barely see its pumping if the valve is not opening and closing
6
Q
What is Arrhythmogenic Right/Left ventricular cardiomyopathy (ARVC/ALVC) usually caused by?
A
desmosome gene mutations
ARVC (arrhythmogenic right ventricular cardiomyopathy), fatty fibrosing replacement of the muscle, programmed replacement in the heart muscle, ECG has epsilon waves, late potential, a factor contributing to arrhythmia
7
Q
What is the main feature of arrhythmogenic cardiomyopathy?
A
Arrhythmia
8
Q
All cardiomyopathies carry an arrhythmic risk.
True/False?
A
True!
9
Q
What is Inherited arrhythmia (channelopathy) usually caused by?
A
ion channel protein gene mutations
10
Q
Talk about Channelopathies.
A
These usually relate to potassium, sodium or calcium channels
- Channelopathies include long QT, short QT, Brugada and CPVT (Catecholaminergic polymorphic ventricular tachycardia)- abnormally fast heartbeat, respond extremely well to beta blockers
- Channelopathies have a structurally normal heart
- Channelopathies may present with recurrent syncope
11
Q
Why should we be aware of QT prolonging drugs?
A
they can kill people with long QT syndrome
12
Q
Sudden cardiac death in young people is often due to?
A
an inherited condition
- If so this is most likely a cardiomyopathy or ion channelopathy
13
Q
Sudden arrhythmic death syndrome (SADS) usually refers to ?
A
normal heart/arrhythmia
14
Q
Talk about FH (familial hypercholesterolaemia).
A
- Familial hypercholesterolaemia (FH) is an inherited abnormality of cholesterol metabolism
- FH leads to serious premature coronary and other vascular disease
- Receptor issues, LDL receptor problems, massive risk of MI, Coronary artery disease, genetic, dominantly inherited, manifestation within the family will be different eventho all have the disease, age-related penetrance
15
Q
Aortic aneurysm or dissection is often inherited.
True/False?
A
True!
16
Q
What does Aortovascular syndromes include?
A
Marfan, Loeys-Dietz, vascular Ehler Danlos (EDS)
Marfan: Marfan syndrome is a disorder of the body’s connective tissues, a group of tissues that maintain the structure of the body and support internal organs and other tissues.
Loeys-Dietz syndrome is a connective tissue disorder that was first described in 2005. Most individuals with this disorder have craniofacial feature
Vascular Ehler Danlos: Vascular EDS (vEDS) is a rare type of EDS and is often considered to be the most serious. It affects the blood vessels and internal organs, which can cause them to split open and lead to life-threatening bleeding. People with vEDS may have: skin that bruises very easily.
17
Q
Inherited Cardiac Conditions (ICC) are usually inherited dominantly or recessively?
A
- dominantly!
- offspring have 50% risk of inheritance
18
Q
What are some life-saving treatments that are available for inherited cardiac conditions (ICC)?
A
(ICD, beta-blockers, statins, vascular surgery)
19
Q
Is Naxos disease dominantly inherited or recessively inherited?
A
Naxos disease is a recessively inherited condition with arrhythmogenic right ventricular dysplasia/cardiomyopathy (ARVD/C) and a cutaneous phenotype, characterised by peculiar woolly hair and palmoplantar keratoderma.
20
Q
What happens to the heart when patient died from alarm clock ?
A
Long QT can trigger ventricular arrhythmia- alarm clock lmao
21
Q
Hypertension is the major risk factor of?
A
> Stroke – ischaemic and haemorrhagic
Myocardial infarction
Heart failure
Chronic renal disease
Cognitive decline
Premature death
22
Q
Hypertension can increase the risk of what kind of heart condition?
A
Atrial fibrillation (independent stroke risk)
23
Q
Each 2 mmHg rise in systolic BP is associated with how many % of risk of IHD and Stroke?
A
7% increased mortality from ischaemic heart disease
10% increased mortality from stroke
24
Q
What is the hypertension BP?
A
Suspected hypertension:
- Clinic BP 140/90 mmHg or higher
People with suspected hypertension are offered ambulatory blood pressure monitoring (ABPM) to confirm a diagnosis of hypertension
25
Talk about Stage 1 hypertension, Stage 2 hypertension and severe hypertension.
Clinic BP APBM
Stage 1 hypertension 140/90 and 135/85
Stage 2 hypertension 160/100 and 150/95
Severe hypertension SBP 180
or DBP 110
26
What is the general type of treatment for patients with primary hypertension?
Lifestyle modification
Antihypertensive drug therapy
27
Talk about initiating treatment in patients with hypertension.
Offer antihypertensive drug treatment to people aged under 80 years with stage 1 hypertension who have one or more of the following:
1. Target organ damage
2. Established cardiovascular disease
3. Renal disease
4. Diabetes
5. A 10-year cardiovascular risk of 20% or greater.
*************
Offer antihypertensive drug treatment to people of any age with stage 2 hypertension.
28
Talk about mechanism of BP control?
Cardiac output and Peripheral Resistance
2. Interplay between:
a. Renin-Angiotensin-Aldosterone system
b. Sympathetic nervous system (noradrenaline)
3. Local vascular vasoconstrictor and vasodilator mediators
29
What can sympathetic nervous system do? (noradrenaline)
- increase renin in RAAS system
- increase peripheral resistance
- increase cardiac output
30
Talk about ACEi.
Main clinical indications
- Hypertension
- Heart failure
- Diabetic nephropathy
> Ramipril
> Enalapril
> Perindopril
> Trandolapril
Main adverse effects:
1. Related to reduced angiotensin II formation
a. Hypotension
b. Acute renal failure
c. Hyperkalaemia
d. Teratogenic effects in pregnancy
2. Related to increased kinin production
Cough
b. Rash
c. Anaphylactoid reactions
31
Talk about Angiotensin II Receptor Blockers (ARB).
Main clinical indications
> Hypertension
> Diabetic nephropathy
> Heart failure (when ACE-I contraindicated)
- Candesartan
- Losartan
- Valsartan
- Irbesartan
- Telmisartan
Main adverse effects
- Symptomatic hypotension (especially volume deplete patients)
- Hyperkalaemia
- Potential for renal dysfunction
- Rash
- Angio-oedema
- Contraindicated in pregnancy
- Generally very well tolerated
32
Talk about Calcium Channel Blockers.
Main clinical indications
- Hypertension
- Ischaemic heart disease (IHD) – angina
- Arrhythmia (tachycardia)
L-type calcium channel blockers:
1. Dihydropyridines: nifedipine, amlodipine, felodipine, lacidipine
> Preferentially affect vascular smooth muscle
> Peripheral arterial vasodilators
2. Phenylalkylamines: verapamil
> Main effects on the heart
> Negatively chronotropic, negatively inotropic
3. Benzothiazepines: diltiazem
> Intermediate heart/peripheral vascular effects
33
Talk about the adverse effect of Calcium Channel Blocker.
Due to peripheral vasodilatation (mainly dihydropyridines)
- Flushing
- Headache
- Oedema
- Palpitations
Due to negatively chronotropic effects (mainly verapamil/diltiazem)
- Bradycardia
- Atrioventricular block
Due to negatively inotropic effects (mainly verapamil)
- Worsening of cardiac failure
Verapamil causes constipation
34
Talk about Beta-adrenoceptor blockers (BB).
Main clinical indications
- Ischaemic heart disease (IHD) – angina
- Heart failure
- Arrhythmia
- Hypertension
Selectivity:
1. Beta 1 selective:
- metoprolol
- bisoprolol
2. Beta1/Beta 2 non-selective:
- propanolol
- nadolol
- carvedilol
3. Intermediate
- Atenolol
35
What is the main adverse effect of Beta-adrenoceptor blockers (BB)?
Fatigue
Headache
Sleep disturbance/nightmares
Bradycardia
Hypotension
Cold peripheries
Erectile dysfunction
Worsening of:
- Asthma (may be severe) or COPD
- PVD – Claudication or Raynaud’s
- Heart failure – if given in standard dose or acutely
36
Talk about diuretics.
Main clinical indications:
> Hypertension
> Heart failure
Classes:
> Thiazides and related drugs (distal tubule)
- BENDROFLUMETHIAZIDE
- HYDROCHLOROTHIAZIDE
- CHLORTHALIDONE
> Loop diuretics (loop of Henle)
- FUROSEMIDE
- BUMETANIDE
> Potassium-sparing diuretics
- SPIRONOLACTONE
- EPLERENONE
- AMILORIDE
> Aldosterone antagonists
37
What is the main adverse effect of diuretics?
Hypovolaemia(mainly loop diuretics)
Hypotension (mainly loop diuretics)
Low serum potassium (hypokalaemia)
Low serum sodium (hyponatraemia)
Low serum magnesium (hypomagnesaemia)
Low serum calcium (hypocalcaemia)
Raised uric acid (hyperuricaemia – gout)
Erectile dysfunction (mainly thiazides)
Impaired glucose tolerance ( mainly thiazides_
38
Talk about other non-common antihypertensives.
α-1 adrenoceptor blockers
Centrally acting anti-hypertensives
Direct renin inhibitor
39
Talk about standard treatment of hypertension.
Step 1: Under 55: ACEi/ARB
Above 55: Calcium Channel Blocker
Step 2: ACEi/ARB + CCB
Step 3: ACEi/ARB + CCB + Thiazide-like diuretics
Step 4: Resistant Hypertension
Consider addition of
Spironolactone, high dose thiazide-like diuretic, Alpha blocker, beta blocker, (others)
40
What are the different types of heart failure?
Heart failure due to left ventricular systolic dysfunction - LVSD
Heart failure with preserved ejection fraction (diastolic failure) – HFPEF
Acute heart failure / Chronic heart failure
41
Talk about Heart Failure.
Heart failure is a complex clinical syndrome of symptoms and signs that suggest the efficiency of the heart as a pump is impaired.
It is caused by structural or functional abnormalities of the heart.
Most common cause is coronary artery disease
Causes morbidity, mortality, hospital admissions and substantial cost
Most of the evidence for pharmacology is in chronic heart failure due to LVSD
Main benefit is with vasodilator therapy via neurohumoral blockade (RAAS - SNS) and not from LV stimulants
42
Talk about basic pharmacology of heart failure.
Symptomatic treatment of congestion:
> Diuretics (usually loop)
Disease influencing therapy – neurohumoral blockade
> Inhibition of renin-angiotensin-aldosterone system
> Inhibition of the sympathetic nervous system
a. First line:
> ACE inhibitors and beta blocker therapy
> Low dose and slow uptitration
b.Aldosterone antagonists
c. ACE-I intolerant:
-Angiotensin receptor blocker
d. ACE-I and ARB intolerant: Hydralazine/nitrate combination
e. Consider digoxin or ivabradine
43
Talk about nitrates in Chronic Heart Failure
- Arterial and venous dilators
Reduction of preload and afterload
Lower BP
- Main uses
> Ischaemic heart disease (angina)
> Heart failure
Example: GTN Spray, GTN Infusion, ISOSORBIDE MONONITRATE
44
Talk about different type of coronary artery disease.
Coronary Artery Disease
1. Chronic stable angina
Anginal chest pain
Predictable
Exertional
Infrequent
Stable
**************
2. Unstable angina / acute coronary syndrome (NSTEMI)
Unpredictable
May be at rest
Frequent
Unstable
**************
3. ST elevation Myocardial Infarction (STEMI)
Unpredictable
Rest pain
Persistent
Unstable
45
Talk about management of Chronic Stable Angina.
1. Antiplatelet therapy
- Aspirin
- Clopidogrel if aspirin intolerant
2. Lipid-lowering therapy
- Statins (simvastatin, atorvastatin, rosuvastatin, pravastatin)
3. Short acting nitrate: GTN spray for acute attack
4. First line treatment: Beta Blocker or Calcium Channel Blocker
5. If intolerant: Switch
6. If not controlled:Combine
7. If intolerant or uncontrolled, consider monotherapy or combinations with: Long acting nitrate
Ivabradine
Nicorandil
Ranolazine
46
Talk about the management for Acute coronary syndromes (NSTEMI and STEMI).
1. Pain relief: GTN spray
Opiates – diamorphine
2. Dual antiplatelet therapy:
Aspirin plus ticagrelor or prasugrel or clopidogrel
3. Antithrombin therapy: Fondaparinux
4. Consider Glycoprotein IIb IIIa inhibitor (high risk cases): tirofiban, eptifibatide, abciximab
5. Background angina therapy: beta blocker, long acting nitrate, calcium channel blocker
6. Lipid lowering therapy: Statins
7. Therapy for LVSD/heart failure as required: ACE-I, beta blocker, aldosterone antagonist
47
Talk about Vaughan Williams classification
of antiarrhythmic drugs.
Class I: Sodium channel blockers
Ia - disopyramide, quinidine, procainamide
Ib - lidocaine, mexilitene
Ic - flecainide, propafenone
Class II: Beta adrenoceptor antagonists
- propranolol, nadolol, carvedilol (non-selective)
- bisoprolol, metoprolol (β1-selective)
Class III: Prolong the action potential
- amiodarone, sotalol
Class IV: Calcium channel blockers
- verapamil, diltiazem
48
Talk about digoxin.
Digitalis Glycoside
Inhibit Na/K pump
Main effects are on the heart:
Bradycardia (increased vagal tone)
Slowing of atrioventricular conduction (increased vagal tone)
Increased ectopic activity
Increased force of contraction (by increased intracellular Ca)
Narrow therapeutic range
Nausea, vomiting, diarrhoea, confusion
Used in atrial fibrillation (AF) to reduce ventricular rate response
Use in severe heart failure as positively inotropic
Digoxin has two principal mechanisms of action, which are selectively employed depending on the indication:
1. Positive Ionotropic: It increases the force of contraction of the heart by reversibly inhibiting the activity of the myocardial Na-K ATPase pump, an enzyme that controls the movement of ions into the heart. Digoxin induces an increase in intracellular sodium that will drive an influx of calcium in the heart and cause an increase in contractility. Cardiac output increases with a subsequent decrease in ventricular filling pressures.
2. AV Node Inhibition: Digoxin has vagomimetic effects on the AV node. By stimulating the parasympathetic nervous system, it slows electrical conduction in the atrioventricular node, therefore, decreasing the heart rate. The rise in calcium levels leads to prolongation of phase 4 and phase 0 of the cardiac action potential, thus increasing the AV node's refractory period. Slower conduction through the AV node carries a decreased ventricular response.
49
Why do we not use LV stimulants in heart failure?
Heart failure, sympathetic nervous system is gone, need RAAS, brain thought fluid or blood loss, then they will activate the sympathetic nervous system, NOT LV STIMULANTS!!
50
Relate spirinolactone with Gynaecomastia.
man has a small amount of breast tissue, but it can be enlarged, aldosterone antagonist - spirinolactone has a small amount of androgens
51
Sacubitril and Valsartan is a combination of drugs.
True/False?
True!
52
What is the difference between preload and afterload?
Preload is the initial stretching of the cardiac myocytes (muscle cells) prior to contraction. It is related to ventricular filling.
Afterload is the force or load against which the heart has to contract to eject the blood.
53
Why is plateau phase significant in membrane potential mechanism graph?
Refractory period
54
What are the 2 example of drugs that prolong QT interval and shouldnt be given to patients with long QT interval.
Amiodarone and sotalol
55
Talk about worm/helminth in general.
Adult worms cannot usually reproduce without a period of development outside the body. This may involve specific environmental conditions, animal hosts and/or vectors. Thus, although they usually produce innumerable larvae or eggs (which may themselves cause disease), the total worm burden cannot increase without constant re-exposure to infection. The PRE-PATENT PERIOD is the interval between infection and the appearance of eggs in the stool.
56
Helminths are divided into three groups, which three groups?
- Nematodes (roundworms)
1. Intestinal
2. Larva migrans
3. Tissue (filaria) - some people consider this as a 4th group
- Trematodes (flatworms, flukes)
1. Blood
2. Liver
3. Lung
4. Intestinal
- Cestodes (tapeworms)
1. non-invasive (just sit in your gut)
2. invasive (invade your gut and go somewhere)
57
Talk about Intestinal nematodes.
- soil-transmitted varieties
- faecal-oral spread
58
Talk about Ascaris lumbricoides: the large roundworm.
- found worldwide, mainly tropics
- 600 cases per annum in the UK
- small intestine > produce egg, grow out of your gut to the lung, then go into trachae then swallow it
- Symptoms/signs: Loeffler’s syndrome (Löffler's syndrome is **a disease in which eosinophils accumulate in the lung in response to a parasitic infection)**
- often asymtomatic, mechanical obstruction, biliary/pancreatic obstruction or malnutrition
- well known for disrupting surgical anastomoses after intra-abdominal durgery
- odd presentations-emerging from nose, perforated eardrum
- diagnosis: stool microscopy for eggs, seeing the worm itself
- Drugs: piperazine, pyrantel, mebendazole, levasimole
59
Talk about the hookworm.
1. Ancyclostoma duodenale (west/SE asia, mediterranean, middle east)
2. Necator americanus (USA, central/south america, central africa, india)
- small white worm, 1cm in length, life expectancy: 1-5 years
- cause of anaemia
- worm hooked in the bowel wall
- does not get into mouth
- clinical features:
> Ground itch - papules at the site of entry of larvae, eg on feet
> Pulmonary symptoms L mild due to pulmonary migration
- Diagnosis: Stool microscopy for eggs
- Treatment: Iron supplement: pyrantel, mebendazole
60
Talk about Enterobius vermicularis(the pinworm or threadworm).`
- very common in UK
- only common helminth infestation in UK
- doesnt invade the body, get in from the mouth, get around FAMILY, get it from door knobs or paedetrician wards
- Life cycle: adult is resident in the large bowel
- the female emerges at the anus at night to lay egg at the perineum
- the egg become infectious after 4 hours,
- pruritis ani
- appendicitis
- vaginal penetration (infertility, endometriosis salpingitis
- paranasal sinuses
- diagnoses and treatment: microscopy and sellotape strip
- piperizine
61
Talk about Whipworms.
- might often cause rectal prolapse
- trichuris trichiura
- found worldwide
- 2-5cm long and live around a year PPP is 70-90 dyas
- adult is partly buried in the mucosal membrane of the large bowel
- eggs are passed into the environment in the host’s faeces
- found in the caecum, ascending colon
- clinicaql factorsL often asymptomatic, coexist with ascaris lumbricoides
- trichuriasis
- Diagnosis: stool microscopy
- Mebendazole, albendazole
62
Talk about Strongyloides stercoralis.
- cause strongyloidiasis
- worldwide
- adult is 2mm long, lies buried in the small intestinal mucosa
- PPP is 17-28 days
- crawl into skin, goes all over the body
- can AUTOINFECT - lavatory infection
- pruritis, pulmonary symptoms, gut symptoms (malnutrition), larva currens (skin rashes with auto infection, last <24 hours)
> Hyperinfection syndrome
- autoinfection associated and in immunocompromised state
- advance HIVv
- alcoholism
- immunocompromisation and corticosteroid therapy
- diarrhoea, weight loss, malabsorption, paralytic ileus, peritonitis, bacterial problems, (gram-negative septicaemia, meningitis, pulmonary disease)
- See no eosinophils, larvae found in stools and sputum (and potentially in all tissues)
- Diagnosis : stool- larval forms (eggs rarely seen), serology, eosinophila (swallow string, leave it in bowel, then take it out and see the larvae under the microscope)
63
Talk about Larva migrans.
- Visceral larva migrans (VLM)
- caused by Toxocara canis (dog roundworm) and T. cati (cat roundworm)
- Life cycle: a dead end, eggs are ingested> develop into larvae > invade tissue for 1-2 years (the organism can develop no further)
- Clinical: mainly a disease of children and see fever, hepatomegaly, eosinophilia, asthma (the first 3 signs and symptoms mimic leukaemia which is not true)
- Diagnosis:eosinophiliaa, serology
- Treatment: mebendazole, albendazole
64
Talk about Ocular toxocariasis (human).
- larvae become trapped in the retina
- see a granulomatous reaction
- Clinical: retinal mass, blindness (diff diagnosis: retinoblastoma)
- Diagnosis: serology/antigen detection in/of aqueous humour, biopsy (NB> no eosinophilia)
- Treatment: mebendazole, albendazole
65
Talk about Cutaneous larva migrans.
- creeping itchy skin eruption
- Due to dog hookworms
- ancycuistoma canium/braziliense
- lesions at the sites where larvae penetrate
- cutaneous larva migrans (hot, painful, extremely itchy)
66
Talk about Anisakiasis on endoscopy.
salmon/sushi, raw seafood, crustaceans, fish, squid, octopus
67
Talk about Dracunculus medinensis.
- the guinea worm or medina worm
- adult is up to 100 cm long, and lives for one year subcutaneously
- the incubation period is about one year, one case per year in the UK
- about 3 million cases per annum worldwide (eradication proposed by WHO)
- Blister in the leg, the worm will crawl out, the worm might discharge eggs
- other sites of emergence include the axillae and the vagina or any human orifice
- contaminated fresh water, crustaceans,
- solution: filter/sieve any drinking water through 2 layers of Muslin clothes, can prevent this disease
- can develop sepsis
- tetanus
- joint problems, peritomnitis
- diagnosis: ulcer promotes egg release
- treatment: wind out the worm
- mebendazole
- caduceus
68
Talk about Tissue Nematodes: The filaria.
- Wuchereria bancroftii
- Elephantiasis, endemic in the tropics, insect borne, adults live in the lymphatic system for like 30 years
- Diagnosis: demonstration of microfilaria in blood, needs to be taken at the right time of day (usually 2300pm to 0100am), varies with the geographical location, DEC provocation test, the larvae of these worm come up at night as more acidic pH sleeping at night, sucking your blood
- serology
- Treatment: DEC (Diethylcarbamazine) Ivermectin
> Onchocerciasis (aka hanging groin, river blindness, caused by fly), usually south africa
> Loa loa
- mainly in West Africa
- that worm is under the surface of the
conjunctiva
- Tail details under microscope
> Trichinella spiralis
- cause of trichinosis
- a zoonesis of rats that ciruclates in rats
and various carnivores, a “dead-end”
- Asymptomatic
- GI disturbances with transiet worm
development
- fever, headache, cough at eight weeks
- periorbital oedema etc
- brugia malayi
69
Talk about tapworms.
Tap worm
- 5-10m long, lives up to 30 years
- PPP is 12 weeks
- weight loss
- Life cycle: caught by eating undercooked beef containing cyts
- asymptomatic
- progllottids can emerge from human anus
- diagnosis: stools for eggs and proglottids
- Treatment: niclosamide, praziquantel
- Neurocysticercosis (pork tapeworm)
70
Talk about other tapworms.
Other tapworms
> echinococcus granulosus
- the dog tapeworm
- cause of hydatid disease (in humans, cattle, and sheep)
> Echinoccosu multilocularis
- cause of alveococcosis
> Diphyllobothrium latum
- the fish tapeworm
- cause of sparganosis
- vitamin B12 deficiency
71
Talk about blood flukes.
- schistosoma
- snail - to other species
- schistosomiasis
- adult fluke- 12cm long
- normal life span of 3-5 years (but up to 30 years)
- katayama fever (initial immune complex mediated illness 2-4 weeks)
- pathology - egg related, live in the liver, resemble alcholic cirrhosis, shistosoma haematobium
- can cuase bladder disease, massice fibrosis in the liver and squamous cell cancer in the liver not a transitional carcinoma
- calcified bladder
- renal calculi
- cor pulmonale (pulmonary hypertension, ccf)
- may cause obstructive uropathy - reversible if short duration and treated
- EXAM QUESTION
- Diagnosis - serology urine
- treatmentL complete vs incomplete cure
- praziquantel, isoquinoone metirphonate, osamniqione
- vaccine being developed
- control/prevention, reduced contamination byeducation, snanition, prevent egg transmisison
72
Why do we have to know about structural heart defect/congenital heart disease?
Fairly common
Although primarily a cardiac defect, implications for all sorts of other specialities
> Anaesthetics
> Dentistry
> Obs and gynae
> Paediatrics
> General practice
> Palliative care
> Radiology
> Haematology
> Respiratory medicine
> Neurology
73
What are the Care issues in congenital heart patients?
> Intellectual disability in 10%
> Psychosocial issues
> Transition
> Explaining the lesion and the prognosis
> Building independence/ self reliance
74
Talk about the genetic transmission probability of congenital heart defects.
Foetal recurrence
Background population 1%
Father with Congen HD 2.2%
Mother with Congen HD 5.7%
Tetralogy of Fallot 3%
AV septal Defect 10% - 14%
Foetal echocardiography at 18-22 weeks
75
What are some severe congenital heart defect that we would advise the patient to not go through pregnancy?
Severe risk
Maternal mortality expected in up to 50%
Pulmonary hypertension
Severe left heart obstruction
Systemic ventricular impairment (Ejection fraction < 30%)
Marfans syndrome with aortic root diameter > 47 mm
Moderate risk:
Unrepaired coarctation
Repaired coarctation with residual obstruction and hypertension
Repaired tetralogy of fallot with poor haemodynamic result, severe PR and RV dysfunction
Very severe PS
Moderate to severe aortic stenosis
Transposition of the great arteries (Mustard or Senning operations) ccTGA (congenitally corrected Transposition of the Great Arteries)
Well balanced single ventricle (depends on degree of cyanosis, and presence or absence of pulmonary hypertension)
Fontan circulation
Mechanical heart valves
Marfans syndrome with dilated aortic root >40mm < 47 mm
76
What are the 4 main defects in Tetralogy of Fallot?
1. Ventricular septal defect
2. Pulmonary stenosis
3. Hypertrophy of right ventricle
4. Overriding of aorta
The key issue is anterior dislocation of the septum below the pulmonary outflow which causes the other issues
77
Is patients with Tetralogy of Fallot blue? Why?
The stenosis of the RV outflow leads to the RV being at higher pressure than the left
Therefore blue blood passes from the RV to the LV
The patients are BLUE
78
How many percentage is Tetralogy of Fallot in congenital heart defects?
10%
then theres 1/1000 of prevalence
79
Talk about the surgical repair of Tetralogy of Fallot.
The Blalock-Taussig Shunt 1944
Walter Lillehei first ‘complete repair’ on a boy aged 11 – rebore the RVOT and patch VSD
1986 first repair in infancy
Now mostly repaired before the age of two years
Mostly do very well
Often get pulmonary valve regurgitation in adult life and require redo surgery
80
Talk about VSD.
Abnormal connection between the two ventricles
Common – 20% of all congenital heart defects – 1-4/1000 live births
Many close spontaneously during childhood
High pressure LV
Low pressure RV
Blood flows from high pressure chamber to low pressure chamber
Therefore NOT blue
Increased blood flow through the lungs
81
Talk about what are the effects of small and large VSD.
Large
Very high pulmonary blood flow in infancy
Breathless, poor feeding, failure to thrive
Require fixing in infancy (PA band, complete repair)
May lead to Eisenmengers syndrome
Small
Small increase in pulmonary blood flow only
Asymptomatic
Endocarditis risk
Need no intervention
82
Talk about clinical sign of small and large VSD.
Large
Small breathless skinny baby
Increased respiratory rate
Tachycardia
Big heart on chest X ray
Murmur varies in intensity
Small
Loud systolic murmur
Thrill (buzzing sensation)
Well grown
Normal heart rate
Normal heart size
83
Talk about Eisenmengers syndrome.
Initially theres left to right shunt due to the VSD
High pressure pulmonary blood flow
Damages to delicate pulmonary vasculature
The resistance to blood flow through the lungs increases
The RV pressure increases
The shunt direction reverses
The patient becomes BLUE
84
Talk about ASD.
- Abnormal connection between the two atria (primum, secundum, sinus venosus)
- Common
- Often present in adulthood
- Slightly higher pressure in the LA than the RA
- Shunt is left to right
- Therefore NOT blue
- Increased flow into right heart and lungs
85
Talk about the physiology in large and small ASD.
Large
- Significant increased flow through the right heart and lungs in childhood
- Right heart dilatation
- SOBOE
- Increased chest infections
- If any stretch on the right heart should be closed
Small
- Small increase in flow
- No right heart dilatation
- No symptoms
- Leave alone
NB. The shunt on small to moderate sized defects increases with age
86
Talk about clinical signs of ASD.
Pulmonary flow murmur
Fixed split second heart sound (delayed closure of PV because more blood has to get out)
Big pulmonary arteries on CXR
Big heart on chest X ray
87
What are the 2 ways to close ASD?
Surgical
Percutaneous (key hole technique)
88
Talk about Atrio-Ventricular Septal Defects - AVSD.
- 2 per 10 000 live births
- Often Downs syndrome
- Basically a hole in the very centre of the heart
- Involves the ventricular septum, the atrial septum, the mitral and tricuspid valves
- Can be complete or partial
- Instead of two separate AV valves there is one big malformed one
- It usually leaks to a greater or lesser degree
89
Talk about the physiology of complete and partial defect of AVSD.
Complete defect:
- Breathless as neonate
- Poor weight gain
- Poor feeding
- Torrential pulmonary blood flow
- Needs repair or PA band in infancy
- Repair is surgically challenging
Partial defect:
- Can present in late adulthood
- Presents like a small VSD / ASD
- May be left alone if there is no right heart dilatation
90
What are the clinical signs of patent ductus arteriosus?
- Continuous ‘machinery’ murmur
- If large, big heart, breathless
- Eisenmenger’s syndrome
- Differential cyanosis (clubbed and blue toes, but pink not clubbed fingers)
91
Talk about the physiology of patent ductus arteriosus.
Large
Torrential flow from the aorta to the pulmonary arteries in infancy
Breathless, poor feeding, failure to thrive
More common in prem babies
Need to be closed (surgically)
Small
Little flow from the aorta to Pas
Usually asymptomatic
Murmur found incidentally
Endocarditis risk
92
Talk about the closure of patent ductus arteriosus.
Surgical or percutaneous
Local anaesthetic
Venous approach (sometimes requires an AV loop)
Low risk of complications
93
What are the different types of congenital heart defect/ structural cardiac defect out there?
Ventricular septal defect
Atrial septal defect
Atrio-ventricular septal defects
Patent ductus arteriosus
Coarctaction of the aorta
Bicuspid aortic valve and aortopathy
Pulmonary stenosis
Tetralogy of Fallot
Eisenmenger syndrome
94
Talk about the coarctation of the aorta.
Narrowing of the aorta at the site of insertion of the ductus arteriosus
95
Talk about the physiology of mild and severe coarctation of the aorta.
Severe
Complete or almost complete obstruction to aortic flow
Collapse with heart failure
Needs urgent repair
Mild
Presents with hypertension
Incidental murmur
Should be repaired to try to prevent problems in the long term
96
What are the clinical signs of coarctation of the aorta?
Right arm hypertension
Bruits (buzzes) over the scapulae and back from collateral vessels
Murmur
97
Talk about the long-term problem of coarctation.
Hypertension
Early coronary artery disease
Early strokes
Sub arachnoid haemorrhage
Re-coarctation requiring repeat intervention
Aneurysm formation at the site of repair
98
Talk about the repair of coarctation of the aorta.
Surgical vs percutaneous repair
- Subclavian flap repair
- End to end repair
99
Talk about the bicuspid Aortic valve.
Normal AV has three cusps (looks like a Mercedes emblem)
Bicuspid AVs are common
1-2% of the population (M>F)
Can be severely stenotic in infancy or childhood
Degenerate quicker than normal valves
Become regurgitant earlier than normal valves
Are associated with coarctation and dilatation of the ascending aorta
100
Talk about pulmonary stenosis.
Narrowing of the outflow of the right ventricle
Valvar
Sub valvar
Supra valvar
Branch
8-12 % of all congenital heart defects
101
Talk about severe and moderate/mild pulmonary stenosis.
Severe
Right ventricular failure as neonate
Collapse
Poor pulmonary blood flow
RV hypertrophy
Tricuspid regurgitation
Moderate / mild
Well tolerated for many years
Right ventricular hypertrophy
102
Talk about pulmonary stenosis.
Treatment:
- Balloon valvuloplasty
- Open valvotomy
- Open trans-annular patch
- Shunt (to bypass the blockage)
103
Criteria for hypertension screening?
- early onset <30 yo and no risk factors
- hypertension resistant to 3 drugs
- malignant hypertension
- specific features e.g. phaeochromocytoma (endocrine tumour on your adrenal gland)
104
What can commonly cause hypokalaemia?
- diuretics commonly cause hypokalemia
- aldosterone causes high blood pressure and low potassium
- >spontaneous hypokaelemia or in response to thiazides might suggest hyperaldosteronism
- >primary or secondary to things like sleep apneoa
105
When there is high blood pressure, what are the body parts that need to be examined and could possibly be impaired?
- Kidney
- Eyes- retinohaemorrhages (emergency), will be dead if not treated
- Evidence of immediate damage (papilloedema, acute stroke, acute kidney injury)
106
How big of response would you expect from one tablet of atenolol?
- systolic : 8-10 mmHg
- diastolic 4-6 mmHg
107
How to investigate patient's home blood pressure?
- one way is to measure it at home (need to have done it with regular time/structure)
- alternative way is to fix patient with a machine and wear for 24 hours
- BP measurement modalities
- clinic/surgery measures
- unattended automated office BP
home self-measurement
- Ambulatory BP measurement
108
At what threshold of blood pressure does patient need treatment?
- For pt at low CVD risk 160/100 mmHg
- at high CVD risk 140/90 mmHg
- (these are clinic threshold)
109
Female or Male higher risk for high BP?
Male
110
Treating the high BP does not make you feel any better.
True/False?
True!
- Its more of prevention of bad things
- High BP has not signs and symptoms
- the only symptomatic benefit of treatment is a reduction of headaches (this is of importance if a patient has, or perceives that they have side-effects)
111
How far do we want to lower down patient's blood pressure?
- Routine - <140/90mmHg
- previous stroke - <130/80mmHg
- heavy porteinuria - <130/80mmHg
- CKD AND diabetes - <130/80mmHg
- Older patients - <150/90mmHg (why dont want to drop too down, the problem is if lower bp, they tend to fall over)
112
How many drugs do patients with high blood pressure usually take?
- most patient need 2 or more tablets
- one drug - 39%
- 2 drugs - 40%
- three drugs - 16%
- four drugs 4%
- 4+ drugs - 1%
113
What can hypertension cause?
ischemic heart disease, MI, angina, stroke, chronic kidney disease, dementia, aortic dissection (less clear-cut evidence), heart failure,renal failure, peripheral vascular disease
114
How can hypertension affect life span?
- with reated hyperntension
- 50 yo male 5 years loss of life, 7 years of disease free life
115
How much benefit will get from lowering high BP?
- average gain
- increase in life expectancy of 5 years
- reduction instroke 40%
- reduction in MI 30%
116
are there any lifestyle changes by which eric might lower his BP without drug treatment?
- high salt - hypertension
- weight is by far the strongest of high blood pressure
- exercise is a risk factor
- stress
- alcohol
- Weight loss (6kg) - 8-10 mmHg; salt restirction moderate - 4 mmHg; exercise 3 hours/week = 8 mmHg; alcohol - reduction of 6-3 umits per night = 7 mmHg
117
What are the BP lowering drugs ?
- Calcium channel blockers (non-rate limiting- “dipine” and rate-limiting- mainly vasodilators)
- ACEi/ ARBs- block formation/action of angiotensin
- diuretics- reduce circulating sodium
- B-blockers - reduce renin release/ cardiac contractility
118
Are there any other factors which might be contributing to eric’s high BP?
- Drugs which icnrease blood pressure
- NSAID, SNRI like venlafaxine, corticosteroids like prednisolone, oestrogen containing oral contraceptives, stimulants like methylphenidate, anti-anxiety drugs like Gabapentin, anti-TFNs, anti-cancer drugs
119
How long will eric need to take treatment for?
- Treatment withdrawal leads to rebound in BP
- treatment of pre-hypertension did not prevent the later development od hypertension’
- therefore treatment needed lifelong
120
What possible reasons for loss of control and how common it is?
- Not taking tablets (20-30% not taking meds; 40-60% taking some but not all)
- Changes in lifestyle- increased weight or new drugs
- Progression of an underlying cause - patients with resistant or progressive high blood pressure more likely to have secondary hypertension
121
How often do you check whether pt is taking his tablet and he isnt what do you do about it?
checking concordance - ask him, checking prescribing log, check urine mass spec analysis
122
What is electrocardiogram?
The Electrocardiogram is a record of the electrical activity of the heart
123
What is ECG is useful to diagnose ?
What are the common clinical presentation that needs an ECG?
Provide information on
Cardiac arrhythmia
Acute/chronic cardiac ischaemia
Myocardial disease
Electrolyte disturbance
Useful in a broad range of clinical scenarios
Chest pain
Palpitation
Breathlessness
Blackout
124
Talk about the cardiac position of the heart.
Lying 2/3 to the left and 1/3 to the right
125
Talk about the conducting system of the heart.
SA Node> AV Node> Bundle of His> Right and Left Bundle Branches, For left bundle branches there is Anterior and Posterior fascicle
126
Talk about the deflection and direction of PQRST wave.
Amplitude of deflection is related to mass of myocardium
Width of deflection reflects speed of conduction
Positive deflection is towards the lead/vector
127
What is the normal QRS axis ?
-30 to +90 degrees
Left axis deviation -30 to -90 degrees
- Left anterior fascicular block
- Left bundle branch block
- Left ventricular hypertrophy
Right axis deviation 90 to 180 degrees
- Left posterior fascicular block
- Right heart hypertrophy/strain
Indeterminate axis
-90 to 180
128
Talk about P wave
Positive inferior leads
Positive in lead I
Negative in aVR
Biphasic in V1
Normally <120 ms wide
<0.3mV (3 small sq) tall
129
Talk about abnormalities of P wave
Low amplitude
Atrial fibrosis, obesity, hyperkalaemia
High amplitude ‘Tall’
Right atrial enlargement
Broad notched ‘Bifid’
Left atrial enlargement
Alternative pacemaker foci
Focal atrial tacycardias
‘wandering pacemaker’
130
Talk about PR interval.
Consists of atrial depolarisation and conduction from atria to ventricles
Normally 120-200 ms
Prolonged in disorders of AV node and specialised conducting tissue
Shorter in younger patients or in pre-excitation (Wolf-Parkinson-White)
131
Talk about QRS.
Ventricular depolarisation
Normally <120ms
Size of complexes related to myocardial mass
Predominantly negative S wave in V1, transitioning to positive R wave by V6
Normal frontal axis -30 to +90 (positive in leads I, II)
132
Talk about QRS abnormalities.
Broad QRS
Ventricular conduction delay / bundle branch block
Pre-excitation
Small QRS complexes
Obese patient
Pericardial effusion
Infiltrative cardiac disease
Tall QRS complexes
Left ventricular hypertrophy
(S wave in V1 and R wave in V5/V6 >35mm)
Thin patient
133
Talk about QT interval.
From start of QRS to end of T wave
Represents ventricular depolarisation and repolarisation
Corrected for heart rate (380 – 450ms)
Excessively rapid or slow repolarisation can be arrhythmogenic
“Long QT” or “Short QT” syndromes
Congenital, drugs, electrolyte disturbances
134
Talk about ST segment
From end of QRS (“J point”) to start of T wave
Normally isoelectric
Can be elevated in early repolarisation, myocardial infarction, pericarditis/myocarditis,
135
Talk about T wave.
Height of T wave normally less than QRS
T waves usually inverted in aVR, can be inverted in III
T wave changes (inversion) are non-specific but can indicate:
Ischaemia/infarction
Myocardial strain (hypertrophy)
Myocardial disease (cardiomyopathy)
136
Talk about the abnormalities of rate and rhythm.
“Normal heart rate” 60-100 beats / min
Tachycardias
Atrial fibrillation, Atrial Flutter
Supraventricular tachycardia
Ventricular tachycardia
Ventricular fibrillation
137
Talk about bradycardia?
Can occur at any level in the conducting system
Causes
Conduction tissue fibrosis
Ischaemia
Inflammation/infiltrative disease
Drugs
138
Talk about AV conduction problems:
1. Normal
2. First degree AV block
3. Second degree AV block (Mobitz Type 1 and Type 2)
4. Complete (third degree heart block)
139
For second degree heart block, talk about the Mobitz Type 1 and Type 2.
Mobitz Type 1:
PR interval gradually increases until AV nodes fail completely and no QRS wave is seen. Starts all over again, PR interval gradually lengthens.
Mobitz Type 2:
PR interval is constant but every nth QRS complex is mixing.
Sudden unpredictable loss of AV conduction and loss of QRS.
Due to loss of conduction in Bundle of His, Purkinje fibres.
140
How can left bundle branch block presents on ECG?
William
V1: W
V6: M
141
How can right bundle branch block presents on ECG.
William
V1: M
V6: W
142
Talk about ischemia and infarction.
T wave flattening inversion
ST segment depression
ST segment elevation
Q waves – old infarction
143
What are the main coronary arteries.
1. Right coronary artery
2. Left circumflex artery (left coronary artery)
3. Left Anterior Descending artery (left coronary artery)
144
Talk about electrolyte disturbance.
Potassium
Hyperkalaemia: Tall T waves, flattening of P waves, broadening of QRS… eventually ‘sine wave pattern’
Hypokalaemia: Flattening of T wave, QT prolongation
Calcium
Hypercalcaemia: QT shortening
Hypocalcaemia: QT prolongation
145
What is the systemic approach to ECG?
Rate
Rhythm
Axis
P, PR, QRS, ST, QT
146
Talk about ectopic beats
Very Common
Non sustained beats arising from ectopic regions of atria or ventricles
Generally benign
High burden VE can cause heart failure
High burden AE can progress to AF
Most patients will gain symptomatic relief from reassurance/betablockers
Who to refer
High burden ectopy (>5%, though risk prob not increased till >20%)
Refractory to BB
Structural heart disease
Syncope
147
Talk about the mechanism of ectopic beats.
Triggered activity - Abnormal activation during or after repolarisation
Early - during repolarisation (phase 2&3)
Delayed – after phase 3 relating to intracellular calcium overloading
Favoured by high catecholamine states, hypokalaemia, ischaemia
Abnormal automaticity
- Change in rate of diastolic current leak
148
Talk about atrial fibrillation
Commonest sustained arrhythmia
Paroxysmal (self terminating) OR
Persistent (continues without intervention)
Rapid chaotic firing causes
Loss of atrial mechanical contraction
Irregular often rapid ventricular response
149
Talk about medical treatment for Atrial Fibrillation.
Treat underlying cause
Alcohol, Thyroid disease, Hypertension, Valve disease, Heart failure, Obesity, Excessive exercise, Infection etc.
Rate control (accept AF)
Beta blockers
Calcium channel blockers
(Digoxin)
Restore sinus rhythm acutely
Electrical cardioversion (acutely / after anticoagulation)
Pharmacological cardioversion (flecainide / amiodarone)
Maintain sinus rhythm
Flecainide
Dronedarone
Sotalol
Amiodarone
150
What test can be used to assess Atrial Fibrillation risk.
CHADS-VASC >1 = formal anticoagulation with warfarin / DOAC
151
Talk about Novel oral agents on anticoagulant.
Direct Xa inhibitors:
Rivaroxaban
Apixaban
Edoxaban
Direct Thrombin Inhibitor:
Dabigatran
152
Talk about supraventricular tachycardia.
Advice on valsalva manoeuvres
Can try beta blocker/CCB
Who to refer:
Frequent / sustained episodes
Needed adenosine for termination
Abnormal ECG (pre-excitation)
153
Talk about Catheter ablation AVNRT.
Radiofrequency energy directed at slow pathway
95% success rate and long term cure
Risks: PPM 1%
154
Talk about accessory pathway.
Congenital remnant muscle strands between atrium and ventricle
Can be manifest (pre-excitation on ECG)
Or concealed (ECG normal, only conduct retrogradely and only detected at EP study)
155
Talk about AP mediated arrhythmia.
AVRT – can be narrow or broad complex
“orthodromic” - narrow
“antidromic” – broad (fully preexcited)
156
Talk about myocardial substrate.
Diseased ventricles
Myocardial infarction
Cardiomyopathy
157
Talk about electrical storm.
3 or more sustained episodes of VT or VF, or appropriate ICD shocks during a 24-hour period
High risk / poor prognosis
Manage on CCU/ITU
Treatment
Correct any provoking factors e.g. electrolyte (K/Mg), ischaemia, infection, heart failure
Beta blockers, sedation
Amiodarone +/- lignocaine
Overdrive pacing
General anaesthesia / Neuraxial blockade
Catheter ablation
158
Talk about Catheter ablation of VT.
Catheter ablation can be used to
reduce episodes of VT or frequency of ICD shocks
Can be curative for ‘normal heart VT’
159
Talk about narrow and broad complex of tachycardia.
Narrow complex
SVT
AF/flutter
Broad complex
VT
SVT with BBB/preexcitation
160
What are the common scenarios where ECG is useful?
Chest pain
Acute MI, Pericarditis,
(Pulmonary embolus/Aortic dissection)
Palpitations
Ectopic beats, SVT, VT, AF
Breathless
Heart failure/previous MI/LBBB
Blackout
Conduction disease/bradycardia/ Extreme tachycardia
161
What is heart failure?
An inability of the heart to deliver blood (and O2) at a rate commensurate with the requirements of the metabolising tissues, despite normal or increased cardiac filling pressures.
162
Talk about aetiology of heart failure.
The commonest cause is myocardial dysfunction.
This usually results from IHD.
Other causes include:
- Hypertension,
- alcohol excess,
- cardiomyopathy,
- valvular,
- endocardial,
- pericardial causes.
163
What are the signs and symptoms of HF?
Symptoms:
Breathlessness
Tiredness
Cold peripheries
Leg swelling
Increased weight
Signs:
Tachycardia
Displaced apex beat
Raised JVP
Added heart sounds and murmurs
Hepatomegaly, especially if pulsatile and tender
Peripheral and sacral oedema
Ascites
164
Talk about NYHA classification of Heart Failure.
Class I: No limitation (Asymptomatic)
Class II: Slight limitation (mild HF)
Class III: Marked limitation (Symptomatically moderate HF)
Class IV: Inability to carry out any physical activity without discomfort (symptomatically severe HF)
165
Talk about HF definition with related condition.
The syndrome of breathlessness, tiredness and fluid overload caused by a form of cardiac dysfunction
HF-REF (left ventricular systolic impairment with LVEF<40%) (reduced ejection fraction)
HF-PEF (LVEF>50%, with dilated LA>34ml/m2 and either E:e’>13 or LVH) (preserved ejection fraction)
HF-PH (pulmonary hypertension)
HF-Valve (severe stenosis or regurgitation)
166
Talk about the Pharmacological interventions Mainly in HFREF.
Diuretics
ACEI
β Blockers
MRA (mineralocorticoid receptor antagonists)
Hydralazine + nitrates
ARB
Digoxin
Ivabradine
Sacubitril-Valsartan
Dapagliflozin
167
What are the 4 main valvular heart disease?
Aortic Stenosis
Mitral regurgitation
Aortic Regurgitation
Mitral Stenosis
168
Talk about aortic stenosis generally.
Normal Aortic Valve Area: 3-4 cm2
Symptoms occur when valve area is 1/4th of normal.
Types:
Supravalvular
Subvalvular
Valvular
BAV:
0.5-2% of general population
Up to 10% of first degree relatives will have BAV
Associated aortopathy and coarctation
169
Talk about Pathophysiology of Aortic Stenosis.
A pressure gradient develops between the left ventricle and the aorta. (increased afterload)
LV function initially maintained by compensatory pressure hypertrophy
When compensatory mechanisms exhausted, LV function declines.
170
Talk about the presentation of aortic stenosis.
Syncope: (exertional) 15%
Angina: (increased myocardial oxygen demand; demand/supply mismatch) 35%
Dyspnoea: on exertion due to heart failure (systolic and diastolic) 50%
Sudden death <2%
171
Talk about the physical sign of aortic stenosis.
Slow rising carotid pulse (pulsus tardus) & decreased pulse amplitude (pulsus parvus)
Heart sounds- soft or absent second heart sound, S4 gallop due to LVH.
Ejection systolic murmur- crescendo-decrescendo character.
“Loudness” does NOT tell you anything about severity
172
Talk about prognosis of aortic stenosis
Angina + AS: 50% survive for 5 years.
Syncope + AS: 50% survive for 3 years,
HF + AS mean survival is <2 years.
Risk of SCD in asymptomatic or minimally symptomatic patients is rare (<2%).
173
Talk about the investigation of aortic stenosis.
Echocardiography
Two measurements obtained are:
Left ventricular size and function: LVH, Dilation, and EF
Doppler derived gradient and valve area (AVA)
174
Talk about the grading of Aortic Stenosis.
Mild >1.5cm2
Moderate 1.0-1.5cm2
Severe<1.0cm2
Severe: mean gradient > 40 mmHg
175
Talk about the management of AS.
General:
Fastidious dental hygiene / care
Consider IE prophylaxis in dental procedures
Medical - limited role since AS is a mechanical problem. Vasodilators are relatively contraindicated in severe AS
Aortic Valve Replacement:
Surgical
TAVI – Transcatheter Aortic Valve Implantation
176
Talk about the indication of intervention in aortic stenosis.
Any SYMPTOMATIC patient with severe AS (includes symptoms with exercise)
Any patient with decreasing EF
Any patient undergoing CABG with moderate or severe AS
Consider intervention if adverse features on exercise testing in asymptomatic patients with severe AS
177
Talk about mitral regurgitation.
Chronic Definition: Backflow of blood from the LV to the LA during systole
Mild (physiological) MR is seen in 80% of normal individuals.
178
Talk about the etiologies of Chronic Mitral Regurgitation
Myxomatous degeneration (MVP)
Ischemic MR
Rheumatic heart disease
Infective Endocarditis
179
Talk about the pathophysiology of MR.
Pure Volume Overload
Compensatory Mechanisms: Left atrial enlargement, LVH and increased contractility
Progressive left atrial dilation and right ventricular dysfunction due to pulmonary hypertension.
Progressive left ventricular volume overload leads to dilatation and progressive heart failure.
180
Talk about the physical sign and symptoms of MR.
Auscultation: pansystolic murmur at the apex radiating to the axilla
S3 (CHF/LA overload)
In chronic MR, the intensity of the murmur does correlate with the severity.
Displaced hyperdynamic apex beat
Exertion Dyspnoea: ( exercise intolerance)
Heart Failure: May coincide with increased hemodynamic burden e.g., pregnancy, infection or atrial fibrillation
181
Talk about the natural history of MR.
Compensatory phase: 10-15 years
Patients with asymptomatic severe MR have a 5%/year mortality rate
Once the patient’s EF becomes <60% and/or becomes symptomatic, mortality rises sharply
Mortality: From progressive dyspnoea and heart failure
182
Talk about the investigation on MR.
ECG: May show, LA enlargement, atrial fibrillation and LV hypertrophy with severe MR
CXR: LA enlargement, central pulmonary artery enlargement.
ECHO: Estimation of LA, LV size and function. Valve structure assessment
TOE v helpful
183
Talk about the management of MR.
Medications
Rate control for atrial fibrillation with -blockers, CCB, digoxin
Anticoagulation in atrial fibrillation and flutter
Nitrates / Diuretics in acute MR
Chronic HF Rx if chronic MR with CCF
No indication for ‘prophylactic’ vasodilators such as ACEI, hydralazine
Serial Echocardiography:
Mild: 2-3 years
Moderate: 1-2 years
Severe: 6-12 months
IE prophylaxis: Patients with prosthetic valves or a Hx of IE for dental procedures.
184
Talk about indications of injury in severe MR.
ANY Symptoms at rest or exercise (repair if feasible)
Asymptomatic:
If EF <60%, LVESD >40mm
If new onset atrial fibrillation/raised PAP >50 mmHg
185
Talk about aortic regurgitation (AR)
Definition: Leakage of blood into LV during diastole due to ineffective coaptation of the aortic cusps
186
Talk about Etiology of Chronic AR.
Bicuspid aortic valve
Rheumatic
Infective endocarditis
187
Talk about Pathophysiology of AR.
Combined pressure AND volume overload
Compensatory Mechanisms: LV dilation, LVH. Progressive dilation leads to heart failure
188
Talk about Physical Exam findings of AR.
Wide pulse pressure: most sensitive
Hyperdynamic and displaced apical impulse
Auscultation-
Diastolic blowing murmur at the left sternal border
Austin flint murmur (apex): Regurgitant jet impinges on anterior MVL causing it to vibrate
Systolic ejection murmur: due to increased flow across the aortic valve
189
Talk about Natural History of AR.
Asymptomatic until 4th or 5th decade
Rate of Progression: 4-6% per year
Progressive Symptoms include:
- Dyspnoea: exertional, orthopnea, and paroxsymal nocturnal dyspnea
Palpitations: due to increased force of contraction and ectopics
190
Talk about the investigation of MR.
CXR: enlarged cardiac silhouette and aortic root enlargement
ECHO: Evaluation of the AV and aortic root with measurements of LV dimensions and function (cornerstone for decision making and follow up evaluation)
191
Talk about the management of MR.
General: consider IE prophylaxis
Medical: Vasodilators (ACEI’s potentially improve stroke volume and reduce regurgitation but indicated only in CCF or HTN
Serial Echocardiograms: to monitor progression.
Surgical Treatment: Definitive Tx
(TAVI in exceptional cases only if unsuitable for SAVR)
192
What are the indication for surgery of MR.
ANY Symptoms at rest or exercise
Asymptomatic treatment if:
EF drops below 50% or LV becomes dilated > 50mm at end systole
193
Talk about the mitral stenosis overview.
Definition: Obstruction of LV inflow that prevents proper filling during diastole
Normal MV Area: 4-6 cm2
Transmitral gradients and symptoms begin at areas less than 2 cm2
Rheumatic carditis is the predominant cause
Prevalence and incidence: decreasing due to a reduction of rheumatic heart disease.
194
Talk about the etiology of Mitral stenosis.
Rheumatic heart disease: 77-99% of all cases
Infective endocarditis: 3.3%
Mitral annular calcification: 2.7%
195
Talk about the pathophysiology of MS.
Progressive Dyspnea (70%): LA dilation pulmonary congestion (reduced emptying)
worse with exercise, fever, tachycardia, and pregnancy
Increased Transmitral Pressures: Leads to left atrial enlargement and atrial fibrillation.
Right heart failure symptoms: due to Pulmonary venous HTN
Hemoptysis: due to rupture of bronchial vessels due to elevated pulmonary pressure
196
Talk about the natural history of MS.
Disease of plateaus:
Mild MS: 10 years after initial RHD insult
Moderate: 10 years later
Severe: 10 years later
Mortality: Due to progressive pulmonary congestion, infection, and thromboembolism.
197
Talk about the physical sign of MS.
prominent "a" wave in jugular venous pulsations: Due to pulmonary hypertension and right ventricular hypertrophy
Signs of right-sided heart failure: in advanced disease
Mitral facies: When MS is severe and the cardiac output is diminished, there is vasoconstriction, resulting in pinkish-purple patches on the cheeks
198
Talk about the heart sound in MS.
Diastolic murmur:
Low-pitched diastolic rumble most prominent at the apex.
Heard best with the patient lying on the left side in held expiration
Intensity of the diastolic murmur does not correlate with the severity of the stenosis
Loud Opening S1 snap: heard at the apex when leaflets are still mobile
Due to the abrupt halt in leaflet motion in early diastole, after rapid initial rapid opening, due to fusion at the leaflet tips.
A shorter S2 to opening snap interval indicates more severe disease.
199
Talk about the investigation of MS.
ECG: may show atrial fibrillation and LA enlargement
CXR: LA enlargement and pulmonary congestion. Occasionally calcified MV
ECHO: The GOLD STANDARD for diagnosis. Asses mitral valve mobility, gradient and mitral valve area
200
What is the management of MS.
Serial echocardiography:
Mild: 3-5 years
Moderate:1-2 years
Severe: yearly
Medications: MS like AS is a mechanical problem and medical therapy does not prevent progression
-blockers, CCBs, Digoxin which control heart rate and hence prolong diastole for improved diastolic filling
Duiretics for fluid overload
Identify patient early who might benefit from percutaneous mitral balloon valvotomy.
IE prophylaxis: Patients with prosthetic valves or a Hx of IE for dental procedures.
201
What are the Indications for Mitral valve replacement in Mitral stenosis
ANY SYMPTOMATIC Patient with NYHA Class III or IV Symptoms
Asymptomatic moderate or Severe MS with a pliable valve suitable for PMBV
202
What is infective endocarditis?
Infection of heart valve/s or other endocardial lined structures within the heart (such as septal defects, pacemaker leads, surgical patches, etc).
A really bad infection, plus showers of infectious material around your bloodstream, and/or damaging the heart valves to cause heart failure.
203
What is the treatment of infective endocarditis?
Mainstay is antibiotics/antimicrobials
May require cardiac surgery to remove the infectious material and/or repair the damage
Treatment of other complications (emboli, arrythmia, heart failure, etc)
204
What are the types of infective endocarditis?
Each type can have different presentations, pathogens and outcomes
Left sided native IE (mitral or aortic)
Left sided prosthetic IE
Right sided IE (rarely prosthetic as rare to have PV or TV replaced)
Device related IE (pacemakers, defibrillators, with or without valve IE
Prosthetic; can be Early (within year) or Late (after a year) post op
205
How to catch infective endocarditis?
Have an abnormal valve; regurgitant or prosthetic valves are most likely to get infected.
Introduce infectious material into the blood stream or directly onto the heart during surgery
Have had IE previously
206
Talk about the epidemiology of infective endocarditis.
Used to be a disease of the young affected by rheumatic heart disease.
Now it is a disease of:
the elderly (in an ageing population)
the young i.v. drug abusers
the young with congenital heart disease.
Anyone with prosthetic heart valves
207
Talk about the incidence of infective endocarditis.
0.6 - 6 per 100,000 person-years.
M:F ratio varies from 2:1 to 9:1.
PVE in the 1st post-op year is 1-4%
PVE after the 1st post-op year is 1%/year
Incidence and mortality have not fallen over 30 years
10 year survival 60-90%
208
Talk about the clinical presentation of infective endocarditis.
Depends on site, organism, etc
Signs of systemic infection (fever, sweats, etc)
Embolisation; stroke, pulmonary embolus, bone infections, kidney dysfunction, myocardial infarction
Valve dysfunction; heart failure, arrythmia
209
Talk about diagnosis of infective endocarditis.
2 Major Criteria
Pathogen grown from blood cultures
evidence of endocarditis on echo, or new valve leak
5 Minor Criteria
Predisposing factors
Fever
Vascular phenomena
Immune phenomena
Equivocal blood cultures
Definite IE
2 major, 1 major+3 minor, 5 minor
Possible IE
1 major, 1 major+3 minor, 5 minor
210
Talk about echocardiography for infective endocarditis.
Transthoracic echo (TTE). Safe, non-invasive, no discomfort, often poor images so lower sensitivity
Transoesophageal (TOE/TEE). Excellent pictures but more invasive. Patients rarely want to have a second TOE. Generally safe but risk of perforation or aspiration.
211
Talk about peripheral stigmata presentation for infective endocarditis.
Petechiae 10 to 15%,
Splinter hemorrhages
Osler’s nodes (small, tender, purple, erythematous subcutaneous nodules are usually found on the pulp of the digits)
Janeway lesions are erythematous, macular, nontender lesions on the fingers, palm, or sole
Roth spots on fundoscopy.
212
Talk about the diagnosis of infective endocarditis.
Cultures may remain negative in 2% to 5% of patients with IE.
Certain organisms: cell media; special media or microbiological methods, or may require long incubtion 7-21/7.
The most common cause for negative blood cultures in patients with IE is prior antimicrobial therapy.
WBC is rarely helpful.
Raised CRP is almost always present.
ECG (ischemia or infarction, new appearance of heart block)
TTE is of crucial importance in detecting a vegetation.
The sensitivity of transthoracic 2-D echocardiography is still only about 60%; may need transoesophageal echo either for diagnosis or to assess complications (severity of valve damage, aortic abscess formation, function of prosthesis)
Transoesophageal echo (TOE) has improved the rate of detection of vegetations on native valves to 90–95%
TOE improves the sensitivity of detecting vegetations on prosthetic valves to up to 96%
A negative TTE/TOE does not eliminate the possibility that IE is present.
213
What is the treatment of infective endocarditis.
Antimicrobials; intravenous for around 6weeks; choice of agent/s based on culture sensitivities
Treat complications; arrhythmia, heart failure, heart block, embolisation, stroke rehab, abscess drainage etc
Surgery
214
When to operate on infective endocarditis patient?
the infection cannot be cured with antibiotics (ie recurs after treatment, or CRP doesn’t fall)
complications (aortic root abscess, severe valve damage
to remove infected devices (always needed)
to replace valve after infection cured (may be weeks/months/years later
To remove large vegetations before they embolise
