Cardiovascular System Flashcards

1
Q

Delayed capillary refill

A

-shock: hypovolemia, sepsis
- hypothermia: Low body temperatures can lead to vasoconstriction and slower CRT.
- peripheral vascular disease
- congestive heart failure
- dehydration
-

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2
Q

Quincke sign due to nail bed pulsation

A
  • aortic regurgitation severe
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3
Q

Blood pressure

A
Wide: - arteriosclerosis 
           - hyperthyroidism 
          - severe anemia
           - aortic regurgitation
           -septic shock
- patent ductus arteriosus 

Possible causes of a wide pulse pressure include anything that increases stroke volume (the amount of blood pumped by the heart per beat) or decreases arterial compliance (the ability of the arteries to expand and contract with changes in pressure). 

Narrow: - Aortic stenosis
               - hyovolemia
- heart failure
- hypovolemia
- cardiac tamponade

Shock may occur if systole is less than 90mmHg

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4
Q

Corrigan’s sign refers to visible carotid artery

A
  • aortic regurgitation
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5
Q

Malar flush

Is a pale, flushed central cyanosis

A
  • systemic lupus erythematous
  • mitral stenosis
  • low cardiac output
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6
Q

Impalpable apex beat

A
  • dextrocardia
  • obesity
  • copd
  • thick chest wall
  • pericardial effusion

Hence roll patient onto the left lateral position this may enable apex beat to be palpated

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7
Q

Radio-femoral delay

A

Coarctation of the aorta

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8
Q

Radio-radial

A

Dissection aneurysm

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9
Q

Graves diseases

A
  • exopthalmus

- goitre

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10
Q

Parasternal heaves

A
  • sustained, thrusting usually felt at the left sternal edge

Right ventricular enlargement
Seen in pulmonary stenosis, cor pulmonale, ASD

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11
Q

Thrill

A

Palpable murmur but felt as a vibration

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12
Q

At the apex auscultation

A
  • pansystolic murmur which radiates to the axilla
  • mitral regurgitation
  • mitral stenosis
  • Aortic stenosis
  • Aortic regurgitation
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13
Q

Nail fold infarcts aka splinter hemorrhage

A
  • vasculitis
  • infective endocarditis
  • systemic lupus erythematous
  • rheumatoid arthritis
  • trauma
  • microemboli
  • sepsis from any source
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14
Q

Postural hypertension

A

Refers to a drop in systole greater than 20mmHg or diastole greater than 10mmHg upon standing for 3-5 minutes

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15
Q

Heaving

A
  • caused by outflow obstruction leading to left ventricular hypertrophy
  • e.g Aortic stenosis, systemic hypertension, tricuspid regurgitation

Results from pressure overload
Aortic stenosis radiates to the carotid artery

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16
Q

Displaced or thrusting

A
  • caused by volume overload leading to left ventricular hypertrophy
  • e.g Aortic or mitral incompetence
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17
Q

Tapping

A

Has a palpable S1 heart sound

In mitral stenosis

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18
Q

Diffuse apex beat

A
  • left ventricular failure

- dilated cardiomyopathy

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19
Q

Double pulse

A
  • hypertrophic obstructive cardiomyopathy
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20
Q

Causes of bruits

A
  • atherosclerosis In elderly patients

- vasculitis In the young

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21
Q

Auscultation of the bases of the lungs

A
  • basal crackles: fine crackles (pulmonary oedema)
    But in the ward you can hear coarse crackles
  • pleural effusion
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22
Q

Tricuspid stenosis

A

Origin/cause: rheumatic heart disease
Common in females than males
Usually associated with MS
Rheumatic TS is associated in some degree with TR

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23
Q

Spleenomegaly

A

Infective endocarditis

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24
Q

Roth spots

A

Infective endocarditis

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25
Cornea Arcus
- elderly patients | - hyperlipidemia
26
Cvs clubbing
- infective endocarditis | - cyanotic congenital
27
Osler nodes
Tender nodules in finger pulps - infective endocarditis - systemic lupus erythematous - typhoid fever - gonoccocal infection
28
Janeway lesions
Red maculaes on palms - infective endocarditis
29
Cold extremities
- hypo perfusion - peripheral vascular disease - Raynaud phenomenon - congestive heart failure - anxiety
30
Koilynychia
- severe iron deficiency anemia | -
31
Peripheral cyanosis
Cold Raynaud’s phenomenon Congestive heart failure, mainly central but it causes peripheral cyanosis Copd Shock Venous thrombosis
32
Capillary refill 10 | If delayed is due to reduced cardiac output or peripheral vascular disease
- shock - dehydrated - anemia - hypothermia - peripheral vascular disease - Raynaud phenomenon - vasodilator drugs such as beta blocker, calcium channel blocker
33
Pyrexia
Infective endocarditis First three days post MI - malaria Gastroenteritis’s
34
Pulse rate
Tachycardia: exercise, anxiety, pregnancy, hyperthermia, heart failure, pulmonary embolism, CO2 retention, thyrotoxicosis, hypovolemic shock, congenital (wolf Parkinson’s white syndrome) Bradycardia: drugs such as beta blockers, calcium channel blockers; hypothyroidism, sick sinus syndrome, vasovagal stimulation, increased intracranial pressure, in athletes (normal)
35
Pulse rhythm
- regular: normal sinus rhythm - regularly irregular: second degree heart block, sinus arrhythmia, ventricular extrasystole, ventricular bigeminus - irregularly irregular: atrial fibrillation, multiple ventricular extra systole, atrial flutter with variable block, self limiting paroxysmal arrhythmia
36
Atrial fibrillation | FM
- hypertension - cardiac failure - myocardial infarction - thyrotoxicosis - alcoholic heart disease - mitral Valve disease - infection - following cardio thoracic surgery
37
Pulse volume
Low/ thready: low cardiac output (aortic stenosis, aortic dissection, arterial occlusion, mitral stenosis, coarctation of the aorta), pump failure ( heart failure, cardiomyopathy, tacharrythmia, cardiac tamponade) aortic stenosis Bounding: thyrotoxicosis, Co2 retention, aortic regurgitation, sepsis, exercise, pregnancy, anxiety, severe anemia, fever, patent ductus arteriosus
38
Collapsing pulse or Watson’s water hammer pulse
- exercise - beriberi - pregnancy - anxiety - fever - thyrotoxicosis - aortic regurgitation - severe anemia - sepsis - chronic alcoholism - Co2 retention - patent ductus arteriosus - ventricular septal defect - atrial septal defect - arterioventricular malformations
39
Palpable arterial wall
Atherosclerosis Arterial aneurysm Arterititis as seen in Takayasu arteritis, temporal arteritis Old age
40
Cordlike pulse- a pulse that is thickened and not compressible
- artherosclerosis
41
Macroglossia
Amyloidosis Beckwith Weidemann syndrome Congenital hypothyroidism ( cretinism) Down syndrome Acromegaly Angioedema Neurofibromatosis
42
Marfan syndrome
- arachynodactyl - high arched palate - lens displacement superior temporal - long limbs - tall for age or tall stature - mitral valve prolapse leading to a mitral regurgitation - curved spine - chest abnormalities: Pectus carinatum or Pectus excavatum
43
Corrigan’s sign
Prominent carotid pulsations seen in Aortic regurgitation
44
Gum disease
- malnutrition
45
Infective endocarditis
- Osler nodes - Janeway lesions - bad oral hygiene - Roth spots - spleenomegaly
46
Elevated JVP is above 4cm above the sternal angle
Fluid overload: excessive IV fluids, renal disease, heart failure Right ventricular systolic failure: cor pulmomale, left ventricular failure Right ventricular diastolic failure:constrictive pericarditis and tamponade Pulmonary hypertension Exercise Walking Pericardial effusion Tricuspid regurgitation internal jugular vein acts as a capricious manometer of right atrial pressure. Look for the right internal jugular vein as it passes just medial to the clavicular head of the sternocleidomastoid up behind the angle of the jaw to the earlobes. Pressure at zero (at the sternal angle) is 5cm, so add the height of the JVP with 5cm to obtain the right heart filling pressure in cm of water. A pressure above 9cm (4cm above the sternal angle at 45°) is elevated.
47
The carotid is not palpated at the same time
- in order to prevent stimulating reflex bradycardia due to brain hypoxia
48
Pulses
Pulsus tardes et parvus: Aortic stenosis Plateau pulse: Aortic stenosis , poorly functioning left ventricule Anacrotic pulse: Aortic stenosis Pulsus alternates: left ventricular failure Pulsus bisferans: Aortic stenosis, aortic regurgitation, hypertrophic cardiomyopathy, subaortic stenosis Pulsus bigeminus: family history, caffeine, nicotine, recreational drugs, herbal medicine, over the counter drugs, thyroid disease
49
Bounding pulse
- anxiety - fever - exercise - thyrotoxicosis - hypertension - aortic regurgitation - arteriosus venous fistula - CO2 retention - patent ductus arteriosus - liver failure - sepsis
50
Pulsus paradoxus
- asthma - copd - superior vena cava obstruction - pericardial constriction - cardiac tamponade - obstructive sleep apnea systolic pressure weakens in inspiration by >10mmHg). it's an exaggeration of the normal decrease in blood pressure that occurs when a person inhales. Pulsus paradoxus is often associated with conditions that impede the filling of the heart or that restrict heart function.
51
Positive hepatojugular
- right heart failure - tricuspid regurgitation - cardiac tamponade - pericarditis - inferior vena cava obstruction
52
Displaced apex beat laterally
- Cardiomegaly - left ventricular dilation - mediastinal shift: massive pleural effusion and tension pneumothorax
53
Parasternal heaves
- right ventricular hypertrophy
54
Investigations done in cvs | 8
- electrocardiograph - echocardiogram - ambulatory ecg - cardiac catherization - coronary angiopathy - cardiac stress imaging - chest X-rays - Ct scan and MRI
55
Tapping apex beat
Mitral stenosis
56
Mask and oxygen delivery
Patient is being given oxygen via a …. At a rate of …. L/min Nasal prongs- 4-6l/min Simple face mask- 8-10l/min Rebreather or Venturi mask- 12-14l/min Non-rebreather mask: 15l/min
57
Midline sternotomy scar
1. Cardiac surgery: open heart surgery procedures such as CABG, heart valve repair, heart transplantation 2. Thoracic surgery: thymectomy, mediastinal tumor resection, treatment for Pectus excavatum Lung surgery: lung transplantation Trauma for surgical exploration
58
Aortic regurgitation
The symptoms and signs of aortic regurgitation can vary widely, from none to severe, and may include: Dyspnea: Shortness of breath, particularly with exertion or when lying down. Orthopnea: Difficulty breathing while lying flat. Paroxysmal Nocturnal Dyspnea: Waking up at night with difficulty breathing. Fatigue or weakness: Particularly with physical exertion. Pulmonary edema: Fluid build-up in the lungs, causing breathlessness. Chest pain: Usually described as a pressure or tightness in the chest, typically increasing with activity and decreasing with rest. There are also several characteristic physical examination findings, including: Diastolic Murmur: An early high pitched diastolic decrescendo blowing murmur heard best along the left sternal border with the patient sitting up, leaning forward, and holding their breath after exhaling. Wide Pulse Pressure: The difference between systolic and diastolic blood pressure can be large, causing bounding or "water-hammer" pulses. Corrigan's pulse: A rapid and forceful distension of the arterial pulse with a quick collapse. De Musset's sign: Bobbing of the head in time with the heartbeat. Austin Flint murmur: A mid-diastolic rumble at the cardiac apex due to the regurgitant flow of blood interfering with the flow of blood into the ventricle from the atrium. Quincke's pulse: Capillary pulsations seen on the fingernails when light is shone on them. Traube's sign: pistol shot’ femorals, a booming sound heard over the femorals. Duroziez's sign: to and fro diastolic murmur heard when compressing the femo- rals proximally with the stethoscope. Hill's sign: A higher systolic blood pressure in the legs compared to the arms. Müller’s sign—systolic pulsations of the uvula. Have a wide pulse pressure, bounding pulse, long diastolic murmur
59
Cardiac tamponade 1
- rapid accumulation of fluid in the pericardium. It is a pathophysiological process whereby elevated intrapericardial pressure from a pericardial effusion causes compression of the heart (especially the right ventricle) - causes squeezing of the chambers of the right side of the heart more than the left side - presentation: hypotension, tachycardia, jugular venous distension, muffled heart sounds, pulses paradosus, pallor, cold sweats, left ventricular failure, symptoms of right heart failure, obstructive shock- no venous return , cardiac arrest, dyspneic Beck’s triad? Pulses paradoxus: it is a misnomer, it is an exaggerated drop in systolic arterial BP more than 10mmhg which occurs during inspiration
60
Cardiac tamponade 2
- Unstable patients with suspected tamponade: Do not delay treatment for extensive diagnostic workup; proceed directly with quick pericardial fluid drainage, through either pericardiocentesis or surgery - In stable patients, confirm the diagnosis with echocardiography (either TTE or FAST). treatment focuses on the underlying disease. - Aetiology: Hemopericardium: accumulation of blood in pericardial space Cardiac wall rupture (e.g., complication of post- myocardial infarction) Chest trauma (traumatic cardiac tamponade) Aortic dissection Cardiac surgery (e.g., heart valve surgery, coronary bypass surgery) Serous or serosanguinous pericardial effusion Idiopathic Acute pericarditis (especially viral- coxsackie b virus, novel Covid-19 but also fungal, tuberculous or bacterial) Malignancy- lymphoma, breast ca, radiation therapy Postpericardiotomy syndrome Uremia Autoimmune disorders such as SLE, rheumatoid arthritis Hypothyroidism Right heart failure
61
Cardiac tamponade 3
Diagnosis: chest X-ray- enlargement of the heart (cardiomegaly) 12 lead ECG: Transthoracic Echo: pericardial effusion, during diastole right atrium and ventricular collapse, septum bounce, during systole more blood will pass through the tricuspid as compared to the mitral - Pericardiocentesis which improves a hemodynamically unstable patient is cardiac tamponade RX: in a haemodynamic ally unstable pt before pericardiocentesis is done 1. An inotrope such as dobutamine can be given to help with the contractility of the heart. Be careful as it can cause bradycardia via vasodilatation 2. Vasopressors: norepinephrine or epinephrine 3. Be careful when giving fluids 4. When pressure is stabilized, pericardiocentesis can be done. 5. If there is an underlying problem then a chest tube can be placed in
62
Ddx of cyanosis
Lung pathology: intra liminal obstruction such as copd, asthma, pulmonary edema, pulmonary embolism, pneumonia. Solved: when supplementatry oxygen is given Heart: 5T’s and VSD with Eisenmenger syndrome Rare: methaemoglobinemia
63
Skin discoloration Ddx
- Addison’s disease - ACTH in bronchial carcinoma - chronic kidney disease (when urea is raised) - malabsorption - cholasma (in pregnancy) - haemochromatosis (bronze diabetes) -
64
Obesity
- BMI of over 30kg/m2. - higher waist to hip ratio, indicating central fat distribution, - It is associated with diabetes mellitus type 2, ischaemic heart disease, dyslipidemia, osteoarthritis, Conditions associated with obesity: Cushing syndrome, hypothyroidism, Lifestyle change is key to treatment, to increase energy expenditure and reduce intake Medica- tion ± surgery may be considered if the patient fulfils strict criteria
65
Enlarged lymph nodes
Reactive lymphadenopathy specifically refers to the enlargement of lymph nodes in response to an infection or inflammation. Ddx: - infections: Bacteria- tb, STIs such as syphyllis Viral: infective mononucleosis (EBV), HIV, CMV, infectious hepatitis Others: toxoplasmosis Non infective: sarcoidosis, amyloidosis, Dermatology: eczema, psoriasis Drugs: phenytoin - autoimmune dx: dx where the body mistakenly attacks itself- rheumatoid arthritis, SLE Infiltrative lymphadenopathy refers to a condition where lymph nodes are infiltrated by abnormal cells, which could be due to malignancies or certain infectious or inflammatory conditions. Malignant Lymphoma or leukemia: ALL, AML, CLL Metastatic from breast, lung, prostate, kidney
66
Oedema Ddx
Increased hydrostatic pressure: DVT, right heart failure Decreased oncotic pressure: low plasma protein such as: protein losing enteropathy, cirrhosis, nephrotic syndrome, Periorbital edema: the eyelid skin is very thin so periorbital oedema is usually the first sign—think of al- lergies (contact dermatitis, eg from stings), angioedema (can be hereditary, ACEI), Non- pitting edema: lymphoedema due to poor lymphatic drainage. Filariasis
67
Weight loss
- Malnutrition - Malignancy - infections such as TB- bronchoscopy samples for ZN stain and TB culture. , HIV, - diabetes Type 2 - hyperthyroidism in cases of increased appetite -
68
Cachexia in cardiac failure
- cardiac cachexia
69
Chest pain with heart burn
heartburn’ more likely if ‘burning’, onset after eating/drinking, worse lying flat, or associated with dysphagia.
70
Syncope
- loss of consciousness for a short duration as a result of hypoperfusion. Causes: AV block, aortic stenosis - how long did it last for - is there any warning before (pre syncope) - what was the patient doing (was it gradual or sudden) - associated with confusion, tongue bites, incontinence , loss of memory pre/post - any witnesses Prodromal symptoms: Chest pain, palpitations, or dyspnoea point to a cardiac cause, eg ar- rhythmia. Aura, headache, dysarthria, and limb weakness indicate CNS causes. During the episode: Limb jerking, tongue biting, or urinary incon- tinence? NB: hypoxia from lack of cerebral perfusion may cause seizures. Recovery: Was this rapid (arrhythmia) or prolonged, with drowsiness (seizure)?
71
Vertiligo
illusion of rotation of either the patient or their sur- roundings ± difficulty walking/standing, patients may fall over.
72
Imbalance and faintness
Imbalance, a difficulty in walking straight but without vertigo, from peripheral nerve, posterior column, cerebellar, or other central pathway failure. Faintness ie ‘light-headedness’, seen in anaemia, BP, postural hypotension, hypoglycaemia, carotid sinus hypersensitivity, and epilepsy.
73
Intermittent claudication
Pain in the buttock, thigh, calf, foot How long can patient walk before experiencing the pain - rest pain Ddx: DVT
74
Ischaemic heart disease risk factors
- hypertension - smoking - diabetes mellitus - family history hyperlipidemia
75
Wide pulse pressure
- aortic regurgitation - anaemia - exercise - pregnancy - hyperthyroidism - obstructive sleep apnea - arteriosclerosis - septic shock
76
Narrow pulse pressure
- aortic stenosis - hypovolemia - Cardiogenic shock - cardiac tamponade - advanced HF
77
Impalpable heart
- Dextrocardia - COPD -
78
A thrill
Palpable murmur
79
Polydactyl
Atrial septal defect
80
Cuff size
- Optimal cuff width is 40% of the arm circumference. -
81
Postural hypotension
- This is an important cause of falls and faints in the elderly. It is defined as a drop in systolic BP >20mmHg or diastolic >10mmHg after standing for 3min vs lying. Ddx: Hypovolaemia (early sign); drugs, eg nitrates, diuretics, antihypertensives, antipsychotics; Addison’s ; hypopituitarism ; autonomic neuropathy (DM, multisystem atrophy); after a marathon run (peripheral resistance is low for some hours); idiopathic.
82
Small volume pulses
- aortic stenosis - shock - pericardial effusion
83
Slow rising (anacrotic) pulse
Also known as parvus et tardus This causes the pulse to rise to its peak more slowly and less forcefully than normal - aortic stenosis
84
Bisferiens pulse
- combination of aortic stenosis and aortic regurgitation , HOCM, patent ductus arteriosus pulse that feels like a double peak or "two beats" during one cardiac cycle, i.e., with each heartbeat. It is often associated with conditions that cause an irregular flow of blood out of the heart.
85
Pulsus alterans
alternating strong and weak beats) suggests LVF, cardiomyopathy, or aortic stenosis.
86
Jerky pulses
Hypertrophic CM
87
No pulse
- occluded artery - death
88
Differentiating arterial pulse from venous pulse (JVP)
- Usually impalpable - obliterated by finger pressure on the vessel. • Rises transiently with pressure on abdomen (abdominojugular reflux) or on liver (hepatojugular reflux) - alters with posture and respiration (disappears when patient sits from lying flat).
89
Abnormalities with JVP
Raised JVP with normal waveform: Fluid overload, right heart failure. • Fixed raised JVP with absent pulsation (non pulsatile): SVC obstruction (p528). • Large a wave: Pulmonary hypertension, pulmonary stenosis. This is due to atrial dilatation and the atrium pumping against an increased pressure in the right ventricle • Cannon a wave: When the right atrium contracts against a closed tricuspid valve, large ‘cannon’ a waves result. Causes—complete heart block, single chamber ventricular pacing, ventricular arrhythmias/ectopics.seen when an atrium contracts against a closed tricuspid valve because the ventricle is also contracting • Absent a wave: Atrial fibrillation. • Large v waves: Tricuspid regurgitation—look for earlobe movement. • Constrictive pericarditis: High plateau of JVP (which rises on inspiration—Kuss- maul’s sign) with deep x and y descents. • Absent JVP: When lying flat, the jugular vein should be filled. If there is reduced circulatory volume (eg dehydration, haemorrhage) the JVP may be absent. provides valuable information about the function of the right side of the heart and the volume status in the body.
90
Heart sounds abnormalities Ddx
Loud S1: mitral stenosis (tapping apex), diastolic filling time is short (short PR interval), tachycardia, exercise, hyper dynamic state such as fever, pregnancy, sepsis Soft S1: mitral regurgitation, diastolic filling time is longer The intensity of S1 is variable in AV block, AF, and nodal or ventricular tachycardia. Loud A2: loud in tachycardia, hypertension, and transposition, but this is probably not a useful clinical entity. P2 is loud in pulmonary hypertension and soft in pulmonary stenosis. A2 is softening in aortic stenosis. splitting and P2 are heard best in the pulmonary area.
91
Additional heart sounds Ddx
3rd heart sound (S3) may occur just after S2: -S3 is pathological over the age of 30yrs. - A loud S3 occurs in a dilated left ventricle with rapid ventricular filling (mitral regurgitation, VSD) or poor LV function (post MI, dilated cardiomyopathy). In constrictive pericarditis or restrictive cardiomyopathy it occurs early and is more high pitched (‘pericardial knock’). 4th heart sound (S4) occurs just before S1. Always abnormal, it represents atrial contraction against a ventricle made stiff by any cause, eg aortic stenosis or hyper- tensive heart disease. Triple and gallop rhythms A 3rd or 4th heart sound occurring with a sinus tachycar- dia may give the impression of galloping hooves. Seen in pulmonary embolism An ejection systolic click is heard early in systole with bicuspid aortic valves, and if high BP. The right heart equivalent lesions may also cause clicks. Mid-systolic clicks occur in mitral valve prolapse An opening snap precedes the mid-diastolic murmur of mitral (and tricuspid) steno- sis. It indicates a pliable (non-calcified) valve. Prosthetic sounds are caused by non-biological valves, on opening and closing: rum- bling sounds ≈ ball and cage valves (eg Starr–Edwards); single clicks ≈ tilting disc valve (eg single disc: Bjork Shiley; bileaflet: St Jude—often quieter). Prosthetic mitral valve clicks occur in time with S1, aortic valve clicks in time with S2.
92
High pitched (best heard with diaphragm) vs low pitched (best heard with bell)
Low pitched: S3, S4, stenotic valves High pitched: S1, S2, regurgitation,
93
Mnemonic for murmur characterization
S – Site: where is the murmur loudest? C – Character: soft / blowing / crescendo (getting louder) / decrescendo (getting quieter) / crescendo-decrescendo (louder then quieter) R – Radiation: can you hear the murmur over the carotids (aortic stenosis) or left axilla (mitral regurgitation)? I – Intensity: what grade is the murmur? P – Pitch: is it high-pitched or low and rumbling? Pitch indicates velocity. T – Timing: is it systolic or diastolic? Eg: The patient has a grade 3 pansystolic murmur, best heard at the mitral area, it radiated to the axilla and is a high pitched murmur. This is a mitral regurgitation murmur This patient has a harsh / soft / blowing, Grade …, systolic / diastolic murmur, heard loudest in the aortic / mitral / tricuspid / pulmonary area, that does not / radiates to the carotids / left axilla. It is high / low pitched and has a crescendo / decrescendo / crescendo-decrescendo shape. This is suggestive of a diagnosis of mitral stenosis / aortic stenosis.”
94
Character and timing of murmur
- Ejection systolic murmur: crescendo- decrescendo, aortic stenosis, pulmonary stenosis, HOCM - Pansystolic murmur: mitral regurgitation, tricuspid regurgitation (soft S1), VSD Mitral valve prolapse; midshstolic click - Mid diastolic murmur: occur in mitral stenosis (accentuated presystolically if heart still in sinus rhythm), rheumatic fever (Carey Coombs’ murmur: due to thickening of the mitral valve leaflets), and aortic regurgitation (Austin Flint murmur: due to the fluttering of the anterior mitral valve cusp caused by the regurgitant stream).
95
Area of loudest murmur (location)
Though an unreliable sign, mitral murmurs tend to be loudest over the apex, in contrast to the area of greatest intensity from lesions of the aortic (right 2nd intercostal space), pulmonary (left 2nd intercostal space), and tricuspid (lower left sternal edge) valves.
96
Radiation
aortic stenosis classically radiates to the carotids, in contrast to the PSM of mitral regurgitation, which radiates to the axilla.
97
Accentuating maneuvers
Movements that bring the relevant part of the heart closer to the stethoscope ac- centuate murmurs (eg leaning forward for aortic regurgitation, left lateral position for mitral stenosis). • Expiration increases blood flow to the left side of the heart and therefore accentu- ates left-sided murmurs. Inspiration has the opposite effect. • Valsalva manoeuvre (forced expiration against a closed glottis) decreases sys- temic venous return, accentuating mitral valve prolapse and H(O)CM, but softening mitral regurgitation and aortic stenosis. Squatting has exactly the opposite effect. Exercise accentuates the murmur of mitral stenosis.
98
Grading of murmur
1/6 Very soft, only heard after listening for a while 2/6 Soft, but detectable immediately 3/6 Clearly audible, but no thrill palpable 4/6 Clearly audible, palpable thrill 5/6 Audible with stethoscope only partially touching chest 6/6 Can be heard without placing stethoscope on chest
99
Chest pain cardiac Ddx
- dissecting aneurysm - pericarditis: sharp pleuritic chest pain, worse lying better when sitting, friction rub heard on auscultation, lasts hours to day. ECG: typically diffuse ST elevation - pulmonary embolism - angina pectoris: retrosternal tightness, radiates to neck, jaw, shoulder, arm. Pain is central, squeezing, gripping, heavy, tight, exertional or stress related. Brought on by exertion or emotion, lasts 1-10 mins and is relieved by NTG or rest. ECG: transient ST elevation or depression. Develops into unstable, NSTEMI, STEMI which can lead to heart failure, arrhythmia, renal failure, confusion. - aortic stenosis (degenerative valve disease) : seen over age 60, exertional chest pain, exertional SOB, ejection systolic murmur, palpitations or arrhythmia, heart failure Myocarditis: have an antecedent infection such as TB, coxsackie B virus, SARS COV-2, aspergillus, radiation, malignancy. Presents with chest pain, arrhythmia and heart failure
100
MI
- prolonged dull central crushing pain or pressure. Radiating to the shoulder, either or both arms, or neck/jaw suggests cardiac ischae- mia. If pain is relieved within minutes by rest or glyceryl trinitrate (GTN), suspect angina (GTN relieves oesophageal spasm more slowly). MI may cause nausea, vomiting, or sweating. Angina is caused by coronary artery disease—and also by aortic stenosis, hypertrophic cardiomyopathy (HCM), paroxysmal supraventricular tachycardia (SVT)—and can be exacerbated by anae- mia.
101
Aortic dissection
- The pain of aortic dissection (p654) is classically instantaneous, tearing, and interscapular, but may be retrosternal. - Odd neu- rological symptoms and atypical chest pain—think aortic dissection. - on Ct have a tennis ball sign - RX: surgery - can present as MI, PE (these are emergencies including aortic dissection)
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Chest pain Ddx 2
Constricting suggests angina, oesophageal spasm, anxiety Sharp suggests pain from the pleura, pericardium, chest wall Epigastric pain may be cardiac. (Radiation) Pain associated with cold, exercise, palpitations, or emotion suggests cardiac pain or anxiety; if brought on by food, lying flat, hot drinks, or alcohol, con- sider oesophageal spasm/disease (but meals can also cause angina). Exacerbation antacids help, suspect GI causes. Pericarditic pain improves on leaning forward. Relieving Chest pain with tenderness suggests self-limiting Tietze’s syndrome.1 Odd neu- rological symptoms and atypical chest pain—think aortic dissection. Dyspnoea occurs with cardiac pain, pulmonary emboli, pleurisy, or anxiety. Association Pleuritic pain: chest pain exacerbated by inspiration. Implies inflammation of the pleura from pulmonary infection, inflammation, or infarction. It causes us to ‘catch our breath’. Ddx: musculoskeletal pain;1 fractured rib (pain on respiration, exacerbated by gentle pressure on the sternum); subdiaphragmatic pathology (eg gallstones). RX: Admit patient. Perform basic resuscitation. Give O2 and do a 12 lead ecg within 5 mins of patient’s arrival. Relieve pain (eg 5–10mg IV morphine) • Cardiac monitor • 12-lead ECG • CXR • Arterial blood gas (ABG)
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Aortic chest pain
- aortic dissection: sudden and severe at the beginning, may be chest and /or back, pulse deficits or aortic valve incompetence. Type 1 aortic dissection is dangerous since it involves the aortic arch Pulse deficits refer to a difference in the strength or presence of pulses between the upper extremities (arms) and lower extremities (legs) Aortic aneurysm: deep steady pain located at site of pressure on musculoskeletal system. May have cough, dysphagia, or sysmptoms from local compression
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Investigations for chest pain
ECG: pericarditis (diffuse STEMI), myocardial infarction (STEMI/NSTEMI) Chest X-ray: aortic dissection, aneurysm, pericarditis (globular heart) Upper GI series or endoscopy: GERD, ulcer Abdominal ultrasound: gallstones, biliary colic, Chest CT/MRI: aortic disease Ventilation perfusion VQ scan/CT angiogram: pulmonary embolus Stress test/CT angiogram: angina Echo: pericardial effusion, aortic dissection,
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Angina criteria
Typical angina - constricting discomfort in the front of the chest, in the neck, jaw, shoulder, arm - precipitated by physical exertion - relieved by rest or nitrate within 5 mins Atypical angina Meets two of these criteria. Atypical presentation include SOB, fatigue Non- angina chest pain Meets only one or none of this criteria
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Dyspnea Ddx
- left ventricular failure - pulmonary embolism - asthma - copd - anaemia - pain - anxiety - Pulmonary embolism is associated with acute onset of dyspnoea and pleuritic chest pain; ask about risk factors for DVT.
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Palpitations Ddx
- atrial fibrillation - supraventricular tachycardia - ventricular tachycardia - thyrotoxicosis - anxiety Phaechromocytoma
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Phaechromocytoma triad
- However, it is important to note that this triad is not present in all cases, and the presentation of pheochromocytoma can vary widely among individuals. The triad includes the following symptoms: Headache: Severe, recurrent, and sudden-onset headaches are a common feature of pheochromocytoma. - palpitations - excessive sweating Other presentations High blood pressure (hypertension) Anxiety or panic attacks Tremors or shaking Flushing (reddening of the skin) Weight loss Abdominal pain or discomfort Nausea and vomiting
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Tietze syndrome
Tietze’s syndrome: self-limiting costochondritis ± costosternal joint swelling. Causes: idiopathic; microtrauma; infection; psoriatic/rheumatoid arthritis. RX : NSAIDS or steroid injections. Tenderness is also caused by: fibrositis, lymphoma, chondrosarcoma, myeloma, metastases, rib TB. Imaging: bone scintigraphy; CT.
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Easy fatiguability
Due to low cardiac output
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Ascites in heart disease
Massive in: - constructive pericarditis - endomyocardial fibrosis - liver congestion from right sided heart failure leading to cirrhosis of the liver Right hypochondria l pain due to hepatomegaly as a result of stretching of the liver capsule Early satiety due to portal venous congestion
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Hemoptysis in heart failure
- pulmonary edema (pinkish frothy sputum) - rupture of the pulmonary vein
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Right sided heart failure presentation
- oedema - right hypochondriac pain - anorexia - early satiety
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Presentation of left sided heart failure
- exertional dyspnea. NHYA 2-4 - orthopnea - paroxysmal nocturnal dyspnea - wheezing - cough with frothy sputum which may be blood stained - fatigue
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Presentation of disturbance of cardiac rhythm
- palpitations - pre/syncope
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Inadequate cardiac output
Fatigue - pre/syncope
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Peripheral vascular disease
- oedema - intermittent claudication - cold extermities
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S3 pathology
- seen after 40 years of age - signifies stiffness or change in ventricular compliance This results in LV diastolic dysfunction Ddx: constrictive pericarditis, left ventricular failure, pericardial effusion, mitral regurgitation, Normal in young people, high output states such as beriberi, fever, sepsis, thyrotoxicosis
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S4 pathology
Associated with reduced ventricular distensibility Ddx: heart failure Hypertension Hypertrophic cardiomyopathy Aortic stenosis
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Grading of dyspnea
1: No dyspnea on physical activity 2: Dyspnea on extraordinary activity 3: Dyspnea on ordinary activity 4: Dyspnea at rest
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Cough in cvs
Cough n Due to pulmonary congestion n Dry in early stages n Productive of frothy sputum, which may be blood-stained (haemoptysis) from a ruptured pulmonary vein
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ECG essentials p wave
- depolarization towards positive electrode results in upward deflection, away from the electrode downward deflection - the size of deflection reflects the volume/amplitude of depolarized muscle - SA node: 60-100; AV node: 40-60; ventricular cells: 20-45 bpm P wave: atrial contraction. It is a wave of depolarization. In a normal ECG, the P wave is typically upright (positive) in leads I, II, III, aVF (augmented vector foot), and V3 to V6. This means that the electrical depolarization is predominantly moving from the superior aspect of the atria (from high to low) to the inferior aspect of the atria (from top to bottom). The P wave may appear inverted (negative) or biphasic (partially positive and partially negative) in lead aVR (augmented vector right) due to its orientation away from the leads that typically show positive P waves. The p wave is inferiorly to the left ie towards leads 1 and 2. Therefore P wave is upright in leads 1 and 2 Negative P wave in lead 1 1) incorrect lead placement 2) dextrocardia 3) ectopic atrial foci
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A paradoxical increase in JVP
- constrictive pericarditis - pericardial effusion
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Decreased JVP
- hypovolaemia via dehydration or hemorrhage
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A shifted apex beat
- cardiomegaly (LVH, RVH) - mediastinal shift: massive pleural effusion, tension pneumothorax, fibrotic lung, massive hemothorax
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Aetiology of pericarditis
- idiopathic - virus such as coxsackie virus - autoimmune conditions like SLE, RA - chronic kidney disease/ uraemia - myocardial infarction - tuberculosis - trauma - infiltrated by tumours
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Why the internal jugular vein and not the external jugular vein
- the internal jugular vein is in direct continuity with the atrium - the internal jugular vein has no valves - the internal jugular vein is not tortuous and susceptible to kinking
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QRS complex 1
- direction of electrical impulse: upward deflection (towards positive electrode) or downward deflection (towards negative electrode) - electrical forces generated by ventricular depolarization. QRS complex duration is measured in the lead with the widest complex - QRS <0.11s (3 small sq) Delay in ventricular depolarization gives broad QRS QRS septal depolarization: left side of septum depolarizes first. Impulse sent from left to right. Septal electrodes: V1/V2- small positive deflection of R wave Lateral leads (I, avL, v5,v6)- have small septal Q waves Non- pathological Q waves - <2 small squares deep - < 1 small square wide - < 25% of the amplitude of corresponding R wave
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QRS 2
- lead V1 small initial R wave followed by large negative deflection S wave - lead V6 small initial Q wave followed by large positive deflection - The normal ECG pattern of R wave progression is as follows: V1 and V2: In these leads, the R wave is usually small or absent, and the S wave is predominant. V3: The R wave starts to increase in height, and the S wave decreases in size compared to V1 and V2. V4: The R wave continues to increase in amplitude and becomes the tallest in this lead. It is usually larger than the S wave. V5: The R wave remains tall but may start to decrease in amplitude compared to V4. V6: The R wave is still present, but its height may be further reduced compared to V5. V1,2 are low because current starts from there . This is known as normal R wave progression
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ST segment
- interval between the termination of QRS and the start of T wave - end of ventricular depolarization beginning of ventricular repolarization ST segment should be at the same level (isoelectric) with subsequent TP segment
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ECG changes in AMI
Early: peaked T waves, degrees of ST segment elevation Late: Q wave formation and loss of R wave, T wave inversion
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T wave
T wave inversion: t - wave orientation usually corresponds to QRS complex T wave inversion in V1,2 (septal electrode) is normal Tall T waves- hyper acute eg: AMI Peaked T waves: Metabolic disorders, hyperkalemia
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Qt interval
- measures from beginning of QRS to end of T wave. Made up of the ST segment - total time for depolarization and repolarization - as heart slows, the QT interval widens - QT interval measured relevant to the heart rate. It should not be more than half the R-R distance. Usually <0.44s (11 small sq) Prolonged WR interval predisposes to: Ventricular arrhythmia particularily Torsades de pointes, hypokalemia, hypomagnesemia, hypocalcemia
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Lead placement- chest leads
Anterior chest leads: V1-V6 View heart in horizontal plane Limb leads: I, II, III avR, avL, avF Views heart in a vertical plane Lead anatomy Septal: V1, V2 Inferior: II,III, avF Anterior: V1-V6 (mainly V3-4) Lateral: I, V5-6, avL
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Amplitude of wave is influenced by
- myocardial mass such as LVH - thickness of intervening tissue - distance between electrode and myocardium - net vector depolarization
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Amplitude (low, high)
Low amplitude - copd - obesity - pericardial fluid High amplitude - thi patient - left ventricular hypertrophy
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Irregular heart rate
Easily accessed on Lead 2 (which is a rhythm strip) For irregular HR, calculate rate by counting the number of intervals between WRS complexes * 6
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For calculating rhythm
A rhythm strip is used Lead 2 and V1 In sinus rhythm - normal cardiac rhythm, P wave precedes every QRS, P wave is upright in leads 1 and 2, HR= 60-100 meaning it originates from the SA node In sinus arrhythmia Common in healthy individuals, rate increases with inspiration, vagal Lu mediated. Increased volume of blood returns to the heart in inspiration.
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Supraventricular arrhythmia
- atrial fibrillation - atrial flutter - paroxysmal supraventricylar tachycardia
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Atrial fibrillation 1
- refers to chaotic electrical activity of the aorta from multiple foci (typically the pulmonary vein) in one or both atria with infective atrial contraction - ventricular rhythm is usually irregular wavy baseline - average ventricular rate is 160-180 beats/min - QRS duration is normal (0.06-0.12)- narrow - no normal P waves - impulses do not originate from the sinus node are due to re- entry wavelets conducted between R and L atrium. The AV node allows some of the impulses to pass through at variable intervals - Irregular irregular rhythm due to chaotic atrial activity - commonly affects the elderly - no PR interval
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Atrial flutter
- saw tooth appearance of P waves which is known as FLUTTER waves or F waves - formed at an atrial rate of 250-350 bpm - usually a single, irritable focus in the atria - no P waves or PR interval - QRS normal width - AV node protects the ventricles by blocking most of the atrial impulses
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Paroxysmal supraventricular tachycardia
- the heart rate speeds up and the P waves are lost - rate: from normal to tachycardia Regularity: regular to regular P waves: normal to none - have a narrowed QRS -
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Ventricular arrhythmias
- ventricular tachycardia: increased rate, absent P waves, absent PR interval, QRS duration is wide often bizzare with notching.rhythm is regular and rate-100 to 120 Impulse originates in the ventricles (no P waves, wide QRS). Life threatening. Torsades de pointed is a form of ventricular tachycardia. Three or more beats of irritable foci - ventricular fibrillation: no rate, irregularly irregular, no P waves, no PR interval, QRS is wide, if recognizable Completely abnormal. The ventricular cells are excitable and depolarizing randomly, rapid drop in CO and death occurs if not reversed quickly. Two types coarse and fine ventricular fibrillation. Coarse ventricular fibrillation indicates recent onset and is readily corrected by a defibrillator Fine means a longer period of time since onset and resuscitation is more difficult
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Cardiac axis
- The average direction of spread of the depolarization wave through the ventricles as measured from a zero reference point (lead 1) - Right axis deviation is beyond 90 - Left axis deviation is beyond -30 - Axis lies 90 to equip basic. Determination of axis is helpful in: - conduction defects - broad complex tachycardia - pre-excited conduction - pulmonary embolism
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Bundle branch block
- a block of the bundle branch would be reflected as a change in the QRS complex - Foe BBB two changes will be seen on ECG . QRS complex widens. This is because it will take a longer time for the electrical signal to pass throughout the ventricles . QRS morphology changes A RBBB means the right ventricle depolarizes via non specialized tissue No conduction is seen down the right bundle. Septal depolarization is normal. the right ventricle depolarizes after secondary R wave (RSR pattern) Excitation of left ventricle- S wave in V1
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Right bundle branch 2
Delayed RV activation - prolonged QRS - secondary R wave in leads facing RV (septal leads- V1,V2) - broad S waves in LV leads (lateral- I, aVl, V5,V6) Causes of RBBB - normal in young people - right ventricular strain eg PE, RVH - ischaemic heart disease - atrial septal defect leading to RVH Causes of dominant R wave in V1 - right ventricular hypertrophy - posterior MI - dextrocardia - WPW - RBBB
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Left bundle branch
- delay in activation LV - prolonged QRS - secondary R wave in LV leads (I, avL, V5, V6) - LBB consists of two fascicles Causes of LBBB - always abnormal - ischaemic HD - LVH - aortic valve disease - cardiomyopathy - right ventricular pacemaker
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Sokolow/Lyon criteria for LVH
- precordial leads SV1 + RV5 or RV6 > 35mm (3.5mV) if >35 years old
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Calibration of the ECG
- standard paper speed= 25mm/s - 1 large box= 5mm = 0.20s Amplitude 1mV moves stylus 1 cm vertically. 0.1mV = 1 mm = 1 small sq 1 small square= 1mm = 0.04s 3 sec= 15 big boxes 300 large boxes = 1 min 5 large box= 1 sec Normal QRS <0.11s Delay in ventricular depolarization gives broad QRS complex
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P wave
- sa node initiates atrial depolarization - little muscle mass therefore small deflection - p waves upright in leads 1 and 2 Negative P wave in lead 1 is abnormal (check lead positions)
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Intervals of ECG
- PR interval measured from beginning of P wave to first deflection of QRS - Normal P wave- 0.12-0.2s Qt interval varies with rate prolonged QT interval predisposes to ventricular arrythmia
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Reading ECG
- rate - rhythm - QRS axis - interval - hypertrophy - infarction
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Intrinsic rate of the heart’s electrical system
The sinoatrial (SA) node: 60-100 beats per minute (bpm) The atrioventricular (AV) node: 40-60 bpm The ventricles (Purkinje fibers): 20-40 bpm
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Av note stimulated by what nerve
AV node
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Low amplitude QRS complex causes
- obesity or increased chest wall thickness - emphysema - pericardial effusion - myocardial infarction - cardiomyopathy
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In calculating cardiac axis what lead is used
I) chest lead II) limb lead Ans: Limb lead ( lead 1 and aVF)
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T wave abnormalities
- T wave may be inverted in lead V3 in afrocaribeans - t wave flattened suggests hypokalemia - digoxin May cause ST abnormalities - short PR interval- WPW
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Ejection fraction
EF= amount of blood pumped out of the ventricle/ amount of blood in the ventricle Must be between 40 and 50%
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Groupings of Heart failure
Dysfunction:!Systolic and diastolic dysfunction Ejection fraction: HfrEF (systolic failure) AND HFpEF (Diastolic failure) Presentation: Acute (de novo HF/ decompensated HF) and chronic Nature of symptoms: Left sided HF and Right sided HF and BVF or congestive HF
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Cardiac remodelling
Done by interstitial fibrosis formed in the walls of the heart esp for hypertrophy as seen in hypertension due to pressure overload Concentric LVH- increase wall thickness Eccentric LVH- increase in chamber size
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Right sided heart failure
- pedal swelling - right hypochondriac pain from enlarging liver - abdominal distension from an enlarging liver - anorexia - fullness after taking small amount of food Others which are not specific to right or left: Papitations Dizziness Syncope Chest pain Weight loss
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Signs of heart failure
- tachypnea - tachycardia - basal crackles occasionally rhonchi may be heard - gallop rhythm - the apex beat may be displaced - a murmur May be heard - there may be high blood pressure
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Signs of right heart failure
- tachycardia - dependent pitting edema - ascites - tender, smooth, soft hepatomegaly - raised JVP - gallop rhythm
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Rheumatic HD 1
- streptococcal infection (Group A Hemolytic streptococci- pathogenic strains are M type 1,3,5,6,18 (most virulent mucous strain),24) causes rheumatic fever and RHD - most common cause of VHD is acute rheumatic fever or RHD RHD is the most common cause of HF in Ghana Age group: 5-15 years. Equal in males and females Mitral valve disease and chorea are common in females whilst aortic valve involvement is seen in males Predisposing factors: low socioeconomic status, overcrowding, poor nutrition, poor hygiene Genetic predisposition: certain HLA markers and specific B cell allow tiger (D8/17) Pathogenesis: Molecular mimicry- antibodies cross react with human tissues because of antigenic similarity b/n strep and human connective tissues( hypersensitivity 2) Presentation: bites heart, kick joint and licks brain Symptoms occur 1-5w (an average of 2-3w) after an initial attack of pharyngitis. History of preceding sore throat is present in 50% of the pts Fever, anorexia, lethargy, malaise, fatigue, epistaxis, abdominal pain, anemia, skin rashes, respiratory problems Arthritis: most common and early manifestation, affects knees, ankles, elbows and wrists, asymmetric pain and migratory of the large joints, Carditis: often seen in pts with acute fever, characterized by pancarditis, endocarditis (valvulitis) is a universal finding Skin lesions: erythema marginantum (red macular that fade in the center), occur on trunk and proximal extremities but not the face anddd subcutaneous nodules (small, firm and painless) Sydenham chorea (St. Vitus dance): appears 3months after rheumatic fever, late neurological manifestation, common in females, first feature: emotional breakdown. Have purposeless involuntary movements of face, feet and hands
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Aortic dissection causes
- hypertension - trauma - surgery causing a leak of the vessel - vasculitis from syphyllis or Takayasu arteritis - congenital: connective tissue disorders such as Marfan syndrome, Ehler’s Danlos - coarctation of the aorta Usually occurs in the ascending aorta or aortic arch Presentation Ripping /tearing chest pain, radiation to the back or interscapular (thoracic aortic dissection), neck, hand (aortic arch), radio- radial delay- squeezing on left subclavian artery, hypertension, if hypotension then they are bleeding leading to hemorrhagic shock Complications - hemorrhagic shock if hypotensive (aortic rupture) - cardiac tamponade- compressing the pericardium - stroke- dissecting compressing the arterial artery - mesenteric ischaemia - acute kidney injury - quadriplegia Mgt: - get an ecg to rule out MI Chest X-ray to rule out pneumonia and rule in aortic dissection since they have a wide mediastinum A - CT angiogram (if hemodynamically stable) to confirm dissection. If not stable transoesophageal echo Type A and B A- before the brachiocephalic artery Left common carotid artery B- after the left subclavian artery
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Atrial fibrillation presentation
- ectopic atrial cells firing abnormally thereby producing an abnormal rate and rhythm - presentation: syncopal event, dyspnea, fatigue, palpitations, tachycardia, irregular irregular rhythm, presentation of stroke, renal infarct, splenic infarct, mesenteric ischaemia, pulmonary edema Have embolic phenomenon and Cardiogenic dysfunction These pts are at risk of bleeding when put on anticoagulants (HAZBLEED) to measure their risk if they should be put or not
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Early signs of hypoxia
- Restlessness - Agitation
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Dilated cardiomyopathy
- Elevated BNP (breaking and stretching of the ventricles). 100 or less is normal - RX: increase CO and thereby increasing O2 to the heart
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Digoxin Be careful when giving digoxin
- apical pulse, checking the apical pulse for 60s before giving the drug - potassium levels <3.5 - digoxin toxicity: present with vision changes, dizziness, nausea and vomiting
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Restrictive cardiomyopathy
Causes: Infiltrative: amyloidosis, sarcoidosis, Gaucher’s disease/ lysosomal storage disorder, fatty infiltration Noninfilterative: familial, sleroderma, DM,idiopathic, hypertrophy Storage: hemochromatosis, glycogen storage disease, fairy’s disease Endomyocardial: EMF, carcinoid syndrome, radiation, toxins Inv: usually normal RX: heart transplant Non pharmacological RX D- diet R- rest / stress free E- supervised exercise within tolerance level S- stop smoking or alcohol drinking W- weight loss
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Hypertrophic cardiomyopathy
- most deadly Since it can cause an obstruction of the aortic valve - asymptomatic - echo: septal wall thickening RX: cutting the septum or reducing the BP by giving beta blockers, calcium channel blockers S4 gallop due to stiff ventricles Jerky pulse
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Rheumatic HD
Filet - Jones criteria Mnemonic JONES CAFE PAL Major J- joint involvement O*- O looks like a heart: myocarditis N- nodules subcutaneous E- erythema marginagum S- Sydenham chorea Minor C - CRP increased A- althragia F- fever E- elevated ESR P- prolonged PR interval A- anamnesis of rheumatism L- leukocytosis A and L clinical whilst the rest are laboratory Diagnosis 2 major OR one major plus two minor and supporting evidence of recent Group A Strep infection (eg positive throat culture or elevated anti-streptolysin I, anti- hyaluronidade
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Rheumayic heart disease 2
Duckett- Jones criteria 2 major or 1 major and 2 minor and supporting evidence of recent Group A Streptococcal infection (eg positive throat culture or elected anti-streptolysin O, anti- hyaluronidase JONES CAFE PAL Major J- Joint involvement o*- o resembles the heart, Carditis N- Subcutaneous Nodules E- erythema marginatum S- sydenham chorea Minor C-CRP elevated A- arthralgia F- Fever E- ESR elevated P- Prolonged PR interval A- Anamnesis of rheumatism L- leukocytosis F AND A are clinical manifestations of the minor whilst the rest are laboratory Rx: - oral penicillin 500mg bd* 10d OR A single does of benzathine penicillin 1.2 million units IM Tab erythromycin 250mg bd*10d (penicillin allergy) Arthritis, arthralgia: salicylates or NSAIDs (aspirin 80-100 mg/kg/day in 4-5 divided doses *3-5 weeks Severe carditis: cor tick steroids (prednisolone 1-2mg/kg/d; max 60mg *4-6w, then taper 20-25 mg/wk) Sydenham chorea: haloperidol 0.5 mg/kg/ day Complications - arrhythmia commonly afib Congestive cardiac failure Infective endocarditis - rheumatic valvular heart dx
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Mitral stenosis
Mitral orifice: 4-6cm 2 Symptoms: exertional dyspnea, cough, palpitations, fatigue, orthopnea, PND, dizziness Signs: mitral flush- rosy cheeks, tapping apex beat, apex beat may be normal, Loud S1, accentuated P2, opening snap heard on expiration, Pre- systolic accentuation, low pitched, rumbling, mid-diastolic murmur, heard best at the apex with the patient in the lateral position Can have MS and RV failure Causes - RHD - congenital mitral valve stenosis - mitral annular calcination with extension to the leaflets as seen in elderly patients (degenerative calcifications) - SLE - rheumatoid arthritis - left atrial myxoma - infective endocarditis with large vegetation CRIS DR Hallmark of mitral stenosis: an abnormally elevated left atrioventricular pressure gradient
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Mitral regurgitation
Symptoms: exertional dyspnea, palpitations, fatigue, orthopnea, PND, dizziness, syncope Signs: absent or soft S1, thrusting apex beat, displaced apex beat, murmur Pansystolic, most prominent at the apex and radiates to the axilla Causes Acute: endocarditis, papillary muscle rupture (post MI), trauma, chordal rupture or leaflet flail (MVP/IE) Chronic: RHD, endocarditis (healed), HOCM, dilated cardiomyopathy, degenerative changes to the valve, myxomatous, ischaemic (LV Remodelling, radiation MRDIPProlapse
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Aortic stenosis
Symptoms: exertional dyspnea, angina, palpitations, fatigue, dizziness, syncope, sudden death Signs: slow rising pulse, low systolic pressure, narrow pulse pressure,heaving apex beat (pressure overload), normal in location apex beat, soft S2, diamond shaped, harsh midsystolic ejection murmur, heard best at the aortic area and radiating to the carotids (Gallavardin phenomenon) Associated with HOCM Normal valve orifice: 2-4cm2 Causes RHD Degenerative calcification Congenital Radiation
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Aortic regurgitation presentation
Symptoms: exertional dyspnea, palpitations, fatigue, orthopnea, PND, dizziness, syncope Signs: collapsing pulse, wide pulse pressure, soft S2, heaving apex beat, displaced apex beat, early harsh diastolic murmur, heard best at the 4th left intercostal space with the patient leaning forward Complications - arrhythmia esp atrial fibrillation (blackouts) - stroke (ischaemic due to blood clots) - heart failure because of presentation - infective endocarditis How is it diagnosed - history: high index of suspicion in high risk regions and populations - examination / echocardiography Treatment Medical: diuretics, digoxin (antidote for digoxin toxicity- digibind), antiobiotic prophylaxis. Main: correct arrhythmia Percutaneous transilluminal ballon valvuloplasty Surgery - valve repair - valve replacement: porcine tissues, bioprosthetics - mechanical valves: require anti coagulation with warfarin Prevention Primary - early detection and management of streptococcal throat infection - antibiotic prophylaxis in highly prevalent areas with Benzathine penicillin - health education: improving living conditions, hygiene, avoid overcrowding Secondary Benzathine Pencillin G 1200000U every 3weeks IM Penicillin V 250mg twice daily oral For individuals allergic to penicillin and sulfadiazine give erythromycin
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Micro organism that causes acute rheumatic fever
Group A beta haemolytic S. pyogenes causes infection of the oropharynx
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Valves frequently affected in RHD
Mitral> Aortic > Tricuspid > Pulmonary
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Angina occurs in aortic stenosis t/f
True Occurs in 70% of people with severe AS Angina is usually exertional and generally dosent occur at rest And occurs with orthostatic changes
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Infective endocarditis presentation 1
Types Infective or non- infective Marantic endocarditis (malignancy) Libman-Sacks endocarditis due to SLE Men affected more than women 2.5:1 Leading cardiac conditions. RHD>MVP and MR> Degenrative AV Nosocomical: pacemakers, dialysis shunts, IV catheters (affect the right side) Other risk factors: native valve IE, prosthetic valve IE Oral cavity: S. Viridans, HACEK; gut- enterococcus Pathogenesis: endocarditis is usually due to the presence of bacteria in the blood and abnormal cardiac endothelium facilitating their adherence and growth. Damaged endocardium promotes platelet and fibrin deposition which the organism adheres to and grows leading to vegetation formation Clinical presentation: fever,chills, sweats, anorexia, weight loss, malaise, dyspnea, cough, stroke, headache, nausea/vomiting FROMurmur JAnaemiaNauseaE splinter haemorrhage Signs: fever, murmur, changing/new murmur, neurological abnormalities, embolic event,spleenomegaly, clubbing, peripheral manifestation Diagnosis by Duke’s criteria 2 major criteria 1 major criteria and 3 minor criteria 5 minor criteria Pathological/histological findings Major Positive blood culture: typical microbe from 2 separate cultures Evidence of endocardia’s imvolvement Echo: oscillating intra cardiac mass on valve New regurgitant murmur Minor Predisposition: IVDA fever >38 Vascular: Janeway lesion, petechiae Immunology: GN, Osler’s nodes Blood c/s positive Echo: consistent but not meeting criteria
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Infective endocarditis presentation 2
Complications: embolus, local spread of infection, metastatic spread of infection, formation of antigen-antibody complexes: glomerulonephritis and arthritis Antibiotics: Resistant organisms: vancomycin/Rifampicin/Gentamycin Acute/Staph: IV Cloxacillin/Gentamycin Subacute: Penicillin 12-18months *4/52; Gentamycin 1mg/kg/d x2/53 HÁČEK: IV/IM Ceftriazone 2g/d *4/52 Enterococcus: Ampicillin and Gentamycin Surgery indications - CHF; perivalvular incasive dx; uncontrolled infection despite maximal anti microbial therapy, presence of prosthetic valve endocarditis unless late infection Prophylaxis high risk: prosthetic valve, previous infective endocarditis, cyanosis HD, RHD, MVP with regurgitation or thickened leaflets, undergoing a procedure that Carrie’s a risk of transient bacteremia due to an organism that Caries IE
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HÁČEK
Haemophilus species Aggregatibacter species (formerly Actinobacillus actinomycetemcomitans) Cardiobacterium hominis Eikenella corrodens Kingella species
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Mitral valve prolapse
- also known as : systolic click murmur syndrome, barlow’s syndrome, floppy valve syndrome and billowing, mitral leaflet syndrome - commonly associated with myxomatous degeneration - common in women seen in ages 15-30 - usually asymptomatic - systolic click and murmur with mild prolapse of the posterior leaflet to severe MR due to chordal rupture and leaflet flail (a high pitched late systolic murmur) Presentation: palpitations, light headedness, syncope, sudden death from arrhythmias Commonly seen in Marfan syndrome
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Causes of aortic regurgitation
- RHD - degenerative calcification - myxomatous - endocarditis - trauma - syphyllis - aortic dissection - Marfan syndrome - hypertension - aortitis - CoA
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Tricuspid regurgitation
- causes: right ventricular enlargement from pulmonary artery hypertension, RHD, endomyocardial fibrosis, infective endocarditis, infarction of RV papillary muscles, tricuspid valve prolapse, radiation - TR is often seen in late stages of heart failure due to dilated CMP or CHD with severe PA HTN Clinical features of TS and TR results primarily from systemic venous congestion and reduction of CO TR presentation: distended neck veins, marked hepatomegaly, ascites, pleural effusions, oedema, systolic pulsations of the liver, positive hepatojugular reflex Murmur: right parasternal heaving and a blowing Pansystolic murmur along left lower sternal margin
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Pulmonary valve
- the pulmonic valve is less frequently affected by RHD and infective endocarditis and carcinoid syndrome - regurgitation is the commonest abnormality due to secondary dilatatiok of the pulmonic valve ring due to severe PA hypertension - it also occurs in childhood repair of ToF with reconstruction of the right ventricle outflow tract - pulmonic stenosis usually congenital, regurgitation an occur in normal people
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RX of VHD
- medical - percutaneous - surgery: repair, replacement with prosthetic or mechanical valves requiring anticoagulants
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Causes of arrhythmia
Hypoxia Hypertensive heart disease Rheumatic heart disease/ valvular heart disease Cardiomyopathies Pulmonary embolism Thyrotoxicosis Pericardial disease Coronary Artery disease/ischaemic heart disease Electrolyte imbalance Digoxin toxicity Hypercapnia Presentation: unrecordable BP INVESTIGATIONS: resting ecg, ambulatory ecg, serum electrolytes, echocardiography
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Ventricular premature beat
A single irritable focus within ventricle fibers prematurely giving rise to an ectopic beat. QRS is wide If every other beat is VPB- ventricular bigeminy If every third beat is VPB- ventricular trigeminy If every other fourth beat is VPB- ventricular quadrigeminy A ventricular premature beat that falls on the T wave precipitates VT or VF
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First degree AV block
- prolonged PR interval (0.20s) - most often occurs when there is a prolongation or delay in impulse conduction through the AV node
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Second degree AV block
Two types Morbitz type 1 or Wenkebach second degree AV block: is as a result of intermittent block of the impulse within the AV node, with subsequent failure to conduct an arterial impulse from the atria to the ventricles. Change in PR interval, but PP intervals are constant, RR intervals are not constant Mobitz type 2: no change in PR interval prior to or after the non conducted P wave. Several P waves in a row without QRS complexes
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Third degree AV block or complete heart block
- there is complete failure of the AV node to conduct any impulses from the atria to the ventricles - the P waves are completely dissociated from the QRS complexes on the ecg Atrial rate is faster than ventricular rate
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Treat of arrhythmia
- Anti- arrhythmic drugs Shock therapy: DC cardio version or defibrillator - pacemaker implantation
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Dilated cardiomyopathy 1
Types: idiopathic cardiomyopathy- burnt out hypertension Ischaemic cardiomyopathy Hypertensive CM Valvular CM Nutritional CM- beriberi Diabetes CM Hypo/hyperthyroidism CM Myocarditis-viral (Cox sackie B) Alcoholic CM peripartum CM- occurs late in pregnancy or during early postpartum period (the last trimester or upto the puerperium). Affects women of poor socioeconomic status. Common in high parity and multiple pregnancies. Recover with RX but relapses after subsequent pregnancies. HIV CM, toxoplasmosis Antiretroviral CM Chagasic CM- trypanosomiasis infection Chagas Anthracycline-induced cardiomyopathy is a well-known side effect and can be dose-limiting. The risk increases with the cumulative dose of the medication. Alcohol CM- onset with arrhythmia (recurrent afib), history of prolonged (>10 yr hx) of alcohol intake, RX: cessation of alcohol. Evidence of thiamine deficiency Sickle cell CM: associated with chronic anaemia, heart failure, MI, pulmonary infarction Mnemonic: HIV DM HANS
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Dilated cardiomyopathy 2
- presentation: heart failure, arrhythmias, thromboembolism, sudden death Males more affected Hx of increased alcohol intake and systemic HTN Cardiac enlargement with displaced apex beat Left parasternal heave from RV hypertrophy Apical S3; functional mitral and tricuspid regurgitation hence thrusting Apex beat Complications: systemic and pulmonary embolism (stasis of blood) ECG: LBBB, LAE, abnormal Q in V1-4, arrhythmias- afib
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Restriction CM
- diastolic dysfunction - endocardia’s thickening with or without Marked LA dilatation but normal size LV and thickness - idiopathic or secondary to infiltration Ecg: low voltage QRS, conduction disturbances, arrythmias- SVT, VT HYPERTROPHIC CM - LVH, LAD - abnormal inferior, anterior and lateral Q waves - bizzare QRS complexes CXr: cardiomegaly with HF features
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Endomyocardial fibrosis/ Davies disease/idiopathic mural endocarditis/eosinophilia carditis/topical endomyocarditis/obliterative cardiomyopathy
- common in RV then BV then LV - affects commonly male children of low socioeconomic status (egg on stick appearance) - fibrosis and scarring commonly affects the apex of the ventricles extending to involve the posterior cusps of the AV VALVES. Involvement of AV valves creates regurgitation resulting in grossly distended atria and secondary PHT. Leads to thrombus formation due to stats is of blood. Fibrosis reduces ventricular cavity size and restricts ventricular filling (thus mimicking constrictive pericarditis) Presentation: RHF> LHF, proptosis, tricuspid regurgitation, afib, low blood pressure, no parasternal heave because of RV fibrosis and reduction in contractile activity, signs of pericardial effusion, central cyanosis, finger clubbing, oral gingival, periorbital pigmentation, retarded growth, enlarged parotid glands, delayed central maturity CXr: globular heart Oligaemic king fields due to cyanosis Pericardial or pleural effusion ECG: Sinus rhythm or afib, rsr patterin in V1 Echo Apical fibrosis, dilated outflow tract, severe TR, grossly dilated RA with a thrombi RX: endocardiectomy with valve replacement or cardiac transplant Contraindicated if there is massive ascites and liver fibrosis Palliative care: diuretics, digoxin-afib, anticoagulation, pericardiocentesis
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Cardiac amyloidosis
-pt will have systemic amyloidosis - LVH and RVH - atrial septal thickening - valve thickening, MR and TR - pericardial effusion
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Anticoagulants
Are drugs that inhibit the clotting cascade Enxoparin 40mg SC (low molecular weight heparin) inhibits activated factor 10 and thrombin DOACs such as dabigatran inhibits thrombin Warfarin a vitamin K antagonist inhibits factor 2,7,9,10 Anticoagulants prevent any more clots from forming and stops the clots that are already being formed
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Chest X-ray appearance of heart failure
A: alveolar edema or batwing appearance B: Kerley B lines C: cardiomegaly, increased cardiothoracic ration D: dilated prominent upper lobe vessels E: pleural effusion
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Heart failure principles of mgt
- Ensure adequate tissue perfusion - Fluid management - treat underlying precipitating factor - Counselling- DRESS Avoid mono sodium glutamate (Maggie) Eat a lot of fruits and vegetables and omega 3 fish (SMASH) S- salmon M- mackerel A- anchovies S- sardine H- herring
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Rapid ventricular filling, S3
Heard in Mitral regurgitation Aortic regurgitation Heart failure Thyrotoxicosis Common in children, young adults, athletes and pregnancy
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Hypertension causes
pressure overload
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Metolazone
Potentials the action of loop diuretics because it blocks sodium reputable further down the nephron, but may result in profound hypokalemia and volume depletion
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Inotropic drugs
- milrinone - dobutamine Digoxin*
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Indications of anticoagulants in HF
Absolute - decreased EF and afib - previous cardio-embolic event - recent large MI Relative - dilated LV with severe LVD - intracardiac thrombus - apical aneurysm - spontaneous echocontrast - acute CMP (peripartum, myocarditis, amyloid)
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Rate control drugs in afib
- beta blockers - calcium channel blockers such as diltiazem - digoxin
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Rhythm control for afib
- Amiodarone - flecainide - quinidine - digoxin
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Sudden death caused by
- ventricular tachycardia or ventricular fibrillation - bradyarrythmia . Asystole . Electromechanical dissociation (pulseless electrical activity)
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Surgical management for heart failure patients
- Pacer/AICD- Automatic Implantable Cardioverter Defibrillator/CRT- Cardiac resynchronization therapy - CABG - mechanical ventricular assist and replacement devices - transplantation
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Complications of heart failure
- arrhythmia (afib/VT) - thromboembolism (CVA, DVT) - electrolyte abnormalities - cardiac cirrhosis - muscle wasting - sudden cardiac death
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Causes of readmissions for HF
- diet non- adherence - drug non- adherence - inappropriate drug - failure to seek care
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WHO criteria for AMI
STEMI chest pain or classic symptoms for more than 30 mins ST increased 1 mV in two contiguous leads or new LBBB INC cardiac enzymes levels NSTEMI chest pain or classic symptoms increased 30 mins or more ST dep or T Wave depression Increased cardiac enzymes
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MI wall ischaemia landmarks
Septal wall ischaemia injury or infarct- V1,V2 Anterior wall ischaemia injury or infarct- V3, V4 Lateral wall ischaemia injury or infarct- I, aVL, V5, V6 (also for Cx occlusion) Inferior wall ischaemia injury or infarct- aVF, II, III (also RCA occlusion) LAD occlusion- I through to VI
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Complications of acute heart failure
- atrial fibrillation - hyponatremia - cardiorenal stndrome